cardio/queries.csv

fig_num,sub_section_headings,images-src,image_caption
Figure 7.3,Non-ST segment elevation myocardial infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
Figure 7.4,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
Figure 7.4,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
Figure 7.5,Changes in ECG,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
Figure 7.6,Changes in ECG,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
Figure 7.7,Anterior wall myocardial infarctions (AWMI),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
Figure 7.9,Inferior wall myocardial infarction (IWMI),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
Figure 7.11,Posterior wall myocardial infarction (PWMI),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
Figure 7.1,Text,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
Figure 6.1,Pathophysiology,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
Figure 6.3,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
Figure 6.4,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
Figure 6.5,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
Figure 6.6,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
Figure 6.7,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
Figure 6.8,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
Figure 5.1,unintrusive,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
Figure 5.2,unintrusive,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
Figure 5.1,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
Figure 4.1,Text,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
Figure 4.2,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
Figure 4.3,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
Figure 4.4,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
Figure 4.5,The risk is twofold as the vegetations can:,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
Figure 4.6,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
Figure 4.7,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
Figure 4.8,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
Figure 3.1,JNC,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
Figure 3.1,Systemic abnormalities and EH,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
Figure 3.2,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
Figure 2.1,Text,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
Figure 2.2,Text,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
Figure 2.3,Ejection Fraction in Systolic Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
Figure 2.3,Ejection Fraction in Diastolic Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
Figure 2.4,Ejection Fraction in Diastolic Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
Figure 2.5,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
Figure 2.6,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
Figure 2.7,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
Figure 1.1,USMLE,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
Figure 1.2,fibrillatory,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.