unique_id,web-scraper-start-url,sub_chapters_x,sub_chapters-href,paragraph,is_paragraph,sub_section_headings,fig_num,sub_chapters_y,images-src,image_caption
cfbec522-9844-4f0a-9848-03c1c3818c4d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,Introduction,False,Introduction,,,,
ed66933c-0507-4838-8b90-3e3328daf222,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"It might be worth putting dyspnea in a clinical context. Like pain, dyspnea can occur across a number of pathological conditions. It is the cardinal symptom of lung disease, but it is highly prevalent in heart diseases as well—in fact it is a more common sign of myocardial infarction in women than the classical symptom of chest pain that is more prevalent in men.",True,Introduction,,,,
116f070e-6849-4ded-b300-6139c518706b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Dyspnea is also a strong predictor of mortality in most heart and lung diseases. As well as cardiopulmonary conditions, dyspnea is also prevalent in other conditions that affect breathing or metabolism, and (see figure 18.1) it is prevalent during end-stage disease where it is as common as pain and forms a significant problem for end-of-life care. Despite its prevalence there are few options for treating this symptom. Unlike pain, there are no specific drugs to reduce this sensation.",True,Introduction,Figure 18.1,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
116f070e-6849-4ded-b300-6139c518706b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Dyspnea is also a strong predictor of mortality in most heart and lung diseases. As well as cardiopulmonary conditions, dyspnea is also prevalent in other conditions that affect breathing or metabolism, and (see figure 18.1) it is prevalent during end-stage disease where it is as common as pain and forms a significant problem for end-of-life care. Despite its prevalence there are few options for treating this symptom. Unlike pain, there are no specific drugs to reduce this sensation.",True,Introduction,Figure 18.1,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
116f070e-6849-4ded-b300-6139c518706b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Dyspnea is also a strong predictor of mortality in most heart and lung diseases. As well as cardiopulmonary conditions, dyspnea is also prevalent in other conditions that affect breathing or metabolism, and (see figure 18.1) it is prevalent during end-stage disease where it is as common as pain and forms a significant problem for end-of-life care. Despite its prevalence there are few options for treating this symptom. Unlike pain, there are no specific drugs to reduce this sensation.",True,Introduction,Figure 18.1,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
b3b1d020-d416-41e3-9722-626863e22d96,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,Forms of Dyspnea,False,Forms of Dyspnea,,,,
f5d49a8e-7472-47f2-aa2e-2ae15bf3322c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,So now let us look at the distinguishable sensations that the term dyspnea encompasses and begin to understand how they differ neurologically (see figure 18.2).,True,Forms of Dyspnea,Figure 18.2,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.2.png,Figure 18.2: Types of dyspnea.
f5d49a8e-7472-47f2-aa2e-2ae15bf3322c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,So now let us look at the distinguishable sensations that the term dyspnea encompasses and begin to understand how they differ neurologically (see figure 18.2).,True,Forms of Dyspnea,Figure 18.2,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.2.png,Figure 18.2: Types of dyspnea.
f5d49a8e-7472-47f2-aa2e-2ae15bf3322c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,So now let us look at the distinguishable sensations that the term dyspnea encompasses and begin to understand how they differ neurologically (see figure 18.2).,True,Forms of Dyspnea,Figure 18.2,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.2.png,Figure 18.2: Types of dyspnea.
971f0265-da9a-4606-aaea-3f064a1f4859,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Effort to breathe: The first form of dyspnea is the sensation of work or effort to breathe. The healthy individual is usually unaware of the effort they are putting into breathing until breathing is significantly increased, such as during exercise when ventilation and work of breathing rises. The sensation of the work or effort to breathe is not particularly uncomfortable. If you jogged down the street now you might become more aware of the effort to breathe, but are not disturbed by it.",True,Forms of Dyspnea,,,,
524b2e43-5ae6-4318-96fa-5fced66102e8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,So where does this sensation come from?,False,So where does this sensation come from?,,,,
e6fc31fa-4351-4dd2-bccd-ff4a91ad3da8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"An increase in motor drive is required to activate more tension or movement in any skeletal muscle, including the respiratory muscles. And like other skeletal muscles, such as limb muscles, we believe that the sensation of effort comes from a perception of that increased motor drive. Sensory information from the activated muscles, in our case the respiratory muscles, is thought to generate the sensation of work.",True,So where does this sensation come from?,,,,
133ab222-0225-4d54-bcd5-18c6b4070b00,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Getting laboratory subjects to report work and effort separately is very difficult, so for our purposes right now, we are grouping what might be two sensations together as one.",True,So where does this sensation come from?,,,,
a9e094a8-293b-450f-ba3a-bca93185329f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Chest tightness: The next form of dyspnea is primarily reported by asthmatic patients during bronchoconstriction. Similar to the sensation of work and effort, tightness was originally thought to arise from the increase in respiratory muscle activity associated with a rise in resistive work of breathing. But in 2002 we showed that “tightness” was unrelated to respiratory effort by removing respiratory muscle activity of bronchoconstricted asthmatics with mechanical ventilation. When we did this, “tightness” persisted, despite the respiratory muscles being inactive. So what does cause tightness? The next best, but so far unproven, alternative is that inflammation of the airways associated with an asthma attack leads to activation of airway irritant (or rapidly adapting) receptors, the afferent activity from which is perceived centrally as tightness.",True,So where does this sensation come from?,,,,
52ae02da-d9e8-4763-989e-d5354904f7ee,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Air hunger: Air hunger is arguably the most complex and clinically important form. “Air hunger” is the sensation of suffocation and can be described as a “desperate urge to breathe.” You may have experienced this sensation at the end of a prolonged breath-hold, and it is the unpleasantness of air hunger that made you resume breathing. “Air hunger” is a warning signal that ventilation is insufficient and blood gases are becoming deranged; given the immediate importance of maintaining constant blood gases, air hunger is perhaps our most important homeostatic signal, and it has been referred to as the “suffocation alarm.” The mechanisms underlying air hunger are still unclear, but again, they were once thought to involve the respiratory muscle motor and sensory signals and detection of a disparity between them—that is, the brain perceived that the respiratory muscles were not achieving the work they had been commanded to do. This hypothesis was developed in the sixties and still persists in texts today; however, it is wrong. In two separate labs, one at Harvard University and the other in Australia, pulmonary physiologists completely paralyzed each other to remove all motor activity; when they inhaled carbon dioxide, they still felt air hungry, suggesting the respiratory muscle signals were not essential to generate air hunger. So where does air hunger come from?",True,So where does this sensation come from?,,,,
72bffedf-aac4-414b-a6c7-eea6e2e282ec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"We see air hunger arise when PaCO2 rises, when PaO2 falls, or when arterial pH decreases. These changes are detected by chemoreceptors that reflexly increase the drive to breathe from the brainstem. While we are not usually aware of our reflex breathing drive, we think that once this drive increases to a critical level, a signal is sent upward that is perceived as air hunger.",True,So where does this sensation come from?,,,,
1453b6a2-caa4-4494-848f-1a198da08ae0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"So any signals to the brainstem respiratory networks that increase the drive to breathe are likely to promote air hunger, and these influences may not all be chemical (see figure 18.3). For example, emotions such as anxiety increase the drive to breathe, and this is a pertinent point with clinical ramifications that we will return to.",True,So where does this sensation come from?,Figure 18.3,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
1453b6a2-caa4-4494-848f-1a198da08ae0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"So any signals to the brainstem respiratory networks that increase the drive to breathe are likely to promote air hunger, and these influences may not all be chemical (see figure 18.3). For example, emotions such as anxiety increase the drive to breathe, and this is a pertinent point with clinical ramifications that we will return to.",True,So where does this sensation come from?,Figure 18.3,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
1453b6a2-caa4-4494-848f-1a198da08ae0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"So any signals to the brainstem respiratory networks that increase the drive to breathe are likely to promote air hunger, and these influences may not all be chemical (see figure 18.3). For example, emotions such as anxiety increase the drive to breathe, and this is a pertinent point with clinical ramifications that we will return to.",True,So where does this sensation come from?,Figure 18.3,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
7690de05-839f-42ba-a0b7-de654894948f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Likewise, any influences that reduce the drive to breathe also have a tendency to reduce air hunger (see figure 18.3). Perhaps the most interesting example of this is the effect of pulmonary stretch receptor activity. Pulmonary stretch receptors are mechanoreceptors in the airways that respond to lung inflation. Although this pulmonary afferent activity is thought to have little effect on the control of breathing in man, it reduces the drive to breathe in other species as part of the Hering–Breuer reflex. What we see in humans is that lung inflation, and presumably an increase in pulmonary stretch receptor firing, profoundly reduces air hunger, even in the absence of any blood gas improvements.",True,So where does this sensation come from?,Figure 18.3,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
7690de05-839f-42ba-a0b7-de654894948f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Likewise, any influences that reduce the drive to breathe also have a tendency to reduce air hunger (see figure 18.3). Perhaps the most interesting example of this is the effect of pulmonary stretch receptor activity. Pulmonary stretch receptors are mechanoreceptors in the airways that respond to lung inflation. Although this pulmonary afferent activity is thought to have little effect on the control of breathing in man, it reduces the drive to breathe in other species as part of the Hering–Breuer reflex. What we see in humans is that lung inflation, and presumably an increase in pulmonary stretch receptor firing, profoundly reduces air hunger, even in the absence of any blood gas improvements.",True,So where does this sensation come from?,Figure 18.3,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
7690de05-839f-42ba-a0b7-de654894948f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Likewise, any influences that reduce the drive to breathe also have a tendency to reduce air hunger (see figure 18.3). Perhaps the most interesting example of this is the effect of pulmonary stretch receptor activity. Pulmonary stretch receptors are mechanoreceptors in the airways that respond to lung inflation. Although this pulmonary afferent activity is thought to have little effect on the control of breathing in man, it reduces the drive to breathe in other species as part of the Hering–Breuer reflex. What we see in humans is that lung inflation, and presumably an increase in pulmonary stretch receptor firing, profoundly reduces air hunger, even in the absence of any blood gas improvements.",True,So where does this sensation come from?,Figure 18.3,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
a9f22713-e80c-40c9-ac82-38c879c982a5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"This is easy to demonstrate to yourself by holding your breath; during the breath-hold CO2 will gradually accumulate in your bloodstream and you will feel a gradually increasing urge to breathe that will become increasingly more uncomfortable to a point when it is intolerable and you must begin breathing again. That first big breath you take does not return your arterial CO2 to normal, but despite this you get great relief from air hunger by taking it, probably because that big breath stretched the lung and caused a rapid increase of stretch receptor activity to the brainstem.",True,So where does this sensation come from?,,,,
d3edc83e-0deb-4917-8aeb-ee3ced677ae0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"So air hunger is really affected by a balance of influences: those that increase the drive to breathe (such as hypercapnia and hypoxia) promote air hunger, while inhibitory influences on the drive to breathe tend to promote comfort (see figure 18.4).",True,So where does this sensation come from?,Figure 18.4,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.4.png,Figure 18.4: Balance of pulmonary stretch receptors and chemoreceptor firing.
d3edc83e-0deb-4917-8aeb-ee3ced677ae0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"So air hunger is really affected by a balance of influences: those that increase the drive to breathe (such as hypercapnia and hypoxia) promote air hunger, while inhibitory influences on the drive to breathe tend to promote comfort (see figure 18.4).",True,So where does this sensation come from?,Figure 18.4,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.4.png,Figure 18.4: Balance of pulmonary stretch receptors and chemoreceptor firing.
d3edc83e-0deb-4917-8aeb-ee3ced677ae0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"So air hunger is really affected by a balance of influences: those that increase the drive to breathe (such as hypercapnia and hypoxia) promote air hunger, while inhibitory influences on the drive to breathe tend to promote comfort (see figure 18.4).",True,So where does this sensation come from?,Figure 18.4,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.4.png,Figure 18.4: Balance of pulmonary stretch receptors and chemoreceptor firing.
112711d7-be86-47e8-8d1a-b28752a6f6a9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,Impact of Dyspnea,False,Impact of Dyspnea,,,,
8f30f95b-215b-436b-9512-3ae10768618b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"There are other elements that should be considered when dealing with the air-hungry patient. Probably because of its homeostatic importance, the sensation of air hunger is very effective at getting attention and producing fear and anxiety. Recent comparisons of attentive and emotional impacts suggest air hunger is perceived as much more threatening and worrisome than pain at equivalent intensities. (Ironically we routinely ask about patients’ pain, but rarely about their air hunger.)",True,Impact of Dyspnea,,,,
fb7adc11-d772-4195-b5da-be301bfab084,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"This emotional impact of air hunger is reflected in the regions of the brain that are consistently seen to be activated in recent functional brain imaging studies (see figure 18.5). The amygdala, anterior insula, and anterior cingulate are all persistently seen to activate during air hunger, and all are either associated with the brain’s fear network or generation of emotional responses. The activation of the anterior insula is also interesting as this phylogenically old part of the cortex also responds to other homeostatic imbalances, such as thirst, hunger for food, and pain. Although air hunger itself is unpleasant, it is these emotional components that produce air hunger’s profoundly negative effect on patients’ quality of life and makes end-of-life distressing for both the patient and their loved ones. We will come back to the impact of emotional responses in a moment.",True,Impact of Dyspnea,Figure 18.5,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.5.png,Figure 18.5: Central regions associated with air hunger.
fb7adc11-d772-4195-b5da-be301bfab084,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"This emotional impact of air hunger is reflected in the regions of the brain that are consistently seen to be activated in recent functional brain imaging studies (see figure 18.5). The amygdala, anterior insula, and anterior cingulate are all persistently seen to activate during air hunger, and all are either associated with the brain’s fear network or generation of emotional responses. The activation of the anterior insula is also interesting as this phylogenically old part of the cortex also responds to other homeostatic imbalances, such as thirst, hunger for food, and pain. Although air hunger itself is unpleasant, it is these emotional components that produce air hunger’s profoundly negative effect on patients’ quality of life and makes end-of-life distressing for both the patient and their loved ones. We will come back to the impact of emotional responses in a moment.",True,Impact of Dyspnea,Figure 18.5,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.5.png,Figure 18.5: Central regions associated with air hunger.
fb7adc11-d772-4195-b5da-be301bfab084,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"This emotional impact of air hunger is reflected in the regions of the brain that are consistently seen to be activated in recent functional brain imaging studies (see figure 18.5). The amygdala, anterior insula, and anterior cingulate are all persistently seen to activate during air hunger, and all are either associated with the brain’s fear network or generation of emotional responses. The activation of the anterior insula is also interesting as this phylogenically old part of the cortex also responds to other homeostatic imbalances, such as thirst, hunger for food, and pain. Although air hunger itself is unpleasant, it is these emotional components that produce air hunger’s profoundly negative effect on patients’ quality of life and makes end-of-life distressing for both the patient and their loved ones. We will come back to the impact of emotional responses in a moment.",True,Impact of Dyspnea,Figure 18.5,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.5.png,Figure 18.5: Central regions associated with air hunger.
4b7a8014-6af3-445b-b4be-e857a0bc111a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"So there we are—three different forms of dyspnea, with separate neural mechanisms. That said, it is unlikely that a patient will ever walk into your office and tell you they have “dyspnea,” or pinpoint which form of dyspnea they have. But taking an interest in the subtleties of your patients’ comments may not be a purely academic exercise either. More likely they are likely to use descriptors like those shown in table 18.1. These descriptors that use more common, everyday language have been related to each form of dyspnea. Knowing which form or forms of dyspnea the patient is experiencing can help in diagnosis as the different causes of dyspnea (like those listed in figure 18.1) can produce different levels of each form. For example, chest tightness is much more commonly reported by asthmatics, whereas patients with chronic obstructive pulmonary disease tend to use descriptors more related to effort to breathe and air hunger.",True,Impact of Dyspnea,Figure 18.1,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
4b7a8014-6af3-445b-b4be-e857a0bc111a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"So there we are—three different forms of dyspnea, with separate neural mechanisms. That said, it is unlikely that a patient will ever walk into your office and tell you they have “dyspnea,” or pinpoint which form of dyspnea they have. But taking an interest in the subtleties of your patients’ comments may not be a purely academic exercise either. More likely they are likely to use descriptors like those shown in table 18.1. These descriptors that use more common, everyday language have been related to each form of dyspnea. Knowing which form or forms of dyspnea the patient is experiencing can help in diagnosis as the different causes of dyspnea (like those listed in figure 18.1) can produce different levels of each form. For example, chest tightness is much more commonly reported by asthmatics, whereas patients with chronic obstructive pulmonary disease tend to use descriptors more related to effort to breathe and air hunger.",True,Impact of Dyspnea,Figure 18.1,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
4b7a8014-6af3-445b-b4be-e857a0bc111a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"So there we are—three different forms of dyspnea, with separate neural mechanisms. That said, it is unlikely that a patient will ever walk into your office and tell you they have “dyspnea,” or pinpoint which form of dyspnea they have. But taking an interest in the subtleties of your patients’ comments may not be a purely academic exercise either. More likely they are likely to use descriptors like those shown in table 18.1. These descriptors that use more common, everyday language have been related to each form of dyspnea. Knowing which form or forms of dyspnea the patient is experiencing can help in diagnosis as the different causes of dyspnea (like those listed in figure 18.1) can produce different levels of each form. For example, chest tightness is much more commonly reported by asthmatics, whereas patients with chronic obstructive pulmonary disease tend to use descriptors more related to effort to breathe and air hunger.",True,Impact of Dyspnea,Figure 18.1,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
12aa1d7b-d9ba-4fcb-889e-d4973fa700f7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,Table 18.1: Patient descriptors for the three different forms of dyspnea.,True,Impact of Dyspnea,,,,
5a0b5c38-5d23-49af-be59-525bac0623e2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"While the different forms of dyspnea have been investigated, described, and now explored as their potential as diagnostic tools, the emotional impact of dyspnea is only now receiving more attention. The most immediate complication caused by the emotional component is the potential for a positive feedback loop to form between air hunger and the anxiety it generates. The anxiety that air hunger produces results in an increased drive to breathe; in turn this increased drive to breathe causes the air hunger to increase, which leads to more anxiety and so on (figure 18.6).",True,Impact of Dyspnea,Figure 18.6,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.6-new.png,"Figure 18.6: The cycle of anxiety causing an increase in the drive to breathe and air hunger, which in turn causes more anxiety. Psychological disorders can produce air hunger if they involve anxiety."
5a0b5c38-5d23-49af-be59-525bac0623e2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"While the different forms of dyspnea have been investigated, described, and now explored as their potential as diagnostic tools, the emotional impact of dyspnea is only now receiving more attention. The most immediate complication caused by the emotional component is the potential for a positive feedback loop to form between air hunger and the anxiety it generates. The anxiety that air hunger produces results in an increased drive to breathe; in turn this increased drive to breathe causes the air hunger to increase, which leads to more anxiety and so on (figure 18.6).",True,Impact of Dyspnea,Figure 18.6,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.6-new.png,"Figure 18.6: The cycle of anxiety causing an increase in the drive to breathe and air hunger, which in turn causes more anxiety. Psychological disorders can produce air hunger if they involve anxiety."
5a0b5c38-5d23-49af-be59-525bac0623e2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"While the different forms of dyspnea have been investigated, described, and now explored as their potential as diagnostic tools, the emotional impact of dyspnea is only now receiving more attention. The most immediate complication caused by the emotional component is the potential for a positive feedback loop to form between air hunger and the anxiety it generates. The anxiety that air hunger produces results in an increased drive to breathe; in turn this increased drive to breathe causes the air hunger to increase, which leads to more anxiety and so on (figure 18.6).",True,Impact of Dyspnea,Figure 18.6,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.6-new.png,"Figure 18.6: The cycle of anxiety causing an increase in the drive to breathe and air hunger, which in turn causes more anxiety. Psychological disorders can produce air hunger if they involve anxiety."
c02eb73c-f5b5-4ccd-8113-3e904d9ae87f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Behavioral effects of dyspnea: This cycle can be entered into by different types of patients; those with cardiopulmonary disease enter the cycle at the point of the air hunger, whereas patients with anxiety disorders can enter the cycle at this point and can experience significant air hunger even with apparently perfectly normal lung and heart function. On a more long-term basis the quality of life of air-hungry patients can be diminished by another positive feedback scenario that can produce “respiratory cripples” of cardiopulmonary patients. The air hunger produced by the underlying disease worsens during exertion, so makes exercising uncomfortable. This frequently results in patients avoiding exercise, perhaps starting with taking an elevator instead of the stairs, or driving to the grocery store when previously they might have walked.",True,Impact of Dyspnea,,,,
0701b412-5140-4761-96ac-7ad79d1b62d8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"This reduction in exercise leads to cardiac deconditioning, which in turn makes the air hunger worse and leads to further avoidance of exercise. Along with the progression of the disease, this cycle may leave the patient out-of-breath while simply sitting in a chair.",True,Impact of Dyspnea,,,,
ff30a35d-ec49-4a2b-8402-f685ad7483bb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"The patient’s quality of life becomes severely diminished as their life is ruled by dyspnea that prevents them from leaving the house, interacting with children or grandchildren, and performing simple activities that used to bring enjoyment, such as gardening, wood-working, walking, and more. This reduced quality of life can potentially lead to depression, and the emotional response to dyspnea may be exacerbated.",True,Impact of Dyspnea,,,,
3fa222a8-44f6-40e4-9700-b4c786fbd3df,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"So what can be done to relieve the patient’s air hunger and the associated anxiety? Well, despite its prevalence, the treatment of dyspnea is decades behind the treatment of pain. For too long the approach to treating dyspnea has been to treat the underlying disease with the expectation that the dyspnea will go away. This is true and a perfect course of action for many conditions, but for many diseases that produce dyspnea we have ineffective cures, such as emphysema, lung cancer, and pulmonary fibrosis. How do we make the 49 percent of terminally ill patients who suffer with dyspnea at the end of life more comfortable?",True,Impact of Dyspnea,,,,
96bf1610-7ea3-41bb-83c4-4fe808ffa128,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Opioids: A common practice is to use opioids, but the mechanism of how they might work and indeed their overall efficacy has been disputed. There are a number of routes for how morphine may act, if it indeed does so. Opioids may have a direct inhibitory effect on the central networks that generate air hunger, or at higher dose concentrations they may reduce air hunger indirectly by causing respiratory depression—that is, they tackle air hunger at what we think to be its source. Alternatively, opioids may reduce the affective or emotional component of dyspnea (i.e., the patient may perceive air hunger, but simply is not as bothered by it). Recent work from Harvard University suggests that morphine has a direct effect on both the sensory and affective components of air hunger independent of its effect on ventilatory drive.",True,Impact of Dyspnea,,,,
acd95dde-e94e-456d-b79c-aaf7cda0accb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Anxiolytics: As the emotional component of air hunger is so strong, the fear and anxiety produced can be treated in the absence of any specific drug to treat the air hunger itself. Use of anxiolytics drugs has also produced mixed results that may be complicated by the patient’s underlying condition, and whether the type of anxiolytic causes ventilatory depression.",True,Impact of Dyspnea,,,,
98681128-282c-4676-af4c-e9237fc4b75c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Furosemide: Although there is currently no drug that specifically tackles air hunger, there is a growing body of evidence that inhaled furosemide (the loop diuretic) reduces air hunger by sensitizing pulmonary stretch receptors, meaning they fire more for any given lung volume. This amplifies the stretch receptors’ inhibitory effect on air hunger described earlier, by fooling the brain into thinking the lungs are at a greater volume than they really are.",True,Impact of Dyspnea,,,,
d4f7d731-abe8-4b12-9515-b817f4c6a042,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,Nonpharmaceutical alternatives: A nonpharmaceutical alternative is to simply cool the patient’s face with a fan or wet cloth. This facial cooling initiates the “diving reflex” via the trigeminal nerve. One component of the diving reflex is to reduce ventilatory drive at the brainstem—an ideal response if one is heading underwater.,True,Impact of Dyspnea,,,,
2f2f59dd-03fc-41e1-b326-987748de2c35,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,This inhibition of ventilatory drive is likely responsible for the moderate reduction in air hunger seen with facial cooling.,True,Impact of Dyspnea,,,,
7276f9ff-0abe-46ec-add8-1d0160bf075e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Rehabilitation and desensitization: While dyspnea can be addressed by other methods than those briefly described here, few have been shown to work consistently or effectively. On a more long-term basis, breathing training and pulmonary rehabilitation appear to help patients overcome exacerbations of their disease or even reduce chronic air hunger, but both require patient cooperation and compliance and may have limited effect in severe disease. What can be taken from the literature is that the treatment of dyspnea is in desperate need of more attention. For a symptom that is so common and has such an impact on patients, dyspnea is a clinical issue that is woefully underaddressed.",True,Impact of Dyspnea,,,,
29ba2106-3add-4572-a0ef-2a6e579be8b8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,Text,False,Text,,,,
709e47ee-7a91-414c-81cc-5c3752c06c47,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"American Thoracic Society Committee on Dyspnea. “An Official American Thoracic Society Statement: Update on the Mechanisms, Assessment, and Management of Dyspnea.” American Journal of Respiratory and Critical Care Medicine 185, no. 4: 435–52. https://doi.org/10.1164/rccm.201111-2042ST.",True,Text,,,,
d5f1a15f-0fcf-40e5-aa89-9237e2b68c6a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Impact of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-2,"Banzett, Robert B., Robert W. Lansing, and Andrew P. Binks. “Air Hunger: A Primal Sensation and a Primary Element of Dyspnea.” Comprehensive Physiology 11, no. 2 (April 2021): 1449–83. https://doi.org/10.1002/cphy.c200001.",True,Text,,,,
eaade492-7fea-444d-9904-ee91b6c4c763,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,Introduction,False,Introduction,,,,
bdb87e8e-e91f-4072-ba85-de99a6b70880,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"It might be worth putting dyspnea in a clinical context. Like pain, dyspnea can occur across a number of pathological conditions. It is the cardinal symptom of lung disease, but it is highly prevalent in heart diseases as well—in fact it is a more common sign of myocardial infarction in women than the classical symptom of chest pain that is more prevalent in men.",True,Introduction,,,,
9d5db843-8a44-4447-945f-36c6fbab198d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Dyspnea is also a strong predictor of mortality in most heart and lung diseases. As well as cardiopulmonary conditions, dyspnea is also prevalent in other conditions that affect breathing or metabolism, and (see figure 18.1) it is prevalent during end-stage disease where it is as common as pain and forms a significant problem for end-of-life care. Despite its prevalence there are few options for treating this symptom. Unlike pain, there are no specific drugs to reduce this sensation.",True,Introduction,Figure 18.1,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
9d5db843-8a44-4447-945f-36c6fbab198d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Dyspnea is also a strong predictor of mortality in most heart and lung diseases. As well as cardiopulmonary conditions, dyspnea is also prevalent in other conditions that affect breathing or metabolism, and (see figure 18.1) it is prevalent during end-stage disease where it is as common as pain and forms a significant problem for end-of-life care. Despite its prevalence there are few options for treating this symptom. Unlike pain, there are no specific drugs to reduce this sensation.",True,Introduction,Figure 18.1,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
9d5db843-8a44-4447-945f-36c6fbab198d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Dyspnea is also a strong predictor of mortality in most heart and lung diseases. As well as cardiopulmonary conditions, dyspnea is also prevalent in other conditions that affect breathing or metabolism, and (see figure 18.1) it is prevalent during end-stage disease where it is as common as pain and forms a significant problem for end-of-life care. Despite its prevalence there are few options for treating this symptom. Unlike pain, there are no specific drugs to reduce this sensation.",True,Introduction,Figure 18.1,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
8c6e3dc3-d522-4e5f-b153-fb3adef62022,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,Forms of Dyspnea,False,Forms of Dyspnea,,,,
9e296ac7-ddc9-4c89-be3f-1a242aa2159b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,So now let us look at the distinguishable sensations that the term dyspnea encompasses and begin to understand how they differ neurologically (see figure 18.2).,True,Forms of Dyspnea,Figure 18.2,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.2.png,Figure 18.2: Types of dyspnea.
9e296ac7-ddc9-4c89-be3f-1a242aa2159b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,So now let us look at the distinguishable sensations that the term dyspnea encompasses and begin to understand how they differ neurologically (see figure 18.2).,True,Forms of Dyspnea,Figure 18.2,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.2.png,Figure 18.2: Types of dyspnea.
9e296ac7-ddc9-4c89-be3f-1a242aa2159b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,So now let us look at the distinguishable sensations that the term dyspnea encompasses and begin to understand how they differ neurologically (see figure 18.2).,True,Forms of Dyspnea,Figure 18.2,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.2.png,Figure 18.2: Types of dyspnea.
0d3d65d1-560d-4f64-935d-fba4701f809d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Effort to breathe: The first form of dyspnea is the sensation of work or effort to breathe. The healthy individual is usually unaware of the effort they are putting into breathing until breathing is significantly increased, such as during exercise when ventilation and work of breathing rises. The sensation of the work or effort to breathe is not particularly uncomfortable. If you jogged down the street now you might become more aware of the effort to breathe, but are not disturbed by it.",True,Forms of Dyspnea,,,,
d90119d5-cc03-4706-8f15-065cbc28e1d2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,So where does this sensation come from?,False,So where does this sensation come from?,,,,
4abd05f8-6f80-47a5-96a1-8bb856612e9a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"An increase in motor drive is required to activate more tension or movement in any skeletal muscle, including the respiratory muscles. And like other skeletal muscles, such as limb muscles, we believe that the sensation of effort comes from a perception of that increased motor drive. Sensory information from the activated muscles, in our case the respiratory muscles, is thought to generate the sensation of work.",True,So where does this sensation come from?,,,,
1e7b91ba-600d-49c4-abd0-722d43037ef9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Getting laboratory subjects to report work and effort separately is very difficult, so for our purposes right now, we are grouping what might be two sensations together as one.",True,So where does this sensation come from?,,,,
83bab399-5634-407f-88a6-fb419afa9403,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Chest tightness: The next form of dyspnea is primarily reported by asthmatic patients during bronchoconstriction. Similar to the sensation of work and effort, tightness was originally thought to arise from the increase in respiratory muscle activity associated with a rise in resistive work of breathing. But in 2002 we showed that “tightness” was unrelated to respiratory effort by removing respiratory muscle activity of bronchoconstricted asthmatics with mechanical ventilation. When we did this, “tightness” persisted, despite the respiratory muscles being inactive. So what does cause tightness? The next best, but so far unproven, alternative is that inflammation of the airways associated with an asthma attack leads to activation of airway irritant (or rapidly adapting) receptors, the afferent activity from which is perceived centrally as tightness.",True,So where does this sensation come from?,,,,
82030c7d-3119-47b1-8f2a-046da1c60777,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Air hunger: Air hunger is arguably the most complex and clinically important form. “Air hunger” is the sensation of suffocation and can be described as a “desperate urge to breathe.” You may have experienced this sensation at the end of a prolonged breath-hold, and it is the unpleasantness of air hunger that made you resume breathing. “Air hunger” is a warning signal that ventilation is insufficient and blood gases are becoming deranged; given the immediate importance of maintaining constant blood gases, air hunger is perhaps our most important homeostatic signal, and it has been referred to as the “suffocation alarm.” The mechanisms underlying air hunger are still unclear, but again, they were once thought to involve the respiratory muscle motor and sensory signals and detection of a disparity between them—that is, the brain perceived that the respiratory muscles were not achieving the work they had been commanded to do. This hypothesis was developed in the sixties and still persists in texts today; however, it is wrong. In two separate labs, one at Harvard University and the other in Australia, pulmonary physiologists completely paralyzed each other to remove all motor activity; when they inhaled carbon dioxide, they still felt air hungry, suggesting the respiratory muscle signals were not essential to generate air hunger. So where does air hunger come from?",True,So where does this sensation come from?,,,,
5414e108-78ec-4280-8df6-ba80721c7791,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"We see air hunger arise when PaCO2 rises, when PaO2 falls, or when arterial pH decreases. These changes are detected by chemoreceptors that reflexly increase the drive to breathe from the brainstem. While we are not usually aware of our reflex breathing drive, we think that once this drive increases to a critical level, a signal is sent upward that is perceived as air hunger.",True,So where does this sensation come from?,,,,
9ba2cfdb-0fe8-4808-aea0-2c3525ac291b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"So any signals to the brainstem respiratory networks that increase the drive to breathe are likely to promote air hunger, and these influences may not all be chemical (see figure 18.3). For example, emotions such as anxiety increase the drive to breathe, and this is a pertinent point with clinical ramifications that we will return to.",True,So where does this sensation come from?,Figure 18.3,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
9ba2cfdb-0fe8-4808-aea0-2c3525ac291b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"So any signals to the brainstem respiratory networks that increase the drive to breathe are likely to promote air hunger, and these influences may not all be chemical (see figure 18.3). For example, emotions such as anxiety increase the drive to breathe, and this is a pertinent point with clinical ramifications that we will return to.",True,So where does this sensation come from?,Figure 18.3,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
9ba2cfdb-0fe8-4808-aea0-2c3525ac291b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"So any signals to the brainstem respiratory networks that increase the drive to breathe are likely to promote air hunger, and these influences may not all be chemical (see figure 18.3). For example, emotions such as anxiety increase the drive to breathe, and this is a pertinent point with clinical ramifications that we will return to.",True,So where does this sensation come from?,Figure 18.3,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
661a5130-e210-4b3c-8441-150dee47336d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Likewise, any influences that reduce the drive to breathe also have a tendency to reduce air hunger (see figure 18.3). Perhaps the most interesting example of this is the effect of pulmonary stretch receptor activity. Pulmonary stretch receptors are mechanoreceptors in the airways that respond to lung inflation. Although this pulmonary afferent activity is thought to have little effect on the control of breathing in man, it reduces the drive to breathe in other species as part of the Hering–Breuer reflex. What we see in humans is that lung inflation, and presumably an increase in pulmonary stretch receptor firing, profoundly reduces air hunger, even in the absence of any blood gas improvements.",True,So where does this sensation come from?,Figure 18.3,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
661a5130-e210-4b3c-8441-150dee47336d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Likewise, any influences that reduce the drive to breathe also have a tendency to reduce air hunger (see figure 18.3). Perhaps the most interesting example of this is the effect of pulmonary stretch receptor activity. Pulmonary stretch receptors are mechanoreceptors in the airways that respond to lung inflation. Although this pulmonary afferent activity is thought to have little effect on the control of breathing in man, it reduces the drive to breathe in other species as part of the Hering–Breuer reflex. What we see in humans is that lung inflation, and presumably an increase in pulmonary stretch receptor firing, profoundly reduces air hunger, even in the absence of any blood gas improvements.",True,So where does this sensation come from?,Figure 18.3,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
661a5130-e210-4b3c-8441-150dee47336d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Likewise, any influences that reduce the drive to breathe also have a tendency to reduce air hunger (see figure 18.3). Perhaps the most interesting example of this is the effect of pulmonary stretch receptor activity. Pulmonary stretch receptors are mechanoreceptors in the airways that respond to lung inflation. Although this pulmonary afferent activity is thought to have little effect on the control of breathing in man, it reduces the drive to breathe in other species as part of the Hering–Breuer reflex. What we see in humans is that lung inflation, and presumably an increase in pulmonary stretch receptor firing, profoundly reduces air hunger, even in the absence of any blood gas improvements.",True,So where does this sensation come from?,Figure 18.3,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
d89e02af-3aae-4848-8e72-02dacc120202,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"This is easy to demonstrate to yourself by holding your breath; during the breath-hold CO2 will gradually accumulate in your bloodstream and you will feel a gradually increasing urge to breathe that will become increasingly more uncomfortable to a point when it is intolerable and you must begin breathing again. That first big breath you take does not return your arterial CO2 to normal, but despite this you get great relief from air hunger by taking it, probably because that big breath stretched the lung and caused a rapid increase of stretch receptor activity to the brainstem.",True,So where does this sensation come from?,,,,
ca97042e-4a7f-4721-b666-20e7a311a5be,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"So air hunger is really affected by a balance of influences: those that increase the drive to breathe (such as hypercapnia and hypoxia) promote air hunger, while inhibitory influences on the drive to breathe tend to promote comfort (see figure 18.4).",True,So where does this sensation come from?,Figure 18.4,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.4.png,Figure 18.4: Balance of pulmonary stretch receptors and chemoreceptor firing.
ca97042e-4a7f-4721-b666-20e7a311a5be,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"So air hunger is really affected by a balance of influences: those that increase the drive to breathe (such as hypercapnia and hypoxia) promote air hunger, while inhibitory influences on the drive to breathe tend to promote comfort (see figure 18.4).",True,So where does this sensation come from?,Figure 18.4,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.4.png,Figure 18.4: Balance of pulmonary stretch receptors and chemoreceptor firing.
ca97042e-4a7f-4721-b666-20e7a311a5be,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"So air hunger is really affected by a balance of influences: those that increase the drive to breathe (such as hypercapnia and hypoxia) promote air hunger, while inhibitory influences on the drive to breathe tend to promote comfort (see figure 18.4).",True,So where does this sensation come from?,Figure 18.4,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.4.png,Figure 18.4: Balance of pulmonary stretch receptors and chemoreceptor firing.
47a52736-cce5-4d34-b51d-452c98d06c45,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,Impact of Dyspnea,False,Impact of Dyspnea,,,,
6cc0c240-5720-47e8-a2f1-6ee52c126207,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"There are other elements that should be considered when dealing with the air-hungry patient. Probably because of its homeostatic importance, the sensation of air hunger is very effective at getting attention and producing fear and anxiety. Recent comparisons of attentive and emotional impacts suggest air hunger is perceived as much more threatening and worrisome than pain at equivalent intensities. (Ironically we routinely ask about patients’ pain, but rarely about their air hunger.)",True,Impact of Dyspnea,,,,
43f4ec58-bb49-4438-8ddc-ba97ae7f7cda,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"This emotional impact of air hunger is reflected in the regions of the brain that are consistently seen to be activated in recent functional brain imaging studies (see figure 18.5). The amygdala, anterior insula, and anterior cingulate are all persistently seen to activate during air hunger, and all are either associated with the brain’s fear network or generation of emotional responses. The activation of the anterior insula is also interesting as this phylogenically old part of the cortex also responds to other homeostatic imbalances, such as thirst, hunger for food, and pain. Although air hunger itself is unpleasant, it is these emotional components that produce air hunger’s profoundly negative effect on patients’ quality of life and makes end-of-life distressing for both the patient and their loved ones. We will come back to the impact of emotional responses in a moment.",True,Impact of Dyspnea,Figure 18.5,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.5.png,Figure 18.5: Central regions associated with air hunger.
43f4ec58-bb49-4438-8ddc-ba97ae7f7cda,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"This emotional impact of air hunger is reflected in the regions of the brain that are consistently seen to be activated in recent functional brain imaging studies (see figure 18.5). The amygdala, anterior insula, and anterior cingulate are all persistently seen to activate during air hunger, and all are either associated with the brain’s fear network or generation of emotional responses. The activation of the anterior insula is also interesting as this phylogenically old part of the cortex also responds to other homeostatic imbalances, such as thirst, hunger for food, and pain. Although air hunger itself is unpleasant, it is these emotional components that produce air hunger’s profoundly negative effect on patients’ quality of life and makes end-of-life distressing for both the patient and their loved ones. We will come back to the impact of emotional responses in a moment.",True,Impact of Dyspnea,Figure 18.5,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.5.png,Figure 18.5: Central regions associated with air hunger.
43f4ec58-bb49-4438-8ddc-ba97ae7f7cda,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"This emotional impact of air hunger is reflected in the regions of the brain that are consistently seen to be activated in recent functional brain imaging studies (see figure 18.5). The amygdala, anterior insula, and anterior cingulate are all persistently seen to activate during air hunger, and all are either associated with the brain’s fear network or generation of emotional responses. The activation of the anterior insula is also interesting as this phylogenically old part of the cortex also responds to other homeostatic imbalances, such as thirst, hunger for food, and pain. Although air hunger itself is unpleasant, it is these emotional components that produce air hunger’s profoundly negative effect on patients’ quality of life and makes end-of-life distressing for both the patient and their loved ones. We will come back to the impact of emotional responses in a moment.",True,Impact of Dyspnea,Figure 18.5,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.5.png,Figure 18.5: Central regions associated with air hunger.
7a477793-29e9-420f-b9cf-c1dd41ac199b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"So there we are—three different forms of dyspnea, with separate neural mechanisms. That said, it is unlikely that a patient will ever walk into your office and tell you they have “dyspnea,” or pinpoint which form of dyspnea they have. But taking an interest in the subtleties of your patients’ comments may not be a purely academic exercise either. More likely they are likely to use descriptors like those shown in table 18.1. These descriptors that use more common, everyday language have been related to each form of dyspnea. Knowing which form or forms of dyspnea the patient is experiencing can help in diagnosis as the different causes of dyspnea (like those listed in figure 18.1) can produce different levels of each form. For example, chest tightness is much more commonly reported by asthmatics, whereas patients with chronic obstructive pulmonary disease tend to use descriptors more related to effort to breathe and air hunger.",True,Impact of Dyspnea,Figure 18.1,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
7a477793-29e9-420f-b9cf-c1dd41ac199b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"So there we are—three different forms of dyspnea, with separate neural mechanisms. That said, it is unlikely that a patient will ever walk into your office and tell you they have “dyspnea,” or pinpoint which form of dyspnea they have. But taking an interest in the subtleties of your patients’ comments may not be a purely academic exercise either. More likely they are likely to use descriptors like those shown in table 18.1. These descriptors that use more common, everyday language have been related to each form of dyspnea. Knowing which form or forms of dyspnea the patient is experiencing can help in diagnosis as the different causes of dyspnea (like those listed in figure 18.1) can produce different levels of each form. For example, chest tightness is much more commonly reported by asthmatics, whereas patients with chronic obstructive pulmonary disease tend to use descriptors more related to effort to breathe and air hunger.",True,Impact of Dyspnea,Figure 18.1,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
7a477793-29e9-420f-b9cf-c1dd41ac199b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"So there we are—three different forms of dyspnea, with separate neural mechanisms. That said, it is unlikely that a patient will ever walk into your office and tell you they have “dyspnea,” or pinpoint which form of dyspnea they have. But taking an interest in the subtleties of your patients’ comments may not be a purely academic exercise either. More likely they are likely to use descriptors like those shown in table 18.1. These descriptors that use more common, everyday language have been related to each form of dyspnea. Knowing which form or forms of dyspnea the patient is experiencing can help in diagnosis as the different causes of dyspnea (like those listed in figure 18.1) can produce different levels of each form. For example, chest tightness is much more commonly reported by asthmatics, whereas patients with chronic obstructive pulmonary disease tend to use descriptors more related to effort to breathe and air hunger.",True,Impact of Dyspnea,Figure 18.1,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
a367e323-de34-4578-860c-2055a7c129a6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,Table 18.1: Patient descriptors for the three different forms of dyspnea.,True,Impact of Dyspnea,,,,
86bfed1c-642e-445c-bfe9-2c8dc43de598,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"While the different forms of dyspnea have been investigated, described, and now explored as their potential as diagnostic tools, the emotional impact of dyspnea is only now receiving more attention. The most immediate complication caused by the emotional component is the potential for a positive feedback loop to form between air hunger and the anxiety it generates. The anxiety that air hunger produces results in an increased drive to breathe; in turn this increased drive to breathe causes the air hunger to increase, which leads to more anxiety and so on (figure 18.6).",True,Impact of Dyspnea,Figure 18.6,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.6-new.png,"Figure 18.6: The cycle of anxiety causing an increase in the drive to breathe and air hunger, which in turn causes more anxiety. Psychological disorders can produce air hunger if they involve anxiety."
86bfed1c-642e-445c-bfe9-2c8dc43de598,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"While the different forms of dyspnea have been investigated, described, and now explored as their potential as diagnostic tools, the emotional impact of dyspnea is only now receiving more attention. The most immediate complication caused by the emotional component is the potential for a positive feedback loop to form between air hunger and the anxiety it generates. The anxiety that air hunger produces results in an increased drive to breathe; in turn this increased drive to breathe causes the air hunger to increase, which leads to more anxiety and so on (figure 18.6).",True,Impact of Dyspnea,Figure 18.6,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.6-new.png,"Figure 18.6: The cycle of anxiety causing an increase in the drive to breathe and air hunger, which in turn causes more anxiety. Psychological disorders can produce air hunger if they involve anxiety."
86bfed1c-642e-445c-bfe9-2c8dc43de598,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"While the different forms of dyspnea have been investigated, described, and now explored as their potential as diagnostic tools, the emotional impact of dyspnea is only now receiving more attention. The most immediate complication caused by the emotional component is the potential for a positive feedback loop to form between air hunger and the anxiety it generates. The anxiety that air hunger produces results in an increased drive to breathe; in turn this increased drive to breathe causes the air hunger to increase, which leads to more anxiety and so on (figure 18.6).",True,Impact of Dyspnea,Figure 18.6,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.6-new.png,"Figure 18.6: The cycle of anxiety causing an increase in the drive to breathe and air hunger, which in turn causes more anxiety. Psychological disorders can produce air hunger if they involve anxiety."
aa8c03d6-1096-4831-b55b-71471509a030,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Behavioral effects of dyspnea: This cycle can be entered into by different types of patients; those with cardiopulmonary disease enter the cycle at the point of the air hunger, whereas patients with anxiety disorders can enter the cycle at this point and can experience significant air hunger even with apparently perfectly normal lung and heart function. On a more long-term basis the quality of life of air-hungry patients can be diminished by another positive feedback scenario that can produce “respiratory cripples” of cardiopulmonary patients. The air hunger produced by the underlying disease worsens during exertion, so makes exercising uncomfortable. This frequently results in patients avoiding exercise, perhaps starting with taking an elevator instead of the stairs, or driving to the grocery store when previously they might have walked.",True,Impact of Dyspnea,,,,
889d330a-ce54-482e-88b3-f39f83e51b15,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"This reduction in exercise leads to cardiac deconditioning, which in turn makes the air hunger worse and leads to further avoidance of exercise. Along with the progression of the disease, this cycle may leave the patient out-of-breath while simply sitting in a chair.",True,Impact of Dyspnea,,,,
968e2014-76ce-4617-88c2-63fc08d16fff,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"The patient’s quality of life becomes severely diminished as their life is ruled by dyspnea that prevents them from leaving the house, interacting with children or grandchildren, and performing simple activities that used to bring enjoyment, such as gardening, wood-working, walking, and more. This reduced quality of life can potentially lead to depression, and the emotional response to dyspnea may be exacerbated.",True,Impact of Dyspnea,,,,
2a8e7b14-b0f8-4f02-a0dc-15cc6da50b68,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"So what can be done to relieve the patient’s air hunger and the associated anxiety? Well, despite its prevalence, the treatment of dyspnea is decades behind the treatment of pain. For too long the approach to treating dyspnea has been to treat the underlying disease with the expectation that the dyspnea will go away. This is true and a perfect course of action for many conditions, but for many diseases that produce dyspnea we have ineffective cures, such as emphysema, lung cancer, and pulmonary fibrosis. How do we make the 49 percent of terminally ill patients who suffer with dyspnea at the end of life more comfortable?",True,Impact of Dyspnea,,,,
f6645d28-ee9a-4d10-beee-bd5e0c14f27a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Opioids: A common practice is to use opioids, but the mechanism of how they might work and indeed their overall efficacy has been disputed. There are a number of routes for how morphine may act, if it indeed does so. Opioids may have a direct inhibitory effect on the central networks that generate air hunger, or at higher dose concentrations they may reduce air hunger indirectly by causing respiratory depression—that is, they tackle air hunger at what we think to be its source. Alternatively, opioids may reduce the affective or emotional component of dyspnea (i.e., the patient may perceive air hunger, but simply is not as bothered by it). Recent work from Harvard University suggests that morphine has a direct effect on both the sensory and affective components of air hunger independent of its effect on ventilatory drive.",True,Impact of Dyspnea,,,,
f6d87bbe-ccc1-440c-b839-101f5ed8d991,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Anxiolytics: As the emotional component of air hunger is so strong, the fear and anxiety produced can be treated in the absence of any specific drug to treat the air hunger itself. Use of anxiolytics drugs has also produced mixed results that may be complicated by the patient’s underlying condition, and whether the type of anxiolytic causes ventilatory depression.",True,Impact of Dyspnea,,,,
bbc8e405-12cc-4f02-bd84-1ad9e65dbbe4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Furosemide: Although there is currently no drug that specifically tackles air hunger, there is a growing body of evidence that inhaled furosemide (the loop diuretic) reduces air hunger by sensitizing pulmonary stretch receptors, meaning they fire more for any given lung volume. This amplifies the stretch receptors’ inhibitory effect on air hunger described earlier, by fooling the brain into thinking the lungs are at a greater volume than they really are.",True,Impact of Dyspnea,,,,
cea58fdf-53e0-4737-afb4-ed139b15bfe4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,Nonpharmaceutical alternatives: A nonpharmaceutical alternative is to simply cool the patient’s face with a fan or wet cloth. This facial cooling initiates the “diving reflex” via the trigeminal nerve. One component of the diving reflex is to reduce ventilatory drive at the brainstem—an ideal response if one is heading underwater.,True,Impact of Dyspnea,,,,
a8d7ccb4-487d-49aa-a8bf-2a48449b2067,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,This inhibition of ventilatory drive is likely responsible for the moderate reduction in air hunger seen with facial cooling.,True,Impact of Dyspnea,,,,
6c6661eb-f6dd-4d47-b4d9-03288dfb62b5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Rehabilitation and desensitization: While dyspnea can be addressed by other methods than those briefly described here, few have been shown to work consistently or effectively. On a more long-term basis, breathing training and pulmonary rehabilitation appear to help patients overcome exacerbations of their disease or even reduce chronic air hunger, but both require patient cooperation and compliance and may have limited effect in severe disease. What can be taken from the literature is that the treatment of dyspnea is in desperate need of more attention. For a symptom that is so common and has such an impact on patients, dyspnea is a clinical issue that is woefully underaddressed.",True,Impact of Dyspnea,,,,
efd101d6-9703-42d1-a992-5906d7aaadfe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,Text,False,Text,,,,
a4934104-1f05-45c8-8316-db4c489c54d3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"American Thoracic Society Committee on Dyspnea. “An Official American Thoracic Society Statement: Update on the Mechanisms, Assessment, and Management of Dyspnea.” American Journal of Respiratory and Critical Care Medicine 185, no. 4: 435–52. https://doi.org/10.1164/rccm.201111-2042ST.",True,Text,,,,
722c9e07-0424-477b-8d84-2ee5766a8c5b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/#chapter-61-section-1,"Banzett, Robert B., Robert W. Lansing, and Andrew P. Binks. “Air Hunger: A Primal Sensation and a Primary Element of Dyspnea.” Comprehensive Physiology 11, no. 2 (April 2021): 1449–83. https://doi.org/10.1002/cphy.c200001.",True,Text,,,,
9f87b67d-898b-4ae9-ab20-96c5d9d79c2c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,Introduction,False,Introduction,,,,
9afe3332-8490-4df8-a8ac-0144425560dc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"It might be worth putting dyspnea in a clinical context. Like pain, dyspnea can occur across a number of pathological conditions. It is the cardinal symptom of lung disease, but it is highly prevalent in heart diseases as well—in fact it is a more common sign of myocardial infarction in women than the classical symptom of chest pain that is more prevalent in men.",True,Introduction,,,,
b5a4ddba-a287-4a31-a7a4-4a5fb259630a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Dyspnea is also a strong predictor of mortality in most heart and lung diseases. As well as cardiopulmonary conditions, dyspnea is also prevalent in other conditions that affect breathing or metabolism, and (see figure 18.1) it is prevalent during end-stage disease where it is as common as pain and forms a significant problem for end-of-life care. Despite its prevalence there are few options for treating this symptom. Unlike pain, there are no specific drugs to reduce this sensation.",True,Introduction,Figure 18.1,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
b5a4ddba-a287-4a31-a7a4-4a5fb259630a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Dyspnea is also a strong predictor of mortality in most heart and lung diseases. As well as cardiopulmonary conditions, dyspnea is also prevalent in other conditions that affect breathing or metabolism, and (see figure 18.1) it is prevalent during end-stage disease where it is as common as pain and forms a significant problem for end-of-life care. Despite its prevalence there are few options for treating this symptom. Unlike pain, there are no specific drugs to reduce this sensation.",True,Introduction,Figure 18.1,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
b5a4ddba-a287-4a31-a7a4-4a5fb259630a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Dyspnea is also a strong predictor of mortality in most heart and lung diseases. As well as cardiopulmonary conditions, dyspnea is also prevalent in other conditions that affect breathing or metabolism, and (see figure 18.1) it is prevalent during end-stage disease where it is as common as pain and forms a significant problem for end-of-life care. Despite its prevalence there are few options for treating this symptom. Unlike pain, there are no specific drugs to reduce this sensation.",True,Introduction,Figure 18.1,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
b668f9af-527a-499c-a73c-b79e9cd2f077,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,Forms of Dyspnea,False,Forms of Dyspnea,,,,
ea3e12eb-22fa-46a9-82af-b0541913908b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,So now let us look at the distinguishable sensations that the term dyspnea encompasses and begin to understand how they differ neurologically (see figure 18.2).,True,Forms of Dyspnea,Figure 18.2,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.2.png,Figure 18.2: Types of dyspnea.
ea3e12eb-22fa-46a9-82af-b0541913908b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,So now let us look at the distinguishable sensations that the term dyspnea encompasses and begin to understand how they differ neurologically (see figure 18.2).,True,Forms of Dyspnea,Figure 18.2,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.2.png,Figure 18.2: Types of dyspnea.
ea3e12eb-22fa-46a9-82af-b0541913908b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,So now let us look at the distinguishable sensations that the term dyspnea encompasses and begin to understand how they differ neurologically (see figure 18.2).,True,Forms of Dyspnea,Figure 18.2,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.2.png,Figure 18.2: Types of dyspnea.
bba4bb96-9ce8-4bf4-a6a9-dd9569575f38,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Effort to breathe: The first form of dyspnea is the sensation of work or effort to breathe. The healthy individual is usually unaware of the effort they are putting into breathing until breathing is significantly increased, such as during exercise when ventilation and work of breathing rises. The sensation of the work or effort to breathe is not particularly uncomfortable. If you jogged down the street now you might become more aware of the effort to breathe, but are not disturbed by it.",True,Forms of Dyspnea,,,,
1adbd3da-4bc3-437f-8fa2-e42ead5790b5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,So where does this sensation come from?,False,So where does this sensation come from?,,,,
2b8d03a6-039b-4300-945b-6e50339f4163,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"An increase in motor drive is required to activate more tension or movement in any skeletal muscle, including the respiratory muscles. And like other skeletal muscles, such as limb muscles, we believe that the sensation of effort comes from a perception of that increased motor drive. Sensory information from the activated muscles, in our case the respiratory muscles, is thought to generate the sensation of work.",True,So where does this sensation come from?,,,,
6b8dba32-67db-44c8-adf0-d104563275de,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Getting laboratory subjects to report work and effort separately is very difficult, so for our purposes right now, we are grouping what might be two sensations together as one.",True,So where does this sensation come from?,,,,
2d7c39c9-4a6b-41e1-82fb-335a79c90e98,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Chest tightness: The next form of dyspnea is primarily reported by asthmatic patients during bronchoconstriction. Similar to the sensation of work and effort, tightness was originally thought to arise from the increase in respiratory muscle activity associated with a rise in resistive work of breathing. But in 2002 we showed that “tightness” was unrelated to respiratory effort by removing respiratory muscle activity of bronchoconstricted asthmatics with mechanical ventilation. When we did this, “tightness” persisted, despite the respiratory muscles being inactive. So what does cause tightness? The next best, but so far unproven, alternative is that inflammation of the airways associated with an asthma attack leads to activation of airway irritant (or rapidly adapting) receptors, the afferent activity from which is perceived centrally as tightness.",True,So where does this sensation come from?,,,,
851da94e-ad37-4320-bbe8-bc80ea67cf3a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Air hunger: Air hunger is arguably the most complex and clinically important form. “Air hunger” is the sensation of suffocation and can be described as a “desperate urge to breathe.” You may have experienced this sensation at the end of a prolonged breath-hold, and it is the unpleasantness of air hunger that made you resume breathing. “Air hunger” is a warning signal that ventilation is insufficient and blood gases are becoming deranged; given the immediate importance of maintaining constant blood gases, air hunger is perhaps our most important homeostatic signal, and it has been referred to as the “suffocation alarm.” The mechanisms underlying air hunger are still unclear, but again, they were once thought to involve the respiratory muscle motor and sensory signals and detection of a disparity between them—that is, the brain perceived that the respiratory muscles were not achieving the work they had been commanded to do. This hypothesis was developed in the sixties and still persists in texts today; however, it is wrong. In two separate labs, one at Harvard University and the other in Australia, pulmonary physiologists completely paralyzed each other to remove all motor activity; when they inhaled carbon dioxide, they still felt air hungry, suggesting the respiratory muscle signals were not essential to generate air hunger. So where does air hunger come from?",True,So where does this sensation come from?,,,,
5af7903a-3ead-4d4f-823e-e1b26ce992ba,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"We see air hunger arise when PaCO2 rises, when PaO2 falls, or when arterial pH decreases. These changes are detected by chemoreceptors that reflexly increase the drive to breathe from the brainstem. While we are not usually aware of our reflex breathing drive, we think that once this drive increases to a critical level, a signal is sent upward that is perceived as air hunger.",True,So where does this sensation come from?,,,,
5ecd8638-2ac8-4a92-8c57-21cc41dcc6d5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"So any signals to the brainstem respiratory networks that increase the drive to breathe are likely to promote air hunger, and these influences may not all be chemical (see figure 18.3). For example, emotions such as anxiety increase the drive to breathe, and this is a pertinent point with clinical ramifications that we will return to.",True,So where does this sensation come from?,Figure 18.3,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
5ecd8638-2ac8-4a92-8c57-21cc41dcc6d5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"So any signals to the brainstem respiratory networks that increase the drive to breathe are likely to promote air hunger, and these influences may not all be chemical (see figure 18.3). For example, emotions such as anxiety increase the drive to breathe, and this is a pertinent point with clinical ramifications that we will return to.",True,So where does this sensation come from?,Figure 18.3,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
5ecd8638-2ac8-4a92-8c57-21cc41dcc6d5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"So any signals to the brainstem respiratory networks that increase the drive to breathe are likely to promote air hunger, and these influences may not all be chemical (see figure 18.3). For example, emotions such as anxiety increase the drive to breathe, and this is a pertinent point with clinical ramifications that we will return to.",True,So where does this sensation come from?,Figure 18.3,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
2b6580cc-d652-4ced-8b66-b40aa0fcdbdd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Likewise, any influences that reduce the drive to breathe also have a tendency to reduce air hunger (see figure 18.3). Perhaps the most interesting example of this is the effect of pulmonary stretch receptor activity. Pulmonary stretch receptors are mechanoreceptors in the airways that respond to lung inflation. Although this pulmonary afferent activity is thought to have little effect on the control of breathing in man, it reduces the drive to breathe in other species as part of the Hering–Breuer reflex. What we see in humans is that lung inflation, and presumably an increase in pulmonary stretch receptor firing, profoundly reduces air hunger, even in the absence of any blood gas improvements.",True,So where does this sensation come from?,Figure 18.3,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
2b6580cc-d652-4ced-8b66-b40aa0fcdbdd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Likewise, any influences that reduce the drive to breathe also have a tendency to reduce air hunger (see figure 18.3). Perhaps the most interesting example of this is the effect of pulmonary stretch receptor activity. Pulmonary stretch receptors are mechanoreceptors in the airways that respond to lung inflation. Although this pulmonary afferent activity is thought to have little effect on the control of breathing in man, it reduces the drive to breathe in other species as part of the Hering–Breuer reflex. What we see in humans is that lung inflation, and presumably an increase in pulmonary stretch receptor firing, profoundly reduces air hunger, even in the absence of any blood gas improvements.",True,So where does this sensation come from?,Figure 18.3,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
2b6580cc-d652-4ced-8b66-b40aa0fcdbdd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Likewise, any influences that reduce the drive to breathe also have a tendency to reduce air hunger (see figure 18.3). Perhaps the most interesting example of this is the effect of pulmonary stretch receptor activity. Pulmonary stretch receptors are mechanoreceptors in the airways that respond to lung inflation. Although this pulmonary afferent activity is thought to have little effect on the control of breathing in man, it reduces the drive to breathe in other species as part of the Hering–Breuer reflex. What we see in humans is that lung inflation, and presumably an increase in pulmonary stretch receptor firing, profoundly reduces air hunger, even in the absence of any blood gas improvements.",True,So where does this sensation come from?,Figure 18.3,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.3.png,Figure 18.3: The proposed neural mechanism of air hunger.
7c10a70b-e39b-4e08-ba2e-2f455649cc7e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"This is easy to demonstrate to yourself by holding your breath; during the breath-hold CO2 will gradually accumulate in your bloodstream and you will feel a gradually increasing urge to breathe that will become increasingly more uncomfortable to a point when it is intolerable and you must begin breathing again. That first big breath you take does not return your arterial CO2 to normal, but despite this you get great relief from air hunger by taking it, probably because that big breath stretched the lung and caused a rapid increase of stretch receptor activity to the brainstem.",True,So where does this sensation come from?,,,,
381f6865-cfcb-4a48-8334-67342ffd2e8a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"So air hunger is really affected by a balance of influences: those that increase the drive to breathe (such as hypercapnia and hypoxia) promote air hunger, while inhibitory influences on the drive to breathe tend to promote comfort (see figure 18.4).",True,So where does this sensation come from?,Figure 18.4,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.4.png,Figure 18.4: Balance of pulmonary stretch receptors and chemoreceptor firing.
381f6865-cfcb-4a48-8334-67342ffd2e8a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"So air hunger is really affected by a balance of influences: those that increase the drive to breathe (such as hypercapnia and hypoxia) promote air hunger, while inhibitory influences on the drive to breathe tend to promote comfort (see figure 18.4).",True,So where does this sensation come from?,Figure 18.4,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.4.png,Figure 18.4: Balance of pulmonary stretch receptors and chemoreceptor firing.
381f6865-cfcb-4a48-8334-67342ffd2e8a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"So air hunger is really affected by a balance of influences: those that increase the drive to breathe (such as hypercapnia and hypoxia) promote air hunger, while inhibitory influences on the drive to breathe tend to promote comfort (see figure 18.4).",True,So where does this sensation come from?,Figure 18.4,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.4.png,Figure 18.4: Balance of pulmonary stretch receptors and chemoreceptor firing.
3b8e7363-0a22-4811-a5e8-fb634dd16b81,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,Impact of Dyspnea,False,Impact of Dyspnea,,,,
d94e6e1f-3916-4bca-bda3-b826c491c16f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"There are other elements that should be considered when dealing with the air-hungry patient. Probably because of its homeostatic importance, the sensation of air hunger is very effective at getting attention and producing fear and anxiety. Recent comparisons of attentive and emotional impacts suggest air hunger is perceived as much more threatening and worrisome than pain at equivalent intensities. (Ironically we routinely ask about patients’ pain, but rarely about their air hunger.)",True,Impact of Dyspnea,,,,
29fbdc5f-e0ec-44f9-8577-5c4a41587949,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"This emotional impact of air hunger is reflected in the regions of the brain that are consistently seen to be activated in recent functional brain imaging studies (see figure 18.5). The amygdala, anterior insula, and anterior cingulate are all persistently seen to activate during air hunger, and all are either associated with the brain’s fear network or generation of emotional responses. The activation of the anterior insula is also interesting as this phylogenically old part of the cortex also responds to other homeostatic imbalances, such as thirst, hunger for food, and pain. Although air hunger itself is unpleasant, it is these emotional components that produce air hunger’s profoundly negative effect on patients’ quality of life and makes end-of-life distressing for both the patient and their loved ones. We will come back to the impact of emotional responses in a moment.",True,Impact of Dyspnea,Figure 18.5,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.5.png,Figure 18.5: Central regions associated with air hunger.
29fbdc5f-e0ec-44f9-8577-5c4a41587949,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"This emotional impact of air hunger is reflected in the regions of the brain that are consistently seen to be activated in recent functional brain imaging studies (see figure 18.5). The amygdala, anterior insula, and anterior cingulate are all persistently seen to activate during air hunger, and all are either associated with the brain’s fear network or generation of emotional responses. The activation of the anterior insula is also interesting as this phylogenically old part of the cortex also responds to other homeostatic imbalances, such as thirst, hunger for food, and pain. Although air hunger itself is unpleasant, it is these emotional components that produce air hunger’s profoundly negative effect on patients’ quality of life and makes end-of-life distressing for both the patient and their loved ones. We will come back to the impact of emotional responses in a moment.",True,Impact of Dyspnea,Figure 18.5,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.5.png,Figure 18.5: Central regions associated with air hunger.
29fbdc5f-e0ec-44f9-8577-5c4a41587949,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"This emotional impact of air hunger is reflected in the regions of the brain that are consistently seen to be activated in recent functional brain imaging studies (see figure 18.5). The amygdala, anterior insula, and anterior cingulate are all persistently seen to activate during air hunger, and all are either associated with the brain’s fear network or generation of emotional responses. The activation of the anterior insula is also interesting as this phylogenically old part of the cortex also responds to other homeostatic imbalances, such as thirst, hunger for food, and pain. Although air hunger itself is unpleasant, it is these emotional components that produce air hunger’s profoundly negative effect on patients’ quality of life and makes end-of-life distressing for both the patient and their loved ones. We will come back to the impact of emotional responses in a moment.",True,Impact of Dyspnea,Figure 18.5,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.5.png,Figure 18.5: Central regions associated with air hunger.
1df1c3a7-6c73-4a83-812e-134b38f81fb9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"So there we are—three different forms of dyspnea, with separate neural mechanisms. That said, it is unlikely that a patient will ever walk into your office and tell you they have “dyspnea,” or pinpoint which form of dyspnea they have. But taking an interest in the subtleties of your patients’ comments may not be a purely academic exercise either. More likely they are likely to use descriptors like those shown in table 18.1. These descriptors that use more common, everyday language have been related to each form of dyspnea. Knowing which form or forms of dyspnea the patient is experiencing can help in diagnosis as the different causes of dyspnea (like those listed in figure 18.1) can produce different levels of each form. For example, chest tightness is much more commonly reported by asthmatics, whereas patients with chronic obstructive pulmonary disease tend to use descriptors more related to effort to breathe and air hunger.",True,Impact of Dyspnea,Figure 18.1,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
1df1c3a7-6c73-4a83-812e-134b38f81fb9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"So there we are—three different forms of dyspnea, with separate neural mechanisms. That said, it is unlikely that a patient will ever walk into your office and tell you they have “dyspnea,” or pinpoint which form of dyspnea they have. But taking an interest in the subtleties of your patients’ comments may not be a purely academic exercise either. More likely they are likely to use descriptors like those shown in table 18.1. These descriptors that use more common, everyday language have been related to each form of dyspnea. Knowing which form or forms of dyspnea the patient is experiencing can help in diagnosis as the different causes of dyspnea (like those listed in figure 18.1) can produce different levels of each form. For example, chest tightness is much more commonly reported by asthmatics, whereas patients with chronic obstructive pulmonary disease tend to use descriptors more related to effort to breathe and air hunger.",True,Impact of Dyspnea,Figure 18.1,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
1df1c3a7-6c73-4a83-812e-134b38f81fb9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"So there we are—three different forms of dyspnea, with separate neural mechanisms. That said, it is unlikely that a patient will ever walk into your office and tell you they have “dyspnea,” or pinpoint which form of dyspnea they have. But taking an interest in the subtleties of your patients’ comments may not be a purely academic exercise either. More likely they are likely to use descriptors like those shown in table 18.1. These descriptors that use more common, everyday language have been related to each form of dyspnea. Knowing which form or forms of dyspnea the patient is experiencing can help in diagnosis as the different causes of dyspnea (like those listed in figure 18.1) can produce different levels of each form. For example, chest tightness is much more commonly reported by asthmatics, whereas patients with chronic obstructive pulmonary disease tend to use descriptors more related to effort to breathe and air hunger.",True,Impact of Dyspnea,Figure 18.1,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.1.png,Figure 18.1: Conditions that can produce dyspnea. ARDS: Acute respiratory distress syndrome.
b0d9d34f-36f8-491c-a99e-7aa374d5a228,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,Table 18.1: Patient descriptors for the three different forms of dyspnea.,True,Impact of Dyspnea,,,,
5444abc9-f2a2-49b0-bf46-8d5693ddc377,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"While the different forms of dyspnea have been investigated, described, and now explored as their potential as diagnostic tools, the emotional impact of dyspnea is only now receiving more attention. The most immediate complication caused by the emotional component is the potential for a positive feedback loop to form between air hunger and the anxiety it generates. The anxiety that air hunger produces results in an increased drive to breathe; in turn this increased drive to breathe causes the air hunger to increase, which leads to more anxiety and so on (figure 18.6).",True,Impact of Dyspnea,Figure 18.6,Impact of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.6-new.png,"Figure 18.6: The cycle of anxiety causing an increase in the drive to breathe and air hunger, which in turn causes more anxiety. Psychological disorders can produce air hunger if they involve anxiety."
5444abc9-f2a2-49b0-bf46-8d5693ddc377,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"While the different forms of dyspnea have been investigated, described, and now explored as their potential as diagnostic tools, the emotional impact of dyspnea is only now receiving more attention. The most immediate complication caused by the emotional component is the potential for a positive feedback loop to form between air hunger and the anxiety it generates. The anxiety that air hunger produces results in an increased drive to breathe; in turn this increased drive to breathe causes the air hunger to increase, which leads to more anxiety and so on (figure 18.6).",True,Impact of Dyspnea,Figure 18.6,Occurrence and Forms of Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.6-new.png,"Figure 18.6: The cycle of anxiety causing an increase in the drive to breathe and air hunger, which in turn causes more anxiety. Psychological disorders can produce air hunger if they involve anxiety."
5444abc9-f2a2-49b0-bf46-8d5693ddc377,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"While the different forms of dyspnea have been investigated, described, and now explored as their potential as diagnostic tools, the emotional impact of dyspnea is only now receiving more attention. The most immediate complication caused by the emotional component is the potential for a positive feedback loop to form between air hunger and the anxiety it generates. The anxiety that air hunger produces results in an increased drive to breathe; in turn this increased drive to breathe causes the air hunger to increase, which leads to more anxiety and so on (figure 18.6).",True,Impact of Dyspnea,Figure 18.6,18. Dyspnea,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/18.6-new.png,"Figure 18.6: The cycle of anxiety causing an increase in the drive to breathe and air hunger, which in turn causes more anxiety. Psychological disorders can produce air hunger if they involve anxiety."
3f011ac2-c345-4b74-9e81-bbd88dc74356,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Behavioral effects of dyspnea: This cycle can be entered into by different types of patients; those with cardiopulmonary disease enter the cycle at the point of the air hunger, whereas patients with anxiety disorders can enter the cycle at this point and can experience significant air hunger even with apparently perfectly normal lung and heart function. On a more long-term basis the quality of life of air-hungry patients can be diminished by another positive feedback scenario that can produce “respiratory cripples” of cardiopulmonary patients. The air hunger produced by the underlying disease worsens during exertion, so makes exercising uncomfortable. This frequently results in patients avoiding exercise, perhaps starting with taking an elevator instead of the stairs, or driving to the grocery store when previously they might have walked.",True,Impact of Dyspnea,,,,
90d88064-7d18-4183-be7c-f79196141514,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"This reduction in exercise leads to cardiac deconditioning, which in turn makes the air hunger worse and leads to further avoidance of exercise. Along with the progression of the disease, this cycle may leave the patient out-of-breath while simply sitting in a chair.",True,Impact of Dyspnea,,,,
a14d52eb-4596-4a56-b6b6-47a9a96ccdc1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"The patient’s quality of life becomes severely diminished as their life is ruled by dyspnea that prevents them from leaving the house, interacting with children or grandchildren, and performing simple activities that used to bring enjoyment, such as gardening, wood-working, walking, and more. This reduced quality of life can potentially lead to depression, and the emotional response to dyspnea may be exacerbated.",True,Impact of Dyspnea,,,,
57540af4-a642-4ef6-816c-3dabf9c184ee,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"So what can be done to relieve the patient’s air hunger and the associated anxiety? Well, despite its prevalence, the treatment of dyspnea is decades behind the treatment of pain. For too long the approach to treating dyspnea has been to treat the underlying disease with the expectation that the dyspnea will go away. This is true and a perfect course of action for many conditions, but for many diseases that produce dyspnea we have ineffective cures, such as emphysema, lung cancer, and pulmonary fibrosis. How do we make the 49 percent of terminally ill patients who suffer with dyspnea at the end of life more comfortable?",True,Impact of Dyspnea,,,,
5ea9ed2d-f33f-4768-a4aa-ff1b06c67c8a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Opioids: A common practice is to use opioids, but the mechanism of how they might work and indeed their overall efficacy has been disputed. There are a number of routes for how morphine may act, if it indeed does so. Opioids may have a direct inhibitory effect on the central networks that generate air hunger, or at higher dose concentrations they may reduce air hunger indirectly by causing respiratory depression—that is, they tackle air hunger at what we think to be its source. Alternatively, opioids may reduce the affective or emotional component of dyspnea (i.e., the patient may perceive air hunger, but simply is not as bothered by it). Recent work from Harvard University suggests that morphine has a direct effect on both the sensory and affective components of air hunger independent of its effect on ventilatory drive.",True,Impact of Dyspnea,,,,
cbfc963f-5681-40a4-a555-e7ed8959bef2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Anxiolytics: As the emotional component of air hunger is so strong, the fear and anxiety produced can be treated in the absence of any specific drug to treat the air hunger itself. Use of anxiolytics drugs has also produced mixed results that may be complicated by the patient’s underlying condition, and whether the type of anxiolytic causes ventilatory depression.",True,Impact of Dyspnea,,,,
494e2215-b599-48a8-beb9-9219b29d28b8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Furosemide: Although there is currently no drug that specifically tackles air hunger, there is a growing body of evidence that inhaled furosemide (the loop diuretic) reduces air hunger by sensitizing pulmonary stretch receptors, meaning they fire more for any given lung volume. This amplifies the stretch receptors’ inhibitory effect on air hunger described earlier, by fooling the brain into thinking the lungs are at a greater volume than they really are.",True,Impact of Dyspnea,,,,
e6628cbb-b296-4342-8b23-a8441915f849,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,Nonpharmaceutical alternatives: A nonpharmaceutical alternative is to simply cool the patient’s face with a fan or wet cloth. This facial cooling initiates the “diving reflex” via the trigeminal nerve. One component of the diving reflex is to reduce ventilatory drive at the brainstem—an ideal response if one is heading underwater.,True,Impact of Dyspnea,,,,
7128e63c-682a-479e-be6e-2e24f678b6ae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,This inhibition of ventilatory drive is likely responsible for the moderate reduction in air hunger seen with facial cooling.,True,Impact of Dyspnea,,,,
cb33d6c4-9bf3-4cfe-97b2-aa92e7070b8a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Rehabilitation and desensitization: While dyspnea can be addressed by other methods than those briefly described here, few have been shown to work consistently or effectively. On a more long-term basis, breathing training and pulmonary rehabilitation appear to help patients overcome exacerbations of their disease or even reduce chronic air hunger, but both require patient cooperation and compliance and may have limited effect in severe disease. What can be taken from the literature is that the treatment of dyspnea is in desperate need of more attention. For a symptom that is so common and has such an impact on patients, dyspnea is a clinical issue that is woefully underaddressed.",True,Impact of Dyspnea,,,,
8794f04b-822d-4e01-bcdb-9dce3ae2ceaa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,Text,False,Text,,,,
e9d2bcf4-5588-4d5a-bb7c-edaae5b6e82b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"American Thoracic Society Committee on Dyspnea. “An Official American Thoracic Society Statement: Update on the Mechanisms, Assessment, and Management of Dyspnea.” American Journal of Respiratory and Critical Care Medicine 185, no. 4: 435–52. https://doi.org/10.1164/rccm.201111-2042ST.",True,Text,,,,
a339d70a-4d99-47be-a532-bd44589df203,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,18. Dyspnea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dyspnea/,"Banzett, Robert B., Robert W. Lansing, and Andrew P. Binks. “Air Hunger: A Primal Sensation and a Primary Element of Dyspnea.” Comprehensive Physiology 11, no. 2 (April 2021): 1449–83. https://doi.org/10.1002/cphy.c200001.",True,Text,,,,
1309d9c9-be85-4cc5-904c-48cff097dcee,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,Introduction,False,Introduction,,,,
eaf7bcbf-edca-4466-9a42-b46c6949eff1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,In this chapter we will have a look at the regions of the nervous system that control breathing and how they interact or override each other.,True,Introduction,,,,
0265f0d7-d3b1-473b-999c-5b7194a761da,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,The Role of the Brainstem,False,The Role of the Brainstem,,,,
45109a72-ff09-4e18-a1a0-2ed04fe649a5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"It has long been known that the brainstem contains critical centers for the control of breathing. These regions produce what is often referred to as the reflex drive to breathe, or brainstem drive to breathe. Despite its critical nature for survival, this involuntary motor drive that operates the respiratory muscles is barely understood.",True,The Role of the Brainstem,,,,
595fcd21-2569-4627-86c5-5d68eb0636ed,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,What we will do here is summarize some basic information to create a coherent and accurate overview.,True,The Role of the Brainstem,,,,
e86d1c9f-5259-49bb-b6f4-405933b1bf97,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The reflex drive to breathe is a typical reflex arch, with receptors in the vasculature and lung reporting to a central controller in the brainstem that implements its effects via the respiratory muscles. What is different from most simple reflexes is that the controller is rather complex and can be thought of as a central hub that integrates inputs from multiple sources.",True,The Role of the Brainstem,,,,
d4768435-0fdd-4197-8f2a-aab985042149,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Many visceral sensors supplying the controller in the brainstem send their afferent signals via the glossopharyngeal and vagus nerves to the nucleus tractus solitaries, or NTS. This input station is part of an anatomically indistinct region on the dorsal surface of the medulla, called the dorsal respiratory group or DRG. The DRG connects to motor neurons that lead to the inspiratory muscles.",True,The Role of the Brainstem,,,,
c8c80c23-07e4-421d-aeee-1c419d5441b1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,NTS,False,NTS,,,,
b610698c-7867-40bf-9f03-839655118614,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"These DRG (figure 17.1) neurons show ramp-like bursts of activity that cause inspiratory muscle contraction to induce inspiration, then stop, allowing the inspiratory muscles to relax and passive exhalation to begin. This intermittent ramp of activity can be modulated by input from the sensors or other regions of the central nervous system, but it is not spontaneous; rather this activity is initiated by another respiratory pacemaker. It was this pacemaker that eluded physiologists for decades.",True,NTS,Figure 17.1,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
b610698c-7867-40bf-9f03-839655118614,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"These DRG (figure 17.1) neurons show ramp-like bursts of activity that cause inspiratory muscle contraction to induce inspiration, then stop, allowing the inspiratory muscles to relax and passive exhalation to begin. This intermittent ramp of activity can be modulated by input from the sensors or other regions of the central nervous system, but it is not spontaneous; rather this activity is initiated by another respiratory pacemaker. It was this pacemaker that eluded physiologists for decades.",True,NTS,Figure 17.1,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
b610698c-7867-40bf-9f03-839655118614,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"These DRG (figure 17.1) neurons show ramp-like bursts of activity that cause inspiratory muscle contraction to induce inspiration, then stop, allowing the inspiratory muscles to relax and passive exhalation to begin. This intermittent ramp of activity can be modulated by input from the sensors or other regions of the central nervous system, but it is not spontaneous; rather this activity is initiated by another respiratory pacemaker. It was this pacemaker that eluded physiologists for decades.",True,NTS,Figure 17.1,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
d8b83920-c9e5-4c00-94ef-666420f6e650,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"On the other side of medulla is the ventral respiratory group (figure 17.1), which has been known for a long time to contain circuits that contribute to the control of breathing within its rostral, intermediate, and caudal regions. Within the intermediate region a cluster of neurons called the pre-Bötzinger complex (figure 17.1) with apparently spontaneous activity is currently thought to be the respiratory pacemaker. The pre-bötzinger complex is likely responsible for the activity of the DRG inspiratory neurons to produce the ramping activity.",True,NTS,Figure 17.1,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
d8b83920-c9e5-4c00-94ef-666420f6e650,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"On the other side of medulla is the ventral respiratory group (figure 17.1), which has been known for a long time to contain circuits that contribute to the control of breathing within its rostral, intermediate, and caudal regions. Within the intermediate region a cluster of neurons called the pre-Bötzinger complex (figure 17.1) with apparently spontaneous activity is currently thought to be the respiratory pacemaker. The pre-bötzinger complex is likely responsible for the activity of the DRG inspiratory neurons to produce the ramping activity.",True,NTS,Figure 17.1,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
d8b83920-c9e5-4c00-94ef-666420f6e650,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"On the other side of medulla is the ventral respiratory group (figure 17.1), which has been known for a long time to contain circuits that contribute to the control of breathing within its rostral, intermediate, and caudal regions. Within the intermediate region a cluster of neurons called the pre-Bötzinger complex (figure 17.1) with apparently spontaneous activity is currently thought to be the respiratory pacemaker. The pre-bötzinger complex is likely responsible for the activity of the DRG inspiratory neurons to produce the ramping activity.",True,NTS,Figure 17.1,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
2df7f090-b158-430f-8cd9-56d9c8d73c02,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,Bötzinger,False,Bötzinger,,,,
40061455-d94f-4a55-a8d6-2d476e24a6c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,bötzinger,False,bötzinger,,,,
5964420c-b5bc-46f6-9eda-53aa0a34e0cc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The ventral respiratory group also contains neurons with inspiratory-related activity and connections to the inspiratory motor neurons. It is better known for its expiratory neurons, however, which are capable of activating the expiratory muscles when expiration must become active rather than remain passive. During quiet resting breathing, these expiratory neurons remain dormant.",True,bötzinger,,,,
c90b1cb4-2cce-4fac-aff5-e33efe169340,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,This medullary circuitry can be influenced by other brainstem centers thought to be responsible for fine-tuning the breathing rhythm.,True,bötzinger,,,,
54677cd2-0ea5-437f-a884-bdf43ab1c066,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The Apneustic center in the lower pons (figure 17.1) excites the inspiratory neurons and prolongs the ramp activity they produce; this inevitably produces a prolonged inspiratory period. Higher up in the pons is the Pneumotaxic center (figure 17.1), which acts as an off switch for inspiratory neurons; thus it regulates inspiratory volume and indirectly influences the rate of breathing, tending to increase it. This is a very basic overview of the breathing circuitry that is capable of generating inspiration and active expiration when needed. But these centers take information and direction from other neural influences, including chemoreceptors, receptors in the lung, and higher brain centers. We will look at the latter two now.",True,bötzinger,Figure 17.1,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
54677cd2-0ea5-437f-a884-bdf43ab1c066,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The Apneustic center in the lower pons (figure 17.1) excites the inspiratory neurons and prolongs the ramp activity they produce; this inevitably produces a prolonged inspiratory period. Higher up in the pons is the Pneumotaxic center (figure 17.1), which acts as an off switch for inspiratory neurons; thus it regulates inspiratory volume and indirectly influences the rate of breathing, tending to increase it. This is a very basic overview of the breathing circuitry that is capable of generating inspiration and active expiration when needed. But these centers take information and direction from other neural influences, including chemoreceptors, receptors in the lung, and higher brain centers. We will look at the latter two now.",True,bötzinger,Figure 17.1,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
54677cd2-0ea5-437f-a884-bdf43ab1c066,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The Apneustic center in the lower pons (figure 17.1) excites the inspiratory neurons and prolongs the ramp activity they produce; this inevitably produces a prolonged inspiratory period. Higher up in the pons is the Pneumotaxic center (figure 17.1), which acts as an off switch for inspiratory neurons; thus it regulates inspiratory volume and indirectly influences the rate of breathing, tending to increase it. This is a very basic overview of the breathing circuitry that is capable of generating inspiration and active expiration when needed. But these centers take information and direction from other neural influences, including chemoreceptors, receptors in the lung, and higher brain centers. We will look at the latter two now.",True,bötzinger,Figure 17.1,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
56e1699c-4262-4f47-88a8-530015ad2680,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,Pulmonary and Higher Brain Influences,False,Pulmonary and Higher Brain Influences,,,,
131d0e8e-0e90-43eb-bd29-2da7eadc4a8f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The brainstem drive to breathe can be modulated from above and from below. The literature about whether these influences increase or decrease the drive to breathe is often confused, perhaps because of the wide range of experiments performed and the different species used. We will have a look at some of the most consistent and clinically pertinent aspects here, starting in the lung and three populations of intrapulmonary neural receptors.",True,Pulmonary and Higher Brain Influences,,,,
b9b6f27e-0866-410e-b07c-8c8539553429,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Pulmonary stretch receptors are mechanoreceptors found in airway walls and smooth muscle. As their name suggests, they respond to expansion of the lung, and their afferent activity to the brainstem increases with lung volume, as figure 17.2 shows. Upon arrival at the NTS the PSR activity tends to inhibit inspiratory neurons and can stop inspiratory activity completely in other species (the Hering–Breuer reflex). However, their influence on the control of breathing in humans is weak, and while they might not contribute to the control of breathing in man, they likely influence respiratory sensations, such as shortness of breath.",True,Pulmonary and Higher Brain Influences,Figure 17.2,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.2.png,"Figure 17.2: Lung volume and pulmonary stretch receptor firing. The top tracing represents lung volume with two full inflations followed by a sustained inflation. In response to the increases in lung volume, pulmonary stretch receptors depolarize, producing action potentials, which are shown in the lower trace as upward spikes. The increase in action potentials with increased lung volume is seen as more densely clustered spikes. Note how the sustained inflation causes an initial high frequency of action potentials that gradually falls as the receptor adapts to the high lung volume."
b9b6f27e-0866-410e-b07c-8c8539553429,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Pulmonary stretch receptors are mechanoreceptors found in airway walls and smooth muscle. As their name suggests, they respond to expansion of the lung, and their afferent activity to the brainstem increases with lung volume, as figure 17.2 shows. Upon arrival at the NTS the PSR activity tends to inhibit inspiratory neurons and can stop inspiratory activity completely in other species (the Hering–Breuer reflex). However, their influence on the control of breathing in humans is weak, and while they might not contribute to the control of breathing in man, they likely influence respiratory sensations, such as shortness of breath.",True,Pulmonary and Higher Brain Influences,Figure 17.2,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.2.png,"Figure 17.2: Lung volume and pulmonary stretch receptor firing. The top tracing represents lung volume with two full inflations followed by a sustained inflation. In response to the increases in lung volume, pulmonary stretch receptors depolarize, producing action potentials, which are shown in the lower trace as upward spikes. The increase in action potentials with increased lung volume is seen as more densely clustered spikes. Note how the sustained inflation causes an initial high frequency of action potentials that gradually falls as the receptor adapts to the high lung volume."
b9b6f27e-0866-410e-b07c-8c8539553429,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Pulmonary stretch receptors are mechanoreceptors found in airway walls and smooth muscle. As their name suggests, they respond to expansion of the lung, and their afferent activity to the brainstem increases with lung volume, as figure 17.2 shows. Upon arrival at the NTS the PSR activity tends to inhibit inspiratory neurons and can stop inspiratory activity completely in other species (the Hering–Breuer reflex). However, their influence on the control of breathing in humans is weak, and while they might not contribute to the control of breathing in man, they likely influence respiratory sensations, such as shortness of breath.",True,Pulmonary and Higher Brain Influences,Figure 17.2,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.2.png,"Figure 17.2: Lung volume and pulmonary stretch receptor firing. The top tracing represents lung volume with two full inflations followed by a sustained inflation. In response to the increases in lung volume, pulmonary stretch receptors depolarize, producing action potentials, which are shown in the lower trace as upward spikes. The increase in action potentials with increased lung volume is seen as more densely clustered spikes. Note how the sustained inflation causes an initial high frequency of action potentials that gradually falls as the receptor adapts to the high lung volume."
9a879c60-0390-4150-b2e0-feb665277246,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Irritant receptors are found in the airway epithelium and are ideally placed to perform their role of detecting harmful substances entering the lungs, such as noxious gases, particulates, and even cold air. They generally have an inhibitory influence on the drive to breathe, perhaps as an attempt to limit the amount of noxious substance entering the lung. Other components to their defensive strategies are bronchoconstriction and induction of the cough reflex. Their response to inflammatory mediators also suggests they may play a role in asthma.",True,Pulmonary and Higher Brain Influences,,,,
0d90f985-2aad-4750-9b34-83804b15cdcf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"J-receptors, or Juxtacapillary receptors, are found at the junction of the pulmonary capillaries and alveoli. These receptors respond to increases in interstitial pressure so are likely to play a role in the response to pulmonary edema. Their effect on the drive to breathe can be regarded as excitatory as they cause an increase in breathing rate as part of the J-reflex, which includes cardiac components and is intended to prevent over-exercising and cardiopulmonary collapse. As such the J-receptors may also contribute to generating the sensation of shortness of breath.",True,Pulmonary and Higher Brain Influences,,,,
c259f790-0487-49a7-a758-669eee1efafa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"These three pulmonary receptor groups are the three that usually appear in textbooks, perhaps because of their clinical pertinence, but perhaps because we know most about these. Others exist, and details can be found in other sources. We will now focus briefly on the influence of higher centers on breathing, and these are generally all positive (i.e., cause an increase in breathing). Cortical influences are numerous and undefined, that collectively they produce what is referred to as the wakeful drive to breath. The extent of cortical influence is best illustrated by sleep, when the higher brain is unconscious and any wakeful drive is removed. During sleep breathing is significantly reduced—enough so that arterial PCO2 is several mmHg higher than during wakefulness. This suggests that cortical influences on breathing are enough to cause a lower PaCO2 than would be determined by chemoreflexes alone.",True,Pulmonary and Higher Brain Influences,,,,
13ceda45-b561-4824-94d2-3a4322b069eb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,PaCO2,False,PaCO2,,,,
39d62e67-bec0-4e7e-af31-d09054aac299,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"More specific influences from higher centers include emotions; anger, anxiety, sadness, happiness, and sexual arousal all influence the drive and pattern of breathing. This is perhaps best exemplified by emotionally driven sighs or the frankly bizarre activity of laughter. But the list of higher center influences does not stop there; indeed it is likely that we still yet do not know where it stops. Changes in light changes breathing, a sudden loud sound changes breathing, doing a mathematical problem changes breathing… and so on. And unfortunately for clinicians and pulmonary physiologists, the act of measuring breathing changes breathing. So it is likely that all those textbook numbers for normal respiratory rate and depth are all too high, as telling someone you are going to measure their breathing usually causes them to hyperventilate.",True,PaCO2,,,,
586782ef-9a4f-4ff2-a0f7-601efb0c851d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Breathing is also a rare incidence of being able to voluntarily control a normally reflex activity (e.g., we can willfully override reflex breathing to perform speech or a breath-hold). In fact, we have as precise control over our respiratory muscles as we have control over the muscles in our hands. Humans maybe be exclusive in this respect because of our elaborate speech, but again, this is another unknown. However, eventually reflex breathing will always reclaim its command over breathing—as anyone who has performed a prolonged breath-hold will know.",True,PaCO2,,,,
64fb2def-5dd7-49f9-92ac-bb4abee466d8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,Summary,False,Summary,,,,
c9b06272-d486-4a78-a571-8018c1ba6ce2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"So we have seen that at the heart of the control of breathing there is a pacemaker establishing a basic rhythm and depth of breathing, but this is influenced by numerous other factors from both the lung and higher brain. These influences adjust breathing via the brainstem to produce respiratory responses to the environment and changes in emotional state, and contribute to efficient and appropriate levels of ventilation.",True,Summary,,,,
5792e63a-7f9b-453d-86eb-f45665f949a9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,Chemical Control of Breathing,False,Chemical Control of Breathing,,,,
4b40d226-7425-49f8-b741-e4f66e18c57a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"It perhaps comes as no surprise that the major influence on the reflex drive to breathe comes from the homeostatic need to match ventilation with metabolic demand and maintain blood O2, CO2, and pH within narrow ranges. The chemoreflexes are therefore capable of sensing changes in arterial oxygen, carbon dioxide, and pH, modifying the activity of the brainstem respiratory centers and affecting an appropriate change in alveolar ventilation. These reflexes all act as classical negative feedback circuits and are capable of maintaining despite large changes in O2 consumption and CO2 production by metabolizing tissue.",True,Chemical Control of Breathing,,,,
ec911790-4994-421d-95fb-f8cb2839638c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Before getting into the details of the chemoreceptors, let us take a quick overview of the basic circuitry of the chemoreflexes (figure 17.3). There are two sets of sensors in our circuit: the peripheral chemoreceptors that are in the vasculature, and the central chemoreceptors that are found on the surface of the brainstem. The central chemoreceptors are capable of detecting changes in arterial CO2, while the peripheral chemoreceptors respond to changes in CO2, O2, and arterial pH.",True,Chemical Control of Breathing,Figure 17.3,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.3.png,Figure 17.3: Chemoreflex circuit.
ec911790-4994-421d-95fb-f8cb2839638c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Before getting into the details of the chemoreceptors, let us take a quick overview of the basic circuitry of the chemoreflexes (figure 17.3). There are two sets of sensors in our circuit: the peripheral chemoreceptors that are in the vasculature, and the central chemoreceptors that are found on the surface of the brainstem. The central chemoreceptors are capable of detecting changes in arterial CO2, while the peripheral chemoreceptors respond to changes in CO2, O2, and arterial pH.",True,Chemical Control of Breathing,Figure 17.3,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.3.png,Figure 17.3: Chemoreflex circuit.
ec911790-4994-421d-95fb-f8cb2839638c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Before getting into the details of the chemoreceptors, let us take a quick overview of the basic circuitry of the chemoreflexes (figure 17.3). There are two sets of sensors in our circuit: the peripheral chemoreceptors that are in the vasculature, and the central chemoreceptors that are found on the surface of the brainstem. The central chemoreceptors are capable of detecting changes in arterial CO2, while the peripheral chemoreceptors respond to changes in CO2, O2, and arterial pH.",True,Chemical Control of Breathing,Figure 17.3,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.3.png,Figure 17.3: Chemoreflex circuit.
621a5b3a-b03b-456f-8755-29de9f879f11,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Upon excitation by changes in blood gas values, the receptors fire back to the reflex’s controller, the respiratory centers in the brainstem. This results in an increase in reflex ventilatory drive and a greater motor signal to the respiratory muscles. This produces an increase in alveolar ventilation that corrects the blood gas disturbances and stops the chemoreceptors from firing.",True,Chemical Control of Breathing,,,,
14e4f4f0-e774-4f43-852e-b59d08bff992,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"With that basic circuit in mind, let us now look more closely at the chemoreceptors and the ventilatory responses they can induce.",True,Chemical Control of Breathing,,,,
f62d59a0-948e-4ec5-95a0-70d12d0488e1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,Central Chemoreceptors,False,Central Chemoreceptors,,,,
b7f684d1-4ed5-4149-8ea1-c6198879fb0d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,We will start with the central chemoreceptors. The central chemoreceptors are comprised of chemosensitive neurons on the ventral surface of the medulla found close to the entry points of the glossopharyngeal and vagus nerves (coincidentally these are the nerves bringing in afferent information from the peripheral chemoreceptors and the pulmonary mechanoreceptors).,True,Central Chemoreceptors,,,,
0795dcc1-1692-44cd-a472-fe878343915c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Although the central chemoreceptors do not respond to hypoxemia and only respond to rises in arterial CO2, their activity accounts for about 80 percent of the hypercapnic ventilatory response. Given the critical importance of maintaining a normal PaCO2, these are considered the most important chemoreceptors for minute-by-minute regulation of ventilation. Ironically they do not respond to CO2 directly, but rather to changes in pH of the cerebrospinal fluid (CSF).",True,Central Chemoreceptors,,,,
65c5fe4d-2b9c-4e95-bb01-2949d3470676,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"This complication comes from the fact that the central chemoreceptors are not exposed to the blood, but rather are behind the blood brain barrier and bathed in CSF. Hydrogen ions and bicarbonate cannot pass through the blood brain barrier, but CO2 can. Once through the blood brain barrier, CO2 forms carbonic acid in the reaction that is very familiar to you. It is the hydrogen ion from the dissociated carbonic acid that stimulates the chemoreceptors. So the central chemoreceptors respond to a rise in arterial CO2 via a change in CSF pH. Because there is little protein in the CSF, there is little buffering capability, and pH changes here tend to be greater than in the blood where plasma proteins are plentiful. This makes the central chemoreceptors quite sensitive and partly explains their substantial role in CO2 control.",True,Central Chemoreceptors,,,,
43102078-7420-47e1-ac1f-8ee18dc62425,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Prolonged exposure to high CO2, such as in chronic lung disease, can lead to a rise in CSF bicarbonate. This bicarbonate buffers hydrogen ions and reduces the sensitivity of the central chemoreceptors. This partly explains why the hypercapnic ventilatory response diminishes over time in chronic lung patients, such as those with COPD.",True,Central Chemoreceptors,,,,
22cedeec-024e-491c-b4e1-c830ca1cce30,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,Peripheral Chemoreceptors,False,Peripheral Chemoreceptors,,,,
53bcaa8e-3968-4dd6-af8f-0b7263f68ef2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The peripheral chemoreceptors are directly exposed to arterial blood and are capable of responding to changes in CO2, O2, and pH. There are two populations of chemoreceptive cells in the vasculature (see figure 17.4). One population is found in the aortic arch and is referred to as the aortic bodies. These are wired into the brainstem through afferent fibers that project to and join the vagus nerve. The other chemoreceptor is comprised of the carotid bodies, found in the bifurcation of the common carotid arteries. These connect to the brainstem through the carotid sinus and the glossopharyngeal nerves. The carotid bodies are by far the most important in humans, with the aortic bodies contributing very little to any ventilatory response.",True,Peripheral Chemoreceptors,Figure 17.4,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.4.png,Figure 17.4: Peripheral chemoreceptors.
53bcaa8e-3968-4dd6-af8f-0b7263f68ef2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The peripheral chemoreceptors are directly exposed to arterial blood and are capable of responding to changes in CO2, O2, and pH. There are two populations of chemoreceptive cells in the vasculature (see figure 17.4). One population is found in the aortic arch and is referred to as the aortic bodies. These are wired into the brainstem through afferent fibers that project to and join the vagus nerve. The other chemoreceptor is comprised of the carotid bodies, found in the bifurcation of the common carotid arteries. These connect to the brainstem through the carotid sinus and the glossopharyngeal nerves. The carotid bodies are by far the most important in humans, with the aortic bodies contributing very little to any ventilatory response.",True,Peripheral Chemoreceptors,Figure 17.4,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.4.png,Figure 17.4: Peripheral chemoreceptors.
53bcaa8e-3968-4dd6-af8f-0b7263f68ef2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The peripheral chemoreceptors are directly exposed to arterial blood and are capable of responding to changes in CO2, O2, and pH. There are two populations of chemoreceptive cells in the vasculature (see figure 17.4). One population is found in the aortic arch and is referred to as the aortic bodies. These are wired into the brainstem through afferent fibers that project to and join the vagus nerve. The other chemoreceptor is comprised of the carotid bodies, found in the bifurcation of the common carotid arteries. These connect to the brainstem through the carotid sinus and the glossopharyngeal nerves. The carotid bodies are by far the most important in humans, with the aortic bodies contributing very little to any ventilatory response.",True,Peripheral Chemoreceptors,Figure 17.4,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.4.png,Figure 17.4: Peripheral chemoreceptors.
105e0bd6-ef24-40ab-8c61-0cb33135cca7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Although the carotid bodies play little role in reflex response to CO2, their response to hypercapnia is more rapid than the central chemoreceptors and so they are capable of breath-by-breath regulation and responding to abrupt changes in arterial PCO2. More importantly the peripheral chemoreceptors are entirely responsible for the response to hypoxia. The mechanism as to how these receptors work is unclear, but cells within the carotid bodies have very high metabolic rates and receive a proportionately high blood flow. It is likely that a decline in oxygen interrupts their metabolism and reduces their inhibitory interaction on neurotransmitter-filled neighboring cells, allowing excitation of the carotid sinus nerve. Their response to a decline in blood oxygen is far from linear. A decline in PO2 below 100 mmHg causes little change in action potential firing, but the rate of firing rapidly increases at PO2s below 50. This is reflected in the hypoxic ventilatory response illustrated in the graph in figure 17.5.",True,Peripheral Chemoreceptors,Figure 17.5,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.5.png,"Figure 17.5: Hypoxic ventilatory response. BTPS: body temperature and pressure, saturated."
105e0bd6-ef24-40ab-8c61-0cb33135cca7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Although the carotid bodies play little role in reflex response to CO2, their response to hypercapnia is more rapid than the central chemoreceptors and so they are capable of breath-by-breath regulation and responding to abrupt changes in arterial PCO2. More importantly the peripheral chemoreceptors are entirely responsible for the response to hypoxia. The mechanism as to how these receptors work is unclear, but cells within the carotid bodies have very high metabolic rates and receive a proportionately high blood flow. It is likely that a decline in oxygen interrupts their metabolism and reduces their inhibitory interaction on neurotransmitter-filled neighboring cells, allowing excitation of the carotid sinus nerve. Their response to a decline in blood oxygen is far from linear. A decline in PO2 below 100 mmHg causes little change in action potential firing, but the rate of firing rapidly increases at PO2s below 50. This is reflected in the hypoxic ventilatory response illustrated in the graph in figure 17.5.",True,Peripheral Chemoreceptors,Figure 17.5,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.5.png,"Figure 17.5: Hypoxic ventilatory response. BTPS: body temperature and pressure, saturated."
105e0bd6-ef24-40ab-8c61-0cb33135cca7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Although the carotid bodies play little role in reflex response to CO2, their response to hypercapnia is more rapid than the central chemoreceptors and so they are capable of breath-by-breath regulation and responding to abrupt changes in arterial PCO2. More importantly the peripheral chemoreceptors are entirely responsible for the response to hypoxia. The mechanism as to how these receptors work is unclear, but cells within the carotid bodies have very high metabolic rates and receive a proportionately high blood flow. It is likely that a decline in oxygen interrupts their metabolism and reduces their inhibitory interaction on neurotransmitter-filled neighboring cells, allowing excitation of the carotid sinus nerve. Their response to a decline in blood oxygen is far from linear. A decline in PO2 below 100 mmHg causes little change in action potential firing, but the rate of firing rapidly increases at PO2s below 50. This is reflected in the hypoxic ventilatory response illustrated in the graph in figure 17.5.",True,Peripheral Chemoreceptors,Figure 17.5,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.5.png,"Figure 17.5: Hypoxic ventilatory response. BTPS: body temperature and pressure, saturated."
7d454584-4e63-4a14-bc6f-e71196169e7b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Because of this, the hypoxic ventilatory response normally plays little role in the control of breathing in humans. The hypoxic ventilatory response becomes more significant at altitude when inspired PO2 is low, or more pertinently in lung disease, where alveolar ventilation or gas exchange is compromised.",True,Peripheral Chemoreceptors,,,,
439b2a3b-9500-414a-aa44-02adc653c5fd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The hypercapnic ventilatory response (figure 17.6) is much more influential on breathing in humans on a normal day-to-day basis. The response is very linear, with a rise in PCO2 producing a proportionate rise in ventilation, driven of course primarily by the central chemoreceptors, but also contributed to by the afferent activity of the peripheral receptors.",True,Peripheral Chemoreceptors,Figure 17.6,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.6.png,Figure 17.6: Hypercapnic ventilatory response.
439b2a3b-9500-414a-aa44-02adc653c5fd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The hypercapnic ventilatory response (figure 17.6) is much more influential on breathing in humans on a normal day-to-day basis. The response is very linear, with a rise in PCO2 producing a proportionate rise in ventilation, driven of course primarily by the central chemoreceptors, but also contributed to by the afferent activity of the peripheral receptors.",True,Peripheral Chemoreceptors,Figure 17.6,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.6.png,Figure 17.6: Hypercapnic ventilatory response.
439b2a3b-9500-414a-aa44-02adc653c5fd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The hypercapnic ventilatory response (figure 17.6) is much more influential on breathing in humans on a normal day-to-day basis. The response is very linear, with a rise in PCO2 producing a proportionate rise in ventilation, driven of course primarily by the central chemoreceptors, but also contributed to by the afferent activity of the peripheral receptors.",True,Peripheral Chemoreceptors,Figure 17.6,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.6.png,Figure 17.6: Hypercapnic ventilatory response.
b4e8594d-4342-429e-a1d3-29deb926f070,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The central and peripheral chemoreceptors keep arterial PCO2 within very fine limits, primarily because of CO2‘s effect on pH. Alveolar ventilation rapidly increases with even a moderate rise in arterial CO2, but can completely stop (apnea) if arterial CO2 falls below normal (~40 mmHg). The wakeful drive to breathe tends to keep CO2 a little lower than the set-point of the chemoreceptors—a point illustrated during sleep, when the brainstem has complete control of breathing and PaCO2 is seen to rise a few mmHg.",True,Peripheral Chemoreceptors,,,,
64b429be-4d21-4cce-b4be-01fbc2ba73c4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The hypercapnic ventilatory response adapts to chronically elevated arterial CO2, such as in severe lung disease. Here we not only see the CSF increase its buffering capacity with increased bicarbonate, but we also see the chemoreceptors change their set-point. It is not uncommon to see COPD patients with arterial PCO2s above 60.",True,Peripheral Chemoreceptors,,,,
a7b008bd-dbb5-41e3-9c1e-334d7f944f71,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Finally, the hypoxic and hypercapnic ventilatory responses are not independent, and when they are both present at the same time a potentiation is seen (i.e., the response to hypoxic and hypercapnia is greater than the sum of the two individual responses).",True,Peripheral Chemoreceptors,,,,
f5c85927-3e75-41d5-a3dc-748f9aab2b25,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The hypoxic ventilatory response we have just looked at was measured at an alveolar PCO2 of 35.8 mmHg. If the same test is performed at higher PCO2s (figure 17.7), then the hypoxic ventilatory response is much greater, as shown by these upwardly shifted lines when alveolar PCO2 is set to 43.7 mmHg and 48.7 mmHg.",True,Peripheral Chemoreceptors,Figure 17.7,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.7-1.png,Figure 17.7: Hypoxic ventilatory responses with varying degrees of hypercapnia.
f5c85927-3e75-41d5-a3dc-748f9aab2b25,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The hypoxic ventilatory response we have just looked at was measured at an alveolar PCO2 of 35.8 mmHg. If the same test is performed at higher PCO2s (figure 17.7), then the hypoxic ventilatory response is much greater, as shown by these upwardly shifted lines when alveolar PCO2 is set to 43.7 mmHg and 48.7 mmHg.",True,Peripheral Chemoreceptors,Figure 17.7,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.7-1.png,Figure 17.7: Hypoxic ventilatory responses with varying degrees of hypercapnia.
f5c85927-3e75-41d5-a3dc-748f9aab2b25,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The hypoxic ventilatory response we have just looked at was measured at an alveolar PCO2 of 35.8 mmHg. If the same test is performed at higher PCO2s (figure 17.7), then the hypoxic ventilatory response is much greater, as shown by these upwardly shifted lines when alveolar PCO2 is set to 43.7 mmHg and 48.7 mmHg.",True,Peripheral Chemoreceptors,Figure 17.7,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.7-1.png,Figure 17.7: Hypoxic ventilatory responses with varying degrees of hypercapnia.
4b57208b-e130-430c-bd66-a47e7bc49def,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Likewise, the hypercapnic ventilatory response is exaggerated in the presence of hypoxia (see figure 17.8). The hypercapnic ventilatory response we have just looked at was measured at a “normal” alveolar PO2 of 110 mmHg. If the hypercapnic response is measured in the presence of hypoxia, then the curve shifts upward, as shown by the upper lines when alveolar PO2 is reduced to 47 mmHg and 37 mmHg. This potentiation likely comes from the peripheral chemoreceptors, whose firing rate is potentiated in the presence of both stimuli. Consequently, when a patient is both hypoxic and hypercapnic, then they are likely to have a very high drive to breathe, and when this occurs they are likely to feel very short of breath—the topic of the last chapter.",True,Peripheral Chemoreceptors,Figure 17.8,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.8.png,Figure 17.8: Hypercapnic ventilatory responses with varying degrees of hypoxia.
4b57208b-e130-430c-bd66-a47e7bc49def,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Likewise, the hypercapnic ventilatory response is exaggerated in the presence of hypoxia (see figure 17.8). The hypercapnic ventilatory response we have just looked at was measured at a “normal” alveolar PO2 of 110 mmHg. If the hypercapnic response is measured in the presence of hypoxia, then the curve shifts upward, as shown by the upper lines when alveolar PO2 is reduced to 47 mmHg and 37 mmHg. This potentiation likely comes from the peripheral chemoreceptors, whose firing rate is potentiated in the presence of both stimuli. Consequently, when a patient is both hypoxic and hypercapnic, then they are likely to have a very high drive to breathe, and when this occurs they are likely to feel very short of breath—the topic of the last chapter.",True,Peripheral Chemoreceptors,Figure 17.8,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.8.png,Figure 17.8: Hypercapnic ventilatory responses with varying degrees of hypoxia.
4b57208b-e130-430c-bd66-a47e7bc49def,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Likewise, the hypercapnic ventilatory response is exaggerated in the presence of hypoxia (see figure 17.8). The hypercapnic ventilatory response we have just looked at was measured at a “normal” alveolar PO2 of 110 mmHg. If the hypercapnic response is measured in the presence of hypoxia, then the curve shifts upward, as shown by the upper lines when alveolar PO2 is reduced to 47 mmHg and 37 mmHg. This potentiation likely comes from the peripheral chemoreceptors, whose firing rate is potentiated in the presence of both stimuli. Consequently, when a patient is both hypoxic and hypercapnic, then they are likely to have a very high drive to breathe, and when this occurs they are likely to feel very short of breath—the topic of the last chapter.",True,Peripheral Chemoreceptors,Figure 17.8,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.8.png,Figure 17.8: Hypercapnic ventilatory responses with varying degrees of hypoxia.
d1eb2ee4-c45e-4b70-bebb-601f16788991,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"The chemoreflexes modulate breathing to maintain constant arterial blood gases and pH. These reflexes are initiated by central sensors that respond to hypoxia and peripheral sensors that respond to hypercapnia, hypoxia, and changes in arterial pH. Together these sensors can maintain arterial blood gases within narrow ranges despite large changes in oxygen consumption and CO2 production associated with changes in metabolic rate.",True,Peripheral Chemoreceptors,,,,
281430cb-1129-4654-acf6-973a05c82828,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,Text,False,Text,,,,
114c8441-5da7-4816-9a98-ebe7006695e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Levitsky, Michael G. “Chapter 9: Control of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
73bce2fb-98ad-41f3-8101-4bf9af7e048d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"West, John B. “Chapter 8: Control of Ventilation—How Gas Exchange Is Regulated.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
b8d4a9c3-0d94-4647-88e2-309c65d3b974,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-2,"Widdicombe, John G., and Andrew S. Davis. “Chapter 8” and “Chapter 9.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
42db5006-363c-4d78-9181-4fa147fbff7b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,Introduction,False,Introduction,,,,
0008886d-cbca-4769-ba8a-c687af9088d5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,In this chapter we will have a look at the regions of the nervous system that control breathing and how they interact or override each other.,True,Introduction,,,,
e0e7d56d-00d1-4645-9e3e-9a97ec8d4c66,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,The Role of the Brainstem,False,The Role of the Brainstem,,,,
0d5c16db-1928-4b05-a1fc-97b1dfb63d26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"It has long been known that the brainstem contains critical centers for the control of breathing. These regions produce what is often referred to as the reflex drive to breathe, or brainstem drive to breathe. Despite its critical nature for survival, this involuntary motor drive that operates the respiratory muscles is barely understood.",True,The Role of the Brainstem,,,,
76217236-2506-4820-be05-839091a8969d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,What we will do here is summarize some basic information to create a coherent and accurate overview.,True,The Role of the Brainstem,,,,
38e6aba5-d078-46af-aa1c-d76540cf0250,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The reflex drive to breathe is a typical reflex arch, with receptors in the vasculature and lung reporting to a central controller in the brainstem that implements its effects via the respiratory muscles. What is different from most simple reflexes is that the controller is rather complex and can be thought of as a central hub that integrates inputs from multiple sources.",True,The Role of the Brainstem,,,,
37be5b07-f34d-4f81-948d-689db28559f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Many visceral sensors supplying the controller in the brainstem send their afferent signals via the glossopharyngeal and vagus nerves to the nucleus tractus solitaries, or NTS. This input station is part of an anatomically indistinct region on the dorsal surface of the medulla, called the dorsal respiratory group or DRG. The DRG connects to motor neurons that lead to the inspiratory muscles.",True,The Role of the Brainstem,,,,
1b37cf61-81f3-4562-9e15-d05eec26a611,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,NTS,False,NTS,,,,
6899fdee-8cd0-44c6-a512-15f0e858278f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"These DRG (figure 17.1) neurons show ramp-like bursts of activity that cause inspiratory muscle contraction to induce inspiration, then stop, allowing the inspiratory muscles to relax and passive exhalation to begin. This intermittent ramp of activity can be modulated by input from the sensors or other regions of the central nervous system, but it is not spontaneous; rather this activity is initiated by another respiratory pacemaker. It was this pacemaker that eluded physiologists for decades.",True,NTS,Figure 17.1,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
6899fdee-8cd0-44c6-a512-15f0e858278f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"These DRG (figure 17.1) neurons show ramp-like bursts of activity that cause inspiratory muscle contraction to induce inspiration, then stop, allowing the inspiratory muscles to relax and passive exhalation to begin. This intermittent ramp of activity can be modulated by input from the sensors or other regions of the central nervous system, but it is not spontaneous; rather this activity is initiated by another respiratory pacemaker. It was this pacemaker that eluded physiologists for decades.",True,NTS,Figure 17.1,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
6899fdee-8cd0-44c6-a512-15f0e858278f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"These DRG (figure 17.1) neurons show ramp-like bursts of activity that cause inspiratory muscle contraction to induce inspiration, then stop, allowing the inspiratory muscles to relax and passive exhalation to begin. This intermittent ramp of activity can be modulated by input from the sensors or other regions of the central nervous system, but it is not spontaneous; rather this activity is initiated by another respiratory pacemaker. It was this pacemaker that eluded physiologists for decades.",True,NTS,Figure 17.1,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
4cfdf8e8-5d5f-434d-b7a3-a05933436843,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"On the other side of medulla is the ventral respiratory group (figure 17.1), which has been known for a long time to contain circuits that contribute to the control of breathing within its rostral, intermediate, and caudal regions. Within the intermediate region a cluster of neurons called the pre-Bötzinger complex (figure 17.1) with apparently spontaneous activity is currently thought to be the respiratory pacemaker. The pre-bötzinger complex is likely responsible for the activity of the DRG inspiratory neurons to produce the ramping activity.",True,NTS,Figure 17.1,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
4cfdf8e8-5d5f-434d-b7a3-a05933436843,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"On the other side of medulla is the ventral respiratory group (figure 17.1), which has been known for a long time to contain circuits that contribute to the control of breathing within its rostral, intermediate, and caudal regions. Within the intermediate region a cluster of neurons called the pre-Bötzinger complex (figure 17.1) with apparently spontaneous activity is currently thought to be the respiratory pacemaker. The pre-bötzinger complex is likely responsible for the activity of the DRG inspiratory neurons to produce the ramping activity.",True,NTS,Figure 17.1,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
4cfdf8e8-5d5f-434d-b7a3-a05933436843,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"On the other side of medulla is the ventral respiratory group (figure 17.1), which has been known for a long time to contain circuits that contribute to the control of breathing within its rostral, intermediate, and caudal regions. Within the intermediate region a cluster of neurons called the pre-Bötzinger complex (figure 17.1) with apparently spontaneous activity is currently thought to be the respiratory pacemaker. The pre-bötzinger complex is likely responsible for the activity of the DRG inspiratory neurons to produce the ramping activity.",True,NTS,Figure 17.1,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
1430fe42-605a-435a-82f5-19900fe7abe1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,Bötzinger,False,Bötzinger,,,,
11cd3cb9-677a-413c-9196-57d0f4def86f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,bötzinger,False,bötzinger,,,,
1db4dd50-408d-4769-aaea-e5e0b509291e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The ventral respiratory group also contains neurons with inspiratory-related activity and connections to the inspiratory motor neurons. It is better known for its expiratory neurons, however, which are capable of activating the expiratory muscles when expiration must become active rather than remain passive. During quiet resting breathing, these expiratory neurons remain dormant.",True,bötzinger,,,,
00e2789e-fe1c-4546-b1e7-ba99e78856ee,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,This medullary circuitry can be influenced by other brainstem centers thought to be responsible for fine-tuning the breathing rhythm.,True,bötzinger,,,,
2795cbfb-0fa9-469b-86d3-c154181ee6c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The Apneustic center in the lower pons (figure 17.1) excites the inspiratory neurons and prolongs the ramp activity they produce; this inevitably produces a prolonged inspiratory period. Higher up in the pons is the Pneumotaxic center (figure 17.1), which acts as an off switch for inspiratory neurons; thus it regulates inspiratory volume and indirectly influences the rate of breathing, tending to increase it. This is a very basic overview of the breathing circuitry that is capable of generating inspiration and active expiration when needed. But these centers take information and direction from other neural influences, including chemoreceptors, receptors in the lung, and higher brain centers. We will look at the latter two now.",True,bötzinger,Figure 17.1,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
2795cbfb-0fa9-469b-86d3-c154181ee6c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The Apneustic center in the lower pons (figure 17.1) excites the inspiratory neurons and prolongs the ramp activity they produce; this inevitably produces a prolonged inspiratory period. Higher up in the pons is the Pneumotaxic center (figure 17.1), which acts as an off switch for inspiratory neurons; thus it regulates inspiratory volume and indirectly influences the rate of breathing, tending to increase it. This is a very basic overview of the breathing circuitry that is capable of generating inspiration and active expiration when needed. But these centers take information and direction from other neural influences, including chemoreceptors, receptors in the lung, and higher brain centers. We will look at the latter two now.",True,bötzinger,Figure 17.1,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
2795cbfb-0fa9-469b-86d3-c154181ee6c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The Apneustic center in the lower pons (figure 17.1) excites the inspiratory neurons and prolongs the ramp activity they produce; this inevitably produces a prolonged inspiratory period. Higher up in the pons is the Pneumotaxic center (figure 17.1), which acts as an off switch for inspiratory neurons; thus it regulates inspiratory volume and indirectly influences the rate of breathing, tending to increase it. This is a very basic overview of the breathing circuitry that is capable of generating inspiration and active expiration when needed. But these centers take information and direction from other neural influences, including chemoreceptors, receptors in the lung, and higher brain centers. We will look at the latter two now.",True,bötzinger,Figure 17.1,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
1b2b1f0b-327d-4917-b539-58c1a30db7ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,Pulmonary and Higher Brain Influences,False,Pulmonary and Higher Brain Influences,,,,
91c5c329-d2c8-4276-98e2-4fa3e13aadc5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The brainstem drive to breathe can be modulated from above and from below. The literature about whether these influences increase or decrease the drive to breathe is often confused, perhaps because of the wide range of experiments performed and the different species used. We will have a look at some of the most consistent and clinically pertinent aspects here, starting in the lung and three populations of intrapulmonary neural receptors.",True,Pulmonary and Higher Brain Influences,,,,
904cb9d0-01c2-459f-b08a-c116960c5864,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Pulmonary stretch receptors are mechanoreceptors found in airway walls and smooth muscle. As their name suggests, they respond to expansion of the lung, and their afferent activity to the brainstem increases with lung volume, as figure 17.2 shows. Upon arrival at the NTS the PSR activity tends to inhibit inspiratory neurons and can stop inspiratory activity completely in other species (the Hering–Breuer reflex). However, their influence on the control of breathing in humans is weak, and while they might not contribute to the control of breathing in man, they likely influence respiratory sensations, such as shortness of breath.",True,Pulmonary and Higher Brain Influences,Figure 17.2,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.2.png,"Figure 17.2: Lung volume and pulmonary stretch receptor firing. The top tracing represents lung volume with two full inflations followed by a sustained inflation. In response to the increases in lung volume, pulmonary stretch receptors depolarize, producing action potentials, which are shown in the lower trace as upward spikes. The increase in action potentials with increased lung volume is seen as more densely clustered spikes. Note how the sustained inflation causes an initial high frequency of action potentials that gradually falls as the receptor adapts to the high lung volume."
904cb9d0-01c2-459f-b08a-c116960c5864,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Pulmonary stretch receptors are mechanoreceptors found in airway walls and smooth muscle. As their name suggests, they respond to expansion of the lung, and their afferent activity to the brainstem increases with lung volume, as figure 17.2 shows. Upon arrival at the NTS the PSR activity tends to inhibit inspiratory neurons and can stop inspiratory activity completely in other species (the Hering–Breuer reflex). However, their influence on the control of breathing in humans is weak, and while they might not contribute to the control of breathing in man, they likely influence respiratory sensations, such as shortness of breath.",True,Pulmonary and Higher Brain Influences,Figure 17.2,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.2.png,"Figure 17.2: Lung volume and pulmonary stretch receptor firing. The top tracing represents lung volume with two full inflations followed by a sustained inflation. In response to the increases in lung volume, pulmonary stretch receptors depolarize, producing action potentials, which are shown in the lower trace as upward spikes. The increase in action potentials with increased lung volume is seen as more densely clustered spikes. Note how the sustained inflation causes an initial high frequency of action potentials that gradually falls as the receptor adapts to the high lung volume."
904cb9d0-01c2-459f-b08a-c116960c5864,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Pulmonary stretch receptors are mechanoreceptors found in airway walls and smooth muscle. As their name suggests, they respond to expansion of the lung, and their afferent activity to the brainstem increases with lung volume, as figure 17.2 shows. Upon arrival at the NTS the PSR activity tends to inhibit inspiratory neurons and can stop inspiratory activity completely in other species (the Hering–Breuer reflex). However, their influence on the control of breathing in humans is weak, and while they might not contribute to the control of breathing in man, they likely influence respiratory sensations, such as shortness of breath.",True,Pulmonary and Higher Brain Influences,Figure 17.2,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.2.png,"Figure 17.2: Lung volume and pulmonary stretch receptor firing. The top tracing represents lung volume with two full inflations followed by a sustained inflation. In response to the increases in lung volume, pulmonary stretch receptors depolarize, producing action potentials, which are shown in the lower trace as upward spikes. The increase in action potentials with increased lung volume is seen as more densely clustered spikes. Note how the sustained inflation causes an initial high frequency of action potentials that gradually falls as the receptor adapts to the high lung volume."
64ea5187-67c1-450d-8859-aa6f995d2c99,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Irritant receptors are found in the airway epithelium and are ideally placed to perform their role of detecting harmful substances entering the lungs, such as noxious gases, particulates, and even cold air. They generally have an inhibitory influence on the drive to breathe, perhaps as an attempt to limit the amount of noxious substance entering the lung. Other components to their defensive strategies are bronchoconstriction and induction of the cough reflex. Their response to inflammatory mediators also suggests they may play a role in asthma.",True,Pulmonary and Higher Brain Influences,,,,
454f260d-1bcc-4656-b40d-9a9dbda2e39e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"J-receptors, or Juxtacapillary receptors, are found at the junction of the pulmonary capillaries and alveoli. These receptors respond to increases in interstitial pressure so are likely to play a role in the response to pulmonary edema. Their effect on the drive to breathe can be regarded as excitatory as they cause an increase in breathing rate as part of the J-reflex, which includes cardiac components and is intended to prevent over-exercising and cardiopulmonary collapse. As such the J-receptors may also contribute to generating the sensation of shortness of breath.",True,Pulmonary and Higher Brain Influences,,,,
a9050777-dc29-4c19-bba7-b71bc0702dbe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"These three pulmonary receptor groups are the three that usually appear in textbooks, perhaps because of their clinical pertinence, but perhaps because we know most about these. Others exist, and details can be found in other sources. We will now focus briefly on the influence of higher centers on breathing, and these are generally all positive (i.e., cause an increase in breathing). Cortical influences are numerous and undefined, that collectively they produce what is referred to as the wakeful drive to breath. The extent of cortical influence is best illustrated by sleep, when the higher brain is unconscious and any wakeful drive is removed. During sleep breathing is significantly reduced—enough so that arterial PCO2 is several mmHg higher than during wakefulness. This suggests that cortical influences on breathing are enough to cause a lower PaCO2 than would be determined by chemoreflexes alone.",True,Pulmonary and Higher Brain Influences,,,,
1f73d323-1e66-4800-988f-1851d545855f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,PaCO2,False,PaCO2,,,,
522f625f-5f55-432c-a390-3a93aba5bf70,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"More specific influences from higher centers include emotions; anger, anxiety, sadness, happiness, and sexual arousal all influence the drive and pattern of breathing. This is perhaps best exemplified by emotionally driven sighs or the frankly bizarre activity of laughter. But the list of higher center influences does not stop there; indeed it is likely that we still yet do not know where it stops. Changes in light changes breathing, a sudden loud sound changes breathing, doing a mathematical problem changes breathing… and so on. And unfortunately for clinicians and pulmonary physiologists, the act of measuring breathing changes breathing. So it is likely that all those textbook numbers for normal respiratory rate and depth are all too high, as telling someone you are going to measure their breathing usually causes them to hyperventilate.",True,PaCO2,,,,
8028f2c4-0652-4702-83b0-ba9abb7f81eb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Breathing is also a rare incidence of being able to voluntarily control a normally reflex activity (e.g., we can willfully override reflex breathing to perform speech or a breath-hold). In fact, we have as precise control over our respiratory muscles as we have control over the muscles in our hands. Humans maybe be exclusive in this respect because of our elaborate speech, but again, this is another unknown. However, eventually reflex breathing will always reclaim its command over breathing—as anyone who has performed a prolonged breath-hold will know.",True,PaCO2,,,,
31138ea0-a188-4c5b-82dd-9c9fec88e0c3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,Summary,False,Summary,,,,
0a8269f3-b7cb-428b-ae68-4b8dd62012b1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"So we have seen that at the heart of the control of breathing there is a pacemaker establishing a basic rhythm and depth of breathing, but this is influenced by numerous other factors from both the lung and higher brain. These influences adjust breathing via the brainstem to produce respiratory responses to the environment and changes in emotional state, and contribute to efficient and appropriate levels of ventilation.",True,Summary,,,,
d3369978-01b1-4f72-b1dc-65095725d7b5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,Chemical Control of Breathing,False,Chemical Control of Breathing,,,,
027941f3-8f3d-4043-828f-4808018c74d4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"It perhaps comes as no surprise that the major influence on the reflex drive to breathe comes from the homeostatic need to match ventilation with metabolic demand and maintain blood O2, CO2, and pH within narrow ranges. The chemoreflexes are therefore capable of sensing changes in arterial oxygen, carbon dioxide, and pH, modifying the activity of the brainstem respiratory centers and affecting an appropriate change in alveolar ventilation. These reflexes all act as classical negative feedback circuits and are capable of maintaining despite large changes in O2 consumption and CO2 production by metabolizing tissue.",True,Chemical Control of Breathing,,,,
4600494d-efb5-49eb-9d2d-fcbc8e45d0b7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Before getting into the details of the chemoreceptors, let us take a quick overview of the basic circuitry of the chemoreflexes (figure 17.3). There are two sets of sensors in our circuit: the peripheral chemoreceptors that are in the vasculature, and the central chemoreceptors that are found on the surface of the brainstem. The central chemoreceptors are capable of detecting changes in arterial CO2, while the peripheral chemoreceptors respond to changes in CO2, O2, and arterial pH.",True,Chemical Control of Breathing,Figure 17.3,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.3.png,Figure 17.3: Chemoreflex circuit.
4600494d-efb5-49eb-9d2d-fcbc8e45d0b7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Before getting into the details of the chemoreceptors, let us take a quick overview of the basic circuitry of the chemoreflexes (figure 17.3). There are two sets of sensors in our circuit: the peripheral chemoreceptors that are in the vasculature, and the central chemoreceptors that are found on the surface of the brainstem. The central chemoreceptors are capable of detecting changes in arterial CO2, while the peripheral chemoreceptors respond to changes in CO2, O2, and arterial pH.",True,Chemical Control of Breathing,Figure 17.3,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.3.png,Figure 17.3: Chemoreflex circuit.
4600494d-efb5-49eb-9d2d-fcbc8e45d0b7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Before getting into the details of the chemoreceptors, let us take a quick overview of the basic circuitry of the chemoreflexes (figure 17.3). There are two sets of sensors in our circuit: the peripheral chemoreceptors that are in the vasculature, and the central chemoreceptors that are found on the surface of the brainstem. The central chemoreceptors are capable of detecting changes in arterial CO2, while the peripheral chemoreceptors respond to changes in CO2, O2, and arterial pH.",True,Chemical Control of Breathing,Figure 17.3,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.3.png,Figure 17.3: Chemoreflex circuit.
0c355a5c-04d9-418b-8a24-38db9b7e5d43,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Upon excitation by changes in blood gas values, the receptors fire back to the reflex’s controller, the respiratory centers in the brainstem. This results in an increase in reflex ventilatory drive and a greater motor signal to the respiratory muscles. This produces an increase in alveolar ventilation that corrects the blood gas disturbances and stops the chemoreceptors from firing.",True,Chemical Control of Breathing,,,,
fb852303-d01b-4e5c-a673-8e48c41767d0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"With that basic circuit in mind, let us now look more closely at the chemoreceptors and the ventilatory responses they can induce.",True,Chemical Control of Breathing,,,,
4bce527f-e80b-445a-893f-a071b439e7c0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,Central Chemoreceptors,False,Central Chemoreceptors,,,,
7892596a-af6f-4263-9fdc-649f91e889d8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,We will start with the central chemoreceptors. The central chemoreceptors are comprised of chemosensitive neurons on the ventral surface of the medulla found close to the entry points of the glossopharyngeal and vagus nerves (coincidentally these are the nerves bringing in afferent information from the peripheral chemoreceptors and the pulmonary mechanoreceptors).,True,Central Chemoreceptors,,,,
173d8cf4-0c3d-4af5-b6ca-e0229435336b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Although the central chemoreceptors do not respond to hypoxemia and only respond to rises in arterial CO2, their activity accounts for about 80 percent of the hypercapnic ventilatory response. Given the critical importance of maintaining a normal PaCO2, these are considered the most important chemoreceptors for minute-by-minute regulation of ventilation. Ironically they do not respond to CO2 directly, but rather to changes in pH of the cerebrospinal fluid (CSF).",True,Central Chemoreceptors,,,,
c3777bda-3bb5-421f-bcdf-f3157ad1e8eb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"This complication comes from the fact that the central chemoreceptors are not exposed to the blood, but rather are behind the blood brain barrier and bathed in CSF. Hydrogen ions and bicarbonate cannot pass through the blood brain barrier, but CO2 can. Once through the blood brain barrier, CO2 forms carbonic acid in the reaction that is very familiar to you. It is the hydrogen ion from the dissociated carbonic acid that stimulates the chemoreceptors. So the central chemoreceptors respond to a rise in arterial CO2 via a change in CSF pH. Because there is little protein in the CSF, there is little buffering capability, and pH changes here tend to be greater than in the blood where plasma proteins are plentiful. This makes the central chemoreceptors quite sensitive and partly explains their substantial role in CO2 control.",True,Central Chemoreceptors,,,,
a799b257-a47e-432e-833e-00b79d60e223,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Prolonged exposure to high CO2, such as in chronic lung disease, can lead to a rise in CSF bicarbonate. This bicarbonate buffers hydrogen ions and reduces the sensitivity of the central chemoreceptors. This partly explains why the hypercapnic ventilatory response diminishes over time in chronic lung patients, such as those with COPD.",True,Central Chemoreceptors,,,,
dc5b1437-feb5-44e8-a67e-28c25876c04a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,Peripheral Chemoreceptors,False,Peripheral Chemoreceptors,,,,
04baf62e-2d59-4067-85c3-a11763bae21e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The peripheral chemoreceptors are directly exposed to arterial blood and are capable of responding to changes in CO2, O2, and pH. There are two populations of chemoreceptive cells in the vasculature (see figure 17.4). One population is found in the aortic arch and is referred to as the aortic bodies. These are wired into the brainstem through afferent fibers that project to and join the vagus nerve. The other chemoreceptor is comprised of the carotid bodies, found in the bifurcation of the common carotid arteries. These connect to the brainstem through the carotid sinus and the glossopharyngeal nerves. The carotid bodies are by far the most important in humans, with the aortic bodies contributing very little to any ventilatory response.",True,Peripheral Chemoreceptors,Figure 17.4,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.4.png,Figure 17.4: Peripheral chemoreceptors.
04baf62e-2d59-4067-85c3-a11763bae21e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The peripheral chemoreceptors are directly exposed to arterial blood and are capable of responding to changes in CO2, O2, and pH. There are two populations of chemoreceptive cells in the vasculature (see figure 17.4). One population is found in the aortic arch and is referred to as the aortic bodies. These are wired into the brainstem through afferent fibers that project to and join the vagus nerve. The other chemoreceptor is comprised of the carotid bodies, found in the bifurcation of the common carotid arteries. These connect to the brainstem through the carotid sinus and the glossopharyngeal nerves. The carotid bodies are by far the most important in humans, with the aortic bodies contributing very little to any ventilatory response.",True,Peripheral Chemoreceptors,Figure 17.4,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.4.png,Figure 17.4: Peripheral chemoreceptors.
04baf62e-2d59-4067-85c3-a11763bae21e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The peripheral chemoreceptors are directly exposed to arterial blood and are capable of responding to changes in CO2, O2, and pH. There are two populations of chemoreceptive cells in the vasculature (see figure 17.4). One population is found in the aortic arch and is referred to as the aortic bodies. These are wired into the brainstem through afferent fibers that project to and join the vagus nerve. The other chemoreceptor is comprised of the carotid bodies, found in the bifurcation of the common carotid arteries. These connect to the brainstem through the carotid sinus and the glossopharyngeal nerves. The carotid bodies are by far the most important in humans, with the aortic bodies contributing very little to any ventilatory response.",True,Peripheral Chemoreceptors,Figure 17.4,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.4.png,Figure 17.4: Peripheral chemoreceptors.
b2901034-e057-48dd-9467-99da79077047,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Although the carotid bodies play little role in reflex response to CO2, their response to hypercapnia is more rapid than the central chemoreceptors and so they are capable of breath-by-breath regulation and responding to abrupt changes in arterial PCO2. More importantly the peripheral chemoreceptors are entirely responsible for the response to hypoxia. The mechanism as to how these receptors work is unclear, but cells within the carotid bodies have very high metabolic rates and receive a proportionately high blood flow. It is likely that a decline in oxygen interrupts their metabolism and reduces their inhibitory interaction on neurotransmitter-filled neighboring cells, allowing excitation of the carotid sinus nerve. Their response to a decline in blood oxygen is far from linear. A decline in PO2 below 100 mmHg causes little change in action potential firing, but the rate of firing rapidly increases at PO2s below 50. This is reflected in the hypoxic ventilatory response illustrated in the graph in figure 17.5.",True,Peripheral Chemoreceptors,Figure 17.5,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.5.png,"Figure 17.5: Hypoxic ventilatory response. BTPS: body temperature and pressure, saturated."
b2901034-e057-48dd-9467-99da79077047,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Although the carotid bodies play little role in reflex response to CO2, their response to hypercapnia is more rapid than the central chemoreceptors and so they are capable of breath-by-breath regulation and responding to abrupt changes in arterial PCO2. More importantly the peripheral chemoreceptors are entirely responsible for the response to hypoxia. The mechanism as to how these receptors work is unclear, but cells within the carotid bodies have very high metabolic rates and receive a proportionately high blood flow. It is likely that a decline in oxygen interrupts their metabolism and reduces their inhibitory interaction on neurotransmitter-filled neighboring cells, allowing excitation of the carotid sinus nerve. Their response to a decline in blood oxygen is far from linear. A decline in PO2 below 100 mmHg causes little change in action potential firing, but the rate of firing rapidly increases at PO2s below 50. This is reflected in the hypoxic ventilatory response illustrated in the graph in figure 17.5.",True,Peripheral Chemoreceptors,Figure 17.5,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.5.png,"Figure 17.5: Hypoxic ventilatory response. BTPS: body temperature and pressure, saturated."
b2901034-e057-48dd-9467-99da79077047,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Although the carotid bodies play little role in reflex response to CO2, their response to hypercapnia is more rapid than the central chemoreceptors and so they are capable of breath-by-breath regulation and responding to abrupt changes in arterial PCO2. More importantly the peripheral chemoreceptors are entirely responsible for the response to hypoxia. The mechanism as to how these receptors work is unclear, but cells within the carotid bodies have very high metabolic rates and receive a proportionately high blood flow. It is likely that a decline in oxygen interrupts their metabolism and reduces their inhibitory interaction on neurotransmitter-filled neighboring cells, allowing excitation of the carotid sinus nerve. Their response to a decline in blood oxygen is far from linear. A decline in PO2 below 100 mmHg causes little change in action potential firing, but the rate of firing rapidly increases at PO2s below 50. This is reflected in the hypoxic ventilatory response illustrated in the graph in figure 17.5.",True,Peripheral Chemoreceptors,Figure 17.5,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.5.png,"Figure 17.5: Hypoxic ventilatory response. BTPS: body temperature and pressure, saturated."
a4626340-64f9-4e98-9bb3-c1c6456ec0b3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Because of this, the hypoxic ventilatory response normally plays little role in the control of breathing in humans. The hypoxic ventilatory response becomes more significant at altitude when inspired PO2 is low, or more pertinently in lung disease, where alveolar ventilation or gas exchange is compromised.",True,Peripheral Chemoreceptors,,,,
74ecd8c8-56f4-4efb-adbf-5a752109f03e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The hypercapnic ventilatory response (figure 17.6) is much more influential on breathing in humans on a normal day-to-day basis. The response is very linear, with a rise in PCO2 producing a proportionate rise in ventilation, driven of course primarily by the central chemoreceptors, but also contributed to by the afferent activity of the peripheral receptors.",True,Peripheral Chemoreceptors,Figure 17.6,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.6.png,Figure 17.6: Hypercapnic ventilatory response.
74ecd8c8-56f4-4efb-adbf-5a752109f03e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The hypercapnic ventilatory response (figure 17.6) is much more influential on breathing in humans on a normal day-to-day basis. The response is very linear, with a rise in PCO2 producing a proportionate rise in ventilation, driven of course primarily by the central chemoreceptors, but also contributed to by the afferent activity of the peripheral receptors.",True,Peripheral Chemoreceptors,Figure 17.6,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.6.png,Figure 17.6: Hypercapnic ventilatory response.
74ecd8c8-56f4-4efb-adbf-5a752109f03e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The hypercapnic ventilatory response (figure 17.6) is much more influential on breathing in humans on a normal day-to-day basis. The response is very linear, with a rise in PCO2 producing a proportionate rise in ventilation, driven of course primarily by the central chemoreceptors, but also contributed to by the afferent activity of the peripheral receptors.",True,Peripheral Chemoreceptors,Figure 17.6,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.6.png,Figure 17.6: Hypercapnic ventilatory response.
03166d05-e2cd-4c09-9f4f-d2cdfb739da4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The central and peripheral chemoreceptors keep arterial PCO2 within very fine limits, primarily because of CO2‘s effect on pH. Alveolar ventilation rapidly increases with even a moderate rise in arterial CO2, but can completely stop (apnea) if arterial CO2 falls below normal (~40 mmHg). The wakeful drive to breathe tends to keep CO2 a little lower than the set-point of the chemoreceptors—a point illustrated during sleep, when the brainstem has complete control of breathing and PaCO2 is seen to rise a few mmHg.",True,Peripheral Chemoreceptors,,,,
4e082c33-8560-4f18-9acc-caf26836c1b3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The hypercapnic ventilatory response adapts to chronically elevated arterial CO2, such as in severe lung disease. Here we not only see the CSF increase its buffering capacity with increased bicarbonate, but we also see the chemoreceptors change their set-point. It is not uncommon to see COPD patients with arterial PCO2s above 60.",True,Peripheral Chemoreceptors,,,,
5fca2cc3-dbc9-432c-b6b1-775faf192a2b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Finally, the hypoxic and hypercapnic ventilatory responses are not independent, and when they are both present at the same time a potentiation is seen (i.e., the response to hypoxic and hypercapnia is greater than the sum of the two individual responses).",True,Peripheral Chemoreceptors,,,,
2b15d8e4-47c8-43b2-a904-d5b8157dc76b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The hypoxic ventilatory response we have just looked at was measured at an alveolar PCO2 of 35.8 mmHg. If the same test is performed at higher PCO2s (figure 17.7), then the hypoxic ventilatory response is much greater, as shown by these upwardly shifted lines when alveolar PCO2 is set to 43.7 mmHg and 48.7 mmHg.",True,Peripheral Chemoreceptors,Figure 17.7,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.7-1.png,Figure 17.7: Hypoxic ventilatory responses with varying degrees of hypercapnia.
2b15d8e4-47c8-43b2-a904-d5b8157dc76b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The hypoxic ventilatory response we have just looked at was measured at an alveolar PCO2 of 35.8 mmHg. If the same test is performed at higher PCO2s (figure 17.7), then the hypoxic ventilatory response is much greater, as shown by these upwardly shifted lines when alveolar PCO2 is set to 43.7 mmHg and 48.7 mmHg.",True,Peripheral Chemoreceptors,Figure 17.7,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.7-1.png,Figure 17.7: Hypoxic ventilatory responses with varying degrees of hypercapnia.
2b15d8e4-47c8-43b2-a904-d5b8157dc76b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The hypoxic ventilatory response we have just looked at was measured at an alveolar PCO2 of 35.8 mmHg. If the same test is performed at higher PCO2s (figure 17.7), then the hypoxic ventilatory response is much greater, as shown by these upwardly shifted lines when alveolar PCO2 is set to 43.7 mmHg and 48.7 mmHg.",True,Peripheral Chemoreceptors,Figure 17.7,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.7-1.png,Figure 17.7: Hypoxic ventilatory responses with varying degrees of hypercapnia.
23250657-4fd9-4709-a0f2-7575019d4f25,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Likewise, the hypercapnic ventilatory response is exaggerated in the presence of hypoxia (see figure 17.8). The hypercapnic ventilatory response we have just looked at was measured at a “normal” alveolar PO2 of 110 mmHg. If the hypercapnic response is measured in the presence of hypoxia, then the curve shifts upward, as shown by the upper lines when alveolar PO2 is reduced to 47 mmHg and 37 mmHg. This potentiation likely comes from the peripheral chemoreceptors, whose firing rate is potentiated in the presence of both stimuli. Consequently, when a patient is both hypoxic and hypercapnic, then they are likely to have a very high drive to breathe, and when this occurs they are likely to feel very short of breath—the topic of the last chapter.",True,Peripheral Chemoreceptors,Figure 17.8,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.8.png,Figure 17.8: Hypercapnic ventilatory responses with varying degrees of hypoxia.
23250657-4fd9-4709-a0f2-7575019d4f25,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Likewise, the hypercapnic ventilatory response is exaggerated in the presence of hypoxia (see figure 17.8). The hypercapnic ventilatory response we have just looked at was measured at a “normal” alveolar PO2 of 110 mmHg. If the hypercapnic response is measured in the presence of hypoxia, then the curve shifts upward, as shown by the upper lines when alveolar PO2 is reduced to 47 mmHg and 37 mmHg. This potentiation likely comes from the peripheral chemoreceptors, whose firing rate is potentiated in the presence of both stimuli. Consequently, when a patient is both hypoxic and hypercapnic, then they are likely to have a very high drive to breathe, and when this occurs they are likely to feel very short of breath—the topic of the last chapter.",True,Peripheral Chemoreceptors,Figure 17.8,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.8.png,Figure 17.8: Hypercapnic ventilatory responses with varying degrees of hypoxia.
23250657-4fd9-4709-a0f2-7575019d4f25,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Likewise, the hypercapnic ventilatory response is exaggerated in the presence of hypoxia (see figure 17.8). The hypercapnic ventilatory response we have just looked at was measured at a “normal” alveolar PO2 of 110 mmHg. If the hypercapnic response is measured in the presence of hypoxia, then the curve shifts upward, as shown by the upper lines when alveolar PO2 is reduced to 47 mmHg and 37 mmHg. This potentiation likely comes from the peripheral chemoreceptors, whose firing rate is potentiated in the presence of both stimuli. Consequently, when a patient is both hypoxic and hypercapnic, then they are likely to have a very high drive to breathe, and when this occurs they are likely to feel very short of breath—the topic of the last chapter.",True,Peripheral Chemoreceptors,Figure 17.8,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.8.png,Figure 17.8: Hypercapnic ventilatory responses with varying degrees of hypoxia.
8a56fb29-53dc-4371-9288-93228d24fecb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"The chemoreflexes modulate breathing to maintain constant arterial blood gases and pH. These reflexes are initiated by central sensors that respond to hypoxia and peripheral sensors that respond to hypercapnia, hypoxia, and changes in arterial pH. Together these sensors can maintain arterial blood gases within narrow ranges despite large changes in oxygen consumption and CO2 production associated with changes in metabolic rate.",True,Peripheral Chemoreceptors,,,,
c23605e9-9dee-4f9b-ae37-13cb3df9c5b1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,Text,False,Text,,,,
75abbe57-5a7c-4c59-8133-abb995a3a959,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Levitsky, Michael G. “Chapter 9: Control of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
137034ee-564a-4a3f-b996-a079bf6eb660,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"West, John B. “Chapter 8: Control of Ventilation—How Gas Exchange Is Regulated.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
4de10d5a-5a97-47fd-8187-309f75e413e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Central Control Mechanisms,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/#chapter-59-section-1,"Widdicombe, John G., and Andrew S. Davis. “Chapter 8” and “Chapter 9.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
8b9329d4-4ac1-473d-b82d-421a47260e06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,Introduction,False,Introduction,,,,
0ca720f5-4db1-4dde-b36a-61771b0bc770,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,In this chapter we will have a look at the regions of the nervous system that control breathing and how they interact or override each other.,True,Introduction,,,,
32122958-543e-4359-adfe-36a86f15a31c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,The Role of the Brainstem,False,The Role of the Brainstem,,,,
559cc404-6092-4291-b037-4a55007f2f4f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"It has long been known that the brainstem contains critical centers for the control of breathing. These regions produce what is often referred to as the reflex drive to breathe, or brainstem drive to breathe. Despite its critical nature for survival, this involuntary motor drive that operates the respiratory muscles is barely understood.",True,The Role of the Brainstem,,,,
8ebfd7b8-6c3b-4ebe-9551-e5d43551266c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,What we will do here is summarize some basic information to create a coherent and accurate overview.,True,The Role of the Brainstem,,,,
55b9f1c7-b1fa-47dc-a328-b717a03510f6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The reflex drive to breathe is a typical reflex arch, with receptors in the vasculature and lung reporting to a central controller in the brainstem that implements its effects via the respiratory muscles. What is different from most simple reflexes is that the controller is rather complex and can be thought of as a central hub that integrates inputs from multiple sources.",True,The Role of the Brainstem,,,,
561e712c-0b64-4468-a3ae-a08c121e1540,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Many visceral sensors supplying the controller in the brainstem send their afferent signals via the glossopharyngeal and vagus nerves to the nucleus tractus solitaries, or NTS. This input station is part of an anatomically indistinct region on the dorsal surface of the medulla, called the dorsal respiratory group or DRG. The DRG connects to motor neurons that lead to the inspiratory muscles.",True,The Role of the Brainstem,,,,
a167f293-eb5b-47e3-bae7-cbcdcb4ba54e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,NTS,False,NTS,,,,
9165141a-8e94-470b-ae44-f7d1a5d66f28,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"These DRG (figure 17.1) neurons show ramp-like bursts of activity that cause inspiratory muscle contraction to induce inspiration, then stop, allowing the inspiratory muscles to relax and passive exhalation to begin. This intermittent ramp of activity can be modulated by input from the sensors or other regions of the central nervous system, but it is not spontaneous; rather this activity is initiated by another respiratory pacemaker. It was this pacemaker that eluded physiologists for decades.",True,NTS,Figure 17.1,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
9165141a-8e94-470b-ae44-f7d1a5d66f28,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"These DRG (figure 17.1) neurons show ramp-like bursts of activity that cause inspiratory muscle contraction to induce inspiration, then stop, allowing the inspiratory muscles to relax and passive exhalation to begin. This intermittent ramp of activity can be modulated by input from the sensors or other regions of the central nervous system, but it is not spontaneous; rather this activity is initiated by another respiratory pacemaker. It was this pacemaker that eluded physiologists for decades.",True,NTS,Figure 17.1,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
9165141a-8e94-470b-ae44-f7d1a5d66f28,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"These DRG (figure 17.1) neurons show ramp-like bursts of activity that cause inspiratory muscle contraction to induce inspiration, then stop, allowing the inspiratory muscles to relax and passive exhalation to begin. This intermittent ramp of activity can be modulated by input from the sensors or other regions of the central nervous system, but it is not spontaneous; rather this activity is initiated by another respiratory pacemaker. It was this pacemaker that eluded physiologists for decades.",True,NTS,Figure 17.1,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
a53878a6-b88e-48df-abb5-c428202008f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"On the other side of medulla is the ventral respiratory group (figure 17.1), which has been known for a long time to contain circuits that contribute to the control of breathing within its rostral, intermediate, and caudal regions. Within the intermediate region a cluster of neurons called the pre-Bötzinger complex (figure 17.1) with apparently spontaneous activity is currently thought to be the respiratory pacemaker. The pre-bötzinger complex is likely responsible for the activity of the DRG inspiratory neurons to produce the ramping activity.",True,NTS,Figure 17.1,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
a53878a6-b88e-48df-abb5-c428202008f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"On the other side of medulla is the ventral respiratory group (figure 17.1), which has been known for a long time to contain circuits that contribute to the control of breathing within its rostral, intermediate, and caudal regions. Within the intermediate region a cluster of neurons called the pre-Bötzinger complex (figure 17.1) with apparently spontaneous activity is currently thought to be the respiratory pacemaker. The pre-bötzinger complex is likely responsible for the activity of the DRG inspiratory neurons to produce the ramping activity.",True,NTS,Figure 17.1,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
a53878a6-b88e-48df-abb5-c428202008f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"On the other side of medulla is the ventral respiratory group (figure 17.1), which has been known for a long time to contain circuits that contribute to the control of breathing within its rostral, intermediate, and caudal regions. Within the intermediate region a cluster of neurons called the pre-Bötzinger complex (figure 17.1) with apparently spontaneous activity is currently thought to be the respiratory pacemaker. The pre-bötzinger complex is likely responsible for the activity of the DRG inspiratory neurons to produce the ramping activity.",True,NTS,Figure 17.1,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
efebd834-d539-48e7-8934-0cf3db5e3576,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,Bötzinger,False,Bötzinger,,,,
32a3ee99-9815-4873-8882-617c21997b1b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,bötzinger,False,bötzinger,,,,
9afb0f5a-72ef-4141-af2c-db3d51743a71,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The ventral respiratory group also contains neurons with inspiratory-related activity and connections to the inspiratory motor neurons. It is better known for its expiratory neurons, however, which are capable of activating the expiratory muscles when expiration must become active rather than remain passive. During quiet resting breathing, these expiratory neurons remain dormant.",True,bötzinger,,,,
bed23e05-5617-4c48-a47f-0cbfc0e76e50,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,This medullary circuitry can be influenced by other brainstem centers thought to be responsible for fine-tuning the breathing rhythm.,True,bötzinger,,,,
2a12f462-c18f-4d26-a58d-4403b4255998,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The Apneustic center in the lower pons (figure 17.1) excites the inspiratory neurons and prolongs the ramp activity they produce; this inevitably produces a prolonged inspiratory period. Higher up in the pons is the Pneumotaxic center (figure 17.1), which acts as an off switch for inspiratory neurons; thus it regulates inspiratory volume and indirectly influences the rate of breathing, tending to increase it. This is a very basic overview of the breathing circuitry that is capable of generating inspiration and active expiration when needed. But these centers take information and direction from other neural influences, including chemoreceptors, receptors in the lung, and higher brain centers. We will look at the latter two now.",True,bötzinger,Figure 17.1,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
2a12f462-c18f-4d26-a58d-4403b4255998,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The Apneustic center in the lower pons (figure 17.1) excites the inspiratory neurons and prolongs the ramp activity they produce; this inevitably produces a prolonged inspiratory period. Higher up in the pons is the Pneumotaxic center (figure 17.1), which acts as an off switch for inspiratory neurons; thus it regulates inspiratory volume and indirectly influences the rate of breathing, tending to increase it. This is a very basic overview of the breathing circuitry that is capable of generating inspiration and active expiration when needed. But these centers take information and direction from other neural influences, including chemoreceptors, receptors in the lung, and higher brain centers. We will look at the latter two now.",True,bötzinger,Figure 17.1,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
2a12f462-c18f-4d26-a58d-4403b4255998,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The Apneustic center in the lower pons (figure 17.1) excites the inspiratory neurons and prolongs the ramp activity they produce; this inevitably produces a prolonged inspiratory period. Higher up in the pons is the Pneumotaxic center (figure 17.1), which acts as an off switch for inspiratory neurons; thus it regulates inspiratory volume and indirectly influences the rate of breathing, tending to increase it. This is a very basic overview of the breathing circuitry that is capable of generating inspiration and active expiration when needed. But these centers take information and direction from other neural influences, including chemoreceptors, receptors in the lung, and higher brain centers. We will look at the latter two now.",True,bötzinger,Figure 17.1,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.1.png,Figure 17.1: Brainstem respiratory network.
06abdd2e-93b3-4583-9beb-b162e217d186,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,Pulmonary and Higher Brain Influences,False,Pulmonary and Higher Brain Influences,,,,
1d920cfe-d5a9-419e-8365-6a80e110c79d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The brainstem drive to breathe can be modulated from above and from below. The literature about whether these influences increase or decrease the drive to breathe is often confused, perhaps because of the wide range of experiments performed and the different species used. We will have a look at some of the most consistent and clinically pertinent aspects here, starting in the lung and three populations of intrapulmonary neural receptors.",True,Pulmonary and Higher Brain Influences,,,,
70cd5359-8128-459a-bc0f-800976e67835,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Pulmonary stretch receptors are mechanoreceptors found in airway walls and smooth muscle. As their name suggests, they respond to expansion of the lung, and their afferent activity to the brainstem increases with lung volume, as figure 17.2 shows. Upon arrival at the NTS the PSR activity tends to inhibit inspiratory neurons and can stop inspiratory activity completely in other species (the Hering–Breuer reflex). However, their influence on the control of breathing in humans is weak, and while they might not contribute to the control of breathing in man, they likely influence respiratory sensations, such as shortness of breath.",True,Pulmonary and Higher Brain Influences,Figure 17.2,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.2.png,"Figure 17.2: Lung volume and pulmonary stretch receptor firing. The top tracing represents lung volume with two full inflations followed by a sustained inflation. In response to the increases in lung volume, pulmonary stretch receptors depolarize, producing action potentials, which are shown in the lower trace as upward spikes. The increase in action potentials with increased lung volume is seen as more densely clustered spikes. Note how the sustained inflation causes an initial high frequency of action potentials that gradually falls as the receptor adapts to the high lung volume."
70cd5359-8128-459a-bc0f-800976e67835,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Pulmonary stretch receptors are mechanoreceptors found in airway walls and smooth muscle. As their name suggests, they respond to expansion of the lung, and their afferent activity to the brainstem increases with lung volume, as figure 17.2 shows. Upon arrival at the NTS the PSR activity tends to inhibit inspiratory neurons and can stop inspiratory activity completely in other species (the Hering–Breuer reflex). However, their influence on the control of breathing in humans is weak, and while they might not contribute to the control of breathing in man, they likely influence respiratory sensations, such as shortness of breath.",True,Pulmonary and Higher Brain Influences,Figure 17.2,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.2.png,"Figure 17.2: Lung volume and pulmonary stretch receptor firing. The top tracing represents lung volume with two full inflations followed by a sustained inflation. In response to the increases in lung volume, pulmonary stretch receptors depolarize, producing action potentials, which are shown in the lower trace as upward spikes. The increase in action potentials with increased lung volume is seen as more densely clustered spikes. Note how the sustained inflation causes an initial high frequency of action potentials that gradually falls as the receptor adapts to the high lung volume."
70cd5359-8128-459a-bc0f-800976e67835,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Pulmonary stretch receptors are mechanoreceptors found in airway walls and smooth muscle. As their name suggests, they respond to expansion of the lung, and their afferent activity to the brainstem increases with lung volume, as figure 17.2 shows. Upon arrival at the NTS the PSR activity tends to inhibit inspiratory neurons and can stop inspiratory activity completely in other species (the Hering–Breuer reflex). However, their influence on the control of breathing in humans is weak, and while they might not contribute to the control of breathing in man, they likely influence respiratory sensations, such as shortness of breath.",True,Pulmonary and Higher Brain Influences,Figure 17.2,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.2.png,"Figure 17.2: Lung volume and pulmonary stretch receptor firing. The top tracing represents lung volume with two full inflations followed by a sustained inflation. In response to the increases in lung volume, pulmonary stretch receptors depolarize, producing action potentials, which are shown in the lower trace as upward spikes. The increase in action potentials with increased lung volume is seen as more densely clustered spikes. Note how the sustained inflation causes an initial high frequency of action potentials that gradually falls as the receptor adapts to the high lung volume."
80d9a2be-1c37-41b9-88a2-6beef7e8d5df,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Irritant receptors are found in the airway epithelium and are ideally placed to perform their role of detecting harmful substances entering the lungs, such as noxious gases, particulates, and even cold air. They generally have an inhibitory influence on the drive to breathe, perhaps as an attempt to limit the amount of noxious substance entering the lung. Other components to their defensive strategies are bronchoconstriction and induction of the cough reflex. Their response to inflammatory mediators also suggests they may play a role in asthma.",True,Pulmonary and Higher Brain Influences,,,,
58707d89-78dd-4db1-9ab7-aeb635ac9dc2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"J-receptors, or Juxtacapillary receptors, are found at the junction of the pulmonary capillaries and alveoli. These receptors respond to increases in interstitial pressure so are likely to play a role in the response to pulmonary edema. Their effect on the drive to breathe can be regarded as excitatory as they cause an increase in breathing rate as part of the J-reflex, which includes cardiac components and is intended to prevent over-exercising and cardiopulmonary collapse. As such the J-receptors may also contribute to generating the sensation of shortness of breath.",True,Pulmonary and Higher Brain Influences,,,,
5cd59a61-c62e-432e-adc6-80c7d1a10ebc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"These three pulmonary receptor groups are the three that usually appear in textbooks, perhaps because of their clinical pertinence, but perhaps because we know most about these. Others exist, and details can be found in other sources. We will now focus briefly on the influence of higher centers on breathing, and these are generally all positive (i.e., cause an increase in breathing). Cortical influences are numerous and undefined, that collectively they produce what is referred to as the wakeful drive to breath. The extent of cortical influence is best illustrated by sleep, when the higher brain is unconscious and any wakeful drive is removed. During sleep breathing is significantly reduced—enough so that arterial PCO2 is several mmHg higher than during wakefulness. This suggests that cortical influences on breathing are enough to cause a lower PaCO2 than would be determined by chemoreflexes alone.",True,Pulmonary and Higher Brain Influences,,,,
49c5ea46-d7f2-4fb8-b11c-6918bf029465,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,PaCO2,False,PaCO2,,,,
c12c2b26-3bb6-4090-88c5-77e4ed3118a9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"More specific influences from higher centers include emotions; anger, anxiety, sadness, happiness, and sexual arousal all influence the drive and pattern of breathing. This is perhaps best exemplified by emotionally driven sighs or the frankly bizarre activity of laughter. But the list of higher center influences does not stop there; indeed it is likely that we still yet do not know where it stops. Changes in light changes breathing, a sudden loud sound changes breathing, doing a mathematical problem changes breathing… and so on. And unfortunately for clinicians and pulmonary physiologists, the act of measuring breathing changes breathing. So it is likely that all those textbook numbers for normal respiratory rate and depth are all too high, as telling someone you are going to measure their breathing usually causes them to hyperventilate.",True,PaCO2,,,,
34dd848b-72a5-46ef-94d1-8f63ba0caab2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Breathing is also a rare incidence of being able to voluntarily control a normally reflex activity (e.g., we can willfully override reflex breathing to perform speech or a breath-hold). In fact, we have as precise control over our respiratory muscles as we have control over the muscles in our hands. Humans maybe be exclusive in this respect because of our elaborate speech, but again, this is another unknown. However, eventually reflex breathing will always reclaim its command over breathing—as anyone who has performed a prolonged breath-hold will know.",True,PaCO2,,,,
7020f11f-3853-4d54-9802-d5e926783a2f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,Summary,False,Summary,,,,
7acf2414-922c-4818-af7b-d9be313fa658,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"So we have seen that at the heart of the control of breathing there is a pacemaker establishing a basic rhythm and depth of breathing, but this is influenced by numerous other factors from both the lung and higher brain. These influences adjust breathing via the brainstem to produce respiratory responses to the environment and changes in emotional state, and contribute to efficient and appropriate levels of ventilation.",True,Summary,,,,
ef0ab30d-e51c-43ec-8920-214db6adabd6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,Chemical Control of Breathing,False,Chemical Control of Breathing,,,,
d8d14e12-f923-44b5-8d68-48e808586a2d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"It perhaps comes as no surprise that the major influence on the reflex drive to breathe comes from the homeostatic need to match ventilation with metabolic demand and maintain blood O2, CO2, and pH within narrow ranges. The chemoreflexes are therefore capable of sensing changes in arterial oxygen, carbon dioxide, and pH, modifying the activity of the brainstem respiratory centers and affecting an appropriate change in alveolar ventilation. These reflexes all act as classical negative feedback circuits and are capable of maintaining despite large changes in O2 consumption and CO2 production by metabolizing tissue.",True,Chemical Control of Breathing,,,,
fa5a6750-8584-45fe-9998-896489636bd1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Before getting into the details of the chemoreceptors, let us take a quick overview of the basic circuitry of the chemoreflexes (figure 17.3). There are two sets of sensors in our circuit: the peripheral chemoreceptors that are in the vasculature, and the central chemoreceptors that are found on the surface of the brainstem. The central chemoreceptors are capable of detecting changes in arterial CO2, while the peripheral chemoreceptors respond to changes in CO2, O2, and arterial pH.",True,Chemical Control of Breathing,Figure 17.3,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.3.png,Figure 17.3: Chemoreflex circuit.
fa5a6750-8584-45fe-9998-896489636bd1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Before getting into the details of the chemoreceptors, let us take a quick overview of the basic circuitry of the chemoreflexes (figure 17.3). There are two sets of sensors in our circuit: the peripheral chemoreceptors that are in the vasculature, and the central chemoreceptors that are found on the surface of the brainstem. The central chemoreceptors are capable of detecting changes in arterial CO2, while the peripheral chemoreceptors respond to changes in CO2, O2, and arterial pH.",True,Chemical Control of Breathing,Figure 17.3,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.3.png,Figure 17.3: Chemoreflex circuit.
fa5a6750-8584-45fe-9998-896489636bd1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Before getting into the details of the chemoreceptors, let us take a quick overview of the basic circuitry of the chemoreflexes (figure 17.3). There are two sets of sensors in our circuit: the peripheral chemoreceptors that are in the vasculature, and the central chemoreceptors that are found on the surface of the brainstem. The central chemoreceptors are capable of detecting changes in arterial CO2, while the peripheral chemoreceptors respond to changes in CO2, O2, and arterial pH.",True,Chemical Control of Breathing,Figure 17.3,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.3.png,Figure 17.3: Chemoreflex circuit.
795cd244-bdea-4d63-829f-6bf6191e3ae8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Upon excitation by changes in blood gas values, the receptors fire back to the reflex’s controller, the respiratory centers in the brainstem. This results in an increase in reflex ventilatory drive and a greater motor signal to the respiratory muscles. This produces an increase in alveolar ventilation that corrects the blood gas disturbances and stops the chemoreceptors from firing.",True,Chemical Control of Breathing,,,,
47a68651-28c5-4a52-a9e9-58dd87b83815,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"With that basic circuit in mind, let us now look more closely at the chemoreceptors and the ventilatory responses they can induce.",True,Chemical Control of Breathing,,,,
3b1ea015-9e2a-48c8-8849-44f526d8040a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,Central Chemoreceptors,False,Central Chemoreceptors,,,,
4bd254f0-6caa-461d-b1aa-2b8fd22cb4f1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,We will start with the central chemoreceptors. The central chemoreceptors are comprised of chemosensitive neurons on the ventral surface of the medulla found close to the entry points of the glossopharyngeal and vagus nerves (coincidentally these are the nerves bringing in afferent information from the peripheral chemoreceptors and the pulmonary mechanoreceptors).,True,Central Chemoreceptors,,,,
47f4ff30-982e-46a1-bdac-809539f37522,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Although the central chemoreceptors do not respond to hypoxemia and only respond to rises in arterial CO2, their activity accounts for about 80 percent of the hypercapnic ventilatory response. Given the critical importance of maintaining a normal PaCO2, these are considered the most important chemoreceptors for minute-by-minute regulation of ventilation. Ironically they do not respond to CO2 directly, but rather to changes in pH of the cerebrospinal fluid (CSF).",True,Central Chemoreceptors,,,,
49911305-524d-449b-b9f6-eb677c19a40e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"This complication comes from the fact that the central chemoreceptors are not exposed to the blood, but rather are behind the blood brain barrier and bathed in CSF. Hydrogen ions and bicarbonate cannot pass through the blood brain barrier, but CO2 can. Once through the blood brain barrier, CO2 forms carbonic acid in the reaction that is very familiar to you. It is the hydrogen ion from the dissociated carbonic acid that stimulates the chemoreceptors. So the central chemoreceptors respond to a rise in arterial CO2 via a change in CSF pH. Because there is little protein in the CSF, there is little buffering capability, and pH changes here tend to be greater than in the blood where plasma proteins are plentiful. This makes the central chemoreceptors quite sensitive and partly explains their substantial role in CO2 control.",True,Central Chemoreceptors,,,,
bbbe48e3-2b68-40e3-8744-93c7588f02f6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Prolonged exposure to high CO2, such as in chronic lung disease, can lead to a rise in CSF bicarbonate. This bicarbonate buffers hydrogen ions and reduces the sensitivity of the central chemoreceptors. This partly explains why the hypercapnic ventilatory response diminishes over time in chronic lung patients, such as those with COPD.",True,Central Chemoreceptors,,,,
2de48d9e-203f-4411-a8cd-86fb4f6dcaf8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,Peripheral Chemoreceptors,False,Peripheral Chemoreceptors,,,,
e140b6b0-db01-454f-8a03-3f3fdb66ea7a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The peripheral chemoreceptors are directly exposed to arterial blood and are capable of responding to changes in CO2, O2, and pH. There are two populations of chemoreceptive cells in the vasculature (see figure 17.4). One population is found in the aortic arch and is referred to as the aortic bodies. These are wired into the brainstem through afferent fibers that project to and join the vagus nerve. The other chemoreceptor is comprised of the carotid bodies, found in the bifurcation of the common carotid arteries. These connect to the brainstem through the carotid sinus and the glossopharyngeal nerves. The carotid bodies are by far the most important in humans, with the aortic bodies contributing very little to any ventilatory response.",True,Peripheral Chemoreceptors,Figure 17.4,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.4.png,Figure 17.4: Peripheral chemoreceptors.
e140b6b0-db01-454f-8a03-3f3fdb66ea7a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The peripheral chemoreceptors are directly exposed to arterial blood and are capable of responding to changes in CO2, O2, and pH. There are two populations of chemoreceptive cells in the vasculature (see figure 17.4). One population is found in the aortic arch and is referred to as the aortic bodies. These are wired into the brainstem through afferent fibers that project to and join the vagus nerve. The other chemoreceptor is comprised of the carotid bodies, found in the bifurcation of the common carotid arteries. These connect to the brainstem through the carotid sinus and the glossopharyngeal nerves. The carotid bodies are by far the most important in humans, with the aortic bodies contributing very little to any ventilatory response.",True,Peripheral Chemoreceptors,Figure 17.4,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.4.png,Figure 17.4: Peripheral chemoreceptors.
e140b6b0-db01-454f-8a03-3f3fdb66ea7a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The peripheral chemoreceptors are directly exposed to arterial blood and are capable of responding to changes in CO2, O2, and pH. There are two populations of chemoreceptive cells in the vasculature (see figure 17.4). One population is found in the aortic arch and is referred to as the aortic bodies. These are wired into the brainstem through afferent fibers that project to and join the vagus nerve. The other chemoreceptor is comprised of the carotid bodies, found in the bifurcation of the common carotid arteries. These connect to the brainstem through the carotid sinus and the glossopharyngeal nerves. The carotid bodies are by far the most important in humans, with the aortic bodies contributing very little to any ventilatory response.",True,Peripheral Chemoreceptors,Figure 17.4,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.4.png,Figure 17.4: Peripheral chemoreceptors.
21a8a92f-8e2d-4340-93aa-d4f3da6c4a6e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Although the carotid bodies play little role in reflex response to CO2, their response to hypercapnia is more rapid than the central chemoreceptors and so they are capable of breath-by-breath regulation and responding to abrupt changes in arterial PCO2. More importantly the peripheral chemoreceptors are entirely responsible for the response to hypoxia. The mechanism as to how these receptors work is unclear, but cells within the carotid bodies have very high metabolic rates and receive a proportionately high blood flow. It is likely that a decline in oxygen interrupts their metabolism and reduces their inhibitory interaction on neurotransmitter-filled neighboring cells, allowing excitation of the carotid sinus nerve. Their response to a decline in blood oxygen is far from linear. A decline in PO2 below 100 mmHg causes little change in action potential firing, but the rate of firing rapidly increases at PO2s below 50. This is reflected in the hypoxic ventilatory response illustrated in the graph in figure 17.5.",True,Peripheral Chemoreceptors,Figure 17.5,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.5.png,"Figure 17.5: Hypoxic ventilatory response. BTPS: body temperature and pressure, saturated."
21a8a92f-8e2d-4340-93aa-d4f3da6c4a6e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Although the carotid bodies play little role in reflex response to CO2, their response to hypercapnia is more rapid than the central chemoreceptors and so they are capable of breath-by-breath regulation and responding to abrupt changes in arterial PCO2. More importantly the peripheral chemoreceptors are entirely responsible for the response to hypoxia. The mechanism as to how these receptors work is unclear, but cells within the carotid bodies have very high metabolic rates and receive a proportionately high blood flow. It is likely that a decline in oxygen interrupts their metabolism and reduces their inhibitory interaction on neurotransmitter-filled neighboring cells, allowing excitation of the carotid sinus nerve. Their response to a decline in blood oxygen is far from linear. A decline in PO2 below 100 mmHg causes little change in action potential firing, but the rate of firing rapidly increases at PO2s below 50. This is reflected in the hypoxic ventilatory response illustrated in the graph in figure 17.5.",True,Peripheral Chemoreceptors,Figure 17.5,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.5.png,"Figure 17.5: Hypoxic ventilatory response. BTPS: body temperature and pressure, saturated."
21a8a92f-8e2d-4340-93aa-d4f3da6c4a6e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Although the carotid bodies play little role in reflex response to CO2, their response to hypercapnia is more rapid than the central chemoreceptors and so they are capable of breath-by-breath regulation and responding to abrupt changes in arterial PCO2. More importantly the peripheral chemoreceptors are entirely responsible for the response to hypoxia. The mechanism as to how these receptors work is unclear, but cells within the carotid bodies have very high metabolic rates and receive a proportionately high blood flow. It is likely that a decline in oxygen interrupts their metabolism and reduces their inhibitory interaction on neurotransmitter-filled neighboring cells, allowing excitation of the carotid sinus nerve. Their response to a decline in blood oxygen is far from linear. A decline in PO2 below 100 mmHg causes little change in action potential firing, but the rate of firing rapidly increases at PO2s below 50. This is reflected in the hypoxic ventilatory response illustrated in the graph in figure 17.5.",True,Peripheral Chemoreceptors,Figure 17.5,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.5.png,"Figure 17.5: Hypoxic ventilatory response. BTPS: body temperature and pressure, saturated."
82429396-6cb9-4758-b6bc-4314a19b8918,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Because of this, the hypoxic ventilatory response normally plays little role in the control of breathing in humans. The hypoxic ventilatory response becomes more significant at altitude when inspired PO2 is low, or more pertinently in lung disease, where alveolar ventilation or gas exchange is compromised.",True,Peripheral Chemoreceptors,,,,
c978ed2a-13b4-4201-9161-e1339c8c45d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The hypercapnic ventilatory response (figure 17.6) is much more influential on breathing in humans on a normal day-to-day basis. The response is very linear, with a rise in PCO2 producing a proportionate rise in ventilation, driven of course primarily by the central chemoreceptors, but also contributed to by the afferent activity of the peripheral receptors.",True,Peripheral Chemoreceptors,Figure 17.6,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.6.png,Figure 17.6: Hypercapnic ventilatory response.
c978ed2a-13b4-4201-9161-e1339c8c45d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The hypercapnic ventilatory response (figure 17.6) is much more influential on breathing in humans on a normal day-to-day basis. The response is very linear, with a rise in PCO2 producing a proportionate rise in ventilation, driven of course primarily by the central chemoreceptors, but also contributed to by the afferent activity of the peripheral receptors.",True,Peripheral Chemoreceptors,Figure 17.6,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.6.png,Figure 17.6: Hypercapnic ventilatory response.
c978ed2a-13b4-4201-9161-e1339c8c45d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The hypercapnic ventilatory response (figure 17.6) is much more influential on breathing in humans on a normal day-to-day basis. The response is very linear, with a rise in PCO2 producing a proportionate rise in ventilation, driven of course primarily by the central chemoreceptors, but also contributed to by the afferent activity of the peripheral receptors.",True,Peripheral Chemoreceptors,Figure 17.6,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.6.png,Figure 17.6: Hypercapnic ventilatory response.
582e794b-f321-4645-ae28-f0507f120b0b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The central and peripheral chemoreceptors keep arterial PCO2 within very fine limits, primarily because of CO2‘s effect on pH. Alveolar ventilation rapidly increases with even a moderate rise in arterial CO2, but can completely stop (apnea) if arterial CO2 falls below normal (~40 mmHg). The wakeful drive to breathe tends to keep CO2 a little lower than the set-point of the chemoreceptors—a point illustrated during sleep, when the brainstem has complete control of breathing and PaCO2 is seen to rise a few mmHg.",True,Peripheral Chemoreceptors,,,,
1dd4ff43-f61d-451f-a063-472df079311e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The hypercapnic ventilatory response adapts to chronically elevated arterial CO2, such as in severe lung disease. Here we not only see the CSF increase its buffering capacity with increased bicarbonate, but we also see the chemoreceptors change their set-point. It is not uncommon to see COPD patients with arterial PCO2s above 60.",True,Peripheral Chemoreceptors,,,,
47ef2801-b20a-473b-add5-cce3a55fd2d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Finally, the hypoxic and hypercapnic ventilatory responses are not independent, and when they are both present at the same time a potentiation is seen (i.e., the response to hypoxic and hypercapnia is greater than the sum of the two individual responses).",True,Peripheral Chemoreceptors,,,,
1145e40a-f16c-41b7-b1f2-4785ef673431,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The hypoxic ventilatory response we have just looked at was measured at an alveolar PCO2 of 35.8 mmHg. If the same test is performed at higher PCO2s (figure 17.7), then the hypoxic ventilatory response is much greater, as shown by these upwardly shifted lines when alveolar PCO2 is set to 43.7 mmHg and 48.7 mmHg.",True,Peripheral Chemoreceptors,Figure 17.7,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.7-1.png,Figure 17.7: Hypoxic ventilatory responses with varying degrees of hypercapnia.
1145e40a-f16c-41b7-b1f2-4785ef673431,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The hypoxic ventilatory response we have just looked at was measured at an alveolar PCO2 of 35.8 mmHg. If the same test is performed at higher PCO2s (figure 17.7), then the hypoxic ventilatory response is much greater, as shown by these upwardly shifted lines when alveolar PCO2 is set to 43.7 mmHg and 48.7 mmHg.",True,Peripheral Chemoreceptors,Figure 17.7,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.7-1.png,Figure 17.7: Hypoxic ventilatory responses with varying degrees of hypercapnia.
1145e40a-f16c-41b7-b1f2-4785ef673431,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The hypoxic ventilatory response we have just looked at was measured at an alveolar PCO2 of 35.8 mmHg. If the same test is performed at higher PCO2s (figure 17.7), then the hypoxic ventilatory response is much greater, as shown by these upwardly shifted lines when alveolar PCO2 is set to 43.7 mmHg and 48.7 mmHg.",True,Peripheral Chemoreceptors,Figure 17.7,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.7-1.png,Figure 17.7: Hypoxic ventilatory responses with varying degrees of hypercapnia.
31e35a20-7574-49b4-9e32-091542efbba2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Likewise, the hypercapnic ventilatory response is exaggerated in the presence of hypoxia (see figure 17.8). The hypercapnic ventilatory response we have just looked at was measured at a “normal” alveolar PO2 of 110 mmHg. If the hypercapnic response is measured in the presence of hypoxia, then the curve shifts upward, as shown by the upper lines when alveolar PO2 is reduced to 47 mmHg and 37 mmHg. This potentiation likely comes from the peripheral chemoreceptors, whose firing rate is potentiated in the presence of both stimuli. Consequently, when a patient is both hypoxic and hypercapnic, then they are likely to have a very high drive to breathe, and when this occurs they are likely to feel very short of breath—the topic of the last chapter.",True,Peripheral Chemoreceptors,Figure 17.8,Chemical Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.8.png,Figure 17.8: Hypercapnic ventilatory responses with varying degrees of hypoxia.
31e35a20-7574-49b4-9e32-091542efbba2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Likewise, the hypercapnic ventilatory response is exaggerated in the presence of hypoxia (see figure 17.8). The hypercapnic ventilatory response we have just looked at was measured at a “normal” alveolar PO2 of 110 mmHg. If the hypercapnic response is measured in the presence of hypoxia, then the curve shifts upward, as shown by the upper lines when alveolar PO2 is reduced to 47 mmHg and 37 mmHg. This potentiation likely comes from the peripheral chemoreceptors, whose firing rate is potentiated in the presence of both stimuli. Consequently, when a patient is both hypoxic and hypercapnic, then they are likely to have a very high drive to breathe, and when this occurs they are likely to feel very short of breath—the topic of the last chapter.",True,Peripheral Chemoreceptors,Figure 17.8,Central Control Mechanisms,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.8.png,Figure 17.8: Hypercapnic ventilatory responses with varying degrees of hypoxia.
31e35a20-7574-49b4-9e32-091542efbba2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Likewise, the hypercapnic ventilatory response is exaggerated in the presence of hypoxia (see figure 17.8). The hypercapnic ventilatory response we have just looked at was measured at a “normal” alveolar PO2 of 110 mmHg. If the hypercapnic response is measured in the presence of hypoxia, then the curve shifts upward, as shown by the upper lines when alveolar PO2 is reduced to 47 mmHg and 37 mmHg. This potentiation likely comes from the peripheral chemoreceptors, whose firing rate is potentiated in the presence of both stimuli. Consequently, when a patient is both hypoxic and hypercapnic, then they are likely to have a very high drive to breathe, and when this occurs they are likely to feel very short of breath—the topic of the last chapter.",True,Peripheral Chemoreceptors,Figure 17.8,17. Control of Breathing,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/17.8.png,Figure 17.8: Hypercapnic ventilatory responses with varying degrees of hypoxia.
930141ab-dbdf-4562-bc75-e18a5e060da3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"The chemoreflexes modulate breathing to maintain constant arterial blood gases and pH. These reflexes are initiated by central sensors that respond to hypoxia and peripheral sensors that respond to hypercapnia, hypoxia, and changes in arterial pH. Together these sensors can maintain arterial blood gases within narrow ranges despite large changes in oxygen consumption and CO2 production associated with changes in metabolic rate.",True,Peripheral Chemoreceptors,,,,
f7e25553-c58f-4b17-8385-51d76ff9febf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,Text,False,Text,,,,
eb2d64a9-4425-41ec-a4a7-7c433faedc13,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Levitsky, Michael G. “Chapter 9: Control of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
096ba32c-db71-4daf-9e91-7d46cf736ecc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"West, John B. “Chapter 8: Control of Ventilation—How Gas Exchange Is Regulated.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
1d2b69f8-97f5-4d0f-a1d6-0eec14766a5e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,17. Control of Breathing,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/control-of-breathing/,"Widdicombe, John G., and Andrew S. Davis. “Chapter 8” and “Chapter 9.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
db0a65e0-e669-4647-b737-5a183e68a90c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The hemoglobin molecule consists of four polypeptide chains, two alpha and two beta (figure 16.1). These proteins comprise the “globin” part of the molecule but are not simply structural as they contain sites that are capable of receiving CO2 and also hydrogen ions—a handy function, as you might imagine. Some anemias, such as sickle cell anemia, involve a conformational change in these proteins and diminish the molecule’s gas carrying ability.",True,Text,Figure 16.1,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.1.png,Figure 16.1: Basic structure of hemoglobin.
db0a65e0-e669-4647-b737-5a183e68a90c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The hemoglobin molecule consists of four polypeptide chains, two alpha and two beta (figure 16.1). These proteins comprise the “globin” part of the molecule but are not simply structural as they contain sites that are capable of receiving CO2 and also hydrogen ions—a handy function, as you might imagine. Some anemias, such as sickle cell anemia, involve a conformational change in these proteins and diminish the molecule’s gas carrying ability.",True,Text,Figure 16.1,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.1.png,Figure 16.1: Basic structure of hemoglobin.
db0a65e0-e669-4647-b737-5a183e68a90c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The hemoglobin molecule consists of four polypeptide chains, two alpha and two beta (figure 16.1). These proteins comprise the “globin” part of the molecule but are not simply structural as they contain sites that are capable of receiving CO2 and also hydrogen ions—a handy function, as you might imagine. Some anemias, such as sickle cell anemia, involve a conformational change in these proteins and diminish the molecule’s gas carrying ability.",True,Text,Figure 16.1,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.1.png,Figure 16.1: Basic structure of hemoglobin.
b3772caa-6325-41b5-beea-7c431fd6d4b3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The heme component of hemoglobin is an iron-containing porphyrin molecule capable of binding with oxygen. Each of the four polypeptide chains contains a heme molecule, meaning that each hemoglobin molecule is capable of transporting four oxygen molecules. It is also worth noting that binding of oxygen to the heme molecule induces a conformational change that results in oxyhemoglobin having some different behaviors and indeed color to deoxyhemoglobin. We will look at some of these differences in behavior later on.",True,Text,,,,
305cc335-e478-4f77-85c3-749b48edc277,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"It is also worth reviewing hemoglobin’s home here as well—the red blood cell (RBC). The red blood cell’s classic biconcave shape provides a large surface area for gas exchange and also means that no hemoglobin molecule inside is very far from the edge of the cell, cutting down on the diffusion distance of gases. The cell is also very flexible, making it capable of squeezing through narrow and twisting capillaries so that its walls and those of the capillary may be in close contact and again diffusion distances are reduced.",True,Text,,,,
396c63b3-8995-41de-a103-31ebc88c8ab7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Each RBC is capable of holding up to 250 million hemoglobin molecules, so consequently is capable of holding one billion oxygen molecules; as such the RBC fulfills its primary role of oxygen transport well. This oxygen transport system fails in anemias that result in either too few red blood cells or too little hemoglobin in each cell (or both). Now let us look at the behavior of hemoglobin.",True,Text,,,,
b3a2853f-4d49-466c-b233-b1e3ad132937,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The behavior of hemoglobin is best described by the oxygen saturation curve (figure 16.2), and this is one of the most important curves to understand in medicine. The curve shows the percentage of hemoglobin that has all of its heme molecules bound with oxygen (i.e., are saturated). So for example a 50 percent saturation would mean that half of the heme sites were occupied by oxygen. The curve shows percentage saturation in relation to oxygen partial pressure, and what should be immediately noticeable is that the higher the partial pressure of oxygen then the greater the saturation. But the relationship is far from linear and its shape offers several important physiological advantages. If it helps understand it, think of this curve as an instruction manual for hemoglobin, telling how saturated it should be at any PO2. In reality it is an enzyme kinetics curve, describing hemoglobin’s affinity for oxygen over a range of PO2.",True,Text,Figure 16.2,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.2.png,Figure 16.2: Hemoglobin saturation curve.
b3a2853f-4d49-466c-b233-b1e3ad132937,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The behavior of hemoglobin is best described by the oxygen saturation curve (figure 16.2), and this is one of the most important curves to understand in medicine. The curve shows the percentage of hemoglobin that has all of its heme molecules bound with oxygen (i.e., are saturated). So for example a 50 percent saturation would mean that half of the heme sites were occupied by oxygen. The curve shows percentage saturation in relation to oxygen partial pressure, and what should be immediately noticeable is that the higher the partial pressure of oxygen then the greater the saturation. But the relationship is far from linear and its shape offers several important physiological advantages. If it helps understand it, think of this curve as an instruction manual for hemoglobin, telling how saturated it should be at any PO2. In reality it is an enzyme kinetics curve, describing hemoglobin’s affinity for oxygen over a range of PO2.",True,Text,Figure 16.2,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.2.png,Figure 16.2: Hemoglobin saturation curve.
b3a2853f-4d49-466c-b233-b1e3ad132937,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The behavior of hemoglobin is best described by the oxygen saturation curve (figure 16.2), and this is one of the most important curves to understand in medicine. The curve shows the percentage of hemoglobin that has all of its heme molecules bound with oxygen (i.e., are saturated). So for example a 50 percent saturation would mean that half of the heme sites were occupied by oxygen. The curve shows percentage saturation in relation to oxygen partial pressure, and what should be immediately noticeable is that the higher the partial pressure of oxygen then the greater the saturation. But the relationship is far from linear and its shape offers several important physiological advantages. If it helps understand it, think of this curve as an instruction manual for hemoglobin, telling how saturated it should be at any PO2. In reality it is an enzyme kinetics curve, describing hemoglobin’s affinity for oxygen over a range of PO2.",True,Text,Figure 16.2,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.2.png,Figure 16.2: Hemoglobin saturation curve.
240bd48e-3307-4e02-a6c4-3980b6721979,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"First let us put the curve in a physiological context. The alveolar PO2 is around 100 mmHg. This means that as blood passes the alveoli and is exposed to this PO2, then oxygen saturation becomes close to 100 percent, about 98 percent. The first important physiological feature of this curve is that PO2 can fall a considerably long way before it has an impact on oxygen saturation. So, taking time to look at the numbers on the graph, let us say, for example, that a patient begins to hypoventilate and alveolar PO2 falls to 70 mmHg; while this is a considerable fall in PO2, the saturation will only fall a few percentage points, and PO2 must fall to 50 before significant loss of saturation, or desaturation, occurs. Below 50, however, notice how the curve rapidly steepens, and now for a small change in PO2, we get a large desaturation.",True,Text,,,,
57274494-19e2-4442-a9f6-72dc7f08e65a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"This steep section of the curve is therefore clinically critical. If your patient’s saturation monitor reads 83 percent what should spring into your mind is it that such a low saturation puts the patient onto the steep part of the curve. It will now take only a small further decline in alveolar PO2 to have a profound effect on saturation, unlike at the top and flat section of the curve where small changes in alveolar PO2 have very little effect on saturation.",True,Text,,,,
ae59bbfa-2b77-438a-a039-3640d3f50564,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"So what is the advantage of having such a steep curve at lower PO2s? Let us look at the physiological situation again. We have already said that the alveolar PO2 of 100 results in a saturation close to 100 percent (i.e., at the lung the hemoglobin has a high affinity for oxygen and becomes fully saturated).",True,Text,,,,
9db43d4c-5e74-4450-aeb0-f34c80abd999,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"At the tissue, however, we want hemoglobin to lose its affinity for oxygen and release some to the metabolizing cells. At the tissue the local PO2 is much lower, around 40, because of the oxygen consumption by the tissue. At the lower PO2, hemoglobin’s affinity for oxygen falls, and it will lose some of its oxygen to the tissue and saturation will fall. This is ideal, as now our oxygen carrier is capable of releasing oxygen where it is needed.",True,Text,,,,
5b86e2bb-12a9-4a32-80fa-554e0dcae3ee,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"If tissue PO2 falls even lower, such as when metabolic rate is high, then more oxygen will be released by hemoglobin as its affinity for oxygen declines with the lower tissue PO2. Therefore the delivery system for oxygen is intrinsically tied to metabolic rate.",True,Text,,,,
56b865af-bc70-47ec-8696-ba94d1f42869,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The shape of this curve makes hemoglobin a remarkable molecule—able to grab oxygen at the oxygen-providing lung, but relinquish it to oxygen-demanding tissue and relinquish more when the tissue needs more. There are other factors that fine-tune the amount of oxygen delivered to tissue to match its oxygen demand. This is summarized in figure 16.3.",True,Text,Figure 16.3,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.3.png,"Figure 16.3: The hemoglobin saturation at the lung (A), at the tissue (B), and at very metabolically active tissue (C)."
56b865af-bc70-47ec-8696-ba94d1f42869,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The shape of this curve makes hemoglobin a remarkable molecule—able to grab oxygen at the oxygen-providing lung, but relinquish it to oxygen-demanding tissue and relinquish more when the tissue needs more. There are other factors that fine-tune the amount of oxygen delivered to tissue to match its oxygen demand. This is summarized in figure 16.3.",True,Text,Figure 16.3,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.3.png,"Figure 16.3: The hemoglobin saturation at the lung (A), at the tissue (B), and at very metabolically active tissue (C)."
56b865af-bc70-47ec-8696-ba94d1f42869,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The shape of this curve makes hemoglobin a remarkable molecule—able to grab oxygen at the oxygen-providing lung, but relinquish it to oxygen-demanding tissue and relinquish more when the tissue needs more. There are other factors that fine-tune the amount of oxygen delivered to tissue to match its oxygen demand. This is summarized in figure 16.3.",True,Text,Figure 16.3,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.3.png,"Figure 16.3: The hemoglobin saturation at the lung (A), at the tissue (B), and at very metabolically active tissue (C)."
96e04902-7f7e-4188-a059-25a5d25aa94e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Shifts in the O2 Saturation Curve,False,Shifts in the O2 Saturation Curve,,,,
fc79ef8e-374a-45ad-b458-bf2beabb7f8e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The metabolic rate of tissue determines its oxygen demand, with more active tissue requiring hemoglobin to relinquish more oxygen. So there are several other factors, beyond low local PO2, that are associated with active tissue that cause hemoglobin to reduce its affinity for oxygen and therefore release it. Tissue with a high metabolic rate tends to have (1) higher temperature, (2) high PCO2, and (3) lower pH. We can look at the effect of each of these factors on the saturation curve.",True,Shifts in the O2 Saturation Curve,,,,
2bb04c75-d144-4a6c-9c8e-4498ac2e1887,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Shifts with temperature: Figure 16.4 shows the saturation curve at difference tissue temperatures. The curve we have just looked at was at 38ºC. Notice that as temperature is reduced, the curve shifts to the left, but more importantly (physiologically) when temperature increases then the curve shifts to the right. Let us look at what this means in terms of hemoglobin’s affinity for oxygen (follow the numbers on the graph again). As before, we will assume that our tissue PO2 is 40 mmHg, and at normal temperatures this results in a saturation of about 70 percent.",True,Shifts in the O2 Saturation Curve,Figure 16.4,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.4.png,Figure 16.4: Effect of temperature on the saturation curve.
2bb04c75-d144-4a6c-9c8e-4498ac2e1887,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Shifts with temperature: Figure 16.4 shows the saturation curve at difference tissue temperatures. The curve we have just looked at was at 38ºC. Notice that as temperature is reduced, the curve shifts to the left, but more importantly (physiologically) when temperature increases then the curve shifts to the right. Let us look at what this means in terms of hemoglobin’s affinity for oxygen (follow the numbers on the graph again). As before, we will assume that our tissue PO2 is 40 mmHg, and at normal temperatures this results in a saturation of about 70 percent.",True,Shifts in the O2 Saturation Curve,Figure 16.4,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.4.png,Figure 16.4: Effect of temperature on the saturation curve.
2bb04c75-d144-4a6c-9c8e-4498ac2e1887,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Shifts with temperature: Figure 16.4 shows the saturation curve at difference tissue temperatures. The curve we have just looked at was at 38ºC. Notice that as temperature is reduced, the curve shifts to the left, but more importantly (physiologically) when temperature increases then the curve shifts to the right. Let us look at what this means in terms of hemoglobin’s affinity for oxygen (follow the numbers on the graph again). As before, we will assume that our tissue PO2 is 40 mmHg, and at normal temperatures this results in a saturation of about 70 percent.",True,Shifts in the O2 Saturation Curve,Figure 16.4,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.4.png,Figure 16.4: Effect of temperature on the saturation curve.
da148794-5848-490d-b6cf-40af24935c19,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Now at the same PO2 but a higher temperature (e.g., 43ºC) the hemoglobin O2 saturation falls to a little over 50 percent, meaning that more oxygen has been relinquished to the tissue (i.e., an increase in temperature reduces hemoglobin’s affinity for oxygen).",True,Shifts in the O2 Saturation Curve,,,,
211cabf9-d406-4501-9908-849d3790c833,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Shifts with CO2: We see a similar situation with a rise in PCO2, shown in figure 16.5 with the saturation curve at different PCO2s. At a normal arterial PCO2 (40 mmHg) we get the same saturation curve that we saw previously. But if PCO2 is raised, such as in the locality of highly active tissue (e.g., 80 mmHg), then the curve shifts rightward. Again this means that hemoglobin’s affinity is lowered at equivalent PO2 and more oxygen is released, resulting in a lower saturation.",True,Shifts in the O2 Saturation Curve,Figure 16.5,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.5.png,Figure 16.5: Effect of PCO2 on the saturation curve.
211cabf9-d406-4501-9908-849d3790c833,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Shifts with CO2: We see a similar situation with a rise in PCO2, shown in figure 16.5 with the saturation curve at different PCO2s. At a normal arterial PCO2 (40 mmHg) we get the same saturation curve that we saw previously. But if PCO2 is raised, such as in the locality of highly active tissue (e.g., 80 mmHg), then the curve shifts rightward. Again this means that hemoglobin’s affinity is lowered at equivalent PO2 and more oxygen is released, resulting in a lower saturation.",True,Shifts in the O2 Saturation Curve,Figure 16.5,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.5.png,Figure 16.5: Effect of PCO2 on the saturation curve.
211cabf9-d406-4501-9908-849d3790c833,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Shifts with CO2: We see a similar situation with a rise in PCO2, shown in figure 16.5 with the saturation curve at different PCO2s. At a normal arterial PCO2 (40 mmHg) we get the same saturation curve that we saw previously. But if PCO2 is raised, such as in the locality of highly active tissue (e.g., 80 mmHg), then the curve shifts rightward. Again this means that hemoglobin’s affinity is lowered at equivalent PO2 and more oxygen is released, resulting in a lower saturation.",True,Shifts in the O2 Saturation Curve,Figure 16.5,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.5.png,Figure 16.5: Effect of PCO2 on the saturation curve.
b7dca429-0ab1-4cc0-8453-0f8954dbb0b6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Shifts with pH: Finally, the same is true for changes in pH, shown in figure 16.6 with the curve at different pHs. When pH falls, as in active tissue, then the curve shifts rightward from its normal position at normal pH (7.4). Again, this result describes a lowered affinity for oxygen, so at equivalent levels of PO2 more oxygen is released when the hemoglobin enters a low pH environment (e.g., 7.2 shown on figure 16.6). Obviously pH and PCO2 are related, and their effect on hemoglobin binding is known as the Bohr effect.",True,Shifts in the O2 Saturation Curve,Figure 16.6,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.6.png,Figure 16.6: Effect of pH on the saturation curve.
b7dca429-0ab1-4cc0-8453-0f8954dbb0b6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Shifts with pH: Finally, the same is true for changes in pH, shown in figure 16.6 with the curve at different pHs. When pH falls, as in active tissue, then the curve shifts rightward from its normal position at normal pH (7.4). Again, this result describes a lowered affinity for oxygen, so at equivalent levels of PO2 more oxygen is released when the hemoglobin enters a low pH environment (e.g., 7.2 shown on figure 16.6). Obviously pH and PCO2 are related, and their effect on hemoglobin binding is known as the Bohr effect.",True,Shifts in the O2 Saturation Curve,Figure 16.6,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.6.png,Figure 16.6: Effect of pH on the saturation curve.
b7dca429-0ab1-4cc0-8453-0f8954dbb0b6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Shifts with pH: Finally, the same is true for changes in pH, shown in figure 16.6 with the curve at different pHs. When pH falls, as in active tissue, then the curve shifts rightward from its normal position at normal pH (7.4). Again, this result describes a lowered affinity for oxygen, so at equivalent levels of PO2 more oxygen is released when the hemoglobin enters a low pH environment (e.g., 7.2 shown on figure 16.6). Obviously pH and PCO2 are related, and their effect on hemoglobin binding is known as the Bohr effect.",True,Shifts in the O2 Saturation Curve,Figure 16.6,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.6.png,Figure 16.6: Effect of pH on the saturation curve.
586eb5e0-d3bf-4f95-8cd4-ded1f58d5fad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"One last factor that causes this rightward shift is 2,3 diphosphoglycerate, or DPG. DPG is an end product of RBC metabolism, and as it increases inside the cell it reduces hemoglobins, affinity for oxygen. Elevated DPG levels are associated with chronic hypoxia, such as experienced at altitude or more pertinently in the presence of chronic lung disease. Conversely, DPG levels are lower in stored blood, so transfused blood may have a problem giving up its oxygen.",True,Shifts in the O2 Saturation Curve,,,,
1fef71c1-4e58-4c5b-a2dd-2ff64270fa82,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,All these factors mean that hemoglobin will deliver more oxygen to busy tissue.,True,Shifts in the O2 Saturation Curve,,,,
3a1b9676-8f37-4ed5-a186-1380b218d734,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Total oxygen carriage: So far we have discussed oxygen transport in terms of hemoglobin only. But despite its lack of solubility, some oxygen can dissolve into the plasma. Realistically this is a very small amount at physiological partial pressures (i.e. at an alveolar PO2 of 100 mmHg only a fraction of a milliliter of oxygen will dissolve into the blood, as figure 16.7 shows).",True,Shifts in the O2 Saturation Curve,Figure 16.7,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.7.png,Figure 16.7: Oxygen carriage.
3a1b9676-8f37-4ed5-a186-1380b218d734,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Total oxygen carriage: So far we have discussed oxygen transport in terms of hemoglobin only. But despite its lack of solubility, some oxygen can dissolve into the plasma. Realistically this is a very small amount at physiological partial pressures (i.e. at an alveolar PO2 of 100 mmHg only a fraction of a milliliter of oxygen will dissolve into the blood, as figure 16.7 shows).",True,Shifts in the O2 Saturation Curve,Figure 16.7,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.7.png,Figure 16.7: Oxygen carriage.
3a1b9676-8f37-4ed5-a186-1380b218d734,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Total oxygen carriage: So far we have discussed oxygen transport in terms of hemoglobin only. But despite its lack of solubility, some oxygen can dissolve into the plasma. Realistically this is a very small amount at physiological partial pressures (i.e. at an alveolar PO2 of 100 mmHg only a fraction of a milliliter of oxygen will dissolve into the blood, as figure 16.7 shows).",True,Shifts in the O2 Saturation Curve,Figure 16.7,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.7.png,Figure 16.7: Oxygen carriage.
4fb823cf-5ec6-4af0-be80-d21a46d8957e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Obviously this amount of oxygen is completely inadequate to support metabolism and illustrates the need for hemoglobin. But this minute amount when added to the O2 combined to the hemoglobin makes up the total O2 content of the blood. When calculating the oxygen content of the blood we must consider both of these compartments—hemoglobin and plasma (figure 16.8).,True,Shifts in the O2 Saturation Curve,Figure 16.8,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.8.png,Figure 16.8: Compartment of blood oxygen content.
4fb823cf-5ec6-4af0-be80-d21a46d8957e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Obviously this amount of oxygen is completely inadequate to support metabolism and illustrates the need for hemoglobin. But this minute amount when added to the O2 combined to the hemoglobin makes up the total O2 content of the blood. When calculating the oxygen content of the blood we must consider both of these compartments—hemoglobin and plasma (figure 16.8).,True,Shifts in the O2 Saturation Curve,Figure 16.8,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.8.png,Figure 16.8: Compartment of blood oxygen content.
4fb823cf-5ec6-4af0-be80-d21a46d8957e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Obviously this amount of oxygen is completely inadequate to support metabolism and illustrates the need for hemoglobin. But this minute amount when added to the O2 combined to the hemoglobin makes up the total O2 content of the blood. When calculating the oxygen content of the blood we must consider both of these compartments—hemoglobin and plasma (figure 16.8).,True,Shifts in the O2 Saturation Curve,Figure 16.8,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.8.png,Figure 16.8: Compartment of blood oxygen content.
d71c9045-47aa-47c4-8a33-9f12e8082617,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Calculating the O2 Content of Blood,False,Calculating the O2 Content of Blood,,,,
69c1fbb3-0b29-4514-8c8a-c0863b81c461,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"To calculate the arterial oxygen content (CaO2) let us first look at the factors affecting the majority of the O2 (i.e., that carried by hemoglobin).",True,Calculating the O2 Content of Blood,,,,
69c2b43e-592a-46b1-96c1-da3fe9945ea7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,(1) This will be determined by the amount of hemoglobin in the blood (measured in mg/dL). So let us start building the equation.,True,Calculating the O2 Content of Blood,,,,
33932dfc-4b2a-4a78-9760-aba3490f8456,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Equation 16.1,True,Calculating the O2 Content of Blood,,,,
d456d8cd-fad4-4ca1-98be-4008fb1eaa32,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,[latex]C_aO_2 = Hb (mg/dL)...[/latex],True,Calculating the O2 Content of Blood,,,,
b5b2dd19-2d9a-4a24-8cf8-f07cb3669f6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"(2) Second, we must consider the oxygen carrying capacity of Hb, which is 1.34 mL O2/gm Hb. So we multiply the amount of Hb by its carrying capacity.",True,Calculating the O2 Content of Blood,,,,
58c0c348-28c4-421e-a673-d53c692e9c56,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Equation 16.2,True,Calculating the O2 Content of Blood,,,,
84fd4d16-1c87-49dc-af8f-00fbbd924a75,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"[latex]C_aO_2 = Hb (mg/dL) \times 1.34\, O_2/gmHb...[/latex]",True,Calculating the O2 Content of Blood,,,,
fb6453fd-b83c-4d3f-8ff2-ab30dd947845,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"(3) But that carrying capacity might not have been reached by all the Hb (i.e., the Hb may not be fully saturated). So to account for this, we multiply by the saturation (SaO2).",True,Calculating the O2 Content of Blood,,,,
7a55c7b8-49eb-41b1-bdaa-390a39806795,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Equation 16.3,True,Calculating the O2 Content of Blood,,,,
30941166-4918-4c1d-a080-a78d798357d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"[latex]C_aO_2 = Hb (mg/dL) \times 1.34\, O_2/gmHb \times S_aO_2...[/latex]",True,Calculating the O2 Content of Blood,,,,
957b8eb3-a276-49c1-a654-407f3a583575,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"(4) So far that takes care of the O2 associated with Hb (normally about 98 percent of the total). Now we must add the O2 in plasma to the equation. We do this by measuring the PaO2 and multiplying it by a solubility coefficient (0.003 mL O2/mmHg/dL) to convert it from a partial pressure to milliliters. Removing the units makes this long but simple equation a little easier to understand. It has two components, representing the two compartments for O2 carriage.",True,Calculating the O2 Content of Blood,,,,
cf6cbe39-934e-4e9f-9bdc-4e65f86ad420,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Equation 16.4,True,Calculating the O2 Content of Blood,,,,
8e138379-435d-4053-a62f-7d8fcdd0fe86,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,[latex]C_aO_2 = (Hb \times 1.34 \times S_aO_2) + (P_aO_2 \times 0.003)[/latex],True,Calculating the O2 Content of Blood,,,,
286888cb-8929-4ded-b263-66f1cfff7b2d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The plasma component is usually inconsequential, but may become more important when blood is exposed to an elevated alveolar PO2, such as during oxygen or hyperbaric therapy.",True,Calculating the O2 Content of Blood,,,,
4ca1b441-ceab-496d-80f2-94e3206739c6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Summary,False,Summary,,,,
4cb10e9b-4aca-4b40-bea4-f60cbbaac50e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"So to summarize, as oxygen’s lack of solubility means metabolic demands cannot be met by dissolved oxygen alone, the vast majority of oxygen is transported by hemoglobin, a molecule that is beautifully designed to pick up oxygen at the lung and release oxygen in proportion to the tissue’s demand. We will see more of hemoglobin’s sophistication when we address CO2 carriage.",True,Summary,,,,
2e673d90-24b6-43a0-a25a-24f82ffd7cd1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,CO2 Transport,False,CO2 Transport,,,,
d9051fb8-839a-427f-beac-fc950efbeb58,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Unlike oxygen, carbon dioxide is soluble enough that it does not need a protein carrier like oxygen needs hemoglobin to enter and exit plasma. However, this does not necessarily mean that CO2 transport is simple. The complication this time is that free dissolved CO2 forms carbonic acid, which can threaten pH homeostasis. So most CO2 is not transported in the dissolved form. Most (approximately 70 percent) of the CO2 that emerges from metabolizing tissue is converted to bicarbonate with the help of enzymes within red blood cells. We will look at this more closely in a moment. About 15–25 percent is transported on hemoglobin.",True,CO2 Transport,,,,
24b87318-a185-4f2a-835a-7964f8ae2adc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Transport on Hemoglobin (15–25 Percent),False,Transport on Hemoglobin (15–25 Percent),,,,
ef098572-d2cf-48dd-8034-55012e836418,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Carbon dioxide can bind to the terminal amine groups of hemoglobin’s polypeptide chains forming carbaminohemoglobin. It is worth noting a couple of points about this. First, CO2 does not compete with oxygen to bind to Hb—the binding sites are completely different and hemoglobin can hold both CO2 and O2 at the same time. Second, deoxyhemoglobin is a better carrier of CO2 than oxyhemoglobin is; consequently at the tissue where hemoglobin is losing its oxygen it is becoming a more efficient CO2 transporter. This is known as the Haldane effect.",True,Transport on Hemoglobin (15–25 Percent),,,,
5f8a0bdf-e46c-40e2-a468-99b7d8542128,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Transport as Dissolved CO2 (About 7 Percent),False,Transport as Dissolved CO2 (About 7 Percent),,,,
f013bd7f-7123-4533-a857-58d2c7ecd296,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"A little CO2 combines with water to produce carbonic acid, the dissociated hydrogen form that must be buffered by plasma proteins, such as albumin.",True,Transport as Dissolved CO2 (About 7 Percent),,,,
52a5f109-3641-4607-b825-aed22e54e09b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Transport as Bicarbonate (About 70 Percent),False,Transport as Bicarbonate (About 70 Percent),,,,
9af068ba-0fe2-4c0e-aac6-8af1be71c06e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Seventy percent of the CO2 enters red blood cells, and once inside a familiar reaction occurs (equation 16.5). The CO2 binds with water in the cytoplasm, producing carbonic acid, which then dissociates into a hydrogen ion and a bicarbonate ion.",True,Transport as Bicarbonate (About 70 Percent),,,,
4f6aba57-0379-4278-ae69-eab956a84a3b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,This reversible reaction is accelerated by the enzyme carbonic anhydrase and is driven rapidly to the right by the high concentration of CO2 at the tissue.,True,Transport as Bicarbonate (About 70 Percent),,,,
7989eb2f-4279-470b-a4a4-98f5f7e69e82,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The hydrogen ion produced helps shift the oxygen saturation curve to the right and so promotes further release of oxygen to the tissue. Hemoglobin then serves yet another purpose by buffering the proton with its polypeptide chains. Deoxyhemoglobin is a better proton acceptor than oxyhemoglobin, so as the hemoglobin loses its oxygen at the tissue it becomes a better pH buffer. This reduces the amount of hydrogen ion on the right side of our equation and moves the equation to the right, promoting the conversion of more CO2.",True,Transport as Bicarbonate (About 70 Percent),,,,
d8839c18-7062-4e13-b4f2-9ad0cc6058b4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Equation 16.5,True,Transport as Bicarbonate (About 70 Percent),,,,
8debef58-2bd0-4963-ac74-2ca1347153e1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],False,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
ce63434c-8f96-4e2f-8362-b545fcf90d39,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,High concentrations of CO2 at the tissue push this equation right to produce bicarbonate.,True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
abd5629c-c673-4e9a-8df0-aa831db05237,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The bicarbonate ion is pumped out of the cell, but without intervention this would leave the inside of the cell too positively charged as the negative charge of the bicarbonate is lost. To maintain electroneutrality the bicarbonate is exchanged for a chloride ion; this process is referred to as the chloride shift. The formation of bicarbonate at the tissue is summarized in figure 16.9.",True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],Figure 16.9,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.9.png,Figure 16.9: Formation of bicarbonate at the tissue.
abd5629c-c673-4e9a-8df0-aa831db05237,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The bicarbonate ion is pumped out of the cell, but without intervention this would leave the inside of the cell too positively charged as the negative charge of the bicarbonate is lost. To maintain electroneutrality the bicarbonate is exchanged for a chloride ion; this process is referred to as the chloride shift. The formation of bicarbonate at the tissue is summarized in figure 16.9.",True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],Figure 16.9,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.9.png,Figure 16.9: Formation of bicarbonate at the tissue.
abd5629c-c673-4e9a-8df0-aa831db05237,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"The bicarbonate ion is pumped out of the cell, but without intervention this would leave the inside of the cell too positively charged as the negative charge of the bicarbonate is lost. To maintain electroneutrality the bicarbonate is exchanged for a chloride ion; this process is referred to as the chloride shift. The formation of bicarbonate at the tissue is summarized in figure 16.9.",True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],Figure 16.9,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.9.png,Figure 16.9: Formation of bicarbonate at the tissue.
fc091c03-7cae-437e-a615-41436e19bee0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,The CO2 now travels through the bloodstream as bicarbonate toward the lungs. At the lungs the process is basically reversed. The partial pressure of CO2 at the lungs is low; consequently our equation is driven toward the left-hand side as CO2 leaves toward the low alveolar PCO2 (equation 16.6).,True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
215659fb-025a-4e62-a33c-af3b48508e3a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Equation 16.6,True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
3f707fe5-c4de-4cec-8f95-5961d44e009b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,←,False,←,,,,
70d42d98-ce38-4c12-9f5b-cd34e4fcc912,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,High bicarbonate and low CO2 at the lung force the equation leftward.,True,←,,,,
b186eeeb-b127-4a4e-aa75-ac5446c366c5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,The high alveolar PO2 also promotes the leftward movement—binding of oxygen to hemoglobin makes hemoglobin a less effective proton binder so it loses the proton and raises the amount of substrate on the right-hand side and thereby promotes reformation of CO2. The Haldane effect is also reversed—as hemoglobin gains oxygen at the lung it loses its affinity for CO2 and releases it into the plasma. This raises plasma PCO2 and promotes diffusion of CO2 into the alveoli for expulsion.,True,←,,,,
43f2b04d-f366-4f0b-87d5-ffafb597f78b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Likewise the chloride shift is reversed and bicarbonate reenters the cell as chloride is pumped back out.,True,←,,,,
9116d612-5ccb-474a-8573-3bf4b72b4eda,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"All these moves help promote the right-to-left direction of our now infamous equation and the re-forming of CO2. Alveolar ventilation gets rid of the re-formed CO2 to the atmosphere, maintaining the alveolar PCO2 at relatively low levels and the direction of the equation right-to-left. The reformation of CO2 at the lungs is summarized in figure 16.10.",True,←,Figure 16.10,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.10.png,Figure 16.10: Reformation of CO2 at the lungs.
9116d612-5ccb-474a-8573-3bf4b72b4eda,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"All these moves help promote the right-to-left direction of our now infamous equation and the re-forming of CO2. Alveolar ventilation gets rid of the re-formed CO2 to the atmosphere, maintaining the alveolar PCO2 at relatively low levels and the direction of the equation right-to-left. The reformation of CO2 at the lungs is summarized in figure 16.10.",True,←,Figure 16.10,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.10.png,Figure 16.10: Reformation of CO2 at the lungs.
9116d612-5ccb-474a-8573-3bf4b72b4eda,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"All these moves help promote the right-to-left direction of our now infamous equation and the re-forming of CO2. Alveolar ventilation gets rid of the re-formed CO2 to the atmosphere, maintaining the alveolar PCO2 at relatively low levels and the direction of the equation right-to-left. The reformation of CO2 at the lungs is summarized in figure 16.10.",True,←,Figure 16.10,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.10.png,Figure 16.10: Reformation of CO2 at the lungs.
b90fb296-7746-4814-8ddb-5bcdf8f39c2c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,The CO2 “Dissociation” Curve,False,The CO2 “Dissociation” Curve,,,,
d819d8c4-d693-44d1-8d35-4c4d37acecb7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"So, for want of a better name, we can also draw a CO2 dissociation or saturation curve, as is shown in figure 16.11. The graph shows the CO2 concentration in blood across a wide range of PCO2 and shows the effect of Hb O2 saturation on CO2 carriage. The CO2 dissociation curve is unlike the oxygen saturation curve and is virtually linear (i.e., the higher the PCO2, the higher the CO2 content of the blood); there is no plateau to the curve as we saw with O2 transport. The ramification of this is that the lower the alveolar PCO2, the lower the blood PCO2, and the higher the alveolar PCO2, the higher the blood PCO2. It is a very simple relationship that ends with the obvious statement that the more you breathe, the lower arterial CO2 becomes. It is worth reminding ourselves here that this is not a relationship seen with oxygen that is limited by the capacity of hemoglobin (breathing more does not necessarily result in more oxygen in the bloodstream). The other aspect to note here is the effect of hemoglobin’s oxygen saturation on carbon dioxide carriage. This has clinical ramifications, so we will look at this more closely.",True,The CO2 “Dissociation” Curve,Figure 16.11,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.11.png,Figure 16.11: CO2 dissociation curve.
d819d8c4-d693-44d1-8d35-4c4d37acecb7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"So, for want of a better name, we can also draw a CO2 dissociation or saturation curve, as is shown in figure 16.11. The graph shows the CO2 concentration in blood across a wide range of PCO2 and shows the effect of Hb O2 saturation on CO2 carriage. The CO2 dissociation curve is unlike the oxygen saturation curve and is virtually linear (i.e., the higher the PCO2, the higher the CO2 content of the blood); there is no plateau to the curve as we saw with O2 transport. The ramification of this is that the lower the alveolar PCO2, the lower the blood PCO2, and the higher the alveolar PCO2, the higher the blood PCO2. It is a very simple relationship that ends with the obvious statement that the more you breathe, the lower arterial CO2 becomes. It is worth reminding ourselves here that this is not a relationship seen with oxygen that is limited by the capacity of hemoglobin (breathing more does not necessarily result in more oxygen in the bloodstream). The other aspect to note here is the effect of hemoglobin’s oxygen saturation on carbon dioxide carriage. This has clinical ramifications, so we will look at this more closely.",True,The CO2 “Dissociation” Curve,Figure 16.11,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.11.png,Figure 16.11: CO2 dissociation curve.
d819d8c4-d693-44d1-8d35-4c4d37acecb7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"So, for want of a better name, we can also draw a CO2 dissociation or saturation curve, as is shown in figure 16.11. The graph shows the CO2 concentration in blood across a wide range of PCO2 and shows the effect of Hb O2 saturation on CO2 carriage. The CO2 dissociation curve is unlike the oxygen saturation curve and is virtually linear (i.e., the higher the PCO2, the higher the CO2 content of the blood); there is no plateau to the curve as we saw with O2 transport. The ramification of this is that the lower the alveolar PCO2, the lower the blood PCO2, and the higher the alveolar PCO2, the higher the blood PCO2. It is a very simple relationship that ends with the obvious statement that the more you breathe, the lower arterial CO2 becomes. It is worth reminding ourselves here that this is not a relationship seen with oxygen that is limited by the capacity of hemoglobin (breathing more does not necessarily result in more oxygen in the bloodstream). The other aspect to note here is the effect of hemoglobin’s oxygen saturation on carbon dioxide carriage. This has clinical ramifications, so we will look at this more closely.",True,The CO2 “Dissociation” Curve,Figure 16.11,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.11.png,Figure 16.11: CO2 dissociation curve.
1a3609d2-2c4e-42a8-8d0c-313f22cb6f86,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"When deoxygenated, hemoglobin’s structure promotes binding of CO2 and buffering of protons by the polypeptide chains. So when O2 saturation is zero, the CO2 and proton carrying capability of Hb is high. As already mentioned, this means that when Hb is in its deoxygenated form at the tissue, its CO2 carrying ability is increased.",True,The CO2 “Dissociation” Curve,,,,
b8b21369-d788-4de9-8042-8259b1d039cf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"When we get to the lung, however, the Hb is exposed to the high alveolar PO2 and oxygen binds to the heme sites and becomes saturated; this causes a conformational change, and the CO2 and proton carrying ability is reduced. So conveniently CO2 release is promoted at the lung.",True,The CO2 “Dissociation” Curve,,,,
da0e740b-9ae7-4eaa-8b46-ed5cadf7fa9c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Although CO2 is highly soluble, very little of it can be transported as dissolved CO2 in plasma because of its effect on pH. The majority is converted to bicarbonate in red blood cells and transported in plasma, while about 25 percent is transported bound to hemoglobin.",True,The CO2 “Dissociation” Curve,,,,
6fcda0a7-cfbe-4ecb-a7dd-93471a531318,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,Text,False,Text,,,,
4ed813be-9b8e-460b-bafa-7979fda65ba0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Levitsky, Michael G. “Chapter 7: Transport of Oxygen and Carbon Dioxide in the Blood.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
d6a16cf9-d059-46b3-b7e2-0261a878af63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"West, John B. “Chapter 6: Gas Transport by the Blood—How Gases Are Moved to the Peripheral Tissues.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
eebcdd0d-d4a0-48ea-b604-9534d41496ed,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,CO2 Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-2,"Widdicombe, John G., and Andrew S. Davis. “Chapter 6.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
791976bc-6385-4d51-86b2-6312519adb76,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The hemoglobin molecule consists of four polypeptide chains, two alpha and two beta (figure 16.1). These proteins comprise the “globin” part of the molecule but are not simply structural as they contain sites that are capable of receiving CO2 and also hydrogen ions—a handy function, as you might imagine. Some anemias, such as sickle cell anemia, involve a conformational change in these proteins and diminish the molecule’s gas carrying ability.",True,Text,Figure 16.1,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.1.png,Figure 16.1: Basic structure of hemoglobin.
791976bc-6385-4d51-86b2-6312519adb76,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The hemoglobin molecule consists of four polypeptide chains, two alpha and two beta (figure 16.1). These proteins comprise the “globin” part of the molecule but are not simply structural as they contain sites that are capable of receiving CO2 and also hydrogen ions—a handy function, as you might imagine. Some anemias, such as sickle cell anemia, involve a conformational change in these proteins and diminish the molecule’s gas carrying ability.",True,Text,Figure 16.1,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.1.png,Figure 16.1: Basic structure of hemoglobin.
791976bc-6385-4d51-86b2-6312519adb76,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The hemoglobin molecule consists of four polypeptide chains, two alpha and two beta (figure 16.1). These proteins comprise the “globin” part of the molecule but are not simply structural as they contain sites that are capable of receiving CO2 and also hydrogen ions—a handy function, as you might imagine. Some anemias, such as sickle cell anemia, involve a conformational change in these proteins and diminish the molecule’s gas carrying ability.",True,Text,Figure 16.1,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.1.png,Figure 16.1: Basic structure of hemoglobin.
a57c00d2-ee81-418d-bb21-a9a6c587aef5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The heme component of hemoglobin is an iron-containing porphyrin molecule capable of binding with oxygen. Each of the four polypeptide chains contains a heme molecule, meaning that each hemoglobin molecule is capable of transporting four oxygen molecules. It is also worth noting that binding of oxygen to the heme molecule induces a conformational change that results in oxyhemoglobin having some different behaviors and indeed color to deoxyhemoglobin. We will look at some of these differences in behavior later on.",True,Text,,,,
4348de8b-3f16-48ad-a6cc-02b74c1cf8b0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"It is also worth reviewing hemoglobin’s home here as well—the red blood cell (RBC). The red blood cell’s classic biconcave shape provides a large surface area for gas exchange and also means that no hemoglobin molecule inside is very far from the edge of the cell, cutting down on the diffusion distance of gases. The cell is also very flexible, making it capable of squeezing through narrow and twisting capillaries so that its walls and those of the capillary may be in close contact and again diffusion distances are reduced.",True,Text,,,,
162ade07-8471-419d-a20a-09b7a0bd95f8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Each RBC is capable of holding up to 250 million hemoglobin molecules, so consequently is capable of holding one billion oxygen molecules; as such the RBC fulfills its primary role of oxygen transport well. This oxygen transport system fails in anemias that result in either too few red blood cells or too little hemoglobin in each cell (or both). Now let us look at the behavior of hemoglobin.",True,Text,,,,
53c8bcb0-90b7-4e6a-904d-0b7a12d94287,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The behavior of hemoglobin is best described by the oxygen saturation curve (figure 16.2), and this is one of the most important curves to understand in medicine. The curve shows the percentage of hemoglobin that has all of its heme molecules bound with oxygen (i.e., are saturated). So for example a 50 percent saturation would mean that half of the heme sites were occupied by oxygen. The curve shows percentage saturation in relation to oxygen partial pressure, and what should be immediately noticeable is that the higher the partial pressure of oxygen then the greater the saturation. But the relationship is far from linear and its shape offers several important physiological advantages. If it helps understand it, think of this curve as an instruction manual for hemoglobin, telling how saturated it should be at any PO2. In reality it is an enzyme kinetics curve, describing hemoglobin’s affinity for oxygen over a range of PO2.",True,Text,Figure 16.2,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.2.png,Figure 16.2: Hemoglobin saturation curve.
53c8bcb0-90b7-4e6a-904d-0b7a12d94287,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The behavior of hemoglobin is best described by the oxygen saturation curve (figure 16.2), and this is one of the most important curves to understand in medicine. The curve shows the percentage of hemoglobin that has all of its heme molecules bound with oxygen (i.e., are saturated). So for example a 50 percent saturation would mean that half of the heme sites were occupied by oxygen. The curve shows percentage saturation in relation to oxygen partial pressure, and what should be immediately noticeable is that the higher the partial pressure of oxygen then the greater the saturation. But the relationship is far from linear and its shape offers several important physiological advantages. If it helps understand it, think of this curve as an instruction manual for hemoglobin, telling how saturated it should be at any PO2. In reality it is an enzyme kinetics curve, describing hemoglobin’s affinity for oxygen over a range of PO2.",True,Text,Figure 16.2,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.2.png,Figure 16.2: Hemoglobin saturation curve.
53c8bcb0-90b7-4e6a-904d-0b7a12d94287,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The behavior of hemoglobin is best described by the oxygen saturation curve (figure 16.2), and this is one of the most important curves to understand in medicine. The curve shows the percentage of hemoglobin that has all of its heme molecules bound with oxygen (i.e., are saturated). So for example a 50 percent saturation would mean that half of the heme sites were occupied by oxygen. The curve shows percentage saturation in relation to oxygen partial pressure, and what should be immediately noticeable is that the higher the partial pressure of oxygen then the greater the saturation. But the relationship is far from linear and its shape offers several important physiological advantages. If it helps understand it, think of this curve as an instruction manual for hemoglobin, telling how saturated it should be at any PO2. In reality it is an enzyme kinetics curve, describing hemoglobin’s affinity for oxygen over a range of PO2.",True,Text,Figure 16.2,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.2.png,Figure 16.2: Hemoglobin saturation curve.
2ce224e9-15c2-4486-9a65-82991d744f6e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"First let us put the curve in a physiological context. The alveolar PO2 is around 100 mmHg. This means that as blood passes the alveoli and is exposed to this PO2, then oxygen saturation becomes close to 100 percent, about 98 percent. The first important physiological feature of this curve is that PO2 can fall a considerably long way before it has an impact on oxygen saturation. So, taking time to look at the numbers on the graph, let us say, for example, that a patient begins to hypoventilate and alveolar PO2 falls to 70 mmHg; while this is a considerable fall in PO2, the saturation will only fall a few percentage points, and PO2 must fall to 50 before significant loss of saturation, or desaturation, occurs. Below 50, however, notice how the curve rapidly steepens, and now for a small change in PO2, we get a large desaturation.",True,Text,,,,
7ef31414-4ffd-41e8-ae10-f844b74edc62,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"This steep section of the curve is therefore clinically critical. If your patient’s saturation monitor reads 83 percent what should spring into your mind is it that such a low saturation puts the patient onto the steep part of the curve. It will now take only a small further decline in alveolar PO2 to have a profound effect on saturation, unlike at the top and flat section of the curve where small changes in alveolar PO2 have very little effect on saturation.",True,Text,,,,
16ed5e68-a70f-43cc-a5be-86fa08eeb92f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"So what is the advantage of having such a steep curve at lower PO2s? Let us look at the physiological situation again. We have already said that the alveolar PO2 of 100 results in a saturation close to 100 percent (i.e., at the lung the hemoglobin has a high affinity for oxygen and becomes fully saturated).",True,Text,,,,
7ff1e491-ba7f-46cb-a214-8cf9b87f1c28,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"At the tissue, however, we want hemoglobin to lose its affinity for oxygen and release some to the metabolizing cells. At the tissue the local PO2 is much lower, around 40, because of the oxygen consumption by the tissue. At the lower PO2, hemoglobin’s affinity for oxygen falls, and it will lose some of its oxygen to the tissue and saturation will fall. This is ideal, as now our oxygen carrier is capable of releasing oxygen where it is needed.",True,Text,,,,
3e8c6302-903d-4c0b-870a-2fe21cbbc8d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"If tissue PO2 falls even lower, such as when metabolic rate is high, then more oxygen will be released by hemoglobin as its affinity for oxygen declines with the lower tissue PO2. Therefore the delivery system for oxygen is intrinsically tied to metabolic rate.",True,Text,,,,
5cae69d7-06ab-47a0-95ad-2be530fa7a33,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The shape of this curve makes hemoglobin a remarkable molecule—able to grab oxygen at the oxygen-providing lung, but relinquish it to oxygen-demanding tissue and relinquish more when the tissue needs more. There are other factors that fine-tune the amount of oxygen delivered to tissue to match its oxygen demand. This is summarized in figure 16.3.",True,Text,Figure 16.3,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.3.png,"Figure 16.3: The hemoglobin saturation at the lung (A), at the tissue (B), and at very metabolically active tissue (C)."
5cae69d7-06ab-47a0-95ad-2be530fa7a33,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The shape of this curve makes hemoglobin a remarkable molecule—able to grab oxygen at the oxygen-providing lung, but relinquish it to oxygen-demanding tissue and relinquish more when the tissue needs more. There are other factors that fine-tune the amount of oxygen delivered to tissue to match its oxygen demand. This is summarized in figure 16.3.",True,Text,Figure 16.3,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.3.png,"Figure 16.3: The hemoglobin saturation at the lung (A), at the tissue (B), and at very metabolically active tissue (C)."
5cae69d7-06ab-47a0-95ad-2be530fa7a33,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The shape of this curve makes hemoglobin a remarkable molecule—able to grab oxygen at the oxygen-providing lung, but relinquish it to oxygen-demanding tissue and relinquish more when the tissue needs more. There are other factors that fine-tune the amount of oxygen delivered to tissue to match its oxygen demand. This is summarized in figure 16.3.",True,Text,Figure 16.3,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.3.png,"Figure 16.3: The hemoglobin saturation at the lung (A), at the tissue (B), and at very metabolically active tissue (C)."
a54c8164-66fa-4f32-82d4-78ec8a7bc36a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Shifts in the O2 Saturation Curve,False,Shifts in the O2 Saturation Curve,,,,
79735da6-bfc1-4403-9542-1095cb936ab5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The metabolic rate of tissue determines its oxygen demand, with more active tissue requiring hemoglobin to relinquish more oxygen. So there are several other factors, beyond low local PO2, that are associated with active tissue that cause hemoglobin to reduce its affinity for oxygen and therefore release it. Tissue with a high metabolic rate tends to have (1) higher temperature, (2) high PCO2, and (3) lower pH. We can look at the effect of each of these factors on the saturation curve.",True,Shifts in the O2 Saturation Curve,,,,
673fee11-02ed-4d07-8892-619d6f422272,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Shifts with temperature: Figure 16.4 shows the saturation curve at difference tissue temperatures. The curve we have just looked at was at 38ºC. Notice that as temperature is reduced, the curve shifts to the left, but more importantly (physiologically) when temperature increases then the curve shifts to the right. Let us look at what this means in terms of hemoglobin’s affinity for oxygen (follow the numbers on the graph again). As before, we will assume that our tissue PO2 is 40 mmHg, and at normal temperatures this results in a saturation of about 70 percent.",True,Shifts in the O2 Saturation Curve,Figure 16.4,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.4.png,Figure 16.4: Effect of temperature on the saturation curve.
673fee11-02ed-4d07-8892-619d6f422272,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Shifts with temperature: Figure 16.4 shows the saturation curve at difference tissue temperatures. The curve we have just looked at was at 38ºC. Notice that as temperature is reduced, the curve shifts to the left, but more importantly (physiologically) when temperature increases then the curve shifts to the right. Let us look at what this means in terms of hemoglobin’s affinity for oxygen (follow the numbers on the graph again). As before, we will assume that our tissue PO2 is 40 mmHg, and at normal temperatures this results in a saturation of about 70 percent.",True,Shifts in the O2 Saturation Curve,Figure 16.4,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.4.png,Figure 16.4: Effect of temperature on the saturation curve.
673fee11-02ed-4d07-8892-619d6f422272,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Shifts with temperature: Figure 16.4 shows the saturation curve at difference tissue temperatures. The curve we have just looked at was at 38ºC. Notice that as temperature is reduced, the curve shifts to the left, but more importantly (physiologically) when temperature increases then the curve shifts to the right. Let us look at what this means in terms of hemoglobin’s affinity for oxygen (follow the numbers on the graph again). As before, we will assume that our tissue PO2 is 40 mmHg, and at normal temperatures this results in a saturation of about 70 percent.",True,Shifts in the O2 Saturation Curve,Figure 16.4,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.4.png,Figure 16.4: Effect of temperature on the saturation curve.
5ec1a448-777c-4b6b-8efd-cb6dfc1a6eb0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Now at the same PO2 but a higher temperature (e.g., 43ºC) the hemoglobin O2 saturation falls to a little over 50 percent, meaning that more oxygen has been relinquished to the tissue (i.e., an increase in temperature reduces hemoglobin’s affinity for oxygen).",True,Shifts in the O2 Saturation Curve,,,,
6b2d2a2f-e968-4c53-9d16-4b1f483ce1ae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Shifts with CO2: We see a similar situation with a rise in PCO2, shown in figure 16.5 with the saturation curve at different PCO2s. At a normal arterial PCO2 (40 mmHg) we get the same saturation curve that we saw previously. But if PCO2 is raised, such as in the locality of highly active tissue (e.g., 80 mmHg), then the curve shifts rightward. Again this means that hemoglobin’s affinity is lowered at equivalent PO2 and more oxygen is released, resulting in a lower saturation.",True,Shifts in the O2 Saturation Curve,Figure 16.5,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.5.png,Figure 16.5: Effect of PCO2 on the saturation curve.
6b2d2a2f-e968-4c53-9d16-4b1f483ce1ae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Shifts with CO2: We see a similar situation with a rise in PCO2, shown in figure 16.5 with the saturation curve at different PCO2s. At a normal arterial PCO2 (40 mmHg) we get the same saturation curve that we saw previously. But if PCO2 is raised, such as in the locality of highly active tissue (e.g., 80 mmHg), then the curve shifts rightward. Again this means that hemoglobin’s affinity is lowered at equivalent PO2 and more oxygen is released, resulting in a lower saturation.",True,Shifts in the O2 Saturation Curve,Figure 16.5,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.5.png,Figure 16.5: Effect of PCO2 on the saturation curve.
6b2d2a2f-e968-4c53-9d16-4b1f483ce1ae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Shifts with CO2: We see a similar situation with a rise in PCO2, shown in figure 16.5 with the saturation curve at different PCO2s. At a normal arterial PCO2 (40 mmHg) we get the same saturation curve that we saw previously. But if PCO2 is raised, such as in the locality of highly active tissue (e.g., 80 mmHg), then the curve shifts rightward. Again this means that hemoglobin’s affinity is lowered at equivalent PO2 and more oxygen is released, resulting in a lower saturation.",True,Shifts in the O2 Saturation Curve,Figure 16.5,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.5.png,Figure 16.5: Effect of PCO2 on the saturation curve.
6a600155-05ee-42c6-864f-0eae339ff555,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Shifts with pH: Finally, the same is true for changes in pH, shown in figure 16.6 with the curve at different pHs. When pH falls, as in active tissue, then the curve shifts rightward from its normal position at normal pH (7.4). Again, this result describes a lowered affinity for oxygen, so at equivalent levels of PO2 more oxygen is released when the hemoglobin enters a low pH environment (e.g., 7.2 shown on figure 16.6). Obviously pH and PCO2 are related, and their effect on hemoglobin binding is known as the Bohr effect.",True,Shifts in the O2 Saturation Curve,Figure 16.6,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.6.png,Figure 16.6: Effect of pH on the saturation curve.
6a600155-05ee-42c6-864f-0eae339ff555,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Shifts with pH: Finally, the same is true for changes in pH, shown in figure 16.6 with the curve at different pHs. When pH falls, as in active tissue, then the curve shifts rightward from its normal position at normal pH (7.4). Again, this result describes a lowered affinity for oxygen, so at equivalent levels of PO2 more oxygen is released when the hemoglobin enters a low pH environment (e.g., 7.2 shown on figure 16.6). Obviously pH and PCO2 are related, and their effect on hemoglobin binding is known as the Bohr effect.",True,Shifts in the O2 Saturation Curve,Figure 16.6,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.6.png,Figure 16.6: Effect of pH on the saturation curve.
6a600155-05ee-42c6-864f-0eae339ff555,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Shifts with pH: Finally, the same is true for changes in pH, shown in figure 16.6 with the curve at different pHs. When pH falls, as in active tissue, then the curve shifts rightward from its normal position at normal pH (7.4). Again, this result describes a lowered affinity for oxygen, so at equivalent levels of PO2 more oxygen is released when the hemoglobin enters a low pH environment (e.g., 7.2 shown on figure 16.6). Obviously pH and PCO2 are related, and their effect on hemoglobin binding is known as the Bohr effect.",True,Shifts in the O2 Saturation Curve,Figure 16.6,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.6.png,Figure 16.6: Effect of pH on the saturation curve.
503f4d47-c5a1-42ce-a959-1f83d614e543,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"One last factor that causes this rightward shift is 2,3 diphosphoglycerate, or DPG. DPG is an end product of RBC metabolism, and as it increases inside the cell it reduces hemoglobins, affinity for oxygen. Elevated DPG levels are associated with chronic hypoxia, such as experienced at altitude or more pertinently in the presence of chronic lung disease. Conversely, DPG levels are lower in stored blood, so transfused blood may have a problem giving up its oxygen.",True,Shifts in the O2 Saturation Curve,,,,
a845200d-a7be-40ec-99e9-ee1ac535e85e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,All these factors mean that hemoglobin will deliver more oxygen to busy tissue.,True,Shifts in the O2 Saturation Curve,,,,
65db2071-bb56-46b0-ac33-eda3e779ead4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Total oxygen carriage: So far we have discussed oxygen transport in terms of hemoglobin only. But despite its lack of solubility, some oxygen can dissolve into the plasma. Realistically this is a very small amount at physiological partial pressures (i.e. at an alveolar PO2 of 100 mmHg only a fraction of a milliliter of oxygen will dissolve into the blood, as figure 16.7 shows).",True,Shifts in the O2 Saturation Curve,Figure 16.7,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.7.png,Figure 16.7: Oxygen carriage.
65db2071-bb56-46b0-ac33-eda3e779ead4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Total oxygen carriage: So far we have discussed oxygen transport in terms of hemoglobin only. But despite its lack of solubility, some oxygen can dissolve into the plasma. Realistically this is a very small amount at physiological partial pressures (i.e. at an alveolar PO2 of 100 mmHg only a fraction of a milliliter of oxygen will dissolve into the blood, as figure 16.7 shows).",True,Shifts in the O2 Saturation Curve,Figure 16.7,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.7.png,Figure 16.7: Oxygen carriage.
65db2071-bb56-46b0-ac33-eda3e779ead4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Total oxygen carriage: So far we have discussed oxygen transport in terms of hemoglobin only. But despite its lack of solubility, some oxygen can dissolve into the plasma. Realistically this is a very small amount at physiological partial pressures (i.e. at an alveolar PO2 of 100 mmHg only a fraction of a milliliter of oxygen will dissolve into the blood, as figure 16.7 shows).",True,Shifts in the O2 Saturation Curve,Figure 16.7,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.7.png,Figure 16.7: Oxygen carriage.
3acd9f68-cfe5-4506-b8ae-408942f00fe2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Obviously this amount of oxygen is completely inadequate to support metabolism and illustrates the need for hemoglobin. But this minute amount when added to the O2 combined to the hemoglobin makes up the total O2 content of the blood. When calculating the oxygen content of the blood we must consider both of these compartments—hemoglobin and plasma (figure 16.8).,True,Shifts in the O2 Saturation Curve,Figure 16.8,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.8.png,Figure 16.8: Compartment of blood oxygen content.
3acd9f68-cfe5-4506-b8ae-408942f00fe2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Obviously this amount of oxygen is completely inadequate to support metabolism and illustrates the need for hemoglobin. But this minute amount when added to the O2 combined to the hemoglobin makes up the total O2 content of the blood. When calculating the oxygen content of the blood we must consider both of these compartments—hemoglobin and plasma (figure 16.8).,True,Shifts in the O2 Saturation Curve,Figure 16.8,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.8.png,Figure 16.8: Compartment of blood oxygen content.
3acd9f68-cfe5-4506-b8ae-408942f00fe2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Obviously this amount of oxygen is completely inadequate to support metabolism and illustrates the need for hemoglobin. But this minute amount when added to the O2 combined to the hemoglobin makes up the total O2 content of the blood. When calculating the oxygen content of the blood we must consider both of these compartments—hemoglobin and plasma (figure 16.8).,True,Shifts in the O2 Saturation Curve,Figure 16.8,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.8.png,Figure 16.8: Compartment of blood oxygen content.
bf1ad935-1498-436c-83ba-d0156ca61759,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Calculating the O2 Content of Blood,False,Calculating the O2 Content of Blood,,,,
4cfa8856-4309-481b-80c5-c9a02b080a81,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"To calculate the arterial oxygen content (CaO2) let us first look at the factors affecting the majority of the O2 (i.e., that carried by hemoglobin).",True,Calculating the O2 Content of Blood,,,,
00629698-3e57-46f1-96a7-1b014ad7d8b5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,(1) This will be determined by the amount of hemoglobin in the blood (measured in mg/dL). So let us start building the equation.,True,Calculating the O2 Content of Blood,,,,
209a9c9a-fe60-418d-b8a0-fce11931509b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Equation 16.1,True,Calculating the O2 Content of Blood,,,,
ffe42a52-90a4-48fe-b2de-b410fe25a9af,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,[latex]C_aO_2 = Hb (mg/dL)...[/latex],True,Calculating the O2 Content of Blood,,,,
c4c1551d-3074-4572-975d-3fba292f4347,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"(2) Second, we must consider the oxygen carrying capacity of Hb, which is 1.34 mL O2/gm Hb. So we multiply the amount of Hb by its carrying capacity.",True,Calculating the O2 Content of Blood,,,,
d267690e-34f2-44be-b7d5-a0c2efe3214b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Equation 16.2,True,Calculating the O2 Content of Blood,,,,
d79a1885-f45a-4fe8-a834-ea42578dfb3f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"[latex]C_aO_2 = Hb (mg/dL) \times 1.34\, O_2/gmHb...[/latex]",True,Calculating the O2 Content of Blood,,,,
992ca9e1-c372-4167-abf1-130368f96cf2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"(3) But that carrying capacity might not have been reached by all the Hb (i.e., the Hb may not be fully saturated). So to account for this, we multiply by the saturation (SaO2).",True,Calculating the O2 Content of Blood,,,,
c5358489-ab6a-4b8b-a354-487cd66cb3a4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Equation 16.3,True,Calculating the O2 Content of Blood,,,,
caa13be0-90c6-4c7f-ab7f-0e9cc1f8da82,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"[latex]C_aO_2 = Hb (mg/dL) \times 1.34\, O_2/gmHb \times S_aO_2...[/latex]",True,Calculating the O2 Content of Blood,,,,
c778feb7-dffb-4672-ba01-e6dfc27bc2c8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"(4) So far that takes care of the O2 associated with Hb (normally about 98 percent of the total). Now we must add the O2 in plasma to the equation. We do this by measuring the PaO2 and multiplying it by a solubility coefficient (0.003 mL O2/mmHg/dL) to convert it from a partial pressure to milliliters. Removing the units makes this long but simple equation a little easier to understand. It has two components, representing the two compartments for O2 carriage.",True,Calculating the O2 Content of Blood,,,,
7cda6ccf-25d5-4de4-9908-3c6597f632ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Equation 16.4,True,Calculating the O2 Content of Blood,,,,
b4c122c6-2751-4f5a-a35e-b83c9bfe9c7c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,[latex]C_aO_2 = (Hb \times 1.34 \times S_aO_2) + (P_aO_2 \times 0.003)[/latex],True,Calculating the O2 Content of Blood,,,,
e7c3a4f2-50ef-476e-8f16-19ea8c8e69db,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The plasma component is usually inconsequential, but may become more important when blood is exposed to an elevated alveolar PO2, such as during oxygen or hyperbaric therapy.",True,Calculating the O2 Content of Blood,,,,
e53ce219-1ee9-4be7-ae18-dd7704b78786,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Summary,False,Summary,,,,
00420728-2f2a-4525-82c0-bed3644f3c80,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"So to summarize, as oxygen’s lack of solubility means metabolic demands cannot be met by dissolved oxygen alone, the vast majority of oxygen is transported by hemoglobin, a molecule that is beautifully designed to pick up oxygen at the lung and release oxygen in proportion to the tissue’s demand. We will see more of hemoglobin’s sophistication when we address CO2 carriage.",True,Summary,,,,
5afc2e99-7c26-4d9a-a0b4-38a46aa5db34,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,CO2 Transport,False,CO2 Transport,,,,
9f7e3ae7-01b0-4345-acf1-25df210d14ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Unlike oxygen, carbon dioxide is soluble enough that it does not need a protein carrier like oxygen needs hemoglobin to enter and exit plasma. However, this does not necessarily mean that CO2 transport is simple. The complication this time is that free dissolved CO2 forms carbonic acid, which can threaten pH homeostasis. So most CO2 is not transported in the dissolved form. Most (approximately 70 percent) of the CO2 that emerges from metabolizing tissue is converted to bicarbonate with the help of enzymes within red blood cells. We will look at this more closely in a moment. About 15–25 percent is transported on hemoglobin.",True,CO2 Transport,,,,
b26c8315-1e7c-47a5-af5c-217dc2f068e6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Transport on Hemoglobin (15–25 Percent),False,Transport on Hemoglobin (15–25 Percent),,,,
976c761a-e451-4b0a-a6fe-1982ac173f4d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Carbon dioxide can bind to the terminal amine groups of hemoglobin’s polypeptide chains forming carbaminohemoglobin. It is worth noting a couple of points about this. First, CO2 does not compete with oxygen to bind to Hb—the binding sites are completely different and hemoglobin can hold both CO2 and O2 at the same time. Second, deoxyhemoglobin is a better carrier of CO2 than oxyhemoglobin is; consequently at the tissue where hemoglobin is losing its oxygen it is becoming a more efficient CO2 transporter. This is known as the Haldane effect.",True,Transport on Hemoglobin (15–25 Percent),,,,
54a1d503-ee99-47bc-804e-a9511a540c36,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Transport as Dissolved CO2 (About 7 Percent),False,Transport as Dissolved CO2 (About 7 Percent),,,,
d6d16d5e-5fce-4038-9b47-1fce292ae6c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"A little CO2 combines with water to produce carbonic acid, the dissociated hydrogen form that must be buffered by plasma proteins, such as albumin.",True,Transport as Dissolved CO2 (About 7 Percent),,,,
748caeed-0fbd-4543-9fcc-6181648dc7b5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Transport as Bicarbonate (About 70 Percent),False,Transport as Bicarbonate (About 70 Percent),,,,
16193f5c-37f2-49c7-bb66-833a9704ccf9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Seventy percent of the CO2 enters red blood cells, and once inside a familiar reaction occurs (equation 16.5). The CO2 binds with water in the cytoplasm, producing carbonic acid, which then dissociates into a hydrogen ion and a bicarbonate ion.",True,Transport as Bicarbonate (About 70 Percent),,,,
d408408c-2eaa-4afd-a3b1-b91e0aaf3fd0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,This reversible reaction is accelerated by the enzyme carbonic anhydrase and is driven rapidly to the right by the high concentration of CO2 at the tissue.,True,Transport as Bicarbonate (About 70 Percent),,,,
8155928a-b200-49c8-ad23-7f85ef6b91b6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The hydrogen ion produced helps shift the oxygen saturation curve to the right and so promotes further release of oxygen to the tissue. Hemoglobin then serves yet another purpose by buffering the proton with its polypeptide chains. Deoxyhemoglobin is a better proton acceptor than oxyhemoglobin, so as the hemoglobin loses its oxygen at the tissue it becomes a better pH buffer. This reduces the amount of hydrogen ion on the right side of our equation and moves the equation to the right, promoting the conversion of more CO2.",True,Transport as Bicarbonate (About 70 Percent),,,,
0a568fd8-826a-4ade-a2fd-f2a5257bff45,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Equation 16.5,True,Transport as Bicarbonate (About 70 Percent),,,,
d902ecde-970c-47bf-8343-7b246cfc99bb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],False,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
aabdc7cd-10bc-4ecf-ab61-003eed47ae30,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,High concentrations of CO2 at the tissue push this equation right to produce bicarbonate.,True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
7db5cd98-ff0b-4722-9989-fe0bb05060ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The bicarbonate ion is pumped out of the cell, but without intervention this would leave the inside of the cell too positively charged as the negative charge of the bicarbonate is lost. To maintain electroneutrality the bicarbonate is exchanged for a chloride ion; this process is referred to as the chloride shift. The formation of bicarbonate at the tissue is summarized in figure 16.9.",True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],Figure 16.9,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.9.png,Figure 16.9: Formation of bicarbonate at the tissue.
7db5cd98-ff0b-4722-9989-fe0bb05060ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The bicarbonate ion is pumped out of the cell, but without intervention this would leave the inside of the cell too positively charged as the negative charge of the bicarbonate is lost. To maintain electroneutrality the bicarbonate is exchanged for a chloride ion; this process is referred to as the chloride shift. The formation of bicarbonate at the tissue is summarized in figure 16.9.",True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],Figure 16.9,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.9.png,Figure 16.9: Formation of bicarbonate at the tissue.
7db5cd98-ff0b-4722-9989-fe0bb05060ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"The bicarbonate ion is pumped out of the cell, but without intervention this would leave the inside of the cell too positively charged as the negative charge of the bicarbonate is lost. To maintain electroneutrality the bicarbonate is exchanged for a chloride ion; this process is referred to as the chloride shift. The formation of bicarbonate at the tissue is summarized in figure 16.9.",True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],Figure 16.9,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.9.png,Figure 16.9: Formation of bicarbonate at the tissue.
247f9340-a3ae-4595-945e-bf9a47e391ba,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,The CO2 now travels through the bloodstream as bicarbonate toward the lungs. At the lungs the process is basically reversed. The partial pressure of CO2 at the lungs is low; consequently our equation is driven toward the left-hand side as CO2 leaves toward the low alveolar PCO2 (equation 16.6).,True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
60ee2f13-4f7e-4fd2-b78a-9f8fa5a77b95,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Equation 16.6,True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
1a19a342-f940-4afe-b662-bdd04c246957,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,←,False,←,,,,
c0258b1c-363d-4565-bf4a-b00969ee798c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,High bicarbonate and low CO2 at the lung force the equation leftward.,True,←,,,,
90fe8a42-b0dd-4135-94c2-2d392beed20c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,The high alveolar PO2 also promotes the leftward movement—binding of oxygen to hemoglobin makes hemoglobin a less effective proton binder so it loses the proton and raises the amount of substrate on the right-hand side and thereby promotes reformation of CO2. The Haldane effect is also reversed—as hemoglobin gains oxygen at the lung it loses its affinity for CO2 and releases it into the plasma. This raises plasma PCO2 and promotes diffusion of CO2 into the alveoli for expulsion.,True,←,,,,
01fbd848-0de3-45c8-b9d2-830e90d8ff08,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Likewise the chloride shift is reversed and bicarbonate reenters the cell as chloride is pumped back out.,True,←,,,,
29c9b5c3-3b65-426b-b172-e5e8b9b4964c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"All these moves help promote the right-to-left direction of our now infamous equation and the re-forming of CO2. Alveolar ventilation gets rid of the re-formed CO2 to the atmosphere, maintaining the alveolar PCO2 at relatively low levels and the direction of the equation right-to-left. The reformation of CO2 at the lungs is summarized in figure 16.10.",True,←,Figure 16.10,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.10.png,Figure 16.10: Reformation of CO2 at the lungs.
29c9b5c3-3b65-426b-b172-e5e8b9b4964c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"All these moves help promote the right-to-left direction of our now infamous equation and the re-forming of CO2. Alveolar ventilation gets rid of the re-formed CO2 to the atmosphere, maintaining the alveolar PCO2 at relatively low levels and the direction of the equation right-to-left. The reformation of CO2 at the lungs is summarized in figure 16.10.",True,←,Figure 16.10,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.10.png,Figure 16.10: Reformation of CO2 at the lungs.
29c9b5c3-3b65-426b-b172-e5e8b9b4964c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"All these moves help promote the right-to-left direction of our now infamous equation and the re-forming of CO2. Alveolar ventilation gets rid of the re-formed CO2 to the atmosphere, maintaining the alveolar PCO2 at relatively low levels and the direction of the equation right-to-left. The reformation of CO2 at the lungs is summarized in figure 16.10.",True,←,Figure 16.10,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.10.png,Figure 16.10: Reformation of CO2 at the lungs.
23f6630d-d833-40d1-966b-83db4b4669e4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,The CO2 “Dissociation” Curve,False,The CO2 “Dissociation” Curve,,,,
3173e1ce-2d06-458e-92cb-f6b49f48fc97,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"So, for want of a better name, we can also draw a CO2 dissociation or saturation curve, as is shown in figure 16.11. The graph shows the CO2 concentration in blood across a wide range of PCO2 and shows the effect of Hb O2 saturation on CO2 carriage. The CO2 dissociation curve is unlike the oxygen saturation curve and is virtually linear (i.e., the higher the PCO2, the higher the CO2 content of the blood); there is no plateau to the curve as we saw with O2 transport. The ramification of this is that the lower the alveolar PCO2, the lower the blood PCO2, and the higher the alveolar PCO2, the higher the blood PCO2. It is a very simple relationship that ends with the obvious statement that the more you breathe, the lower arterial CO2 becomes. It is worth reminding ourselves here that this is not a relationship seen with oxygen that is limited by the capacity of hemoglobin (breathing more does not necessarily result in more oxygen in the bloodstream). The other aspect to note here is the effect of hemoglobin’s oxygen saturation on carbon dioxide carriage. This has clinical ramifications, so we will look at this more closely.",True,The CO2 “Dissociation” Curve,Figure 16.11,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.11.png,Figure 16.11: CO2 dissociation curve.
3173e1ce-2d06-458e-92cb-f6b49f48fc97,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"So, for want of a better name, we can also draw a CO2 dissociation or saturation curve, as is shown in figure 16.11. The graph shows the CO2 concentration in blood across a wide range of PCO2 and shows the effect of Hb O2 saturation on CO2 carriage. The CO2 dissociation curve is unlike the oxygen saturation curve and is virtually linear (i.e., the higher the PCO2, the higher the CO2 content of the blood); there is no plateau to the curve as we saw with O2 transport. The ramification of this is that the lower the alveolar PCO2, the lower the blood PCO2, and the higher the alveolar PCO2, the higher the blood PCO2. It is a very simple relationship that ends with the obvious statement that the more you breathe, the lower arterial CO2 becomes. It is worth reminding ourselves here that this is not a relationship seen with oxygen that is limited by the capacity of hemoglobin (breathing more does not necessarily result in more oxygen in the bloodstream). The other aspect to note here is the effect of hemoglobin’s oxygen saturation on carbon dioxide carriage. This has clinical ramifications, so we will look at this more closely.",True,The CO2 “Dissociation” Curve,Figure 16.11,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.11.png,Figure 16.11: CO2 dissociation curve.
3173e1ce-2d06-458e-92cb-f6b49f48fc97,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"So, for want of a better name, we can also draw a CO2 dissociation or saturation curve, as is shown in figure 16.11. The graph shows the CO2 concentration in blood across a wide range of PCO2 and shows the effect of Hb O2 saturation on CO2 carriage. The CO2 dissociation curve is unlike the oxygen saturation curve and is virtually linear (i.e., the higher the PCO2, the higher the CO2 content of the blood); there is no plateau to the curve as we saw with O2 transport. The ramification of this is that the lower the alveolar PCO2, the lower the blood PCO2, and the higher the alveolar PCO2, the higher the blood PCO2. It is a very simple relationship that ends with the obvious statement that the more you breathe, the lower arterial CO2 becomes. It is worth reminding ourselves here that this is not a relationship seen with oxygen that is limited by the capacity of hemoglobin (breathing more does not necessarily result in more oxygen in the bloodstream). The other aspect to note here is the effect of hemoglobin’s oxygen saturation on carbon dioxide carriage. This has clinical ramifications, so we will look at this more closely.",True,The CO2 “Dissociation” Curve,Figure 16.11,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.11.png,Figure 16.11: CO2 dissociation curve.
06d426f4-4304-4082-ab2e-3dd862807829,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"When deoxygenated, hemoglobin’s structure promotes binding of CO2 and buffering of protons by the polypeptide chains. So when O2 saturation is zero, the CO2 and proton carrying capability of Hb is high. As already mentioned, this means that when Hb is in its deoxygenated form at the tissue, its CO2 carrying ability is increased.",True,The CO2 “Dissociation” Curve,,,,
98abccae-3a37-49a6-a599-f91a928e6225,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"When we get to the lung, however, the Hb is exposed to the high alveolar PO2 and oxygen binds to the heme sites and becomes saturated; this causes a conformational change, and the CO2 and proton carrying ability is reduced. So conveniently CO2 release is promoted at the lung.",True,The CO2 “Dissociation” Curve,,,,
28b70fd8-54cf-49ea-ae16-3f345060621e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Although CO2 is highly soluble, very little of it can be transported as dissolved CO2 in plasma because of its effect on pH. The majority is converted to bicarbonate in red blood cells and transported in plasma, while about 25 percent is transported bound to hemoglobin.",True,The CO2 “Dissociation” Curve,,,,
c898310b-5691-479a-aba9-0c8719969dd3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,Text,False,Text,,,,
5b212f06-0a9f-43a4-ba5b-993fd9d1eabb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Levitsky, Michael G. “Chapter 7: Transport of Oxygen and Carbon Dioxide in the Blood.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
33b333e3-d03f-43e1-8e53-26514d6b1039,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"West, John B. “Chapter 6: Gas Transport by the Blood—How Gases Are Moved to the Peripheral Tissues.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
5cb5a4e9-eca8-49a4-91d0-51ebb00bbb9a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Oxygen Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/#chapter-57-section-1,"Widdicombe, John G., and Andrew S. Davis. “Chapter 6.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
e648c986-3adf-4d4e-99c2-5022dbb9188b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The hemoglobin molecule consists of four polypeptide chains, two alpha and two beta (figure 16.1). These proteins comprise the “globin” part of the molecule but are not simply structural as they contain sites that are capable of receiving CO2 and also hydrogen ions—a handy function, as you might imagine. Some anemias, such as sickle cell anemia, involve a conformational change in these proteins and diminish the molecule’s gas carrying ability.",True,Text,Figure 16.1,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.1.png,Figure 16.1: Basic structure of hemoglobin.
e648c986-3adf-4d4e-99c2-5022dbb9188b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The hemoglobin molecule consists of four polypeptide chains, two alpha and two beta (figure 16.1). These proteins comprise the “globin” part of the molecule but are not simply structural as they contain sites that are capable of receiving CO2 and also hydrogen ions—a handy function, as you might imagine. Some anemias, such as sickle cell anemia, involve a conformational change in these proteins and diminish the molecule’s gas carrying ability.",True,Text,Figure 16.1,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.1.png,Figure 16.1: Basic structure of hemoglobin.
e648c986-3adf-4d4e-99c2-5022dbb9188b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The hemoglobin molecule consists of four polypeptide chains, two alpha and two beta (figure 16.1). These proteins comprise the “globin” part of the molecule but are not simply structural as they contain sites that are capable of receiving CO2 and also hydrogen ions—a handy function, as you might imagine. Some anemias, such as sickle cell anemia, involve a conformational change in these proteins and diminish the molecule’s gas carrying ability.",True,Text,Figure 16.1,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.1.png,Figure 16.1: Basic structure of hemoglobin.
235d7c30-e6b4-4b09-9aef-211be0d5ced0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The heme component of hemoglobin is an iron-containing porphyrin molecule capable of binding with oxygen. Each of the four polypeptide chains contains a heme molecule, meaning that each hemoglobin molecule is capable of transporting four oxygen molecules. It is also worth noting that binding of oxygen to the heme molecule induces a conformational change that results in oxyhemoglobin having some different behaviors and indeed color to deoxyhemoglobin. We will look at some of these differences in behavior later on.",True,Text,,,,
b677e445-6b23-4b88-9908-3d319666812d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"It is also worth reviewing hemoglobin’s home here as well—the red blood cell (RBC). The red blood cell’s classic biconcave shape provides a large surface area for gas exchange and also means that no hemoglobin molecule inside is very far from the edge of the cell, cutting down on the diffusion distance of gases. The cell is also very flexible, making it capable of squeezing through narrow and twisting capillaries so that its walls and those of the capillary may be in close contact and again diffusion distances are reduced.",True,Text,,,,
33ecb120-e12b-4694-b384-d7ca3287055e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Each RBC is capable of holding up to 250 million hemoglobin molecules, so consequently is capable of holding one billion oxygen molecules; as such the RBC fulfills its primary role of oxygen transport well. This oxygen transport system fails in anemias that result in either too few red blood cells or too little hemoglobin in each cell (or both). Now let us look at the behavior of hemoglobin.",True,Text,,,,
7cd6cf5e-be60-49d0-9502-731c566c9c36,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The behavior of hemoglobin is best described by the oxygen saturation curve (figure 16.2), and this is one of the most important curves to understand in medicine. The curve shows the percentage of hemoglobin that has all of its heme molecules bound with oxygen (i.e., are saturated). So for example a 50 percent saturation would mean that half of the heme sites were occupied by oxygen. The curve shows percentage saturation in relation to oxygen partial pressure, and what should be immediately noticeable is that the higher the partial pressure of oxygen then the greater the saturation. But the relationship is far from linear and its shape offers several important physiological advantages. If it helps understand it, think of this curve as an instruction manual for hemoglobin, telling how saturated it should be at any PO2. In reality it is an enzyme kinetics curve, describing hemoglobin’s affinity for oxygen over a range of PO2.",True,Text,Figure 16.2,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.2.png,Figure 16.2: Hemoglobin saturation curve.
7cd6cf5e-be60-49d0-9502-731c566c9c36,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The behavior of hemoglobin is best described by the oxygen saturation curve (figure 16.2), and this is one of the most important curves to understand in medicine. The curve shows the percentage of hemoglobin that has all of its heme molecules bound with oxygen (i.e., are saturated). So for example a 50 percent saturation would mean that half of the heme sites were occupied by oxygen. The curve shows percentage saturation in relation to oxygen partial pressure, and what should be immediately noticeable is that the higher the partial pressure of oxygen then the greater the saturation. But the relationship is far from linear and its shape offers several important physiological advantages. If it helps understand it, think of this curve as an instruction manual for hemoglobin, telling how saturated it should be at any PO2. In reality it is an enzyme kinetics curve, describing hemoglobin’s affinity for oxygen over a range of PO2.",True,Text,Figure 16.2,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.2.png,Figure 16.2: Hemoglobin saturation curve.
7cd6cf5e-be60-49d0-9502-731c566c9c36,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The behavior of hemoglobin is best described by the oxygen saturation curve (figure 16.2), and this is one of the most important curves to understand in medicine. The curve shows the percentage of hemoglobin that has all of its heme molecules bound with oxygen (i.e., are saturated). So for example a 50 percent saturation would mean that half of the heme sites were occupied by oxygen. The curve shows percentage saturation in relation to oxygen partial pressure, and what should be immediately noticeable is that the higher the partial pressure of oxygen then the greater the saturation. But the relationship is far from linear and its shape offers several important physiological advantages. If it helps understand it, think of this curve as an instruction manual for hemoglobin, telling how saturated it should be at any PO2. In reality it is an enzyme kinetics curve, describing hemoglobin’s affinity for oxygen over a range of PO2.",True,Text,Figure 16.2,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.2.png,Figure 16.2: Hemoglobin saturation curve.
873fb003-2251-43f4-90e0-50d6563e3f1d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"First let us put the curve in a physiological context. The alveolar PO2 is around 100 mmHg. This means that as blood passes the alveoli and is exposed to this PO2, then oxygen saturation becomes close to 100 percent, about 98 percent. The first important physiological feature of this curve is that PO2 can fall a considerably long way before it has an impact on oxygen saturation. So, taking time to look at the numbers on the graph, let us say, for example, that a patient begins to hypoventilate and alveolar PO2 falls to 70 mmHg; while this is a considerable fall in PO2, the saturation will only fall a few percentage points, and PO2 must fall to 50 before significant loss of saturation, or desaturation, occurs. Below 50, however, notice how the curve rapidly steepens, and now for a small change in PO2, we get a large desaturation.",True,Text,,,,
0e34dfd6-97c9-4705-b1e8-6daf6798d11e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"This steep section of the curve is therefore clinically critical. If your patient’s saturation monitor reads 83 percent what should spring into your mind is it that such a low saturation puts the patient onto the steep part of the curve. It will now take only a small further decline in alveolar PO2 to have a profound effect on saturation, unlike at the top and flat section of the curve where small changes in alveolar PO2 have very little effect on saturation.",True,Text,,,,
f9351d8b-2353-4276-a0c2-15f9fa5cda04,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"So what is the advantage of having such a steep curve at lower PO2s? Let us look at the physiological situation again. We have already said that the alveolar PO2 of 100 results in a saturation close to 100 percent (i.e., at the lung the hemoglobin has a high affinity for oxygen and becomes fully saturated).",True,Text,,,,
52989a02-4a18-4f48-b036-266ea34063ee,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"At the tissue, however, we want hemoglobin to lose its affinity for oxygen and release some to the metabolizing cells. At the tissue the local PO2 is much lower, around 40, because of the oxygen consumption by the tissue. At the lower PO2, hemoglobin’s affinity for oxygen falls, and it will lose some of its oxygen to the tissue and saturation will fall. This is ideal, as now our oxygen carrier is capable of releasing oxygen where it is needed.",True,Text,,,,
00acfef2-9b1d-4502-8929-744d0dda4398,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"If tissue PO2 falls even lower, such as when metabolic rate is high, then more oxygen will be released by hemoglobin as its affinity for oxygen declines with the lower tissue PO2. Therefore the delivery system for oxygen is intrinsically tied to metabolic rate.",True,Text,,,,
477564c7-2235-4aaa-b245-1f8cf0b57cb8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The shape of this curve makes hemoglobin a remarkable molecule—able to grab oxygen at the oxygen-providing lung, but relinquish it to oxygen-demanding tissue and relinquish more when the tissue needs more. There are other factors that fine-tune the amount of oxygen delivered to tissue to match its oxygen demand. This is summarized in figure 16.3.",True,Text,Figure 16.3,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.3.png,"Figure 16.3: The hemoglobin saturation at the lung (A), at the tissue (B), and at very metabolically active tissue (C)."
477564c7-2235-4aaa-b245-1f8cf0b57cb8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The shape of this curve makes hemoglobin a remarkable molecule—able to grab oxygen at the oxygen-providing lung, but relinquish it to oxygen-demanding tissue and relinquish more when the tissue needs more. There are other factors that fine-tune the amount of oxygen delivered to tissue to match its oxygen demand. This is summarized in figure 16.3.",True,Text,Figure 16.3,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.3.png,"Figure 16.3: The hemoglobin saturation at the lung (A), at the tissue (B), and at very metabolically active tissue (C)."
477564c7-2235-4aaa-b245-1f8cf0b57cb8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The shape of this curve makes hemoglobin a remarkable molecule—able to grab oxygen at the oxygen-providing lung, but relinquish it to oxygen-demanding tissue and relinquish more when the tissue needs more. There are other factors that fine-tune the amount of oxygen delivered to tissue to match its oxygen demand. This is summarized in figure 16.3.",True,Text,Figure 16.3,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.3.png,"Figure 16.3: The hemoglobin saturation at the lung (A), at the tissue (B), and at very metabolically active tissue (C)."
9726e98f-55a3-46be-ac36-606735083576,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Shifts in the O2 Saturation Curve,False,Shifts in the O2 Saturation Curve,,,,
68693162-80d5-4cc0-92ed-ea573f6d1ef3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The metabolic rate of tissue determines its oxygen demand, with more active tissue requiring hemoglobin to relinquish more oxygen. So there are several other factors, beyond low local PO2, that are associated with active tissue that cause hemoglobin to reduce its affinity for oxygen and therefore release it. Tissue with a high metabolic rate tends to have (1) higher temperature, (2) high PCO2, and (3) lower pH. We can look at the effect of each of these factors on the saturation curve.",True,Shifts in the O2 Saturation Curve,,,,
a98f5bd1-6e36-41ad-a54e-d0f5004ecff4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Shifts with temperature: Figure 16.4 shows the saturation curve at difference tissue temperatures. The curve we have just looked at was at 38ºC. Notice that as temperature is reduced, the curve shifts to the left, but more importantly (physiologically) when temperature increases then the curve shifts to the right. Let us look at what this means in terms of hemoglobin’s affinity for oxygen (follow the numbers on the graph again). As before, we will assume that our tissue PO2 is 40 mmHg, and at normal temperatures this results in a saturation of about 70 percent.",True,Shifts in the O2 Saturation Curve,Figure 16.4,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.4.png,Figure 16.4: Effect of temperature on the saturation curve.
a98f5bd1-6e36-41ad-a54e-d0f5004ecff4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Shifts with temperature: Figure 16.4 shows the saturation curve at difference tissue temperatures. The curve we have just looked at was at 38ºC. Notice that as temperature is reduced, the curve shifts to the left, but more importantly (physiologically) when temperature increases then the curve shifts to the right. Let us look at what this means in terms of hemoglobin’s affinity for oxygen (follow the numbers on the graph again). As before, we will assume that our tissue PO2 is 40 mmHg, and at normal temperatures this results in a saturation of about 70 percent.",True,Shifts in the O2 Saturation Curve,Figure 16.4,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.4.png,Figure 16.4: Effect of temperature on the saturation curve.
a98f5bd1-6e36-41ad-a54e-d0f5004ecff4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Shifts with temperature: Figure 16.4 shows the saturation curve at difference tissue temperatures. The curve we have just looked at was at 38ºC. Notice that as temperature is reduced, the curve shifts to the left, but more importantly (physiologically) when temperature increases then the curve shifts to the right. Let us look at what this means in terms of hemoglobin’s affinity for oxygen (follow the numbers on the graph again). As before, we will assume that our tissue PO2 is 40 mmHg, and at normal temperatures this results in a saturation of about 70 percent.",True,Shifts in the O2 Saturation Curve,Figure 16.4,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.4.png,Figure 16.4: Effect of temperature on the saturation curve.
171cfebd-21b7-49f0-9fcf-e883ec52848a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Now at the same PO2 but a higher temperature (e.g., 43ºC) the hemoglobin O2 saturation falls to a little over 50 percent, meaning that more oxygen has been relinquished to the tissue (i.e., an increase in temperature reduces hemoglobin’s affinity for oxygen).",True,Shifts in the O2 Saturation Curve,,,,
b69f14f6-92e8-401f-816e-3af6cede9ae3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Shifts with CO2: We see a similar situation with a rise in PCO2, shown in figure 16.5 with the saturation curve at different PCO2s. At a normal arterial PCO2 (40 mmHg) we get the same saturation curve that we saw previously. But if PCO2 is raised, such as in the locality of highly active tissue (e.g., 80 mmHg), then the curve shifts rightward. Again this means that hemoglobin’s affinity is lowered at equivalent PO2 and more oxygen is released, resulting in a lower saturation.",True,Shifts in the O2 Saturation Curve,Figure 16.5,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.5.png,Figure 16.5: Effect of PCO2 on the saturation curve.
b69f14f6-92e8-401f-816e-3af6cede9ae3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Shifts with CO2: We see a similar situation with a rise in PCO2, shown in figure 16.5 with the saturation curve at different PCO2s. At a normal arterial PCO2 (40 mmHg) we get the same saturation curve that we saw previously. But if PCO2 is raised, such as in the locality of highly active tissue (e.g., 80 mmHg), then the curve shifts rightward. Again this means that hemoglobin’s affinity is lowered at equivalent PO2 and more oxygen is released, resulting in a lower saturation.",True,Shifts in the O2 Saturation Curve,Figure 16.5,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.5.png,Figure 16.5: Effect of PCO2 on the saturation curve.
b69f14f6-92e8-401f-816e-3af6cede9ae3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Shifts with CO2: We see a similar situation with a rise in PCO2, shown in figure 16.5 with the saturation curve at different PCO2s. At a normal arterial PCO2 (40 mmHg) we get the same saturation curve that we saw previously. But if PCO2 is raised, such as in the locality of highly active tissue (e.g., 80 mmHg), then the curve shifts rightward. Again this means that hemoglobin’s affinity is lowered at equivalent PO2 and more oxygen is released, resulting in a lower saturation.",True,Shifts in the O2 Saturation Curve,Figure 16.5,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.5.png,Figure 16.5: Effect of PCO2 on the saturation curve.
3d05083e-b592-4559-8e1d-7eb33c48c12d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Shifts with pH: Finally, the same is true for changes in pH, shown in figure 16.6 with the curve at different pHs. When pH falls, as in active tissue, then the curve shifts rightward from its normal position at normal pH (7.4). Again, this result describes a lowered affinity for oxygen, so at equivalent levels of PO2 more oxygen is released when the hemoglobin enters a low pH environment (e.g., 7.2 shown on figure 16.6). Obviously pH and PCO2 are related, and their effect on hemoglobin binding is known as the Bohr effect.",True,Shifts in the O2 Saturation Curve,Figure 16.6,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.6.png,Figure 16.6: Effect of pH on the saturation curve.
3d05083e-b592-4559-8e1d-7eb33c48c12d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Shifts with pH: Finally, the same is true for changes in pH, shown in figure 16.6 with the curve at different pHs. When pH falls, as in active tissue, then the curve shifts rightward from its normal position at normal pH (7.4). Again, this result describes a lowered affinity for oxygen, so at equivalent levels of PO2 more oxygen is released when the hemoglobin enters a low pH environment (e.g., 7.2 shown on figure 16.6). Obviously pH and PCO2 are related, and their effect on hemoglobin binding is known as the Bohr effect.",True,Shifts in the O2 Saturation Curve,Figure 16.6,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.6.png,Figure 16.6: Effect of pH on the saturation curve.
3d05083e-b592-4559-8e1d-7eb33c48c12d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Shifts with pH: Finally, the same is true for changes in pH, shown in figure 16.6 with the curve at different pHs. When pH falls, as in active tissue, then the curve shifts rightward from its normal position at normal pH (7.4). Again, this result describes a lowered affinity for oxygen, so at equivalent levels of PO2 more oxygen is released when the hemoglobin enters a low pH environment (e.g., 7.2 shown on figure 16.6). Obviously pH and PCO2 are related, and their effect on hemoglobin binding is known as the Bohr effect.",True,Shifts in the O2 Saturation Curve,Figure 16.6,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.6.png,Figure 16.6: Effect of pH on the saturation curve.
8e3554fc-df2c-436e-9813-72bafedeb203,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"One last factor that causes this rightward shift is 2,3 diphosphoglycerate, or DPG. DPG is an end product of RBC metabolism, and as it increases inside the cell it reduces hemoglobins, affinity for oxygen. Elevated DPG levels are associated with chronic hypoxia, such as experienced at altitude or more pertinently in the presence of chronic lung disease. Conversely, DPG levels are lower in stored blood, so transfused blood may have a problem giving up its oxygen.",True,Shifts in the O2 Saturation Curve,,,,
a2946bcc-c6fd-4bbb-ae44-244a64817226,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,All these factors mean that hemoglobin will deliver more oxygen to busy tissue.,True,Shifts in the O2 Saturation Curve,,,,
5343cb7c-3249-4523-b84f-dd4e0c68e96d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Total oxygen carriage: So far we have discussed oxygen transport in terms of hemoglobin only. But despite its lack of solubility, some oxygen can dissolve into the plasma. Realistically this is a very small amount at physiological partial pressures (i.e. at an alveolar PO2 of 100 mmHg only a fraction of a milliliter of oxygen will dissolve into the blood, as figure 16.7 shows).",True,Shifts in the O2 Saturation Curve,Figure 16.7,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.7.png,Figure 16.7: Oxygen carriage.
5343cb7c-3249-4523-b84f-dd4e0c68e96d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Total oxygen carriage: So far we have discussed oxygen transport in terms of hemoglobin only. But despite its lack of solubility, some oxygen can dissolve into the plasma. Realistically this is a very small amount at physiological partial pressures (i.e. at an alveolar PO2 of 100 mmHg only a fraction of a milliliter of oxygen will dissolve into the blood, as figure 16.7 shows).",True,Shifts in the O2 Saturation Curve,Figure 16.7,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.7.png,Figure 16.7: Oxygen carriage.
5343cb7c-3249-4523-b84f-dd4e0c68e96d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Total oxygen carriage: So far we have discussed oxygen transport in terms of hemoglobin only. But despite its lack of solubility, some oxygen can dissolve into the plasma. Realistically this is a very small amount at physiological partial pressures (i.e. at an alveolar PO2 of 100 mmHg only a fraction of a milliliter of oxygen will dissolve into the blood, as figure 16.7 shows).",True,Shifts in the O2 Saturation Curve,Figure 16.7,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.7.png,Figure 16.7: Oxygen carriage.
2cdb7301-2b1b-4427-b0c4-f6bb900cdf09,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Obviously this amount of oxygen is completely inadequate to support metabolism and illustrates the need for hemoglobin. But this minute amount when added to the O2 combined to the hemoglobin makes up the total O2 content of the blood. When calculating the oxygen content of the blood we must consider both of these compartments—hemoglobin and plasma (figure 16.8).,True,Shifts in the O2 Saturation Curve,Figure 16.8,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.8.png,Figure 16.8: Compartment of blood oxygen content.
2cdb7301-2b1b-4427-b0c4-f6bb900cdf09,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Obviously this amount of oxygen is completely inadequate to support metabolism and illustrates the need for hemoglobin. But this minute amount when added to the O2 combined to the hemoglobin makes up the total O2 content of the blood. When calculating the oxygen content of the blood we must consider both of these compartments—hemoglobin and plasma (figure 16.8).,True,Shifts in the O2 Saturation Curve,Figure 16.8,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.8.png,Figure 16.8: Compartment of blood oxygen content.
2cdb7301-2b1b-4427-b0c4-f6bb900cdf09,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Obviously this amount of oxygen is completely inadequate to support metabolism and illustrates the need for hemoglobin. But this minute amount when added to the O2 combined to the hemoglobin makes up the total O2 content of the blood. When calculating the oxygen content of the blood we must consider both of these compartments—hemoglobin and plasma (figure 16.8).,True,Shifts in the O2 Saturation Curve,Figure 16.8,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.8.png,Figure 16.8: Compartment of blood oxygen content.
7152fac2-d6ab-4b43-9ecb-2e79d08acca1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Calculating the O2 Content of Blood,False,Calculating the O2 Content of Blood,,,,
04be6168-8c6f-410d-b09e-417377ff3276,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"To calculate the arterial oxygen content (CaO2) let us first look at the factors affecting the majority of the O2 (i.e., that carried by hemoglobin).",True,Calculating the O2 Content of Blood,,,,
558f00ea-a3d9-4ca8-9489-b408a60f8fc7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,(1) This will be determined by the amount of hemoglobin in the blood (measured in mg/dL). So let us start building the equation.,True,Calculating the O2 Content of Blood,,,,
d9165197-65c4-4f1b-8c84-9713d37dee3e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Equation 16.1,True,Calculating the O2 Content of Blood,,,,
9cc53bb5-c501-4be4-acb0-aec01752c018,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,[latex]C_aO_2 = Hb (mg/dL)...[/latex],True,Calculating the O2 Content of Blood,,,,
583ca34f-d14f-49f9-b947-d7f72a19ab66,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"(2) Second, we must consider the oxygen carrying capacity of Hb, which is 1.34 mL O2/gm Hb. So we multiply the amount of Hb by its carrying capacity.",True,Calculating the O2 Content of Blood,,,,
f7658ea7-5e06-4560-9103-d100102ecac8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Equation 16.2,True,Calculating the O2 Content of Blood,,,,
64cf7dd2-97f4-45f9-abf5-88afd67aed70,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"[latex]C_aO_2 = Hb (mg/dL) \times 1.34\, O_2/gmHb...[/latex]",True,Calculating the O2 Content of Blood,,,,
32c93ba9-5fb6-4fd9-8ba7-9680e5a7926b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"(3) But that carrying capacity might not have been reached by all the Hb (i.e., the Hb may not be fully saturated). So to account for this, we multiply by the saturation (SaO2).",True,Calculating the O2 Content of Blood,,,,
aa7c4959-226a-416b-9d21-7d7672308e46,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Equation 16.3,True,Calculating the O2 Content of Blood,,,,
2c5cd9ad-126e-410f-8571-af4a68a8fa1c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"[latex]C_aO_2 = Hb (mg/dL) \times 1.34\, O_2/gmHb \times S_aO_2...[/latex]",True,Calculating the O2 Content of Blood,,,,
1eca8248-061e-48a8-b56a-9fcd146e9acf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"(4) So far that takes care of the O2 associated with Hb (normally about 98 percent of the total). Now we must add the O2 in plasma to the equation. We do this by measuring the PaO2 and multiplying it by a solubility coefficient (0.003 mL O2/mmHg/dL) to convert it from a partial pressure to milliliters. Removing the units makes this long but simple equation a little easier to understand. It has two components, representing the two compartments for O2 carriage.",True,Calculating the O2 Content of Blood,,,,
58b836fd-a252-4047-9b1d-ecf272f9558d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Equation 16.4,True,Calculating the O2 Content of Blood,,,,
76439a40-bf84-4562-a9f6-883c7ba106ca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,[latex]C_aO_2 = (Hb \times 1.34 \times S_aO_2) + (P_aO_2 \times 0.003)[/latex],True,Calculating the O2 Content of Blood,,,,
6630119f-13ab-4e68-a53b-13204d388db2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The plasma component is usually inconsequential, but may become more important when blood is exposed to an elevated alveolar PO2, such as during oxygen or hyperbaric therapy.",True,Calculating the O2 Content of Blood,,,,
fdf209a1-f395-45e3-b8ff-f92896c52cc3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Summary,False,Summary,,,,
15b4d1f5-94c0-4fbb-aaa1-4f309bb84f2e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"So to summarize, as oxygen’s lack of solubility means metabolic demands cannot be met by dissolved oxygen alone, the vast majority of oxygen is transported by hemoglobin, a molecule that is beautifully designed to pick up oxygen at the lung and release oxygen in proportion to the tissue’s demand. We will see more of hemoglobin’s sophistication when we address CO2 carriage.",True,Summary,,,,
eb65c942-4973-4471-81a0-f2dc0c1f8861,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,CO2 Transport,False,CO2 Transport,,,,
b4fb537f-a187-4895-85c3-991c4fc2405d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Unlike oxygen, carbon dioxide is soluble enough that it does not need a protein carrier like oxygen needs hemoglobin to enter and exit plasma. However, this does not necessarily mean that CO2 transport is simple. The complication this time is that free dissolved CO2 forms carbonic acid, which can threaten pH homeostasis. So most CO2 is not transported in the dissolved form. Most (approximately 70 percent) of the CO2 that emerges from metabolizing tissue is converted to bicarbonate with the help of enzymes within red blood cells. We will look at this more closely in a moment. About 15–25 percent is transported on hemoglobin.",True,CO2 Transport,,,,
a0c3d5f4-93b7-4bb8-8eca-65e90e092329,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Transport on Hemoglobin (15–25 Percent),False,Transport on Hemoglobin (15–25 Percent),,,,
7fab9b4d-0237-4ed9-9018-fc3bc54f822f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Carbon dioxide can bind to the terminal amine groups of hemoglobin’s polypeptide chains forming carbaminohemoglobin. It is worth noting a couple of points about this. First, CO2 does not compete with oxygen to bind to Hb—the binding sites are completely different and hemoglobin can hold both CO2 and O2 at the same time. Second, deoxyhemoglobin is a better carrier of CO2 than oxyhemoglobin is; consequently at the tissue where hemoglobin is losing its oxygen it is becoming a more efficient CO2 transporter. This is known as the Haldane effect.",True,Transport on Hemoglobin (15–25 Percent),,,,
e733c276-0bf7-401a-997a-f15e0a6a5115,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Transport as Dissolved CO2 (About 7 Percent),False,Transport as Dissolved CO2 (About 7 Percent),,,,
d8f75439-6d3a-4c93-9819-946bcbe63f11,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"A little CO2 combines with water to produce carbonic acid, the dissociated hydrogen form that must be buffered by plasma proteins, such as albumin.",True,Transport as Dissolved CO2 (About 7 Percent),,,,
a833dba1-bdc8-4aaa-897e-eb23e98814e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Transport as Bicarbonate (About 70 Percent),False,Transport as Bicarbonate (About 70 Percent),,,,
0b01302e-f2fb-46a4-9a33-ff9649348cbe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Seventy percent of the CO2 enters red blood cells, and once inside a familiar reaction occurs (equation 16.5). The CO2 binds with water in the cytoplasm, producing carbonic acid, which then dissociates into a hydrogen ion and a bicarbonate ion.",True,Transport as Bicarbonate (About 70 Percent),,,,
b37bcb73-29b8-4508-aa86-53339e3bf4bb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,This reversible reaction is accelerated by the enzyme carbonic anhydrase and is driven rapidly to the right by the high concentration of CO2 at the tissue.,True,Transport as Bicarbonate (About 70 Percent),,,,
fe944cac-8d56-4ab9-b4b3-ca800d05983b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The hydrogen ion produced helps shift the oxygen saturation curve to the right and so promotes further release of oxygen to the tissue. Hemoglobin then serves yet another purpose by buffering the proton with its polypeptide chains. Deoxyhemoglobin is a better proton acceptor than oxyhemoglobin, so as the hemoglobin loses its oxygen at the tissue it becomes a better pH buffer. This reduces the amount of hydrogen ion on the right side of our equation and moves the equation to the right, promoting the conversion of more CO2.",True,Transport as Bicarbonate (About 70 Percent),,,,
e176589b-5603-4237-8ab0-eae11539d963,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Equation 16.5,True,Transport as Bicarbonate (About 70 Percent),,,,
88b070d5-b1e1-41cc-8b69-b77555024ae9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],False,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
77952f40-eaf1-4710-8ef3-f4166a2e06b5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,High concentrations of CO2 at the tissue push this equation right to produce bicarbonate.,True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
7af44857-465a-492b-8854-fec3e76bea14,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The bicarbonate ion is pumped out of the cell, but without intervention this would leave the inside of the cell too positively charged as the negative charge of the bicarbonate is lost. To maintain electroneutrality the bicarbonate is exchanged for a chloride ion; this process is referred to as the chloride shift. The formation of bicarbonate at the tissue is summarized in figure 16.9.",True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],Figure 16.9,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.9.png,Figure 16.9: Formation of bicarbonate at the tissue.
7af44857-465a-492b-8854-fec3e76bea14,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The bicarbonate ion is pumped out of the cell, but without intervention this would leave the inside of the cell too positively charged as the negative charge of the bicarbonate is lost. To maintain electroneutrality the bicarbonate is exchanged for a chloride ion; this process is referred to as the chloride shift. The formation of bicarbonate at the tissue is summarized in figure 16.9.",True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],Figure 16.9,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.9.png,Figure 16.9: Formation of bicarbonate at the tissue.
7af44857-465a-492b-8854-fec3e76bea14,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"The bicarbonate ion is pumped out of the cell, but without intervention this would leave the inside of the cell too positively charged as the negative charge of the bicarbonate is lost. To maintain electroneutrality the bicarbonate is exchanged for a chloride ion; this process is referred to as the chloride shift. The formation of bicarbonate at the tissue is summarized in figure 16.9.",True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],Figure 16.9,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.9.png,Figure 16.9: Formation of bicarbonate at the tissue.
98eef1dd-521d-41b3-b209-178b480f3bdf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,The CO2 now travels through the bloodstream as bicarbonate toward the lungs. At the lungs the process is basically reversed. The partial pressure of CO2 at the lungs is low; consequently our equation is driven toward the left-hand side as CO2 leaves toward the low alveolar PCO2 (equation 16.6).,True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
010bed93-03e1-4f8a-baa0-bee95a8469b5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Equation 16.6,True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
b9b975ed-b0f0-4dab-a775-37f9e3101785,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,←,False,←,,,,
b4ed9fc3-e7df-44ec-a70d-0007835cff7d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,High bicarbonate and low CO2 at the lung force the equation leftward.,True,←,,,,
38f70783-6bbb-40e8-9d6a-6a7387c72728,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,The high alveolar PO2 also promotes the leftward movement—binding of oxygen to hemoglobin makes hemoglobin a less effective proton binder so it loses the proton and raises the amount of substrate on the right-hand side and thereby promotes reformation of CO2. The Haldane effect is also reversed—as hemoglobin gains oxygen at the lung it loses its affinity for CO2 and releases it into the plasma. This raises plasma PCO2 and promotes diffusion of CO2 into the alveoli for expulsion.,True,←,,,,
a7fc2a83-b1d9-466f-ba53-4855011aaa56,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Likewise the chloride shift is reversed and bicarbonate reenters the cell as chloride is pumped back out.,True,←,,,,
2a3fd61c-784e-4c8a-b8d7-5fe45dbf3400,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"All these moves help promote the right-to-left direction of our now infamous equation and the re-forming of CO2. Alveolar ventilation gets rid of the re-formed CO2 to the atmosphere, maintaining the alveolar PCO2 at relatively low levels and the direction of the equation right-to-left. The reformation of CO2 at the lungs is summarized in figure 16.10.",True,←,Figure 16.10,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.10.png,Figure 16.10: Reformation of CO2 at the lungs.
2a3fd61c-784e-4c8a-b8d7-5fe45dbf3400,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"All these moves help promote the right-to-left direction of our now infamous equation and the re-forming of CO2. Alveolar ventilation gets rid of the re-formed CO2 to the atmosphere, maintaining the alveolar PCO2 at relatively low levels and the direction of the equation right-to-left. The reformation of CO2 at the lungs is summarized in figure 16.10.",True,←,Figure 16.10,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.10.png,Figure 16.10: Reformation of CO2 at the lungs.
2a3fd61c-784e-4c8a-b8d7-5fe45dbf3400,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"All these moves help promote the right-to-left direction of our now infamous equation and the re-forming of CO2. Alveolar ventilation gets rid of the re-formed CO2 to the atmosphere, maintaining the alveolar PCO2 at relatively low levels and the direction of the equation right-to-left. The reformation of CO2 at the lungs is summarized in figure 16.10.",True,←,Figure 16.10,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.10.png,Figure 16.10: Reformation of CO2 at the lungs.
87096713-dd75-4601-8d0a-03c40da62ed2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,The CO2 “Dissociation” Curve,False,The CO2 “Dissociation” Curve,,,,
1798ddf2-6b4c-4146-a3df-db20ee0ee772,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"So, for want of a better name, we can also draw a CO2 dissociation or saturation curve, as is shown in figure 16.11. The graph shows the CO2 concentration in blood across a wide range of PCO2 and shows the effect of Hb O2 saturation on CO2 carriage. The CO2 dissociation curve is unlike the oxygen saturation curve and is virtually linear (i.e., the higher the PCO2, the higher the CO2 content of the blood); there is no plateau to the curve as we saw with O2 transport. The ramification of this is that the lower the alveolar PCO2, the lower the blood PCO2, and the higher the alveolar PCO2, the higher the blood PCO2. It is a very simple relationship that ends with the obvious statement that the more you breathe, the lower arterial CO2 becomes. It is worth reminding ourselves here that this is not a relationship seen with oxygen that is limited by the capacity of hemoglobin (breathing more does not necessarily result in more oxygen in the bloodstream). The other aspect to note here is the effect of hemoglobin’s oxygen saturation on carbon dioxide carriage. This has clinical ramifications, so we will look at this more closely.",True,The CO2 “Dissociation” Curve,Figure 16.11,CO2 Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.11.png,Figure 16.11: CO2 dissociation curve.
1798ddf2-6b4c-4146-a3df-db20ee0ee772,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"So, for want of a better name, we can also draw a CO2 dissociation or saturation curve, as is shown in figure 16.11. The graph shows the CO2 concentration in blood across a wide range of PCO2 and shows the effect of Hb O2 saturation on CO2 carriage. The CO2 dissociation curve is unlike the oxygen saturation curve and is virtually linear (i.e., the higher the PCO2, the higher the CO2 content of the blood); there is no plateau to the curve as we saw with O2 transport. The ramification of this is that the lower the alveolar PCO2, the lower the blood PCO2, and the higher the alveolar PCO2, the higher the blood PCO2. It is a very simple relationship that ends with the obvious statement that the more you breathe, the lower arterial CO2 becomes. It is worth reminding ourselves here that this is not a relationship seen with oxygen that is limited by the capacity of hemoglobin (breathing more does not necessarily result in more oxygen in the bloodstream). The other aspect to note here is the effect of hemoglobin’s oxygen saturation on carbon dioxide carriage. This has clinical ramifications, so we will look at this more closely.",True,The CO2 “Dissociation” Curve,Figure 16.11,Oxygen Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.11.png,Figure 16.11: CO2 dissociation curve.
1798ddf2-6b4c-4146-a3df-db20ee0ee772,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"So, for want of a better name, we can also draw a CO2 dissociation or saturation curve, as is shown in figure 16.11. The graph shows the CO2 concentration in blood across a wide range of PCO2 and shows the effect of Hb O2 saturation on CO2 carriage. The CO2 dissociation curve is unlike the oxygen saturation curve and is virtually linear (i.e., the higher the PCO2, the higher the CO2 content of the blood); there is no plateau to the curve as we saw with O2 transport. The ramification of this is that the lower the alveolar PCO2, the lower the blood PCO2, and the higher the alveolar PCO2, the higher the blood PCO2. It is a very simple relationship that ends with the obvious statement that the more you breathe, the lower arterial CO2 becomes. It is worth reminding ourselves here that this is not a relationship seen with oxygen that is limited by the capacity of hemoglobin (breathing more does not necessarily result in more oxygen in the bloodstream). The other aspect to note here is the effect of hemoglobin’s oxygen saturation on carbon dioxide carriage. This has clinical ramifications, so we will look at this more closely.",True,The CO2 “Dissociation” Curve,Figure 16.11,16. Gas Transport,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/16.11.png,Figure 16.11: CO2 dissociation curve.
0dd775a2-4d37-4413-9df9-c93c447777d2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"When deoxygenated, hemoglobin’s structure promotes binding of CO2 and buffering of protons by the polypeptide chains. So when O2 saturation is zero, the CO2 and proton carrying capability of Hb is high. As already mentioned, this means that when Hb is in its deoxygenated form at the tissue, its CO2 carrying ability is increased.",True,The CO2 “Dissociation” Curve,,,,
9c2d897f-cdff-4c63-9a97-cc66cf4333ec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"When we get to the lung, however, the Hb is exposed to the high alveolar PO2 and oxygen binds to the heme sites and becomes saturated; this causes a conformational change, and the CO2 and proton carrying ability is reduced. So conveniently CO2 release is promoted at the lung.",True,The CO2 “Dissociation” Curve,,,,
14032563-3799-4fe7-90fb-498dcfd66b07,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Although CO2 is highly soluble, very little of it can be transported as dissolved CO2 in plasma because of its effect on pH. The majority is converted to bicarbonate in red blood cells and transported in plasma, while about 25 percent is transported bound to hemoglobin.",True,The CO2 “Dissociation” Curve,,,,
ce9552a5-eb32-447c-922d-a926988e15a3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,Text,False,Text,,,,
eaf8f867-2857-4e2c-b978-d34dd4391cfe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Levitsky, Michael G. “Chapter 7: Transport of Oxygen and Carbon Dioxide in the Blood.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
95bdd69a-fa20-4250-9d8a-ddba1430d1ed,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"West, John B. “Chapter 6: Gas Transport by the Blood—How Gases Are Moved to the Peripheral Tissues.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
33e7d298-cf3f-4a05-8582-10c5371dc9bc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,16. Gas Transport,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/gas-transport/,"Widdicombe, John G., and Andrew S. Davis. “Chapter 6.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
279562ba-f525-4412-9982-1e9c07d279bb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"There are two circulatory networks that normally form shunts. The bronchial circulation, that supplies the bronchi, empties its venous blood into the pulmonary veins, thereby sending slightly deoxygenated blood back toward the left heart and into the systemic arterial system. Likewise a very small portion of the coronary venous blood is returned to the left ventricle (through the thebesian veins) and thereby bypasses the lung completely before going back in the systemic circulation.",True,Text,,,,
e26d0d11-466b-4a31-bc87-c83397920658,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,These two wayward circulations and the imperfect V/Q matching in the lung serve to suppress arterial oxygen saturation.,True,Text,,,,
71534a84-b0b9-4e60-8220-f5651cdd2910,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,Abnormal Shunts,False,Abnormal Shunts,,,,
2028df86-7d26-41d1-939e-4531335de8be,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Shunts can also be created by abnormal physiology or anatomy. There are several heart structural defects that allow blood from the right heart to enter the systemic circulation and bypass the lungs altogether; one common example is a patent foramen ovale where the incomplete atrial septum between the right and left heart allows deoxygenated venous blood to directly enter the arterial circulation, bypassing, or “shunting,” past the lungs.",True,Abnormal Shunts,,,,
7598457c-5eb4-41de-ac46-a98cdc3b4539,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"In pulmonary disease, areas of the lung may not receive ventilation (e.g., as airways are blocked or collapsed). Perfusion to these areas is therefore wasted as no gas exchange takes place; effectively a right–left physiological shunt has formed, and V/Q approaches zero (i.e., low V and normal Q).",True,Abnormal Shunts,,,,
6a1d93e5-9615-42d3-b2d8-5feebc31550b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,Detecting Shunts,False,Detecting Shunts,,,,
abce3b74-063f-4823-b158-aa4d975f190e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"There is a quick and easy way to detect whether a shunt is contributing to a patient’s low arterial PO2 by giving a patient 100 percent O2 to breathe. The blood passing through capillaries that are exposed to the 100 percent O2 becomes fully saturated. However, any shunted blood never “sees” the high PO2 and consequently stays at venous PO2. When the two routes rejoin and the blood mixes, it remains below 100 percent (i.e., the alveolar–arterial PO2 difference is not abolished by the 100 percent O2, and it never can be as long as the shunt exists).",True,Detecting Shunts,,,,
989d920b-4e5d-4ed6-9069-e8acb68ae263,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,Calculating the Size of a Pulmonary Shunt,False,Calculating the Size of a Pulmonary Shunt,,,,
4ebe9b5f-9a81-497d-b977-d939be39cada,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
4ebe9b5f-9a81-497d-b977-d939be39cada,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
4ebe9b5f-9a81-497d-b977-d939be39cada,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
4ebe9b5f-9a81-497d-b977-d939be39cada,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
4ebe9b5f-9a81-497d-b977-d939be39cada,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
4ebe9b5f-9a81-497d-b977-d939be39cada,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
e553ad86-e664-4ecf-bbb2-9dd8e5e5bf63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
e553ad86-e664-4ecf-bbb2-9dd8e5e5bf63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
e553ad86-e664-4ecf-bbb2-9dd8e5e5bf63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
e553ad86-e664-4ecf-bbb2-9dd8e5e5bf63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
e553ad86-e664-4ecf-bbb2-9dd8e5e5bf63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
e553ad86-e664-4ecf-bbb2-9dd8e5e5bf63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
4068ac99-f409-4266-b009-a69d11e354ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,So know we can use these oxygen concentrations to work out the percentage of shunted blood.,True,Calculating the Size of a Pulmonary Shunt,,,,
f36e6b61-b7bc-468a-86ba-0fcf894754a2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Now let us combine our flow and oxygen concentration and think in terms of absolute oxygen contents in each part of our diagram. (Critical point: The absolute oxygen content is the product of the blood volume and oxygen concentration.) So now thinking of absolute oxygen contents, let us generate a first basic equation (equation 15.1) with what we know—the amount of oxygen in our flow going back to the left heart (QT) equals the oxygen from the pulmonary capillaries, plus that from the shunt.",True,Calculating the Size of a Pulmonary Shunt,,,,
affef48c-01e8-43fd-acbd-4ded7294567f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,Equation 15.1,True,Calculating the Size of a Pulmonary Shunt,,,,
ef3919c8-ac51-40a2-84ca-c3643403fbd4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],False,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],,,,
edf017e4-f8e9-4b25-b8fa-9b71a438769e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
edf017e4-f8e9-4b25-b8fa-9b71a438769e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
edf017e4-f8e9-4b25-b8fa-9b71a438769e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
edf017e4-f8e9-4b25-b8fa-9b71a438769e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
edf017e4-f8e9-4b25-b8fa-9b71a438769e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
edf017e4-f8e9-4b25-b8fa-9b71a438769e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
9ec0dd8c-8545-409c-9501-82b35955ff9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
9ec0dd8c-8545-409c-9501-82b35955ff9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
9ec0dd8c-8545-409c-9501-82b35955ff9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
9ec0dd8c-8545-409c-9501-82b35955ff9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
9ec0dd8c-8545-409c-9501-82b35955ff9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
9ec0dd8c-8545-409c-9501-82b35955ff9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
ad5e9778-4a18-4fb1-a97f-baef972211e6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
ad5e9778-4a18-4fb1-a97f-baef972211e6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
ad5e9778-4a18-4fb1-a97f-baef972211e6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
ad5e9778-4a18-4fb1-a97f-baef972211e6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
ad5e9778-4a18-4fb1-a97f-baef972211e6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
ad5e9778-4a18-4fb1-a97f-baef972211e6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
94eb27ac-ad53-47da-bbf1-abc30fb76ada,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,Let us put those terms into our basic equation (equation 15.2).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],,,,
d71780b8-6e76-4c41-910d-38a5d7cd3e17,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,Equation 15.2,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],,,,
17ae07d9-82fd-4212-8771-9250307f9f54,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],False,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
ed82d5ed-4717-4069-bb0a-103cb5c09a82,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"So at this point we might panic, thinking that we have no measure of flow (Q) for any of these variables, that we only have oxygen concentrations from our blood gases and alveolar gas equation. But panic not. Through the magic of mathematics we can rearrange this equation (15.2) to eliminate our flows (Qs) and be left with an equation that meets our objective of QS/QT.",True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
805a35eb-cf3d-439b-849f-8ebbc99c7e24,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"The shunt equation (equation 15.3) describes the proportion of total perfusion that is passing through the shunt. This is the equation worth remembering: the portion of blood going through the shunt is the difference between the capillary and arterial O2 concentrations, divided by the difference between the capillary and venous oxygen concentrations.",True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
14293145-d6be-46c1-a68d-59db028c08cf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,Equation 15.3,True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
efedbfe6-ffb4-4984-a786-71e19e339f21,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,[latex]Q_T \times C_aO_2 = [(Q_T - Q_S) \times C_CO_2] + [Q_S \times C_VO_2][/latex],True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
ef2c2a52-3094-4f18-9d77-7dde38a95528,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Let us look at an example to put this in context. We have a patient with normal lungs, but a right–left shunt is present. We find out that his arterial blood O2 concentration is 18 mL and venous is 14. Capillary oxygen concentration is calculated to be 20 mL/100 mL. Now we plug the numbers in the equation and see that the proportion of blood going through the shunt is a third, or 33 percent.",True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
03c8b954-bbc4-421a-8222-4d78f99067e3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,Summary,False,Summary,,,,
0c34cf89-7201-4c16-9be7-82f5cfb00ddf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"So to recap, small pulmonary shunts exist even in the normal cardiopulmonary system, but abnormal shunts can arise from a number of different pathological causes. Although the presence of a shunt is relatively easy to detect, it is important to calculate its size, which is also a relatively easy process.",True,Summary,,,,
741a9569-d134-4714-90a4-a8cb8c604c4d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,Text,False,Text,,,,
c0f16823-bf43-4645-9269-c51c6ce26d14,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"Levitsky, Michael G. “Chapter 5: Ventilation–Perfusion Relationships.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
4a3745c2-5916-41da-b111-3377965154c7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-5,"West, John B. “Chapter 5: Ventilation–Perfusion Relationships—How Matching of Gas and Blood Determines Gas Exchange.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
20d1cd91-da2f-4856-8ebc-b53e72a2fd8c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"There are two circulatory networks that normally form shunts. The bronchial circulation, that supplies the bronchi, empties its venous blood into the pulmonary veins, thereby sending slightly deoxygenated blood back toward the left heart and into the systemic arterial system. Likewise a very small portion of the coronary venous blood is returned to the left ventricle (through the thebesian veins) and thereby bypasses the lung completely before going back in the systemic circulation.",True,Text,,,,
0484e324-4905-4135-bc37-25a68dfef4ec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,These two wayward circulations and the imperfect V/Q matching in the lung serve to suppress arterial oxygen saturation.,True,Text,,,,
15dde1b1-b67c-4a3b-b87d-2555db0fac3c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,Abnormal Shunts,False,Abnormal Shunts,,,,
ac6c0ac3-9c92-4cd2-bf5e-3717b1933703,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Shunts can also be created by abnormal physiology or anatomy. There are several heart structural defects that allow blood from the right heart to enter the systemic circulation and bypass the lungs altogether; one common example is a patent foramen ovale where the incomplete atrial septum between the right and left heart allows deoxygenated venous blood to directly enter the arterial circulation, bypassing, or “shunting,” past the lungs.",True,Abnormal Shunts,,,,
60c6e69f-1287-431f-8d6f-bbe56f56de78,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"In pulmonary disease, areas of the lung may not receive ventilation (e.g., as airways are blocked or collapsed). Perfusion to these areas is therefore wasted as no gas exchange takes place; effectively a right–left physiological shunt has formed, and V/Q approaches zero (i.e., low V and normal Q).",True,Abnormal Shunts,,,,
3de66b9d-56b3-40ac-94e7-7853db99f754,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,Detecting Shunts,False,Detecting Shunts,,,,
8230e83c-dcc2-4258-8cbd-e8a33c8f93b5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"There is a quick and easy way to detect whether a shunt is contributing to a patient’s low arterial PO2 by giving a patient 100 percent O2 to breathe. The blood passing through capillaries that are exposed to the 100 percent O2 becomes fully saturated. However, any shunted blood never “sees” the high PO2 and consequently stays at venous PO2. When the two routes rejoin and the blood mixes, it remains below 100 percent (i.e., the alveolar–arterial PO2 difference is not abolished by the 100 percent O2, and it never can be as long as the shunt exists).",True,Detecting Shunts,,,,
64d79420-ef94-4f47-9683-55f955faf147,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,Calculating the Size of a Pulmonary Shunt,False,Calculating the Size of a Pulmonary Shunt,,,,
06d2a3c3-f2b2-4c39-b9fe-49ffb61a70c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
06d2a3c3-f2b2-4c39-b9fe-49ffb61a70c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
06d2a3c3-f2b2-4c39-b9fe-49ffb61a70c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
06d2a3c3-f2b2-4c39-b9fe-49ffb61a70c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
06d2a3c3-f2b2-4c39-b9fe-49ffb61a70c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
06d2a3c3-f2b2-4c39-b9fe-49ffb61a70c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
6a23fb31-2484-4c38-90f8-a8d8704a5eca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
6a23fb31-2484-4c38-90f8-a8d8704a5eca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
6a23fb31-2484-4c38-90f8-a8d8704a5eca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
6a23fb31-2484-4c38-90f8-a8d8704a5eca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
6a23fb31-2484-4c38-90f8-a8d8704a5eca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
6a23fb31-2484-4c38-90f8-a8d8704a5eca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
cf3c7e24-626b-4b03-888c-82f8f240e5b3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,So know we can use these oxygen concentrations to work out the percentage of shunted blood.,True,Calculating the Size of a Pulmonary Shunt,,,,
61f54081-122f-4508-bc4e-7a6f0b0b41ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Now let us combine our flow and oxygen concentration and think in terms of absolute oxygen contents in each part of our diagram. (Critical point: The absolute oxygen content is the product of the blood volume and oxygen concentration.) So now thinking of absolute oxygen contents, let us generate a first basic equation (equation 15.1) with what we know—the amount of oxygen in our flow going back to the left heart (QT) equals the oxygen from the pulmonary capillaries, plus that from the shunt.",True,Calculating the Size of a Pulmonary Shunt,,,,
cb28431c-dc6c-47b4-b5c6-22ef3bc58a29,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,Equation 15.1,True,Calculating the Size of a Pulmonary Shunt,,,,
0d641770-36a3-49f7-b9c0-d58f6dc56012,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],False,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],,,,
943e2e65-d0cc-400d-9ced-e2414e2bbcfe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
943e2e65-d0cc-400d-9ced-e2414e2bbcfe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
943e2e65-d0cc-400d-9ced-e2414e2bbcfe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
943e2e65-d0cc-400d-9ced-e2414e2bbcfe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
943e2e65-d0cc-400d-9ced-e2414e2bbcfe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
943e2e65-d0cc-400d-9ced-e2414e2bbcfe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
0315968a-ee9b-4cb9-872f-3cbc6e340be9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
0315968a-ee9b-4cb9-872f-3cbc6e340be9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
0315968a-ee9b-4cb9-872f-3cbc6e340be9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
0315968a-ee9b-4cb9-872f-3cbc6e340be9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
0315968a-ee9b-4cb9-872f-3cbc6e340be9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
0315968a-ee9b-4cb9-872f-3cbc6e340be9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
a2fbb091-cfc7-48e5-9257-ed44e01d5d61,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
a2fbb091-cfc7-48e5-9257-ed44e01d5d61,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
a2fbb091-cfc7-48e5-9257-ed44e01d5d61,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
a2fbb091-cfc7-48e5-9257-ed44e01d5d61,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
a2fbb091-cfc7-48e5-9257-ed44e01d5d61,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
a2fbb091-cfc7-48e5-9257-ed44e01d5d61,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
3abfa108-fa40-43a3-927f-1f7515df7ff7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,Let us put those terms into our basic equation (equation 15.2).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],,,,
daa602a6-8645-4241-b18e-e74e85788d07,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,Equation 15.2,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],,,,
da30dfee-4f0f-4ca8-8aa6-771f5b46d9d2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],False,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
0508e18d-d4b6-4915-b473-65969fb37d5e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"So at this point we might panic, thinking that we have no measure of flow (Q) for any of these variables, that we only have oxygen concentrations from our blood gases and alveolar gas equation. But panic not. Through the magic of mathematics we can rearrange this equation (15.2) to eliminate our flows (Qs) and be left with an equation that meets our objective of QS/QT.",True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
b2f5ebf5-2918-44de-9c3f-c59dc9863b17,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"The shunt equation (equation 15.3) describes the proportion of total perfusion that is passing through the shunt. This is the equation worth remembering: the portion of blood going through the shunt is the difference between the capillary and arterial O2 concentrations, divided by the difference between the capillary and venous oxygen concentrations.",True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
f8c93609-3723-4596-9748-b03677b6ee91,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,Equation 15.3,True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
d23a9d68-705a-4806-9811-30404abe6874,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,[latex]Q_T \times C_aO_2 = [(Q_T - Q_S) \times C_CO_2] + [Q_S \times C_VO_2][/latex],True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
6e6b798a-4df8-4c38-b290-7a1bf37ce105,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Let us look at an example to put this in context. We have a patient with normal lungs, but a right–left shunt is present. We find out that his arterial blood O2 concentration is 18 mL and venous is 14. Capillary oxygen concentration is calculated to be 20 mL/100 mL. Now we plug the numbers in the equation and see that the proportion of blood going through the shunt is a third, or 33 percent.",True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
70fe9811-7b8c-4ed7-a1c8-1a272326e00f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,Summary,False,Summary,,,,
f730c173-b9d9-4a3b-9b34-ce95cdc820b2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"So to recap, small pulmonary shunts exist even in the normal cardiopulmonary system, but abnormal shunts can arise from a number of different pathological causes. Although the presence of a shunt is relatively easy to detect, it is important to calculate its size, which is also a relatively easy process.",True,Summary,,,,
fc8a8a4a-5fb7-4ce1-8df1-dab9169c6957,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,Text,False,Text,,,,
b248f46a-24fa-4f4d-a1f6-fba436bc750f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"Levitsky, Michael G. “Chapter 5: Ventilation–Perfusion Relationships.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
c8a7a469-669f-4e7c-a5ea-a8e90bd319e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-4,"West, John B. “Chapter 5: Ventilation–Perfusion Relationships—How Matching of Gas and Blood Determines Gas Exchange.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
4679b030-ebc2-4917-a9d1-60a04f0a073b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"There are two circulatory networks that normally form shunts. The bronchial circulation, that supplies the bronchi, empties its venous blood into the pulmonary veins, thereby sending slightly deoxygenated blood back toward the left heart and into the systemic arterial system. Likewise a very small portion of the coronary venous blood is returned to the left ventricle (through the thebesian veins) and thereby bypasses the lung completely before going back in the systemic circulation.",True,Text,,,,
3ff82dc2-2d45-4415-9fd6-cf86bd59a4b5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,These two wayward circulations and the imperfect V/Q matching in the lung serve to suppress arterial oxygen saturation.,True,Text,,,,
966e0e6c-e1b2-4ddb-9294-b86fde64c6ff,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,Abnormal Shunts,False,Abnormal Shunts,,,,
58112c5b-9528-4f28-b294-9fb65ec45bcf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Shunts can also be created by abnormal physiology or anatomy. There are several heart structural defects that allow blood from the right heart to enter the systemic circulation and bypass the lungs altogether; one common example is a patent foramen ovale where the incomplete atrial septum between the right and left heart allows deoxygenated venous blood to directly enter the arterial circulation, bypassing, or “shunting,” past the lungs.",True,Abnormal Shunts,,,,
7a63c4c2-5027-45e7-b7d2-88033b1f465a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"In pulmonary disease, areas of the lung may not receive ventilation (e.g., as airways are blocked or collapsed). Perfusion to these areas is therefore wasted as no gas exchange takes place; effectively a right–left physiological shunt has formed, and V/Q approaches zero (i.e., low V and normal Q).",True,Abnormal Shunts,,,,
9c3a0781-37f0-4fe3-97ec-53bac581c5f3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,Detecting Shunts,False,Detecting Shunts,,,,
de15b5bc-0bcd-40ec-ac3b-cce56acadaec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"There is a quick and easy way to detect whether a shunt is contributing to a patient’s low arterial PO2 by giving a patient 100 percent O2 to breathe. The blood passing through capillaries that are exposed to the 100 percent O2 becomes fully saturated. However, any shunted blood never “sees” the high PO2 and consequently stays at venous PO2. When the two routes rejoin and the blood mixes, it remains below 100 percent (i.e., the alveolar–arterial PO2 difference is not abolished by the 100 percent O2, and it never can be as long as the shunt exists).",True,Detecting Shunts,,,,
5a456eea-333c-4440-b734-3f3db464dd41,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,Calculating the Size of a Pulmonary Shunt,False,Calculating the Size of a Pulmonary Shunt,,,,
f0b86620-3e99-4775-8bea-d0ab2807215e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
f0b86620-3e99-4775-8bea-d0ab2807215e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
f0b86620-3e99-4775-8bea-d0ab2807215e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
f0b86620-3e99-4775-8bea-d0ab2807215e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
f0b86620-3e99-4775-8bea-d0ab2807215e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
f0b86620-3e99-4775-8bea-d0ab2807215e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
5e6b8357-a709-47ac-88b1-b10e034f2f45,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
5e6b8357-a709-47ac-88b1-b10e034f2f45,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
5e6b8357-a709-47ac-88b1-b10e034f2f45,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
5e6b8357-a709-47ac-88b1-b10e034f2f45,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
5e6b8357-a709-47ac-88b1-b10e034f2f45,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
5e6b8357-a709-47ac-88b1-b10e034f2f45,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
4600e7a7-4f2c-4717-81bf-caa326f79c28,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,So know we can use these oxygen concentrations to work out the percentage of shunted blood.,True,Calculating the Size of a Pulmonary Shunt,,,,
b87bfde1-ce6c-4627-9a71-2f9249f66658,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Now let us combine our flow and oxygen concentration and think in terms of absolute oxygen contents in each part of our diagram. (Critical point: The absolute oxygen content is the product of the blood volume and oxygen concentration.) So now thinking of absolute oxygen contents, let us generate a first basic equation (equation 15.1) with what we know—the amount of oxygen in our flow going back to the left heart (QT) equals the oxygen from the pulmonary capillaries, plus that from the shunt.",True,Calculating the Size of a Pulmonary Shunt,,,,
c16092bd-c63f-4542-9b50-5e3af6cba9f6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,Equation 15.1,True,Calculating the Size of a Pulmonary Shunt,,,,
bf9b3c4f-e93b-4bc0-8223-ce479f328480,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],False,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],,,,
8dde4790-b1e0-41fe-a830-00477eb2f026,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
8dde4790-b1e0-41fe-a830-00477eb2f026,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
8dde4790-b1e0-41fe-a830-00477eb2f026,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
8dde4790-b1e0-41fe-a830-00477eb2f026,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
8dde4790-b1e0-41fe-a830-00477eb2f026,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
8dde4790-b1e0-41fe-a830-00477eb2f026,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
dcb29dfe-1380-42b3-bcfa-a51630fd8a9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
dcb29dfe-1380-42b3-bcfa-a51630fd8a9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
dcb29dfe-1380-42b3-bcfa-a51630fd8a9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
dcb29dfe-1380-42b3-bcfa-a51630fd8a9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
dcb29dfe-1380-42b3-bcfa-a51630fd8a9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
dcb29dfe-1380-42b3-bcfa-a51630fd8a9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
0b9c443d-6e92-4e6a-b0ca-d299224704e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
0b9c443d-6e92-4e6a-b0ca-d299224704e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
0b9c443d-6e92-4e6a-b0ca-d299224704e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
0b9c443d-6e92-4e6a-b0ca-d299224704e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
0b9c443d-6e92-4e6a-b0ca-d299224704e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
0b9c443d-6e92-4e6a-b0ca-d299224704e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
faaf9226-b1f0-4e7f-80a5-4b677b72ccca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,Let us put those terms into our basic equation (equation 15.2).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],,,,
1bca73b7-dcee-4433-9567-02b6a470d7bf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,Equation 15.2,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],,,,
a14353bd-aebe-4967-a954-0fe3116ae4d8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],False,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
4b281cbc-b426-4a36-9a76-d0e0bede22f2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"So at this point we might panic, thinking that we have no measure of flow (Q) for any of these variables, that we only have oxygen concentrations from our blood gases and alveolar gas equation. But panic not. Through the magic of mathematics we can rearrange this equation (15.2) to eliminate our flows (Qs) and be left with an equation that meets our objective of QS/QT.",True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
6378e05c-a50f-4f32-9832-04cea30acf7e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"The shunt equation (equation 15.3) describes the proportion of total perfusion that is passing through the shunt. This is the equation worth remembering: the portion of blood going through the shunt is the difference between the capillary and arterial O2 concentrations, divided by the difference between the capillary and venous oxygen concentrations.",True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
e61e4320-bf21-440b-af26-dc05a8f4dfd2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,Equation 15.3,True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
2dc6b6e5-90f7-47ad-bfab-43ee76e15666,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,[latex]Q_T \times C_aO_2 = [(Q_T - Q_S) \times C_CO_2] + [Q_S \times C_VO_2][/latex],True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
29ee3ab3-49cf-46c7-abfc-5b885f78531c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Let us look at an example to put this in context. We have a patient with normal lungs, but a right–left shunt is present. We find out that his arterial blood O2 concentration is 18 mL and venous is 14. Capillary oxygen concentration is calculated to be 20 mL/100 mL. Now we plug the numbers in the equation and see that the proportion of blood going through the shunt is a third, or 33 percent.",True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
e0f5fc2d-351b-4ab5-bdc6-2da6e454f090,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,Summary,False,Summary,,,,
fb90a601-786d-4cfd-925f-8e5389461a05,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"So to recap, small pulmonary shunts exist even in the normal cardiopulmonary system, but abnormal shunts can arise from a number of different pathological causes. Although the presence of a shunt is relatively easy to detect, it is important to calculate its size, which is also a relatively easy process.",True,Summary,,,,
053dd2b3-06d1-44ee-9bac-296102b9be83,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,Text,False,Text,,,,
4cab6cc5-6f79-485f-bb7f-b0003136c03d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"Levitsky, Michael G. “Chapter 5: Ventilation–Perfusion Relationships.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
a7b1f6d2-658d-4130-a7c1-b7819b8bcc91,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Detecting Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-3,"West, John B. “Chapter 5: Ventilation–Perfusion Relationships—How Matching of Gas and Blood Determines Gas Exchange.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
1dd1f475-39de-4f94-8c42-f80cb37efe2d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"There are two circulatory networks that normally form shunts. The bronchial circulation, that supplies the bronchi, empties its venous blood into the pulmonary veins, thereby sending slightly deoxygenated blood back toward the left heart and into the systemic arterial system. Likewise a very small portion of the coronary venous blood is returned to the left ventricle (through the thebesian veins) and thereby bypasses the lung completely before going back in the systemic circulation.",True,Text,,,,
2a582771-2006-49bc-a862-782ed8ff63cc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,These two wayward circulations and the imperfect V/Q matching in the lung serve to suppress arterial oxygen saturation.,True,Text,,,,
de59b7df-422e-45a0-aa0c-d0e92b14b3db,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,Abnormal Shunts,False,Abnormal Shunts,,,,
d9617844-1330-40ce-9058-274e4700a88e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Shunts can also be created by abnormal physiology or anatomy. There are several heart structural defects that allow blood from the right heart to enter the systemic circulation and bypass the lungs altogether; one common example is a patent foramen ovale where the incomplete atrial septum between the right and left heart allows deoxygenated venous blood to directly enter the arterial circulation, bypassing, or “shunting,” past the lungs.",True,Abnormal Shunts,,,,
9f434009-953b-4e99-9c44-322031ce3350,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"In pulmonary disease, areas of the lung may not receive ventilation (e.g., as airways are blocked or collapsed). Perfusion to these areas is therefore wasted as no gas exchange takes place; effectively a right–left physiological shunt has formed, and V/Q approaches zero (i.e., low V and normal Q).",True,Abnormal Shunts,,,,
8535a9f9-4b87-4522-8aa0-a40a7f46faa6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,Detecting Shunts,False,Detecting Shunts,,,,
02c67cf5-71fb-4891-8034-d0a03127cff6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"There is a quick and easy way to detect whether a shunt is contributing to a patient’s low arterial PO2 by giving a patient 100 percent O2 to breathe. The blood passing through capillaries that are exposed to the 100 percent O2 becomes fully saturated. However, any shunted blood never “sees” the high PO2 and consequently stays at venous PO2. When the two routes rejoin and the blood mixes, it remains below 100 percent (i.e., the alveolar–arterial PO2 difference is not abolished by the 100 percent O2, and it never can be as long as the shunt exists).",True,Detecting Shunts,,,,
b903c0cb-9660-4375-80a9-f00636cf8dee,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,Calculating the Size of a Pulmonary Shunt,False,Calculating the Size of a Pulmonary Shunt,,,,
72a7591b-bfd6-43ec-8255-1d39e18f92e2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
72a7591b-bfd6-43ec-8255-1d39e18f92e2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
72a7591b-bfd6-43ec-8255-1d39e18f92e2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
72a7591b-bfd6-43ec-8255-1d39e18f92e2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
72a7591b-bfd6-43ec-8255-1d39e18f92e2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
72a7591b-bfd6-43ec-8255-1d39e18f92e2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
1756323e-4782-4105-9708-8ec662b4a3b1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
1756323e-4782-4105-9708-8ec662b4a3b1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
1756323e-4782-4105-9708-8ec662b4a3b1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
1756323e-4782-4105-9708-8ec662b4a3b1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
1756323e-4782-4105-9708-8ec662b4a3b1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
1756323e-4782-4105-9708-8ec662b4a3b1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
ffa5f05e-3fb8-4b82-b5e5-c496bd7bba17,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,So know we can use these oxygen concentrations to work out the percentage of shunted blood.,True,Calculating the Size of a Pulmonary Shunt,,,,
7d09ed7f-6998-448f-9132-5f4be5339e58,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Now let us combine our flow and oxygen concentration and think in terms of absolute oxygen contents in each part of our diagram. (Critical point: The absolute oxygen content is the product of the blood volume and oxygen concentration.) So now thinking of absolute oxygen contents, let us generate a first basic equation (equation 15.1) with what we know—the amount of oxygen in our flow going back to the left heart (QT) equals the oxygen from the pulmonary capillaries, plus that from the shunt.",True,Calculating the Size of a Pulmonary Shunt,,,,
1831fdad-5079-495c-bee5-5c0e5e5fdd5d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,Equation 15.1,True,Calculating the Size of a Pulmonary Shunt,,,,
edf6e3a5-b827-4737-bdb1-cd8af5ffff74,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,Totaloxygencontent=oxygenfromcapillaries+oxygenfromshunt,False,Totaloxygencontent=oxygenfromcapillaries+oxygenfromshunt,,,,
eb13e75a-5b2d-440d-9298-3ffd78936ccc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,T,False,T,,,,
59b200cb-8221-4634-af86-8c42890e9465,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,o,False,o,,,,
231f5c5e-40fe-49fb-a2d9-0f0a033fc661,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,t,False,t,,,,
ab619d43-cb1b-4ddb-9c42-73c078adc4ae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,a,False,a,,,,
cd05d68d-bc54-4e0d-a9fc-807e72f4703b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,l,False,l,,,,
05d65fcf-179b-44ba-bdfb-8caacca7c83f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,x,False,x,,,,
2800e610-17f1-4e35-a351-0e73033b2115,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,y,False,y,,,,
98f348cf-18a6-4638-9099-c09249e08b46,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,g,False,g,,,,
83ad4a1d-c871-4712-ab06-e220669b5611,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,e,False,e,,,,
63eb39ee-16f5-47b3-b011-2db7c0c3dc71,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,n,False,n,,,,
0e0e2c39-724c-44e0-8388-08297f11d6b0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,c,False,c,,,,
cd4ebe7e-ad7d-4023-a3c7-d72fb52e3df6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,=,False,=,,,,
ab7d0223-1593-4ba7-8688-2db59f8cbbf4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,f,False,f,,,,
475ec566-e76a-4798-bd40-40fd39bc45f3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,r,False,r,,,,
4645f892-ab73-49ab-a604-6ef0bd1efc33,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,m,False,m,,,,
8e930210-4bfa-4ee7-ab42-e0ff6917ec47,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,p,False,p,,,,
a37b3e14-5309-4a59-9214-832890099673,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,i,False,i,,,,
097ba908-5ac3-4d87-86cc-6e8a923813ee,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,s,False,s,,,,
35a4c427-fda1-4e93-982e-1f13fd8ef66f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,+,False,+,,,,
65530c65-a5fb-4846-8a07-a1c5e87f56b9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,h,False,h,,,,
e1a1388b-fa5d-434f-b192-55499d9a817b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,u,False,u,,,,
53790c58-9bca-4756-a539-c0ae32fe237d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,u,Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
53790c58-9bca-4756-a539-c0ae32fe237d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,u,Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
53790c58-9bca-4756-a539-c0ae32fe237d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,u,Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
53790c58-9bca-4756-a539-c0ae32fe237d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,u,Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
53790c58-9bca-4756-a539-c0ae32fe237d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,u,Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
53790c58-9bca-4756-a539-c0ae32fe237d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,u,Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
f70548f4-62ff-4d9f-85f6-c92a0d1db333,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,u,Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
f70548f4-62ff-4d9f-85f6-c92a0d1db333,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,u,Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
f70548f4-62ff-4d9f-85f6-c92a0d1db333,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,u,Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
f70548f4-62ff-4d9f-85f6-c92a0d1db333,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,u,Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
f70548f4-62ff-4d9f-85f6-c92a0d1db333,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,u,Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
f70548f4-62ff-4d9f-85f6-c92a0d1db333,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,u,Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
8e530620-2f8f-4881-858c-332a9ff6759b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,u,Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
8e530620-2f8f-4881-858c-332a9ff6759b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,u,Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
8e530620-2f8f-4881-858c-332a9ff6759b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,u,Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
8e530620-2f8f-4881-858c-332a9ff6759b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,u,Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
8e530620-2f8f-4881-858c-332a9ff6759b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,u,Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
8e530620-2f8f-4881-858c-332a9ff6759b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,u,Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
61f907fd-abe8-4702-91c2-3e98e9aad87b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,Let us put those terms into our basic equation (equation 15.2).,True,u,,,,
c0141032-f8d0-49e3-9210-ca3d4c46df96,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,Equation 15.2,True,u,,,,
cfb3cbc8-3e9f-4fbe-8802-f99e721d9096,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,QSQT=CCO2−CaO2CCO2−CVO2,False,QSQT=CCO2−CaO2CCO2−CVO2,,,,
c7b0ce1a-60c2-499c-8476-8d4ff91be6d4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,QSQT,False,QSQT,,,,
c828b762-d212-4a3f-81d1-b3d095980c5e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,QS,False,QS,,,,
fc55fc96-a857-439f-b353-083266a2ee37,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,Q,False,Q,,,,
e27735ed-724c-4cf3-b7d6-a9e6cb82e8fe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,S,False,S,,,,
8120f6ac-b871-4935-9b39-c92f1a719225,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,QT,False,QT,,,,
c30f8653-75b6-4948-9608-752e30b64779,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,CCO2−CaO2CCO2−CVO2,False,CCO2−CaO2CCO2−CVO2,,,,
7c7f17f0-18e8-4e11-8c55-93d5b70458bb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,CCO2−CaO2,False,CCO2−CaO2,,,,
15ad130a-19b8-41e4-b6c1-795465a298c1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,CC,False,CC,,,,
65522b28-955e-40d7-9994-c2962555bd31,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,C,False,C,,,,
4b7282a5-d879-4896-84b4-675f71483cef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,O2,False,O2,,,,
2b9f0938-1c1c-4073-b830-252cccf6f3ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,O,False,O,,,,
fdc58770-e8a5-4a80-9191-3e2daacc3b6d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,2,False,2,,,,
a636229f-f7a0-4f5f-b811-e9a1a52daf4a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,−,False,−,,,,
4d4a21a0-2886-4d6a-bacf-02308b7a307d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,Ca,False,Ca,,,,
fc6b2008-0e2e-4b2f-b62d-5d46ab2b150a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,CCO2−CVO2,False,CCO2−CVO2,,,,
dbc5a49d-44ea-42d9-ad1b-be56840d8adf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,CV,False,CV,,,,
23745336-a2ae-468a-9615-10cc223fe71d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,V,False,V,,,,
d5a4f6ba-ae97-4c55-81f5-ddc69d8e3b35,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"So at this point we might panic, thinking that we have no measure of flow (Q) for any of these variables, that we only have oxygen concentrations from our blood gases and alveolar gas equation. But panic not. Through the magic of mathematics we can rearrange this equation (15.2) to eliminate our flows (Qs) and be left with an equation that meets our objective of QS/QT.",True,V,,,,
dbbe935b-020b-46da-bbd5-ea38e7bf4b13,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"The shunt equation (equation 15.3) describes the proportion of total perfusion that is passing through the shunt. This is the equation worth remembering: the portion of blood going through the shunt is the difference between the capillary and arterial O2 concentrations, divided by the difference between the capillary and venous oxygen concentrations.",True,V,,,,
b3681cca-27e6-46a3-bc94-443354340a52,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,Equation 15.3,True,V,,,,
d4c747ab-13fa-40d9-86d7-7e2f3c898b6a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,QT×CaO2=[(QT−QS)×CCO2]+[QS×CVO2],False,QT×CaO2=[(QT−QS)×CCO2]+[QS×CVO2],,,,
cd60b846-6f26-42ab-ae27-5088062523f1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,×,False,×,,,,
eabb1c12-f3b6-4d69-a859-e980ecf0c68a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,[,False,[,,,,
a4f234fa-3b7f-4675-8c6a-8d47f5259031,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,(,False,(,,,,
3caa2ac9-c497-4a58-a8f1-f4a58bd6b289,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,),False,),,,,
9d1e63d6-f9f2-47b4-80b3-33236803345b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,],False,],,,,
90acec57-51ab-4d20-983a-e5b26cdeb139,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Let us look at an example to put this in context. We have a patient with normal lungs, but a right–left shunt is present. We find out that his arterial blood O2 concentration is 18 mL and venous is 14. Capillary oxygen concentration is calculated to be 20 mL/100 mL. Now we plug the numbers in the equation and see that the proportion of blood going through the shunt is a third, or 33 percent.",True,],,,,
61c47e98-02c6-4714-a22a-16061872ff50,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,Summary,False,Summary,,,,
e6aa90ba-77c3-444e-a35a-86b896adfa55,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"So to recap, small pulmonary shunts exist even in the normal cardiopulmonary system, but abnormal shunts can arise from a number of different pathological causes. Although the presence of a shunt is relatively easy to detect, it is important to calculate its size, which is also a relatively easy process.",True,Summary,,,,
adaacde8-17b4-4971-a2e0-c4bb9eda2643,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,Text,False,Text,,,,
14f8746b-9434-4da3-b521-48953b7597a4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"Levitsky, Michael G. “Chapter 5: Ventilation–Perfusion Relationships.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
15ddd4ba-eba2-458f-8876-dfb53923e26b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Abnormal Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-2,"West, John B. “Chapter 5: Ventilation–Perfusion Relationships—How Matching of Gas and Blood Determines Gas Exchange.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
de284ee3-f66a-40fe-9c52-d078837825ee,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"There are two circulatory networks that normally form shunts. The bronchial circulation, that supplies the bronchi, empties its venous blood into the pulmonary veins, thereby sending slightly deoxygenated blood back toward the left heart and into the systemic arterial system. Likewise a very small portion of the coronary venous blood is returned to the left ventricle (through the thebesian veins) and thereby bypasses the lung completely before going back in the systemic circulation.",True,Text,,,,
cab42792-33b3-4852-9e63-ba5e1900acf6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,These two wayward circulations and the imperfect V/Q matching in the lung serve to suppress arterial oxygen saturation.,True,Text,,,,
34f8b08b-2315-4047-8f10-f4c5af1b9d26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,Abnormal Shunts,False,Abnormal Shunts,,,,
4be06ae0-411c-4a1a-acb5-8ad2c825114a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Shunts can also be created by abnormal physiology or anatomy. There are several heart structural defects that allow blood from the right heart to enter the systemic circulation and bypass the lungs altogether; one common example is a patent foramen ovale where the incomplete atrial septum between the right and left heart allows deoxygenated venous blood to directly enter the arterial circulation, bypassing, or “shunting,” past the lungs.",True,Abnormal Shunts,,,,
ad0bcae9-022d-42d9-87a7-548c6dc5fb23,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"In pulmonary disease, areas of the lung may not receive ventilation (e.g., as airways are blocked or collapsed). Perfusion to these areas is therefore wasted as no gas exchange takes place; effectively a right–left physiological shunt has formed, and V/Q approaches zero (i.e., low V and normal Q).",True,Abnormal Shunts,,,,
b1bb7474-c791-4c20-a20b-c40f958e26a9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,Detecting Shunts,False,Detecting Shunts,,,,
daecdf71-2d72-40d3-b024-8965b547dde3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"There is a quick and easy way to detect whether a shunt is contributing to a patient’s low arterial PO2 by giving a patient 100 percent O2 to breathe. The blood passing through capillaries that are exposed to the 100 percent O2 becomes fully saturated. However, any shunted blood never “sees” the high PO2 and consequently stays at venous PO2. When the two routes rejoin and the blood mixes, it remains below 100 percent (i.e., the alveolar–arterial PO2 difference is not abolished by the 100 percent O2, and it never can be as long as the shunt exists).",True,Detecting Shunts,,,,
5ff6bc0a-a7a3-4107-bd30-b8b60affc237,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,Calculating the Size of a Pulmonary Shunt,False,Calculating the Size of a Pulmonary Shunt,,,,
8e585f74-6ea0-4fda-8379-c89edbd3575e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
8e585f74-6ea0-4fda-8379-c89edbd3575e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
8e585f74-6ea0-4fda-8379-c89edbd3575e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
8e585f74-6ea0-4fda-8379-c89edbd3575e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
8e585f74-6ea0-4fda-8379-c89edbd3575e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
8e585f74-6ea0-4fda-8379-c89edbd3575e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
7415a8e1-2171-4bcd-a295-edfdb9e7c179,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
7415a8e1-2171-4bcd-a295-edfdb9e7c179,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
7415a8e1-2171-4bcd-a295-edfdb9e7c179,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
7415a8e1-2171-4bcd-a295-edfdb9e7c179,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
7415a8e1-2171-4bcd-a295-edfdb9e7c179,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
7415a8e1-2171-4bcd-a295-edfdb9e7c179,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
afc134d9-1c9d-4745-8c21-580a4111e530,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,So know we can use these oxygen concentrations to work out the percentage of shunted blood.,True,Calculating the Size of a Pulmonary Shunt,,,,
a604662a-b11c-46b9-b515-6b9668001127,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Now let us combine our flow and oxygen concentration and think in terms of absolute oxygen contents in each part of our diagram. (Critical point: The absolute oxygen content is the product of the blood volume and oxygen concentration.) So now thinking of absolute oxygen contents, let us generate a first basic equation (equation 15.1) with what we know—the amount of oxygen in our flow going back to the left heart (QT) equals the oxygen from the pulmonary capillaries, plus that from the shunt.",True,Calculating the Size of a Pulmonary Shunt,,,,
c6737bf5-6e7a-401e-bc80-c2d8c5856d16,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,Equation 15.1,True,Calculating the Size of a Pulmonary Shunt,,,,
88e1cf8a-8b90-42ce-ae6d-9f29111edee2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,Totaloxygencontent=oxygenfromcapillaries+oxygenfromshuntTotaloxygencontent=oxygenfromcapillaries+oxygenfromshunt,False,Totaloxygencontent=oxygenfromcapillaries+oxygenfromshuntTotaloxygencontent=oxygenfromcapillaries+oxygenfromshunt,,,,
c7e540d3-0322-48bc-a731-852bd759c148,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,Totaloxygencontent=oxygenfromcapillaries+oxygenfromshunt,False,Totaloxygencontent=oxygenfromcapillaries+oxygenfromshunt,,,,
89cd7ac0-0b90-4bb2-beb9-a604c2e0bd74,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,T,False,T,,,,
f131bde9-f25e-44cb-8cc5-48bc6b30d02d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,o,False,o,,,,
7ffb105f-28be-4cd9-988b-d316985597da,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,t,False,t,,,,
d05af75f-a5d9-4acf-a69f-fa96cfad36da,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,a,False,a,,,,
c10ac8e8-bf7c-4a04-b301-646f94e6171a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,l,False,l,,,,
6d7ac6c5-375c-4529-a2c0-01914ddaf8f4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,x,False,x,,,,
d6b74884-7fda-4573-848a-08db3800997a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,y,False,y,,,,
3591bb88-cc84-4cdb-bba4-704150c43a49,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,g,False,g,,,,
ee6693ae-1705-47a2-8e4b-5fccaae82f8a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,e,False,e,,,,
8c60366e-ef10-46c6-ad5a-5a853c067d03,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,n,False,n,,,,
f00c40b3-42b7-4150-95ca-bc1a1ab47b58,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,c,False,c,,,,
d80853ba-4f76-4ee9-a6bc-525524f6ef7e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,=,False,=,,,,
aba4838c-3832-461d-a097-16c8a3427034,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,f,False,f,,,,
b5e94988-18db-4305-a976-10a0e99a2896,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,r,False,r,,,,
771bd7a0-7032-4b70-a4c5-f9bc6e9718a7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,m,False,m,,,,
ba40e010-afe4-4cbe-8cfd-19b1640d0055,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,p,False,p,,,,
0e878c41-ff07-41d3-9401-e7066d9a2ca2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,i,False,i,,,,
7812b803-784a-4aa6-9a48-5483ea4514b4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,s,False,s,,,,
764c53dd-c53e-4a58-9957-a83a9164c9bc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,+,False,+,,,,
c867c958-39a5-4063-9971-61d4f2195057,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,h,False,h,,,,
ea33b7aa-8eea-44e6-a092-d80e942c1e05,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,u,False,u,,,,
4934f69c-cd06-4a76-aa73-617e79c4a503,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,u,Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
4934f69c-cd06-4a76-aa73-617e79c4a503,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,u,Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
4934f69c-cd06-4a76-aa73-617e79c4a503,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,u,Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
4934f69c-cd06-4a76-aa73-617e79c4a503,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,u,Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
4934f69c-cd06-4a76-aa73-617e79c4a503,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,u,Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
4934f69c-cd06-4a76-aa73-617e79c4a503,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,u,Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
fe9560d8-9d45-4195-88b4-2fb6c910d3be,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,u,Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
fe9560d8-9d45-4195-88b4-2fb6c910d3be,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,u,Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
fe9560d8-9d45-4195-88b4-2fb6c910d3be,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,u,Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
fe9560d8-9d45-4195-88b4-2fb6c910d3be,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,u,Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
fe9560d8-9d45-4195-88b4-2fb6c910d3be,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,u,Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
fe9560d8-9d45-4195-88b4-2fb6c910d3be,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,u,Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
c7bf4add-cc45-4241-b712-d6cff2331186,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,u,Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
c7bf4add-cc45-4241-b712-d6cff2331186,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,u,Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
c7bf4add-cc45-4241-b712-d6cff2331186,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,u,Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
c7bf4add-cc45-4241-b712-d6cff2331186,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,u,Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
c7bf4add-cc45-4241-b712-d6cff2331186,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,u,Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
c7bf4add-cc45-4241-b712-d6cff2331186,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,u,Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
d987ebef-1676-4f65-bd75-3231f6f2df83,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,Let us put those terms into our basic equation (equation 15.2).,True,u,,,,
73c0ff46-2e0c-44b2-a6ac-37694ea47faa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,Equation 15.2,True,u,,,,
ac8f2018-15ad-4db1-a1fb-0950cf517f5f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,QSQT=CCO2−CaO2CCO2−CVO2QSQT=CCO2−CaO2CCO2−CVO2,False,QSQT=CCO2−CaO2CCO2−CVO2QSQT=CCO2−CaO2CCO2−CVO2,,,,
dea74ee7-4066-445e-9a77-7cc112faa6ca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,QSQT=CCO2−CaO2CCO2−CVO2,False,QSQT=CCO2−CaO2CCO2−CVO2,,,,
35aa67cf-f35c-4050-be86-8a6086e541c7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,QSQT,False,QSQT,,,,
ba0e9402-c031-495c-aa2c-fd7239137512,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,QS,False,QS,,,,
0386da9a-18ab-4910-85a7-4a346fb7a796,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,Q,False,Q,,,,
63d9891d-b4d2-4614-a5f9-6c17f17b9fed,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,S,False,S,,,,
b684e4c0-b3d6-43e1-8f14-e84789d2dff1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,QT,False,QT,,,,
04a3979b-5e90-4b50-8f84-4c186e921dbe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,CCO2−CaO2CCO2−CVO2,False,CCO2−CaO2CCO2−CVO2,,,,
8194d5e5-dae5-46fe-a94d-0219e543cd64,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,CCO2−CaO2,False,CCO2−CaO2,,,,
0df2d7cf-62ca-422d-a49e-425a4791b859,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,CC,False,CC,,,,
c0e25cd9-b113-40bb-a5d2-4186d01c960f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,C,False,C,,,,
fe8b1a76-d3a5-440f-b9f8-593952933357,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,O2,False,O2,,,,
d4850442-1614-45fb-adfb-be0258236a71,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,O,False,O,,,,
7e0ecf90-8859-4ba4-8e39-1625858445a7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,2,False,2,,,,
de145619-9f65-459f-b8ac-e240109211bf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,−,False,−,,,,
4fe44784-ec2d-4a38-a154-933aea04f3d2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,Ca,False,Ca,,,,
27035b7b-635e-47a7-ab4d-084e720a1ccf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,CCO2−CVO2,False,CCO2−CVO2,,,,
2693c8d6-f654-492a-9b2c-87477a8b6b8a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,CV,False,CV,,,,
3908dedd-ae71-422f-9552-6936fa2bf13c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,V,False,V,,,,
9063fd9f-4632-4b14-a9d8-a6fe971c7232,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"So at this point we might panic, thinking that we have no measure of flow (Q) for any of these variables, that we only have oxygen concentrations from our blood gases and alveolar gas equation. But panic not. Through the magic of mathematics we can rearrange this equation (15.2) to eliminate our flows (Qs) and be left with an equation that meets our objective of QS/QT.",True,V,,,,
8a844f41-aad9-45ff-b441-8054748399ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"The shunt equation (equation 15.3) describes the proportion of total perfusion that is passing through the shunt. This is the equation worth remembering: the portion of blood going through the shunt is the difference between the capillary and arterial O2 concentrations, divided by the difference between the capillary and venous oxygen concentrations.",True,V,,,,
8d845987-7400-4764-a0ea-ae85c6275205,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,Equation 15.3,True,V,,,,
7212a675-2de3-45e5-bd6f-4084db3057b0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,QT×CaO2=[(QT−QS)×CCO2]+[QS×CVO2],False,QT×CaO2=[(QT−QS)×CCO2]+[QS×CVO2],,,,
277f18f2-684d-4926-a0b8-493768155083,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,×,False,×,,,,
e21a57aa-6c44-4274-a52a-30e6a9da826a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,[,False,[,,,,
2b116e2a-4b2c-47f5-b0e4-e12eea26b559,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,(,False,(,,,,
5b4569b0-1d2e-476c-b2cc-727398851372,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,),False,),,,,
22afb1fa-0970-4f9b-b9be-0db78adb0ad6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,],False,],,,,
617e981f-104d-4a85-a30d-8a26c65b25b9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Let us look at an example to put this in context. We have a patient with normal lungs, but a right–left shunt is present. We find out that his arterial blood O2 concentration is 18 mL and venous is 14. Capillary oxygen concentration is calculated to be 20 mL/100 mL. Now we plug the numbers in the equation and see that the proportion of blood going through the shunt is a third, or 33 percent.",True,],,,,
26b7c046-e0dd-40aa-b7cd-62369f364800,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,Summary,False,Summary,,,,
e420e5ba-8a3f-476a-8040-9f355accb423,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"So to recap, small pulmonary shunts exist even in the normal cardiopulmonary system, but abnormal shunts can arise from a number of different pathological causes. Although the presence of a shunt is relatively easy to detect, it is important to calculate its size, which is also a relatively easy process.",True,Summary,,,,
17abacea-e377-4f34-9802-7ae046f94d62,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,Text,False,Text,,,,
02c30b2c-c385-42e4-9423-1ef46472c1fe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"Levitsky, Michael G. “Chapter 5: Ventilation–Perfusion Relationships.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
2cac3992-c57e-4b18-a4da-417a5d0b7c29,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/#chapter-55-section-1,"West, John B. “Chapter 5: Ventilation–Perfusion Relationships—How Matching of Gas and Blood Determines Gas Exchange.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
b3e6eb4a-f69f-405f-ad48-21b10b29c036,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"There are two circulatory networks that normally form shunts. The bronchial circulation, that supplies the bronchi, empties its venous blood into the pulmonary veins, thereby sending slightly deoxygenated blood back toward the left heart and into the systemic arterial system. Likewise a very small portion of the coronary venous blood is returned to the left ventricle (through the thebesian veins) and thereby bypasses the lung completely before going back in the systemic circulation.",True,Text,,,,
7f706091-cd9f-499b-b1b7-2ae2d67fac97,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,These two wayward circulations and the imperfect V/Q matching in the lung serve to suppress arterial oxygen saturation.,True,Text,,,,
ccc3dd1b-b8ed-42e9-ac7d-77290e6e7ef1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,Abnormal Shunts,False,Abnormal Shunts,,,,
e4accea5-6492-4e50-a867-7d62a201f35e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Shunts can also be created by abnormal physiology or anatomy. There are several heart structural defects that allow blood from the right heart to enter the systemic circulation and bypass the lungs altogether; one common example is a patent foramen ovale where the incomplete atrial septum between the right and left heart allows deoxygenated venous blood to directly enter the arterial circulation, bypassing, or “shunting,” past the lungs.",True,Abnormal Shunts,,,,
b41fd9ad-9235-40a5-98d8-b5bfa0230d09,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"In pulmonary disease, areas of the lung may not receive ventilation (e.g., as airways are blocked or collapsed). Perfusion to these areas is therefore wasted as no gas exchange takes place; effectively a right–left physiological shunt has formed, and V/Q approaches zero (i.e., low V and normal Q).",True,Abnormal Shunts,,,,
91b7c9b2-a142-4b8e-8893-9b79fea29361,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,Detecting Shunts,False,Detecting Shunts,,,,
1b5cfbd0-1285-49c5-88db-53e9ad17dd2e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"There is a quick and easy way to detect whether a shunt is contributing to a patient’s low arterial PO2 by giving a patient 100 percent O2 to breathe. The blood passing through capillaries that are exposed to the 100 percent O2 becomes fully saturated. However, any shunted blood never “sees” the high PO2 and consequently stays at venous PO2. When the two routes rejoin and the blood mixes, it remains below 100 percent (i.e., the alveolar–arterial PO2 difference is not abolished by the 100 percent O2, and it never can be as long as the shunt exists).",True,Detecting Shunts,,,,
a8f19544-d7c8-4091-af7f-1d7574bd648f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,Calculating the Size of a Pulmonary Shunt,False,Calculating the Size of a Pulmonary Shunt,,,,
aec49db4-e3de-4b2b-b6ae-ef098b28444b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
aec49db4-e3de-4b2b-b6ae-ef098b28444b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
aec49db4-e3de-4b2b-b6ae-ef098b28444b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
aec49db4-e3de-4b2b-b6ae-ef098b28444b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
aec49db4-e3de-4b2b-b6ae-ef098b28444b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
aec49db4-e3de-4b2b-b6ae-ef098b28444b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Because even a small shunt can have a large effect on arterial PO2, it is critical to determine the size of a shunt should one be suspected. Figure 15.1 shows the lungs with blood passing through as normal (QC), while some bypasses the heart (QS) and is shunted back into the systemic circulation. The size of a shunt (QS) is expressed as the percentage of total blood (QT in figure 15.1) (i.e., QS/QT). We will look now at how this is calculated from oxygen concentration. First, let us see what we know.",True,Calculating the Size of a Pulmonary Shunt,Figure 15.1,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.1.png,"Figure 15.1: Schematic of a pulmonary shunt (anatomical or physiological) showing flow (Q) through the pulmonary capillaries (QC), flow through the shunt (QS), and total flow (QT) returning to the left heart."
dde2e7cc-231a-4998-96c8-bd98509b07a8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
dde2e7cc-231a-4998-96c8-bd98509b07a8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
dde2e7cc-231a-4998-96c8-bd98509b07a8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
dde2e7cc-231a-4998-96c8-bd98509b07a8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
dde2e7cc-231a-4998-96c8-bd98509b07a8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
dde2e7cc-231a-4998-96c8-bd98509b07a8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"We can measure the oxygen concentration of the venous system (CVO2 in figure 15.2) and can assume that the shunted blood, having performed no gas exchange, will have the same oxygen concentration. We can also measure the oxygen concentration in the arterial system (CaO2 in figure 15.2), and if we assume that all the blood that passed through the gas exchange capillaries in the lungs equilibrated with the alveolar PO2, we can use the alveolar gas equation to determine the capillary oxygen concentration (CCO2 in figure 15.2).",True,Calculating the Size of a Pulmonary Shunt,Figure 15.2,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.2.png,Figure 15.2: Oxygen concentrations used to calculate the size of a pulmonary shunt.
5825a22e-36d4-4775-af4b-d55a66f45edc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,So know we can use these oxygen concentrations to work out the percentage of shunted blood.,True,Calculating the Size of a Pulmonary Shunt,,,,
b520fe05-1471-474a-b647-bdab19305551,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Now let us combine our flow and oxygen concentration and think in terms of absolute oxygen contents in each part of our diagram. (Critical point: The absolute oxygen content is the product of the blood volume and oxygen concentration.) So now thinking of absolute oxygen contents, let us generate a first basic equation (equation 15.1) with what we know—the amount of oxygen in our flow going back to the left heart (QT) equals the oxygen from the pulmonary capillaries, plus that from the shunt.",True,Calculating the Size of a Pulmonary Shunt,,,,
e955fde4-e1b0-456d-81e8-204157cc450c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,Equation 15.1,True,Calculating the Size of a Pulmonary Shunt,,,,
483a7f74-0aef-4f12-a4fd-4e41f357c627,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],False,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],,,,
3af8cc47-7688-4acd-9334-c38cfc110053,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
3af8cc47-7688-4acd-9334-c38cfc110053,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
3af8cc47-7688-4acd-9334-c38cfc110053,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
3af8cc47-7688-4acd-9334-c38cfc110053,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
3af8cc47-7688-4acd-9334-c38cfc110053,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
3af8cc47-7688-4acd-9334-c38cfc110053,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Let us build on that and put some values in place. The amount of oxygen arriving back in the arterial side must equal the volume of blood multiplied by the arterial oxygen concentration (QT x CaO2), as shown in figure 15.3. And we know that this amount of O2 must be the sum of that from the capillaries, and that from the shunt.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
c806c11d-47ce-475b-8a6b-9ce6560240c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
c806c11d-47ce-475b-8a6b-9ce6560240c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
c806c11d-47ce-475b-8a6b-9ce6560240c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
c806c11d-47ce-475b-8a6b-9ce6560240c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
c806c11d-47ce-475b-8a6b-9ce6560240c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
c806c11d-47ce-475b-8a6b-9ce6560240c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"The amount of oxygen from the shunt is calculated as shunt flow multiplied by the venous oxygen concentration (QS x CVO2), as shown in figure 15.3.",True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
5c0c96a2-6434-449a-87e9-b5fab87078d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
5c0c96a2-6434-449a-87e9-b5fab87078d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Calculating the Size of a Pulmonary Shunt,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
5c0c96a2-6434-449a-87e9-b5fab87078d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Detecting Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
5c0c96a2-6434-449a-87e9-b5fab87078d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Abnormal Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
5c0c96a2-6434-449a-87e9-b5fab87078d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,Normal Anatomical Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
5c0c96a2-6434-449a-87e9-b5fab87078d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,The amount of oxygen going through the pulmonary capillaries can be described as the total volume minus the shunt volume (QT−QS) multiplied by the capillary oxygen concentration (figure 15.3).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],Figure 15.3,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/15.3.png,Figure 15.3: Elements of the shunt equation and where they exist physiologically.
a2cc99a7-0b6c-42d6-bf55-ad21bb6c9960,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,Let us put those terms into our basic equation (equation 15.2).,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],,,,
1e5651d0-24e8-4a9c-8010-4e4052612ac9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,Equation 15.2,True,[latex]Total\:oxygen\:content = oxygen\:from\:capillaries\: + oxygen\:from\:shunt[/latex],,,,
bac725e6-90a9-4928-9bfb-dabed92bd289,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],False,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
9dd30789-e936-4078-8daa-557b29beef31,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"So at this point we might panic, thinking that we have no measure of flow (Q) for any of these variables, that we only have oxygen concentrations from our blood gases and alveolar gas equation. But panic not. Through the magic of mathematics we can rearrange this equation (15.2) to eliminate our flows (Qs) and be left with an equation that meets our objective of QS/QT.",True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
d6e3c88a-f61d-48e5-88d7-1c131df9c0e9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"The shunt equation (equation 15.3) describes the proportion of total perfusion that is passing through the shunt. This is the equation worth remembering: the portion of blood going through the shunt is the difference between the capillary and arterial O2 concentrations, divided by the difference between the capillary and venous oxygen concentrations.",True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
bef2b2f5-3bbc-4e98-989b-4a709cc298ef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,Equation 15.3,True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
974480b6-ecf2-4cc3-b0c0-5d40f736fcb6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,[latex]Q_T \times C_aO_2 = [(Q_T - Q_S) \times C_CO_2] + [Q_S \times C_VO_2][/latex],True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
086c26f9-a73d-4118-977b-9a99209f242c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Let us look at an example to put this in context. We have a patient with normal lungs, but a right–left shunt is present. We find out that his arterial blood O2 concentration is 18 mL and venous is 14. Capillary oxygen concentration is calculated to be 20 mL/100 mL. Now we plug the numbers in the equation and see that the proportion of blood going through the shunt is a third, or 33 percent.",True,[latex]\displaystyle\frac{Q_S}{Q_T} = \frac{C_CO_2 - C_aO_2}{C_CO_2 - C_VO_2}[/latex],,,,
5afc99b5-a553-4019-bb02-627712f40b14,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,Summary,False,Summary,,,,
f214d5d3-40d5-4e20-a7cf-5af7c2a016b7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"So to recap, small pulmonary shunts exist even in the normal cardiopulmonary system, but abnormal shunts can arise from a number of different pathological causes. Although the presence of a shunt is relatively easy to detect, it is important to calculate its size, which is also a relatively easy process.",True,Summary,,,,
be01234e-3a9f-478d-a6c9-09acd35eea22,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,Text,False,Text,,,,
fa3e3b94-ae1d-4236-8726-c4055bc0a1f6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"Levitsky, Michael G. “Chapter 5: Ventilation–Perfusion Relationships.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
1f9ca906-9896-428b-bdf0-924d79d1be07,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,15. Pulmonary Shunts,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-shunts/,"West, John B. “Chapter 5: Ventilation–Perfusion Relationships—How Matching of Gas and Blood Determines Gas Exchange.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
a329a450-96a0-45d4-8482-5adfd0d9a7e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,Introduction,False,Introduction,,,,
5867bf01-6acb-4d92-bac8-5e75bde55544,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,This chapter will describe how the alveolar–arterial PO2 difference is calculated and what assumptions can be made from it.,True,Introduction,,,,
4ef36793-42e1-48cb-be98-c099eb0e004a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Before you start, a quick reminder that an uppercase A refers to alveolar and lowercase to arterial.",True,Introduction,,,,
01ce560a-9f0f-472b-b53b-8580840587ca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,Calculating Alveolar PO₂,False,Calculating Alveolar PO₂,,,,
3fb6de3d-2dcc-42c8-b6d5-1c6e1447a3c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Obviously to measure the alveolar–arterial PO2 difference, we need to know both the alveolar and arterial PO2s. The arterial PO2 is routinely measured as part of a blood gas panel, along with arterial PCO2. However, from your understanding of V/Q distribution across the lung, you might appreciate that the measurement of a “typical” alveolar PO2 is difficult, and it must be calculated as an estimate of the whole lung. This is the role of the alveolar gas equation, and we will look at it now, not just because it may appear on your board exams, but primarily because of its clinical importance. As there are several forms of the equation, we will take the easy way out and use the simplest one (figure 14.1), which is accurate for the vast majority of cases you will ever see.",True,Calculating Alveolar PO₂,Figure 14.1,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.1.png,Figure 14.1: The alveolar gas equation.
3fb6de3d-2dcc-42c8-b6d5-1c6e1447a3c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Obviously to measure the alveolar–arterial PO2 difference, we need to know both the alveolar and arterial PO2s. The arterial PO2 is routinely measured as part of a blood gas panel, along with arterial PCO2. However, from your understanding of V/Q distribution across the lung, you might appreciate that the measurement of a “typical” alveolar PO2 is difficult, and it must be calculated as an estimate of the whole lung. This is the role of the alveolar gas equation, and we will look at it now, not just because it may appear on your board exams, but primarily because of its clinical importance. As there are several forms of the equation, we will take the easy way out and use the simplest one (figure 14.1), which is accurate for the vast majority of cases you will ever see.",True,Calculating Alveolar PO₂,Figure 14.1,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.1.png,Figure 14.1: The alveolar gas equation.
3fb6de3d-2dcc-42c8-b6d5-1c6e1447a3c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Obviously to measure the alveolar–arterial PO2 difference, we need to know both the alveolar and arterial PO2s. The arterial PO2 is routinely measured as part of a blood gas panel, along with arterial PCO2. However, from your understanding of V/Q distribution across the lung, you might appreciate that the measurement of a “typical” alveolar PO2 is difficult, and it must be calculated as an estimate of the whole lung. This is the role of the alveolar gas equation, and we will look at it now, not just because it may appear on your board exams, but primarily because of its clinical importance. As there are several forms of the equation, we will take the easy way out and use the simplest one (figure 14.1), which is accurate for the vast majority of cases you will ever see.",True,Calculating Alveolar PO₂,Figure 14.1,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.1.png,Figure 14.1: The alveolar gas equation.
8f19105f-57c7-497b-94bc-1f0918706586,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,PO2s,False,PO2s,,,,
8ac3033a-fb35-44e7-b15d-9dfe3b1c441b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"The alveolar gas equation estimates whole lung alveolar PO2 as the inspired PO2 minus the arterial PO2 divided by the respiratory exchange ratio. For those interested in the derivation of the equation, more detailed sources are available. But here, we will just look at the factors involved and try and make this simpler to commit to memory (which I suggest you do).",True,PO2s,,,,
c1cb1316-ad14-4e9d-9200-95813f1cab5f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"First let us look at arterial PCO2; this measurement is included in a blood gas panel so will be readily available to you. The alveolar gas equation really needs the alveolar PCO2, but since CO2 is so soluble then we assume that equilibration has taken place and PaCO2 and PACO2 are the same, and we use the number we have at the bedside.",True,PO2s,,,,
cb405ab5-97eb-4cb4-b7c3-d4ec3cef7156,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,PaCO2,False,PaCO2,,,,
3df4a43d-6ee0-4e70-9634-32a0e298c21e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,PACO2,False,PACO2,,,,
fec7dd78-3deb-4a84-ac34-a0ac874d5940,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Now let us look at R, or the respiratory exchange ratio. The respiratory exchange ratio describes how much CO2 is produced per unit of oxygen consumed. (Perhaps you can see why we are using this in conjunction with the arterial PCO2; we are relating CO2 production as a proxy measurement of oxygen consumption.) When utilizing carbohydrate as a fuel (the most common situation) there are eight CO2 molecules produced for every ten oxygen molecules burnt, so R is generally 0.8. Lastly, there is the inspired PO2. Generally, breathing room air at sea level this will be ~150 mmHg. But it is important to note that this might change in the clinic if the patient is given oxygen therapy.",True,PACO2,,,,
a11d47d3-cfc1-4902-951d-3a237d759ce8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"So this simple form of the alveolar gas equation really has two basic halves: the amount of oxygen taken into the alveoli (PIO2), and a reflection of the amount that is taken out (PaCO2/R) to supply metabolism.",True,PACO2,,,,
82060f78-fab1-47c0-85fc-bea05a19eb90,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,PIO2,False,PIO2,,,,
ad307632-7613-4526-acfd-c6fa2fd331c7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"You will find more complex and accurate forms of this equation, but for the vast majority of situations this one is perfectly adequate and is considerably easier to remember, particularly when some of the numbers we plug in are frequently the same. If we look at normal values (equation 14.1), we see that our equation gets us close to what we have learned to be a normal alveolar PO2. Inspired PO2 at sea level and room air is 150 mmHg, we will assume R is 0.8, and a normal arterial PCO2 is 40 mmHg. Here is the alveolar gas equation with normal values:",True,PIO2,,,,
57501364-ceb6-4ed3-942d-91dfd9ecb79b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,Equation 14.1,True,PIO2,,,,
54177776-ab01-416b-bf60-6e2a9729bdfb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,[latex]P_AO_2 = 150 - \frac{40}{0.8} = 100[/latex],True,PIO2,,,,
14dfdb57-bc28-4d38-b6e0-80b8f5bca562,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,Now let us see the clinical use of being able to determine alveolar PO2 and thus calculate any alveolar–arterial PO2 difference.,True,PIO2,,,,
85149e9e-9d25-4f7b-aa1b-ea159491a56f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,False,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,,,,
54b86832-28f0-44d8-9f50-93ffe1c47774,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Not only knowing what the alveolar and arterial PO2s are, but by how much they differ can tell us where a problem in the process of gas exchange might be occurring. So the PAO2–PaO2 difference has great diagnostic value. Let us return to our schematic of a lung with a ventilated and perfused lung unit and look at a few scenarios, starting with the normal state.",True,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,,,,
c7c71fd1-b6b3-4c75-b489-da623faa8c21,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,PAO2,False,PAO2,,,,
081fd1d9-2cb0-4ff2-8520-66977715b831,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,PaO2,False,PaO2,,,,
d8a4e1cb-8727-4554-8087-372ab3bdca8f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Normal lung: With a well-ventilated and perfused lung (figure 14.2), alveolar PO2 is normal, and when there are no problems with diffusion across the membrane into an adequately perfused blood vessel, arterial PO2 is normal as well. Thus the difference between alveolar and arterial PO2 is minimal and normal, and in reality for a young healthy person is no more than 5–10 mmHg (note, however, this difference increases with age).",True,PaO2,Figure 14.2,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.2.png,Figure 14.2: Alveolar and arterial oxygen tensions in the normal state lead to a normal alveolar–arterial PO2 difference.
d8a4e1cb-8727-4554-8087-372ab3bdca8f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Normal lung: With a well-ventilated and perfused lung (figure 14.2), alveolar PO2 is normal, and when there are no problems with diffusion across the membrane into an adequately perfused blood vessel, arterial PO2 is normal as well. Thus the difference between alveolar and arterial PO2 is minimal and normal, and in reality for a young healthy person is no more than 5–10 mmHg (note, however, this difference increases with age).",True,PaO2,Figure 14.2,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.2.png,Figure 14.2: Alveolar and arterial oxygen tensions in the normal state lead to a normal alveolar–arterial PO2 difference.
d8a4e1cb-8727-4554-8087-372ab3bdca8f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Normal lung: With a well-ventilated and perfused lung (figure 14.2), alveolar PO2 is normal, and when there are no problems with diffusion across the membrane into an adequately perfused blood vessel, arterial PO2 is normal as well. Thus the difference between alveolar and arterial PO2 is minimal and normal, and in reality for a young healthy person is no more than 5–10 mmHg (note, however, this difference increases with age).",True,PaO2,Figure 14.2,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.2.png,Figure 14.2: Alveolar and arterial oxygen tensions in the normal state lead to a normal alveolar–arterial PO2 difference.
dfadaa83-f3cc-4495-8e0f-68e356600a1a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Hypoventilation: Now let us look at a case of where the alveolus is inadequately ventilated (figure 14.3): perhaps a patient has been given a high enough dose of opioid for pain relief and it has caused respiratory depression, so the patient no longer breathes enough to achieve sufficient gas exchange. This will lead to a decline in alveolar PO2 and consequently a fall in arterial PO2 as well. However, because the alveolar and arterial PO2s have both decreased, then the difference between the two of them remains the same. So we see low alveolar PO2, low arterial PO2, but a normal A–a PO2 difference.",True,PaO2,Figure 14.3,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.3.png,Figure 14.3: Alveolar and arterial oxygen tensions during hypoventilation result in a normal alveolar–arterial PO2 difference.
dfadaa83-f3cc-4495-8e0f-68e356600a1a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Hypoventilation: Now let us look at a case of where the alveolus is inadequately ventilated (figure 14.3): perhaps a patient has been given a high enough dose of opioid for pain relief and it has caused respiratory depression, so the patient no longer breathes enough to achieve sufficient gas exchange. This will lead to a decline in alveolar PO2 and consequently a fall in arterial PO2 as well. However, because the alveolar and arterial PO2s have both decreased, then the difference between the two of them remains the same. So we see low alveolar PO2, low arterial PO2, but a normal A–a PO2 difference.",True,PaO2,Figure 14.3,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.3.png,Figure 14.3: Alveolar and arterial oxygen tensions during hypoventilation result in a normal alveolar–arterial PO2 difference.
dfadaa83-f3cc-4495-8e0f-68e356600a1a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Hypoventilation: Now let us look at a case of where the alveolus is inadequately ventilated (figure 14.3): perhaps a patient has been given a high enough dose of opioid for pain relief and it has caused respiratory depression, so the patient no longer breathes enough to achieve sufficient gas exchange. This will lead to a decline in alveolar PO2 and consequently a fall in arterial PO2 as well. However, because the alveolar and arterial PO2s have both decreased, then the difference between the two of them remains the same. So we see low alveolar PO2, low arterial PO2, but a normal A–a PO2 difference.",True,PaO2,Figure 14.3,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.3.png,Figure 14.3: Alveolar and arterial oxygen tensions during hypoventilation result in a normal alveolar–arterial PO2 difference.
d84525ab-d131-4bb7-9b3c-544e0c7734e9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Impaired diffusion: Now let us look at a patient with a diffusion abnormality—perhaps some pathological process has caused thickening of the alveolar membranes. Here the alveolus is still adequately ventilated, so alveolar PO2 remains high or at least the same (figure 14.4). But although blood is passing the ventilated region, the thickened membranes prevent diffusion of oxygen into the blood, and arterial PO2 does not equilibrate and so is lower. As a consequence, the A–a difference increases. So this scenario results in a normal alveolar PO2, a low arterial PO2, and an increased difference between the two.",True,PaO2,Figure 14.4,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.4.png,Figure 14.4: Diffusion abnormalities lead to an increased alveolar–arterial PO2 difference.
d84525ab-d131-4bb7-9b3c-544e0c7734e9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Impaired diffusion: Now let us look at a patient with a diffusion abnormality—perhaps some pathological process has caused thickening of the alveolar membranes. Here the alveolus is still adequately ventilated, so alveolar PO2 remains high or at least the same (figure 14.4). But although blood is passing the ventilated region, the thickened membranes prevent diffusion of oxygen into the blood, and arterial PO2 does not equilibrate and so is lower. As a consequence, the A–a difference increases. So this scenario results in a normal alveolar PO2, a low arterial PO2, and an increased difference between the two.",True,PaO2,Figure 14.4,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.4.png,Figure 14.4: Diffusion abnormalities lead to an increased alveolar–arterial PO2 difference.
d84525ab-d131-4bb7-9b3c-544e0c7734e9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Impaired diffusion: Now let us look at a patient with a diffusion abnormality—perhaps some pathological process has caused thickening of the alveolar membranes. Here the alveolus is still adequately ventilated, so alveolar PO2 remains high or at least the same (figure 14.4). But although blood is passing the ventilated region, the thickened membranes prevent diffusion of oxygen into the blood, and arterial PO2 does not equilibrate and so is lower. As a consequence, the A–a difference increases. So this scenario results in a normal alveolar PO2, a low arterial PO2, and an increased difference between the two.",True,PaO2,Figure 14.4,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.4.png,Figure 14.4: Diffusion abnormalities lead to an increased alveolar–arterial PO2 difference.
25cefbc3-5776-4459-9216-f5542ac0cc03,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Inadequate perfusion: Now let us look at a last scenario where perfusion has been stopped, perhaps by a pulmonary embolus (figure 14.5). Ventilation still reaches the region, but there is no perfusion; this is a form of V/Q mismatch. Alveolar PO2 remains normal because air still reaches the region, but with no perfusion and therefore no gas exchange arterial PO2 will fall. This, again, results in an increased A–a PO2 difference.",True,PaO2,Figure 14.5,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.5.png,Figure 14.5: Perfusion abnormalities lead to an increased alveolar–arterial PO2 difference.
25cefbc3-5776-4459-9216-f5542ac0cc03,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Inadequate perfusion: Now let us look at a last scenario where perfusion has been stopped, perhaps by a pulmonary embolus (figure 14.5). Ventilation still reaches the region, but there is no perfusion; this is a form of V/Q mismatch. Alveolar PO2 remains normal because air still reaches the region, but with no perfusion and therefore no gas exchange arterial PO2 will fall. This, again, results in an increased A–a PO2 difference.",True,PaO2,Figure 14.5,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.5.png,Figure 14.5: Perfusion abnormalities lead to an increased alveolar–arterial PO2 difference.
25cefbc3-5776-4459-9216-f5542ac0cc03,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Inadequate perfusion: Now let us look at a last scenario where perfusion has been stopped, perhaps by a pulmonary embolus (figure 14.5). Ventilation still reaches the region, but there is no perfusion; this is a form of V/Q mismatch. Alveolar PO2 remains normal because air still reaches the region, but with no perfusion and therefore no gas exchange arterial PO2 will fall. This, again, results in an increased A–a PO2 difference.",True,PaO2,Figure 14.5,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.5.png,Figure 14.5: Perfusion abnormalities lead to an increased alveolar–arterial PO2 difference.
26823ba2-cc36-4772-85fc-cd9e4662d428,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"So what you should see from the summary in table 14.1 is that all three abnormalities cause a decrease in arterial PO2, so all three patients are likely to present with low arterial saturations. But when blood gases are taken and the alveolar–arterial PO2 difference is calculated, then one or more of our abnormalities could be ruled out. If there is an increased difference, you know it is not hypoventilation. If there is no increase in A–a difference, you know it is neither a diffusion problem nor a V/Q mismatch.",True,PaO2,,,,
a2dfff2e-b3ea-4c25-9e59-aa5613cbb8d2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,Summary,False,Summary,,,,
1957c11e-4181-43fe-b281-d4aa73370133,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"These examples to illustrate the point are rather specific, but generally knowing the alveolar and arterial PO2s and calculating A–a PO2 difference allows you to distinguish whether a decline in arterial PO2 is due to a problem getting oxygen down into the lung, or a problem getting oxygen from lung to blood. So the alveolar equation is a simple equation, but it forms a powerful tool.",True,Summary,,,,
08ea33e3-9037-448b-b892-3f528da57fff,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,Table 14.1: Summary of Alveolar-arterial PO2 difference.,True,Summary,,,,
2e9db90a-66fe-426c-9c6f-2fd4166c7d9f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,Text,False,Text,,,,
0b3f01fc-f893-4c2a-ba14-78f6613e445c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"Levitsky, Michael G. “Chapter 3: Alveolar Ventilation.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
9950f1dc-cf78-4e71-b1ed-7a1a1e6d345d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-2,"West, John B. “Chapter 5: Ventilation–Perfusion Relationships—How Matching of Gas and Blood Determines Gas Exchange.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
21afa531-01e0-45dc-a0b3-00798bc3dd44,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,Introduction,False,Introduction,,,,
8db2388b-ac72-4c2e-9f01-eba392354549,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,This chapter will describe how the alveolar–arterial PO2 difference is calculated and what assumptions can be made from it.,True,Introduction,,,,
e3ed5c9a-b9a4-46f9-bd0d-db287e4d2cb0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Before you start, a quick reminder that an uppercase A refers to alveolar and lowercase to arterial.",True,Introduction,,,,
1febf911-df99-4397-9b3b-14a9280a3a1a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,Calculating Alveolar PO₂,False,Calculating Alveolar PO₂,,,,
e213d9cb-98e2-4f61-8924-071dc855a0c6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Obviously to measure the alveolar–arterial PO2 difference, we need to know both the alveolar and arterial PO2s. The arterial PO2 is routinely measured as part of a blood gas panel, along with arterial PCO2. However, from your understanding of V/Q distribution across the lung, you might appreciate that the measurement of a “typical” alveolar PO2 is difficult, and it must be calculated as an estimate of the whole lung. This is the role of the alveolar gas equation, and we will look at it now, not just because it may appear on your board exams, but primarily because of its clinical importance. As there are several forms of the equation, we will take the easy way out and use the simplest one (figure 14.1), which is accurate for the vast majority of cases you will ever see.",True,Calculating Alveolar PO₂,Figure 14.1,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.1.png,Figure 14.1: The alveolar gas equation.
e213d9cb-98e2-4f61-8924-071dc855a0c6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Obviously to measure the alveolar–arterial PO2 difference, we need to know both the alveolar and arterial PO2s. The arterial PO2 is routinely measured as part of a blood gas panel, along with arterial PCO2. However, from your understanding of V/Q distribution across the lung, you might appreciate that the measurement of a “typical” alveolar PO2 is difficult, and it must be calculated as an estimate of the whole lung. This is the role of the alveolar gas equation, and we will look at it now, not just because it may appear on your board exams, but primarily because of its clinical importance. As there are several forms of the equation, we will take the easy way out and use the simplest one (figure 14.1), which is accurate for the vast majority of cases you will ever see.",True,Calculating Alveolar PO₂,Figure 14.1,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.1.png,Figure 14.1: The alveolar gas equation.
e213d9cb-98e2-4f61-8924-071dc855a0c6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Obviously to measure the alveolar–arterial PO2 difference, we need to know both the alveolar and arterial PO2s. The arterial PO2 is routinely measured as part of a blood gas panel, along with arterial PCO2. However, from your understanding of V/Q distribution across the lung, you might appreciate that the measurement of a “typical” alveolar PO2 is difficult, and it must be calculated as an estimate of the whole lung. This is the role of the alveolar gas equation, and we will look at it now, not just because it may appear on your board exams, but primarily because of its clinical importance. As there are several forms of the equation, we will take the easy way out and use the simplest one (figure 14.1), which is accurate for the vast majority of cases you will ever see.",True,Calculating Alveolar PO₂,Figure 14.1,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.1.png,Figure 14.1: The alveolar gas equation.
02d98daf-9bc9-46fa-b3ed-062952519f10,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,PO2s,False,PO2s,,,,
14a5a69a-ed67-4bfc-af80-93f0e11d3bfe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"The alveolar gas equation estimates whole lung alveolar PO2 as the inspired PO2 minus the arterial PO2 divided by the respiratory exchange ratio. For those interested in the derivation of the equation, more detailed sources are available. But here, we will just look at the factors involved and try and make this simpler to commit to memory (which I suggest you do).",True,PO2s,,,,
1b017c0c-5cad-4361-9c36-ee9a817ffb21,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"First let us look at arterial PCO2; this measurement is included in a blood gas panel so will be readily available to you. The alveolar gas equation really needs the alveolar PCO2, but since CO2 is so soluble then we assume that equilibration has taken place and PaCO2 and PACO2 are the same, and we use the number we have at the bedside.",True,PO2s,,,,
affe77a4-5109-4b1f-827c-b2628f15eae5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,PaCO2,False,PaCO2,,,,
df382318-fc6a-4ba7-b0ef-001a1e4b884e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,PACO2,False,PACO2,,,,
010ba5e6-21a2-481f-9a6c-5a677926fcec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Now let us look at R, or the respiratory exchange ratio. The respiratory exchange ratio describes how much CO2 is produced per unit of oxygen consumed. (Perhaps you can see why we are using this in conjunction with the arterial PCO2; we are relating CO2 production as a proxy measurement of oxygen consumption.) When utilizing carbohydrate as a fuel (the most common situation) there are eight CO2 molecules produced for every ten oxygen molecules burnt, so R is generally 0.8. Lastly, there is the inspired PO2. Generally, breathing room air at sea level this will be ~150 mmHg. But it is important to note that this might change in the clinic if the patient is given oxygen therapy.",True,PACO2,,,,
dc4faa4b-ce65-417a-b99e-21ecc2dc782c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"So this simple form of the alveolar gas equation really has two basic halves: the amount of oxygen taken into the alveoli (PIO2), and a reflection of the amount that is taken out (PaCO2/R) to supply metabolism.",True,PACO2,,,,
833f82bb-2dc1-4f40-b2c5-81976df2f9ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,PIO2,False,PIO2,,,,
18a04ef5-303e-43d9-9ef0-7305b8b83b2e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"You will find more complex and accurate forms of this equation, but for the vast majority of situations this one is perfectly adequate and is considerably easier to remember, particularly when some of the numbers we plug in are frequently the same. If we look at normal values (equation 14.1), we see that our equation gets us close to what we have learned to be a normal alveolar PO2. Inspired PO2 at sea level and room air is 150 mmHg, we will assume R is 0.8, and a normal arterial PCO2 is 40 mmHg. Here is the alveolar gas equation with normal values:",True,PIO2,,,,
af5fcac5-eebb-48b7-9daf-064ca324b858,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,Equation 14.1,True,PIO2,,,,
509a40fa-b90e-40ce-bed4-0b2b31390f8b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,PAO2=150−400.8=100,True,PIO2,,,,
a7ba4f52-4a24-4996-a76b-80590638eed1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,PA,False,PA,,,,
8f32de64-ca63-40f0-b821-b3c485a5bc11,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,P,False,P,,,,
9c6d92eb-335a-4005-8849-5ab89bf60a20,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,A,False,A,,,,
438b0540-74fe-48b8-abc3-8dd4c23cc2d2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,O2,False,O2,,,,
6fe8cd43-5ca0-44b8-b0af-d9b21f14c854,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,O,False,O,,,,
8e4ddf27-425a-4b5b-bb21-456e80f47979,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,2,False,2,,,,
c43d9fe7-4381-4eaa-9f34-7389484ffebd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,=,False,=,,,,
46fc6c48-934c-4b4d-90c8-3a1aba101837,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,150,False,150,,,,
ecb258eb-39f6-448b-b960-81d350b0b241,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,−,False,−,,,,
3148f82d-716f-4a5b-8855-6205d071af92,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,400.8,True,−,,,,
1a2e557e-ce79-4888-9fed-72df5cd6afed,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,40,False,40,,,,
31736771-63ab-4cf7-af41-e14e28195276,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,0.8,True,40,,,,
eedddd0e-3966-4da3-a46e-c8876e05d956,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,100,False,100,,,,
e56e60e4-9236-4f1e-b6f4-6225679747fd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,Now let us see the clinical use of being able to determine alveolar PO2 and thus calculate any alveolar–arterial PO2 difference.,True,100,,,,
47b1202a-f426-4c65-bbdd-18ef2badeeaa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,False,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,,,,
9abd0253-b783-4f04-ad5a-aa827b270dc9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Not only knowing what the alveolar and arterial PO2s are, but by how much they differ can tell us where a problem in the process of gas exchange might be occurring. So the PAO2–PaO2 difference has great diagnostic value. Let us return to our schematic of a lung with a ventilated and perfused lung unit and look at a few scenarios, starting with the normal state.",True,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,,,,
0dfa8650-ff9d-48f6-9343-56abb96576c4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,PAO2,False,PAO2,,,,
e1eca3ad-afcf-4686-9f92-9987bb9ccb37,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,PaO2,False,PaO2,,,,
c8d951bf-773c-4df4-840c-136b0aa382d0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Normal lung: With a well-ventilated and perfused lung (figure 14.2), alveolar PO2 is normal, and when there are no problems with diffusion across the membrane into an adequately perfused blood vessel, arterial PO2 is normal as well. Thus the difference between alveolar and arterial PO2 is minimal and normal, and in reality for a young healthy person is no more than 5–10 mmHg (note, however, this difference increases with age).",True,PaO2,Figure 14.2,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.2.png,Figure 14.2: Alveolar and arterial oxygen tensions in the normal state lead to a normal alveolar–arterial PO2 difference.
c8d951bf-773c-4df4-840c-136b0aa382d0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Normal lung: With a well-ventilated and perfused lung (figure 14.2), alveolar PO2 is normal, and when there are no problems with diffusion across the membrane into an adequately perfused blood vessel, arterial PO2 is normal as well. Thus the difference between alveolar and arterial PO2 is minimal and normal, and in reality for a young healthy person is no more than 5–10 mmHg (note, however, this difference increases with age).",True,PaO2,Figure 14.2,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.2.png,Figure 14.2: Alveolar and arterial oxygen tensions in the normal state lead to a normal alveolar–arterial PO2 difference.
c8d951bf-773c-4df4-840c-136b0aa382d0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Normal lung: With a well-ventilated and perfused lung (figure 14.2), alveolar PO2 is normal, and when there are no problems with diffusion across the membrane into an adequately perfused blood vessel, arterial PO2 is normal as well. Thus the difference between alveolar and arterial PO2 is minimal and normal, and in reality for a young healthy person is no more than 5–10 mmHg (note, however, this difference increases with age).",True,PaO2,Figure 14.2,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.2.png,Figure 14.2: Alveolar and arterial oxygen tensions in the normal state lead to a normal alveolar–arterial PO2 difference.
b0e47d9a-f43c-4cb2-be96-c55b4e209295,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Hypoventilation: Now let us look at a case of where the alveolus is inadequately ventilated (figure 14.3): perhaps a patient has been given a high enough dose of opioid for pain relief and it has caused respiratory depression, so the patient no longer breathes enough to achieve sufficient gas exchange. This will lead to a decline in alveolar PO2 and consequently a fall in arterial PO2 as well. However, because the alveolar and arterial PO2s have both decreased, then the difference between the two of them remains the same. So we see low alveolar PO2, low arterial PO2, but a normal A–a PO2 difference.",True,PaO2,Figure 14.3,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.3.png,Figure 14.3: Alveolar and arterial oxygen tensions during hypoventilation result in a normal alveolar–arterial PO2 difference.
b0e47d9a-f43c-4cb2-be96-c55b4e209295,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Hypoventilation: Now let us look at a case of where the alveolus is inadequately ventilated (figure 14.3): perhaps a patient has been given a high enough dose of opioid for pain relief and it has caused respiratory depression, so the patient no longer breathes enough to achieve sufficient gas exchange. This will lead to a decline in alveolar PO2 and consequently a fall in arterial PO2 as well. However, because the alveolar and arterial PO2s have both decreased, then the difference between the two of them remains the same. So we see low alveolar PO2, low arterial PO2, but a normal A–a PO2 difference.",True,PaO2,Figure 14.3,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.3.png,Figure 14.3: Alveolar and arterial oxygen tensions during hypoventilation result in a normal alveolar–arterial PO2 difference.
b0e47d9a-f43c-4cb2-be96-c55b4e209295,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Hypoventilation: Now let us look at a case of where the alveolus is inadequately ventilated (figure 14.3): perhaps a patient has been given a high enough dose of opioid for pain relief and it has caused respiratory depression, so the patient no longer breathes enough to achieve sufficient gas exchange. This will lead to a decline in alveolar PO2 and consequently a fall in arterial PO2 as well. However, because the alveolar and arterial PO2s have both decreased, then the difference between the two of them remains the same. So we see low alveolar PO2, low arterial PO2, but a normal A–a PO2 difference.",True,PaO2,Figure 14.3,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.3.png,Figure 14.3: Alveolar and arterial oxygen tensions during hypoventilation result in a normal alveolar–arterial PO2 difference.
a09272a0-4fc5-48f5-835d-d960389631d2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Impaired diffusion: Now let us look at a patient with a diffusion abnormality—perhaps some pathological process has caused thickening of the alveolar membranes. Here the alveolus is still adequately ventilated, so alveolar PO2 remains high or at least the same (figure 14.4). But although blood is passing the ventilated region, the thickened membranes prevent diffusion of oxygen into the blood, and arterial PO2 does not equilibrate and so is lower. As a consequence, the A–a difference increases. So this scenario results in a normal alveolar PO2, a low arterial PO2, and an increased difference between the two.",True,PaO2,Figure 14.4,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.4.png,Figure 14.4: Diffusion abnormalities lead to an increased alveolar–arterial PO2 difference.
a09272a0-4fc5-48f5-835d-d960389631d2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Impaired diffusion: Now let us look at a patient with a diffusion abnormality—perhaps some pathological process has caused thickening of the alveolar membranes. Here the alveolus is still adequately ventilated, so alveolar PO2 remains high or at least the same (figure 14.4). But although blood is passing the ventilated region, the thickened membranes prevent diffusion of oxygen into the blood, and arterial PO2 does not equilibrate and so is lower. As a consequence, the A–a difference increases. So this scenario results in a normal alveolar PO2, a low arterial PO2, and an increased difference between the two.",True,PaO2,Figure 14.4,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.4.png,Figure 14.4: Diffusion abnormalities lead to an increased alveolar–arterial PO2 difference.
a09272a0-4fc5-48f5-835d-d960389631d2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Impaired diffusion: Now let us look at a patient with a diffusion abnormality—perhaps some pathological process has caused thickening of the alveolar membranes. Here the alveolus is still adequately ventilated, so alveolar PO2 remains high or at least the same (figure 14.4). But although blood is passing the ventilated region, the thickened membranes prevent diffusion of oxygen into the blood, and arterial PO2 does not equilibrate and so is lower. As a consequence, the A–a difference increases. So this scenario results in a normal alveolar PO2, a low arterial PO2, and an increased difference between the two.",True,PaO2,Figure 14.4,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.4.png,Figure 14.4: Diffusion abnormalities lead to an increased alveolar–arterial PO2 difference.
45c3590a-5b2a-4e02-ad16-f4a1ed245eb8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Inadequate perfusion: Now let us look at a last scenario where perfusion has been stopped, perhaps by a pulmonary embolus (figure 14.5). Ventilation still reaches the region, but there is no perfusion; this is a form of V/Q mismatch. Alveolar PO2 remains normal because air still reaches the region, but with no perfusion and therefore no gas exchange arterial PO2 will fall. This, again, results in an increased A–a PO2 difference.",True,PaO2,Figure 14.5,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.5.png,Figure 14.5: Perfusion abnormalities lead to an increased alveolar–arterial PO2 difference.
45c3590a-5b2a-4e02-ad16-f4a1ed245eb8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Inadequate perfusion: Now let us look at a last scenario where perfusion has been stopped, perhaps by a pulmonary embolus (figure 14.5). Ventilation still reaches the region, but there is no perfusion; this is a form of V/Q mismatch. Alveolar PO2 remains normal because air still reaches the region, but with no perfusion and therefore no gas exchange arterial PO2 will fall. This, again, results in an increased A–a PO2 difference.",True,PaO2,Figure 14.5,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.5.png,Figure 14.5: Perfusion abnormalities lead to an increased alveolar–arterial PO2 difference.
45c3590a-5b2a-4e02-ad16-f4a1ed245eb8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Inadequate perfusion: Now let us look at a last scenario where perfusion has been stopped, perhaps by a pulmonary embolus (figure 14.5). Ventilation still reaches the region, but there is no perfusion; this is a form of V/Q mismatch. Alveolar PO2 remains normal because air still reaches the region, but with no perfusion and therefore no gas exchange arterial PO2 will fall. This, again, results in an increased A–a PO2 difference.",True,PaO2,Figure 14.5,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.5.png,Figure 14.5: Perfusion abnormalities lead to an increased alveolar–arterial PO2 difference.
80f19d1d-5c0a-40e6-821f-a6f25d24789d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"So what you should see from the summary in table 14.1 is that all three abnormalities cause a decrease in arterial PO2, so all three patients are likely to present with low arterial saturations. But when blood gases are taken and the alveolar–arterial PO2 difference is calculated, then one or more of our abnormalities could be ruled out. If there is an increased difference, you know it is not hypoventilation. If there is no increase in A–a difference, you know it is neither a diffusion problem nor a V/Q mismatch.",True,PaO2,,,,
34d59892-6296-440c-bc67-3e082bf146cb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,Summary,False,Summary,,,,
9ba16d6c-19ba-422c-80d6-3247f9ad7e17,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"These examples to illustrate the point are rather specific, but generally knowing the alveolar and arterial PO2s and calculating A–a PO2 difference allows you to distinguish whether a decline in arterial PO2 is due to a problem getting oxygen down into the lung, or a problem getting oxygen from lung to blood. So the alveolar equation is a simple equation, but it forms a powerful tool.",True,Summary,,,,
19e512ab-45d2-4630-9842-c6e05831c0f7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,Table 14.1: Summary of Alveolar-arterial PO2 difference.,True,Summary,,,,
18321207-885b-4c30-8503-2e3c55b55c84,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,Text,False,Text,,,,
796a4fe0-c4eb-4ba5-93f6-d3d54c114260,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"Levitsky, Michael G. “Chapter 3: Alveolar Ventilation.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
4573d66a-a1b2-46f4-b765-ef5318d553d4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/#chapter-53-section-1,"West, John B. “Chapter 5: Ventilation–Perfusion Relationships—How Matching of Gas and Blood Determines Gas Exchange.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
13392019-b8e1-40fa-8aff-19224aec2b7e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,Introduction,False,Introduction,,,,
94533b43-58bb-4696-aa00-79877aff6a0f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,This chapter will describe how the alveolar–arterial PO2 difference is calculated and what assumptions can be made from it.,True,Introduction,,,,
71255eb6-0044-4ed3-aede-c60af90681ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Before you start, a quick reminder that an uppercase A refers to alveolar and lowercase to arterial.",True,Introduction,,,,
7c0ababa-f243-4ab9-be49-0fc4d3fd2734,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,Calculating Alveolar PO₂,False,Calculating Alveolar PO₂,,,,
9f74eb05-1624-4449-b774-eb70d1c96e46,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Obviously to measure the alveolar–arterial PO2 difference, we need to know both the alveolar and arterial PO2s. The arterial PO2 is routinely measured as part of a blood gas panel, along with arterial PCO2. However, from your understanding of V/Q distribution across the lung, you might appreciate that the measurement of a “typical” alveolar PO2 is difficult, and it must be calculated as an estimate of the whole lung. This is the role of the alveolar gas equation, and we will look at it now, not just because it may appear on your board exams, but primarily because of its clinical importance. As there are several forms of the equation, we will take the easy way out and use the simplest one (figure 14.1), which is accurate for the vast majority of cases you will ever see.",True,Calculating Alveolar PO₂,Figure 14.1,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.1.png,Figure 14.1: The alveolar gas equation.
9f74eb05-1624-4449-b774-eb70d1c96e46,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Obviously to measure the alveolar–arterial PO2 difference, we need to know both the alveolar and arterial PO2s. The arterial PO2 is routinely measured as part of a blood gas panel, along with arterial PCO2. However, from your understanding of V/Q distribution across the lung, you might appreciate that the measurement of a “typical” alveolar PO2 is difficult, and it must be calculated as an estimate of the whole lung. This is the role of the alveolar gas equation, and we will look at it now, not just because it may appear on your board exams, but primarily because of its clinical importance. As there are several forms of the equation, we will take the easy way out and use the simplest one (figure 14.1), which is accurate for the vast majority of cases you will ever see.",True,Calculating Alveolar PO₂,Figure 14.1,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.1.png,Figure 14.1: The alveolar gas equation.
9f74eb05-1624-4449-b774-eb70d1c96e46,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Obviously to measure the alveolar–arterial PO2 difference, we need to know both the alveolar and arterial PO2s. The arterial PO2 is routinely measured as part of a blood gas panel, along with arterial PCO2. However, from your understanding of V/Q distribution across the lung, you might appreciate that the measurement of a “typical” alveolar PO2 is difficult, and it must be calculated as an estimate of the whole lung. This is the role of the alveolar gas equation, and we will look at it now, not just because it may appear on your board exams, but primarily because of its clinical importance. As there are several forms of the equation, we will take the easy way out and use the simplest one (figure 14.1), which is accurate for the vast majority of cases you will ever see.",True,Calculating Alveolar PO₂,Figure 14.1,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.1.png,Figure 14.1: The alveolar gas equation.
d4955d7d-aa1d-4992-ac67-b1129b5610ed,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,PO2s,False,PO2s,,,,
7058473f-40eb-468b-aacd-604c811d3536,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"The alveolar gas equation estimates whole lung alveolar PO2 as the inspired PO2 minus the arterial PO2 divided by the respiratory exchange ratio. For those interested in the derivation of the equation, more detailed sources are available. But here, we will just look at the factors involved and try and make this simpler to commit to memory (which I suggest you do).",True,PO2s,,,,
965f4649-200d-42af-9ba6-58ee1d439b58,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"First let us look at arterial PCO2; this measurement is included in a blood gas panel so will be readily available to you. The alveolar gas equation really needs the alveolar PCO2, but since CO2 is so soluble then we assume that equilibration has taken place and PaCO2 and PACO2 are the same, and we use the number we have at the bedside.",True,PO2s,,,,
48cb1ae7-37c9-4b5b-a675-87c3c79d7ce5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,PaCO2,False,PaCO2,,,,
ccca6252-1850-4d98-952c-23968f55b517,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,PACO2,False,PACO2,,,,
872ef67f-168f-4a6e-a73a-8c1eae008db2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Now let us look at R, or the respiratory exchange ratio. The respiratory exchange ratio describes how much CO2 is produced per unit of oxygen consumed. (Perhaps you can see why we are using this in conjunction with the arterial PCO2; we are relating CO2 production as a proxy measurement of oxygen consumption.) When utilizing carbohydrate as a fuel (the most common situation) there are eight CO2 molecules produced for every ten oxygen molecules burnt, so R is generally 0.8. Lastly, there is the inspired PO2. Generally, breathing room air at sea level this will be ~150 mmHg. But it is important to note that this might change in the clinic if the patient is given oxygen therapy.",True,PACO2,,,,
6ca62b87-49c8-429d-8ff4-dee15b138866,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"So this simple form of the alveolar gas equation really has two basic halves: the amount of oxygen taken into the alveoli (PIO2), and a reflection of the amount that is taken out (PaCO2/R) to supply metabolism.",True,PACO2,,,,
476802c8-0b4a-4422-be9f-d44fdd3a6499,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,PIO2,False,PIO2,,,,
6e280721-43f1-45d4-87d4-a3614ebf4d26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"You will find more complex and accurate forms of this equation, but for the vast majority of situations this one is perfectly adequate and is considerably easier to remember, particularly when some of the numbers we plug in are frequently the same. If we look at normal values (equation 14.1), we see that our equation gets us close to what we have learned to be a normal alveolar PO2. Inspired PO2 at sea level and room air is 150 mmHg, we will assume R is 0.8, and a normal arterial PCO2 is 40 mmHg. Here is the alveolar gas equation with normal values:",True,PIO2,,,,
80d5ec2d-6df4-4e9b-9f67-d921ff9af4b6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,Equation 14.1,True,PIO2,,,,
ddfbc373-d881-4302-994b-5a40ac882164,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,[latex]P_AO_2 = 150 - \frac{40}{0.8} = 100[/latex],True,PIO2,,,,
439103c9-7cb4-4c05-ab22-a773a0744c25,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,Now let us see the clinical use of being able to determine alveolar PO2 and thus calculate any alveolar–arterial PO2 difference.,True,PIO2,,,,
9e4a8e13-4be3-4829-ab41-52d393dbce2c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,False,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,,,,
fdb8552f-0bad-4faf-89ef-aa1cb61723b7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Not only knowing what the alveolar and arterial PO2s are, but by how much they differ can tell us where a problem in the process of gas exchange might be occurring. So the PAO2–PaO2 difference has great diagnostic value. Let us return to our schematic of a lung with a ventilated and perfused lung unit and look at a few scenarios, starting with the normal state.",True,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,,,,
6043cef3-21c1-4c03-89e7-1cfd34d164ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,PAO2,False,PAO2,,,,
88b45a3e-43a9-4490-a32f-1b7a8521829e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,PaO2,False,PaO2,,,,
1b29e955-29a6-4825-8999-51084a65a1d8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Normal lung: With a well-ventilated and perfused lung (figure 14.2), alveolar PO2 is normal, and when there are no problems with diffusion across the membrane into an adequately perfused blood vessel, arterial PO2 is normal as well. Thus the difference between alveolar and arterial PO2 is minimal and normal, and in reality for a young healthy person is no more than 5–10 mmHg (note, however, this difference increases with age).",True,PaO2,Figure 14.2,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.2.png,Figure 14.2: Alveolar and arterial oxygen tensions in the normal state lead to a normal alveolar–arterial PO2 difference.
1b29e955-29a6-4825-8999-51084a65a1d8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Normal lung: With a well-ventilated and perfused lung (figure 14.2), alveolar PO2 is normal, and when there are no problems with diffusion across the membrane into an adequately perfused blood vessel, arterial PO2 is normal as well. Thus the difference between alveolar and arterial PO2 is minimal and normal, and in reality for a young healthy person is no more than 5–10 mmHg (note, however, this difference increases with age).",True,PaO2,Figure 14.2,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.2.png,Figure 14.2: Alveolar and arterial oxygen tensions in the normal state lead to a normal alveolar–arterial PO2 difference.
1b29e955-29a6-4825-8999-51084a65a1d8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Normal lung: With a well-ventilated and perfused lung (figure 14.2), alveolar PO2 is normal, and when there are no problems with diffusion across the membrane into an adequately perfused blood vessel, arterial PO2 is normal as well. Thus the difference between alveolar and arterial PO2 is minimal and normal, and in reality for a young healthy person is no more than 5–10 mmHg (note, however, this difference increases with age).",True,PaO2,Figure 14.2,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.2.png,Figure 14.2: Alveolar and arterial oxygen tensions in the normal state lead to a normal alveolar–arterial PO2 difference.
f15fd865-aa9f-4ea1-8642-0042991a3c2b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Hypoventilation: Now let us look at a case of where the alveolus is inadequately ventilated (figure 14.3): perhaps a patient has been given a high enough dose of opioid for pain relief and it has caused respiratory depression, so the patient no longer breathes enough to achieve sufficient gas exchange. This will lead to a decline in alveolar PO2 and consequently a fall in arterial PO2 as well. However, because the alveolar and arterial PO2s have both decreased, then the difference between the two of them remains the same. So we see low alveolar PO2, low arterial PO2, but a normal A–a PO2 difference.",True,PaO2,Figure 14.3,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.3.png,Figure 14.3: Alveolar and arterial oxygen tensions during hypoventilation result in a normal alveolar–arterial PO2 difference.
f15fd865-aa9f-4ea1-8642-0042991a3c2b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Hypoventilation: Now let us look at a case of where the alveolus is inadequately ventilated (figure 14.3): perhaps a patient has been given a high enough dose of opioid for pain relief and it has caused respiratory depression, so the patient no longer breathes enough to achieve sufficient gas exchange. This will lead to a decline in alveolar PO2 and consequently a fall in arterial PO2 as well. However, because the alveolar and arterial PO2s have both decreased, then the difference between the two of them remains the same. So we see low alveolar PO2, low arterial PO2, but a normal A–a PO2 difference.",True,PaO2,Figure 14.3,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.3.png,Figure 14.3: Alveolar and arterial oxygen tensions during hypoventilation result in a normal alveolar–arterial PO2 difference.
f15fd865-aa9f-4ea1-8642-0042991a3c2b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Hypoventilation: Now let us look at a case of where the alveolus is inadequately ventilated (figure 14.3): perhaps a patient has been given a high enough dose of opioid for pain relief and it has caused respiratory depression, so the patient no longer breathes enough to achieve sufficient gas exchange. This will lead to a decline in alveolar PO2 and consequently a fall in arterial PO2 as well. However, because the alveolar and arterial PO2s have both decreased, then the difference between the two of them remains the same. So we see low alveolar PO2, low arterial PO2, but a normal A–a PO2 difference.",True,PaO2,Figure 14.3,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.3.png,Figure 14.3: Alveolar and arterial oxygen tensions during hypoventilation result in a normal alveolar–arterial PO2 difference.
8013826b-799c-4ef6-a8c8-e2af9af734d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Impaired diffusion: Now let us look at a patient with a diffusion abnormality—perhaps some pathological process has caused thickening of the alveolar membranes. Here the alveolus is still adequately ventilated, so alveolar PO2 remains high or at least the same (figure 14.4). But although blood is passing the ventilated region, the thickened membranes prevent diffusion of oxygen into the blood, and arterial PO2 does not equilibrate and so is lower. As a consequence, the A–a difference increases. So this scenario results in a normal alveolar PO2, a low arterial PO2, and an increased difference between the two.",True,PaO2,Figure 14.4,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.4.png,Figure 14.4: Diffusion abnormalities lead to an increased alveolar–arterial PO2 difference.
8013826b-799c-4ef6-a8c8-e2af9af734d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Impaired diffusion: Now let us look at a patient with a diffusion abnormality—perhaps some pathological process has caused thickening of the alveolar membranes. Here the alveolus is still adequately ventilated, so alveolar PO2 remains high or at least the same (figure 14.4). But although blood is passing the ventilated region, the thickened membranes prevent diffusion of oxygen into the blood, and arterial PO2 does not equilibrate and so is lower. As a consequence, the A–a difference increases. So this scenario results in a normal alveolar PO2, a low arterial PO2, and an increased difference between the two.",True,PaO2,Figure 14.4,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.4.png,Figure 14.4: Diffusion abnormalities lead to an increased alveolar–arterial PO2 difference.
8013826b-799c-4ef6-a8c8-e2af9af734d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Impaired diffusion: Now let us look at a patient with a diffusion abnormality—perhaps some pathological process has caused thickening of the alveolar membranes. Here the alveolus is still adequately ventilated, so alveolar PO2 remains high or at least the same (figure 14.4). But although blood is passing the ventilated region, the thickened membranes prevent diffusion of oxygen into the blood, and arterial PO2 does not equilibrate and so is lower. As a consequence, the A–a difference increases. So this scenario results in a normal alveolar PO2, a low arterial PO2, and an increased difference between the two.",True,PaO2,Figure 14.4,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.4.png,Figure 14.4: Diffusion abnormalities lead to an increased alveolar–arterial PO2 difference.
e6d516fe-e1ae-46a7-bdda-126507bbba18,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Inadequate perfusion: Now let us look at a last scenario where perfusion has been stopped, perhaps by a pulmonary embolus (figure 14.5). Ventilation still reaches the region, but there is no perfusion; this is a form of V/Q mismatch. Alveolar PO2 remains normal because air still reaches the region, but with no perfusion and therefore no gas exchange arterial PO2 will fall. This, again, results in an increased A–a PO2 difference.",True,PaO2,Figure 14.5,Alveolar–Arterial PO₂ Difference and its Diagnostic Value,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.5.png,Figure 14.5: Perfusion abnormalities lead to an increased alveolar–arterial PO2 difference.
e6d516fe-e1ae-46a7-bdda-126507bbba18,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Inadequate perfusion: Now let us look at a last scenario where perfusion has been stopped, perhaps by a pulmonary embolus (figure 14.5). Ventilation still reaches the region, but there is no perfusion; this is a form of V/Q mismatch. Alveolar PO2 remains normal because air still reaches the region, but with no perfusion and therefore no gas exchange arterial PO2 will fall. This, again, results in an increased A–a PO2 difference.",True,PaO2,Figure 14.5,Calculating alveolar PO₂,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.5.png,Figure 14.5: Perfusion abnormalities lead to an increased alveolar–arterial PO2 difference.
e6d516fe-e1ae-46a7-bdda-126507bbba18,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Inadequate perfusion: Now let us look at a last scenario where perfusion has been stopped, perhaps by a pulmonary embolus (figure 14.5). Ventilation still reaches the region, but there is no perfusion; this is a form of V/Q mismatch. Alveolar PO2 remains normal because air still reaches the region, but with no perfusion and therefore no gas exchange arterial PO2 will fall. This, again, results in an increased A–a PO2 difference.",True,PaO2,Figure 14.5,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/14.5.png,Figure 14.5: Perfusion abnormalities lead to an increased alveolar–arterial PO2 difference.
d5a60d21-ecb8-48d2-98f0-894ff71362ed,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"So what you should see from the summary in table 14.1 is that all three abnormalities cause a decrease in arterial PO2, so all three patients are likely to present with low arterial saturations. But when blood gases are taken and the alveolar–arterial PO2 difference is calculated, then one or more of our abnormalities could be ruled out. If there is an increased difference, you know it is not hypoventilation. If there is no increase in A–a difference, you know it is neither a diffusion problem nor a V/Q mismatch.",True,PaO2,,,,
c45d632c-a8bc-4cc3-bbd2-d5e47ed9535c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,Summary,False,Summary,,,,
ef73db0a-8353-4d42-a012-691c34bc642b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"These examples to illustrate the point are rather specific, but generally knowing the alveolar and arterial PO2s and calculating A–a PO2 difference allows you to distinguish whether a decline in arterial PO2 is due to a problem getting oxygen down into the lung, or a problem getting oxygen from lung to blood. So the alveolar equation is a simple equation, but it forms a powerful tool.",True,Summary,,,,
40d56a5a-5f35-4ba8-9b65-33fedb2e8cd9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,Table 14.1: Summary of Alveolar-arterial PO2 difference.,True,Summary,,,,
fbe57186-6502-40c9-9fb4-aec2490a9c5a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,Text,False,Text,,,,
116faede-1346-45cc-82d4-805f41d42bad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"Levitsky, Michael G. “Chapter 3: Alveolar Ventilation.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
56f17d5a-5ebb-4379-bf36-883c520eb28b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,14. The Alveolar Gas Equation and Alveolar–Arterial PO2 Difference,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/the-alveolar-gas-equation-and-alveolar-arterial-po2-difference/,"West, John B. “Chapter 5: Ventilation–Perfusion Relationships—How Matching of Gas and Blood Determines Gas Exchange.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
ef7d1b93-3a1e-49fe-8e36-f72ffeb5d196,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"Let us start with a description of the ideal situation, where ventilation to alveoli is matched with the perfusion, then we will see how the lung does not quite achieve this.",True,Text,,,,
20443118-b1a8-481e-b40b-fabc2cdacdae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"This is what we would expect if the lung were perfect, with uniform distribution of ventilation and perfusion to all regions and a V/Q of 1 in all regions.",True,Text,,,,
1266c3d9-2603-4ab5-a23b-c4c09c575487,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"The lung is not a perfect organ, however, and ventilation and perfusion are not equally distributed, and the lung as a whole only achieves an average V/Q of 0.8, which is close to our ideal of 1, but not quite there. Consequently, by the time the blood has passed the alveoli and regrouped in the pulmonary veins, the PO2 of the blood is less than alveolar. This alveolar–arterial PO2 difference is caused by the less-than-perfect matching of V and Q across the lung; but it is not all the lung’s fault, as venous blood that has been through the bronchial and a small section of the coronary circulation (and therefore is deoxygenated) is mixed into the vessels returning to the left heart, which brings down arterial saturation as well. The mixing-in of bronchial and coronary circulations and the less-than-ideal V/Q in the lung as a whole is the reason why your saturation monitors do not read 100 percent, but normal oxygen saturation is considered as 96–98 percent.",True,Text,,,,
10895687-d637-494c-b5c6-7a932ccea4c1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,Partial Pressures and V/Q,False,Partial Pressures and V/Q,,,,
85f0f70d-8677-4678-bea9-07259ce001f8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"When V and Q are matched (V/Q = 1): Atmospheric PO2 is diluted as it descends the airways to give an alveolar PO2 of 100 mmHg, and alveolar PCO2 is 40 mmHg. The blood returning from the tissue has a diminished PO2 of 40 mmHg and a raised PCO2 of 45 mmHg. As this blood passes the alveolus, oxygen moves into the bloodstream down its pressure gradient and CO2 moves into the alveolus down its pressure gradient. As ventilation and perfusion are matched then equilibrium is reached and the blood leaves with arterial gas tensions that are the same as alveolar tensions (figure 13.2).",True,Partial Pressures and V/Q,Figure 13.2,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.2-scaled.jpg,Figure 13.2: Partial pressures when V/Q = 1.
85f0f70d-8677-4678-bea9-07259ce001f8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"When V and Q are matched (V/Q = 1): Atmospheric PO2 is diluted as it descends the airways to give an alveolar PO2 of 100 mmHg, and alveolar PCO2 is 40 mmHg. The blood returning from the tissue has a diminished PO2 of 40 mmHg and a raised PCO2 of 45 mmHg. As this blood passes the alveolus, oxygen moves into the bloodstream down its pressure gradient and CO2 moves into the alveolus down its pressure gradient. As ventilation and perfusion are matched then equilibrium is reached and the blood leaves with arterial gas tensions that are the same as alveolar tensions (figure 13.2).",True,Partial Pressures and V/Q,Figure 13.2,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.2-scaled.jpg,Figure 13.2: Partial pressures when V/Q = 1.
85f0f70d-8677-4678-bea9-07259ce001f8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"When V and Q are matched (V/Q = 1): Atmospheric PO2 is diluted as it descends the airways to give an alveolar PO2 of 100 mmHg, and alveolar PCO2 is 40 mmHg. The blood returning from the tissue has a diminished PO2 of 40 mmHg and a raised PCO2 of 45 mmHg. As this blood passes the alveolus, oxygen moves into the bloodstream down its pressure gradient and CO2 moves into the alveolus down its pressure gradient. As ventilation and perfusion are matched then equilibrium is reached and the blood leaves with arterial gas tensions that are the same as alveolar tensions (figure 13.2).",True,Partial Pressures and V/Q,Figure 13.2,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.2-scaled.jpg,Figure 13.2: Partial pressures when V/Q = 1.
ae9928fc-ebed-484b-9d0e-f106637f0444,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"When V = 0: Now let us look at another and extreme situation, where ventilation (V) is zero so our V/Q is zero (zero divided by anything is zero).",True,Partial Pressures and V/Q,,,,
2004592f-936b-4a32-8de4-acb4a232cda9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"This situation is clinically possible as airways can collapse or become blocked with a mucus plug. Without any ventilation the gas tensions inside the alveolus rapidly equilibrate with the returning venous blood, so alveolar gas tensions end up as a PO2 of 40 mmHg and a PCO2 of 45 mmHg. The venous gas tensions, never having been exposed to a ventilated alveolus, now circulate into the arterial system, and arterial PO2 becomes 40 mmHg and PCO2 becomes 45 mmHg there as well (figure 13.3).",True,Partial Pressures and V/Q,Figure 13.3,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.3.png,Figure 13.3: Partial pressures when V/Q = 0.
2004592f-936b-4a32-8de4-acb4a232cda9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"This situation is clinically possible as airways can collapse or become blocked with a mucus plug. Without any ventilation the gas tensions inside the alveolus rapidly equilibrate with the returning venous blood, so alveolar gas tensions end up as a PO2 of 40 mmHg and a PCO2 of 45 mmHg. The venous gas tensions, never having been exposed to a ventilated alveolus, now circulate into the arterial system, and arterial PO2 becomes 40 mmHg and PCO2 becomes 45 mmHg there as well (figure 13.3).",True,Partial Pressures and V/Q,Figure 13.3,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.3.png,Figure 13.3: Partial pressures when V/Q = 0.
2004592f-936b-4a32-8de4-acb4a232cda9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"This situation is clinically possible as airways can collapse or become blocked with a mucus plug. Without any ventilation the gas tensions inside the alveolus rapidly equilibrate with the returning venous blood, so alveolar gas tensions end up as a PO2 of 40 mmHg and a PCO2 of 45 mmHg. The venous gas tensions, never having been exposed to a ventilated alveolus, now circulate into the arterial system, and arterial PO2 becomes 40 mmHg and PCO2 becomes 45 mmHg there as well (figure 13.3).",True,Partial Pressures and V/Q,Figure 13.3,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.3.png,Figure 13.3: Partial pressures when V/Q = 0.
3daf23a3-a6fa-4dd2-ad9f-81f3a8ecaa97,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"When Q = 0: Now let us go to the other extreme, where perfusion is zero and ventilation is normal (V/Q goes to infinity). Again, this can occur in reality should a pulmonary vessel become blocked by an embolus. In this scenario V/Q becomes infinity—anything divided by zero is infinity. With no perfusion, no gas exchange occurs in this alveolus, and as it is still being ventilated then the alveolar gas tensions equilibrate with the atmosphere (figure 13.4).",True,Partial Pressures and V/Q,Figure 13.4,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.4.png,Figure 13.4: Partial pressures when V/Q is infinite.
3daf23a3-a6fa-4dd2-ad9f-81f3a8ecaa97,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"When Q = 0: Now let us go to the other extreme, where perfusion is zero and ventilation is normal (V/Q goes to infinity). Again, this can occur in reality should a pulmonary vessel become blocked by an embolus. In this scenario V/Q becomes infinity—anything divided by zero is infinity. With no perfusion, no gas exchange occurs in this alveolus, and as it is still being ventilated then the alveolar gas tensions equilibrate with the atmosphere (figure 13.4).",True,Partial Pressures and V/Q,Figure 13.4,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.4.png,Figure 13.4: Partial pressures when V/Q is infinite.
3daf23a3-a6fa-4dd2-ad9f-81f3a8ecaa97,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"When Q = 0: Now let us go to the other extreme, where perfusion is zero and ventilation is normal (V/Q goes to infinity). Again, this can occur in reality should a pulmonary vessel become blocked by an embolus. In this scenario V/Q becomes infinity—anything divided by zero is infinity. With no perfusion, no gas exchange occurs in this alveolus, and as it is still being ventilated then the alveolar gas tensions equilibrate with the atmosphere (figure 13.4).",True,Partial Pressures and V/Q,Figure 13.4,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.4.png,Figure 13.4: Partial pressures when V/Q is infinite.
6b17964d-6a5d-4fb4-a079-5ebef1888fa2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"So going from these extremes of V/Q as zero, passing through the ideal of V/Q of 1 to a V/Q of infinity, we get a range of alveolar gas tensions going from venous gas tensions when V/Q is zero to atmospheric gas tensions when V/Q is infinite.",True,Partial Pressures and V/Q,,,,
3eb035cf-cde4-46d0-9c3b-0f04bc73270a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"This range of alveolar gas tensions is represented by the ventilation–perfusion line (figure 13.5). This graph takes a minute to come to grips with, so let us break it down. The axes of the graph show alveolar PO2 on the X and alveolar PCO2 on the Y. The plot shows the range of V/Q ratios we have just discussed, ranging from zero when there is perfusion but no ventilation, to infinity when there is ventilation but no perfusion. Looking at figure 13.5 more carefully will confirm our numbers. When ventilation and perfusion are present and V/Q is 1, then our alveolar PO2 is 100 mmHg, and the alveolar PCO2 is 40 mmHg—just as we have seen.",True,Partial Pressures and V/Q,Figure 13.5,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.5.png,Figure 13.5: Ventilation–perfusion line.
3eb035cf-cde4-46d0-9c3b-0f04bc73270a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"This range of alveolar gas tensions is represented by the ventilation–perfusion line (figure 13.5). This graph takes a minute to come to grips with, so let us break it down. The axes of the graph show alveolar PO2 on the X and alveolar PCO2 on the Y. The plot shows the range of V/Q ratios we have just discussed, ranging from zero when there is perfusion but no ventilation, to infinity when there is ventilation but no perfusion. Looking at figure 13.5 more carefully will confirm our numbers. When ventilation and perfusion are present and V/Q is 1, then our alveolar PO2 is 100 mmHg, and the alveolar PCO2 is 40 mmHg—just as we have seen.",True,Partial Pressures and V/Q,Figure 13.5,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.5.png,Figure 13.5: Ventilation–perfusion line.
3eb035cf-cde4-46d0-9c3b-0f04bc73270a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"This range of alveolar gas tensions is represented by the ventilation–perfusion line (figure 13.5). This graph takes a minute to come to grips with, so let us break it down. The axes of the graph show alveolar PO2 on the X and alveolar PCO2 on the Y. The plot shows the range of V/Q ratios we have just discussed, ranging from zero when there is perfusion but no ventilation, to infinity when there is ventilation but no perfusion. Looking at figure 13.5 more carefully will confirm our numbers. When ventilation and perfusion are present and V/Q is 1, then our alveolar PO2 is 100 mmHg, and the alveolar PCO2 is 40 mmHg—just as we have seen.",True,Partial Pressures and V/Q,Figure 13.5,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.5.png,Figure 13.5: Ventilation–perfusion line.
010a8427-3fa7-44e2-a0c4-21eefc77ebb8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"If we stop ventilation and go to a V/Q of zero, we again see that the alveolar gas tensions become equal to venous values, with alveolar PO2 at 40 mmHg and PCO2 at 45 mmHg.",True,Partial Pressures and V/Q,,,,
80e28412-7783-4aa2-afe4-4cad6fd00f7a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"And finally, when we stop perfusion and V/Q becomes infinite, then alveolar PO2 becomes 150 mmHg and PCO2 becomes zero (i.e., equilibrates with the atmosphere).",True,Partial Pressures and V/Q,,,,
e2910c28-4e1e-4a52-8eee-22c01143df88,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,Summary,False,Summary,,,,
03247534-2826-4442-8fe8-28952a8e8147,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"In summary, the ventilation–perfusion line show the effect of changing V/Q on alveolar gases. Reduce V/Q toward zero and the alveolar gas tensions tend toward venous gas tensions. Increase V/Q toward infinity and the alveolar gas tensions get closer to atmospheric partial pressures.",True,Summary,,,,
1c4edfae-a845-4cd5-9160-2be7aa42254b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"The importance of understanding this becomes apparent when we see that V/Q changes across the structure of the lung, and if V/Q changes, then alveolar partial pressures change to.",True,Summary,,,,
e5452abd-5a2f-41b6-b3c6-9ef659cd2265,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,Let us look at the distribution of V/Q across the lung and why it changes from apex to base.,True,Summary,,,,
1adb041b-a0e2-42b7-85ca-42ee94490c9b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,Distribution of V/Q,False,Distribution of V/Q,,,,
c8a75611-c00c-4f33-9054-51f0832f74fe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"As you should understand, ventilation increases down the lung so is greatest at the base, and perfusion follows the same pattern—all due to the effects of gravity. But the increase in ventilation down the lung structure is not equal to the increase in perfusion, as can be seen in figure 13.6. You can see here that perfusion is higher than ventilation at the base; it falls off much more rapidly as the lung is ascended, so it ends up being lower than ventilation at the apex.",True,Distribution of V/Q,Figure 13.6,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
c8a75611-c00c-4f33-9054-51f0832f74fe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"As you should understand, ventilation increases down the lung so is greatest at the base, and perfusion follows the same pattern—all due to the effects of gravity. But the increase in ventilation down the lung structure is not equal to the increase in perfusion, as can be seen in figure 13.6. You can see here that perfusion is higher than ventilation at the base; it falls off much more rapidly as the lung is ascended, so it ends up being lower than ventilation at the apex.",True,Distribution of V/Q,Figure 13.6,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
c8a75611-c00c-4f33-9054-51f0832f74fe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"As you should understand, ventilation increases down the lung so is greatest at the base, and perfusion follows the same pattern—all due to the effects of gravity. But the increase in ventilation down the lung structure is not equal to the increase in perfusion, as can be seen in figure 13.6. You can see here that perfusion is higher than ventilation at the base; it falls off much more rapidly as the lung is ascended, so it ends up being lower than ventilation at the apex.",True,Distribution of V/Q,Figure 13.6,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
2255125b-cca4-4f0c-9fc5-f6bcab3bd4c8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"This means there is a range of ventilation–perfusion ratios up the height of the lung (figure 13.6, maroon plot). At the base perfusion is higher than ventilation, so V/Q is less than 1, while toward the apex V/Q rises and becomes greater than 1. At about the level of the third rib, V/Q is perfect (yay!) as ventilation and perfusion are matched, seen here at the points the lines cross. This range of V/Q results in the previously mentioned whole lung average of 0.8.",True,Distribution of V/Q,Figure 13.6,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
2255125b-cca4-4f0c-9fc5-f6bcab3bd4c8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"This means there is a range of ventilation–perfusion ratios up the height of the lung (figure 13.6, maroon plot). At the base perfusion is higher than ventilation, so V/Q is less than 1, while toward the apex V/Q rises and becomes greater than 1. At about the level of the third rib, V/Q is perfect (yay!) as ventilation and perfusion are matched, seen here at the points the lines cross. This range of V/Q results in the previously mentioned whole lung average of 0.8.",True,Distribution of V/Q,Figure 13.6,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
2255125b-cca4-4f0c-9fc5-f6bcab3bd4c8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"This means there is a range of ventilation–perfusion ratios up the height of the lung (figure 13.6, maroon plot). At the base perfusion is higher than ventilation, so V/Q is less than 1, while toward the apex V/Q rises and becomes greater than 1. At about the level of the third rib, V/Q is perfect (yay!) as ventilation and perfusion are matched, seen here at the points the lines cross. This range of V/Q results in the previously mentioned whole lung average of 0.8.",True,Distribution of V/Q,Figure 13.6,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
970159e5-61e1-4e17-9e78-16530fcc8cff,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,yay,False,yay,,,,
71bbd182-2263-4cb5-b087-6aa5f841cd42,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"As you should appreciate from understanding the ventilation–perfusion line, this range of V/Q across the lung results in a range of alveolar gas partial pressures across the lung. The apical alveoli, being relatively overventilated (or underperfused, whichever way you would like to think about it), have a high V/Q and consequently have partial pressures closer to atmospheric partial pressures. On the other extreme, the basal alveoli are relatively underventilated (or overperfused, your choice) and so have a low V/Q, tending toward zero; thus their partial pressures are closer to venous values (figure 13.7).",True,yay,Figure 13.7,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.7.png,Figure 13.7: V/Q and alveolar gas distribution.
71bbd182-2263-4cb5-b087-6aa5f841cd42,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"As you should appreciate from understanding the ventilation–perfusion line, this range of V/Q across the lung results in a range of alveolar gas partial pressures across the lung. The apical alveoli, being relatively overventilated (or underperfused, whichever way you would like to think about it), have a high V/Q and consequently have partial pressures closer to atmospheric partial pressures. On the other extreme, the basal alveoli are relatively underventilated (or overperfused, your choice) and so have a low V/Q, tending toward zero; thus their partial pressures are closer to venous values (figure 13.7).",True,yay,Figure 13.7,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.7.png,Figure 13.7: V/Q and alveolar gas distribution.
71bbd182-2263-4cb5-b087-6aa5f841cd42,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"As you should appreciate from understanding the ventilation–perfusion line, this range of V/Q across the lung results in a range of alveolar gas partial pressures across the lung. The apical alveoli, being relatively overventilated (or underperfused, whichever way you would like to think about it), have a high V/Q and consequently have partial pressures closer to atmospheric partial pressures. On the other extreme, the basal alveoli are relatively underventilated (or overperfused, your choice) and so have a low V/Q, tending toward zero; thus their partial pressures are closer to venous values (figure 13.7).",True,yay,Figure 13.7,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.7.png,Figure 13.7: V/Q and alveolar gas distribution.
3f5715e0-0a23-467c-b144-edc00bb6fd57,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,overventilated,False,overventilated,,,,
9d8cc6a6-4044-4eb4-8083-1baac1cb4a05,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,overperfused,False,overperfused,,,,
3392289c-1e53-4468-8cc4-bf80c8823b52,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"In between these two extremes is a progressive range, so what we see is that alveolar PO2 declines down the lung while alveolar PCO2 rises. As you might imagine, having a range of alveolar gas tensions down the lung has ramifications for gas exchange and particularly for oxygen saturation. This inequality in V/Q resulting in differences in alveolar PO2 is substantial enough to suppress arterial oxygen saturation—and contribute to your oxygen saturation meter never reading 100 percent. Let us see why.",True,overperfused,,,,
3f5defb8-c9c9-4403-bd5c-80eab935516d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"The difference in alveolar PO2 from apex to base is as high as 40 mmHg, as is reflected in this figure. The apical alveoli have a high PO2 (shown in figure 13.8 as 132 mmHg), primarily due to their poor perfusion and relatively high ventilation and thus high V/Q. This produces a high diffusion gradient from 132 mmHg in the apical alveoli, to 40 mmHg in the apical blood. Consequently, what blood does go to the apex becomes fully saturated before it heads back toward the left heart.",True,overperfused,Figure 13.8,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
3f5defb8-c9c9-4403-bd5c-80eab935516d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"The difference in alveolar PO2 from apex to base is as high as 40 mmHg, as is reflected in this figure. The apical alveoli have a high PO2 (shown in figure 13.8 as 132 mmHg), primarily due to their poor perfusion and relatively high ventilation and thus high V/Q. This produces a high diffusion gradient from 132 mmHg in the apical alveoli, to 40 mmHg in the apical blood. Consequently, what blood does go to the apex becomes fully saturated before it heads back toward the left heart.",True,overperfused,Figure 13.8,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
3f5defb8-c9c9-4403-bd5c-80eab935516d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"The difference in alveolar PO2 from apex to base is as high as 40 mmHg, as is reflected in this figure. The apical alveoli have a high PO2 (shown in figure 13.8 as 132 mmHg), primarily due to their poor perfusion and relatively high ventilation and thus high V/Q. This produces a high diffusion gradient from 132 mmHg in the apical alveoli, to 40 mmHg in the apical blood. Consequently, what blood does go to the apex becomes fully saturated before it heads back toward the left heart.",True,overperfused,Figure 13.8,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
f4dbeadd-5730-41ed-9fbe-7bef557b245f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"Down at the base, however, V/Q is low because of the high perfusion and relatively low ventilation. Consequently the PO2 in basal alveoli tend toward venous values, shown in figure 13.8 as 89 mmHg. This lower alveolar PO2 means a diminished diffusion gradient (from 89 in the alveoli to 40 mmHg in the blood), and combined with a shift down the hemoglobin saturation curve (more on this later), this means blood leaving the basal alveoli may not be completely saturated with oxygen.",True,overperfused,Figure 13.8,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
f4dbeadd-5730-41ed-9fbe-7bef557b245f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"Down at the base, however, V/Q is low because of the high perfusion and relatively low ventilation. Consequently the PO2 in basal alveoli tend toward venous values, shown in figure 13.8 as 89 mmHg. This lower alveolar PO2 means a diminished diffusion gradient (from 89 in the alveoli to 40 mmHg in the blood), and combined with a shift down the hemoglobin saturation curve (more on this later), this means blood leaving the basal alveoli may not be completely saturated with oxygen.",True,overperfused,Figure 13.8,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
f4dbeadd-5730-41ed-9fbe-7bef557b245f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"Down at the base, however, V/Q is low because of the high perfusion and relatively low ventilation. Consequently the PO2 in basal alveoli tend toward venous values, shown in figure 13.8 as 89 mmHg. This lower alveolar PO2 means a diminished diffusion gradient (from 89 in the alveoli to 40 mmHg in the blood), and combined with a shift down the hemoglobin saturation curve (more on this later), this means blood leaving the basal alveoli may not be completely saturated with oxygen.",True,overperfused,Figure 13.8,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
cc40646b-880c-45d8-b6b3-f871e00f52bb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"When the blood from the apex and base mix on their journey back to the left heart, the outcome is that the combined oxygen saturation is less than 100 percent, about 97 percent. It is worth making perhaps an obvious but critical point here. The blood from the apex is exposed to a substantially higher PO2 and becomes 100 percent saturated (i.e., it cannot take on any more O2 as it is at its full oxygen carrying capacity). There is no way that it can pick up extra to compensate for the blood coming from basal alveoli, which are not at capacity.",True,overperfused,,,,
640a915e-d9b3-432a-a1da-e6e3361d4808,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"The same is not true for CO2 though. Because of its high solubility, CO2 transport does not rely on a transporter protein like hemoglobin; the transfer of CO2 is really dependent on the diffusion gradient present. So at the apex the lower alveolar PCO2 (slightly less than 30 mmHg looking at our V/Q line) generates a larger diffusion gradient with venous blood, and more CO2 is transferred out the blood, meaning that it can compensate for the low diffusion gradient (perhaps only a few mmHg) that occurs between the alveoli and blood at the lung’s base.",True,overperfused,,,,
3aeac80e-d966-43bc-aa51-84f9ad55e318,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,As a study exercise it may be worthwhile for you to go back to the ventilation–perfusion line and calculate the diffusion gradients for oxygen and carbon dioxide between the alveoli and venous blood at different heights in the lung. I urge you to come to grips with this concept as it is highly pertinent to respiratory disease and can explain clinical-related changes in blood gases.,True,overperfused,,,,
763cc107-131b-4180-9eb7-abc2a42d3dfc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"The take-home message, however, is that even the normal lung is not perfect and has an average V/Q ratio of 0.8, rather than the ideal of 1, and this slight matching of ventilation and perfusion contributes to the arterial saturation being slightly less than 100 percent, but has little effect on arterial CO2. If respiratory disease increases the mismatch, this effect on oxygen saturation can become more pronounced, but the lung has a defense mechanism for this.",True,overperfused,,,,
176c9a3b-64cb-4f98-93e8-641907794de4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,Correcting V/Q Mismatches,False,Correcting V/Q Mismatches,,,,
5ba36db2-9526-4010-9983-6e6b3bd379b3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"In an attempt to maintain V/Q close to 1 and prevent V/Q mismatching, the pulmonary vasculature has an unusual response to hypoxia. While the systemic vasculature responds to local hypoxia with a vasodilation to bring more blood to the area, the pulmonary vasculature constricts in the presence of low oxygen to shunt blood away from hypoxic regions.",True,Correcting V/Q Mismatches,,,,
612b5220-0f54-4d23-a7ec-030ebc728c48,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"Let us look at a common scenario that might occur in a patient with chronic bronchitis. Figure 13.9 represents two regions of the lung. One region becomes blocked by a mucus plug, and ventilation to that region goes to zero.",True,Correcting V/Q Mismatches,Figure 13.9,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.9.png,Figure 13.9: Correcting V/Q mismatches.
612b5220-0f54-4d23-a7ec-030ebc728c48,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"Let us look at a common scenario that might occur in a patient with chronic bronchitis. Figure 13.9 represents two regions of the lung. One region becomes blocked by a mucus plug, and ventilation to that region goes to zero.",True,Correcting V/Q Mismatches,Figure 13.9,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.9.png,Figure 13.9: Correcting V/Q mismatches.
612b5220-0f54-4d23-a7ec-030ebc728c48,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"Let us look at a common scenario that might occur in a patient with chronic bronchitis. Figure 13.9 represents two regions of the lung. One region becomes blocked by a mucus plug, and ventilation to that region goes to zero.",True,Correcting V/Q Mismatches,Figure 13.9,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.9.png,Figure 13.9: Correcting V/Q mismatches.
4e716cd7-2a3d-4ff9-8152-0575cceb89ae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"The alveolar partial pressures will rapidly equilibrate to venous pressures, and desaturated blood goes back to the left heart from this region while the local region around this area becomes mildly hypoxic. The pulmonary vasculature responds to the hypoxia by vasoconstricting, reducing the perfusion to the unventilated region and helping to rematch the V/Q ratio in this region (i.e., low ventilation is matched with low perfusion). In common sense terms, there is no point sending pulmonary blood to an unventilated region, so the hypoxia-driven vasoconstriction prevents this from happening.",True,Correcting V/Q Mismatches,,,,
b29ea3de-4ed5-4b0f-a6bd-6dcf00852fdf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"The distensibility of the pulmonary vasculature means that the blood is shunted to unconstricted vessels (i.e., those supplying ventilated regions). Thus the lung has its own inherent mechanism to optimize V/Q and promote the most effective gas exchange possible.",True,Correcting V/Q Mismatches,,,,
4fde109e-5932-4163-af9e-a45beb0d6c49,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"The unusual response of the pulmonary vasculature is demonstrated in figure 13.10, showing how as alveolar PO2 falls (as occurs with a decline in alveolar ventilation) then blood flow falls—and likewise, the more oxygen in the alveolus, the more pulmonary perfusion it receives.",True,Correcting V/Q Mismatches,Figure 13.10,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.10.png,Figure 13.10: Response of pulmonary vasculature to hypoxia.
4fde109e-5932-4163-af9e-a45beb0d6c49,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"The unusual response of the pulmonary vasculature is demonstrated in figure 13.10, showing how as alveolar PO2 falls (as occurs with a decline in alveolar ventilation) then blood flow falls—and likewise, the more oxygen in the alveolus, the more pulmonary perfusion it receives.",True,Correcting V/Q Mismatches,Figure 13.10,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.10.png,Figure 13.10: Response of pulmonary vasculature to hypoxia.
4fde109e-5932-4163-af9e-a45beb0d6c49,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"The unusual response of the pulmonary vasculature is demonstrated in figure 13.10, showing how as alveolar PO2 falls (as occurs with a decline in alveolar ventilation) then blood flow falls—and likewise, the more oxygen in the alveolus, the more pulmonary perfusion it receives.",True,Correcting V/Q Mismatches,Figure 13.10,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.10.png,Figure 13.10: Response of pulmonary vasculature to hypoxia.
3be15f81-0c88-4ce4-83c2-19c9b755f4da,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"This effect is driven by a hypoxia-sensitive potassium channel found on the albeit sparse smooth muscle of the pulmonary arterioles. This channel is normally open and allows the exit of potassium, which in turn keeps the inside of the muscle cell polarized. When exposed to hypoxia the channel closes, and the outward potassium current stops, allowing the muscle cell’s membrane potential to rise and consequently depolarize to cause a contraction.",True,Correcting V/Q Mismatches,,,,
a3a54ece-31f1-40de-ac3e-9f1e54b27e27,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"So to summarize, the ratio of ventilation and perfusion changes across the lung, and this affects the alveolar and consequently arterial gas tensions from those regions. While the lung does not reach the ideal V/Q ratio, it is capable of shunting pulmonary blood flow away from unventilated areas to optimize gas exchange.",True,Correcting V/Q Mismatches,,,,
a1a1c8f8-60a7-445a-bee5-818669d5e04e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,Text,False,Text,,,,
5c453dd1-8651-4b53-8e6d-dd9c68c742c0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"Levitsky, Michael G. “Chapter 5: Ventilation–Perfusion Relationships.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
1352227c-322f-4845-b526-ab6f8e3d927e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"West, John B. “Chapter 5: Ventilation–Perfusion Relationships—How Matching of Gas and Blood Determines Gas Exchange.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
736d22e3-bd4e-497c-bf9a-992a06cc406d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of V/Q,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-2,"Widdicombe, John G., and Andrew S. Davis. “Chapter 7.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
5c280b22-bbe2-46b5-b5a3-35a58410d99b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"Let us start with a description of the ideal situation, where ventilation to alveoli is matched with the perfusion, then we will see how the lung does not quite achieve this.",True,Text,,,,
33f1592d-8d17-4855-be4f-1827d77b6537,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"This is what we would expect if the lung were perfect, with uniform distribution of ventilation and perfusion to all regions and a V/Q of 1 in all regions.",True,Text,,,,
c62683ab-3826-4177-85d4-4d258d92eb93,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"The lung is not a perfect organ, however, and ventilation and perfusion are not equally distributed, and the lung as a whole only achieves an average V/Q of 0.8, which is close to our ideal of 1, but not quite there. Consequently, by the time the blood has passed the alveoli and regrouped in the pulmonary veins, the PO2 of the blood is less than alveolar. This alveolar–arterial PO2 difference is caused by the less-than-perfect matching of V and Q across the lung; but it is not all the lung’s fault, as venous blood that has been through the bronchial and a small section of the coronary circulation (and therefore is deoxygenated) is mixed into the vessels returning to the left heart, which brings down arterial saturation as well. The mixing-in of bronchial and coronary circulations and the less-than-ideal V/Q in the lung as a whole is the reason why your saturation monitors do not read 100 percent, but normal oxygen saturation is considered as 96–98 percent.",True,Text,,,,
a93213fc-56b3-4520-bc0a-e67a8517eabb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,Partial Pressures and V/Q,False,Partial Pressures and V/Q,,,,
3f1dc7c5-1b53-46cd-adc0-ad9ebb0f6c52,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"When V and Q are matched (V/Q = 1): Atmospheric PO2 is diluted as it descends the airways to give an alveolar PO2 of 100 mmHg, and alveolar PCO2 is 40 mmHg. The blood returning from the tissue has a diminished PO2 of 40 mmHg and a raised PCO2 of 45 mmHg. As this blood passes the alveolus, oxygen moves into the bloodstream down its pressure gradient and CO2 moves into the alveolus down its pressure gradient. As ventilation and perfusion are matched then equilibrium is reached and the blood leaves with arterial gas tensions that are the same as alveolar tensions (figure 13.2).",True,Partial Pressures and V/Q,Figure 13.2,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.2-scaled.jpg,Figure 13.2: Partial pressures when V/Q = 1.
3f1dc7c5-1b53-46cd-adc0-ad9ebb0f6c52,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"When V and Q are matched (V/Q = 1): Atmospheric PO2 is diluted as it descends the airways to give an alveolar PO2 of 100 mmHg, and alveolar PCO2 is 40 mmHg. The blood returning from the tissue has a diminished PO2 of 40 mmHg and a raised PCO2 of 45 mmHg. As this blood passes the alveolus, oxygen moves into the bloodstream down its pressure gradient and CO2 moves into the alveolus down its pressure gradient. As ventilation and perfusion are matched then equilibrium is reached and the blood leaves with arterial gas tensions that are the same as alveolar tensions (figure 13.2).",True,Partial Pressures and V/Q,Figure 13.2,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.2-scaled.jpg,Figure 13.2: Partial pressures when V/Q = 1.
3f1dc7c5-1b53-46cd-adc0-ad9ebb0f6c52,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"When V and Q are matched (V/Q = 1): Atmospheric PO2 is diluted as it descends the airways to give an alveolar PO2 of 100 mmHg, and alveolar PCO2 is 40 mmHg. The blood returning from the tissue has a diminished PO2 of 40 mmHg and a raised PCO2 of 45 mmHg. As this blood passes the alveolus, oxygen moves into the bloodstream down its pressure gradient and CO2 moves into the alveolus down its pressure gradient. As ventilation and perfusion are matched then equilibrium is reached and the blood leaves with arterial gas tensions that are the same as alveolar tensions (figure 13.2).",True,Partial Pressures and V/Q,Figure 13.2,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.2-scaled.jpg,Figure 13.2: Partial pressures when V/Q = 1.
5d472aa0-c2b2-4eb2-a1b4-64f3d1965c7e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"When V = 0: Now let us look at another and extreme situation, where ventilation (V) is zero so our V/Q is zero (zero divided by anything is zero).",True,Partial Pressures and V/Q,,,,
bdb72226-ec05-4496-b97e-15555d6e1c40,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"This situation is clinically possible as airways can collapse or become blocked with a mucus plug. Without any ventilation the gas tensions inside the alveolus rapidly equilibrate with the returning venous blood, so alveolar gas tensions end up as a PO2 of 40 mmHg and a PCO2 of 45 mmHg. The venous gas tensions, never having been exposed to a ventilated alveolus, now circulate into the arterial system, and arterial PO2 becomes 40 mmHg and PCO2 becomes 45 mmHg there as well (figure 13.3).",True,Partial Pressures and V/Q,Figure 13.3,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.3.png,Figure 13.3: Partial pressures when V/Q = 0.
bdb72226-ec05-4496-b97e-15555d6e1c40,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"This situation is clinically possible as airways can collapse or become blocked with a mucus plug. Without any ventilation the gas tensions inside the alveolus rapidly equilibrate with the returning venous blood, so alveolar gas tensions end up as a PO2 of 40 mmHg and a PCO2 of 45 mmHg. The venous gas tensions, never having been exposed to a ventilated alveolus, now circulate into the arterial system, and arterial PO2 becomes 40 mmHg and PCO2 becomes 45 mmHg there as well (figure 13.3).",True,Partial Pressures and V/Q,Figure 13.3,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.3.png,Figure 13.3: Partial pressures when V/Q = 0.
bdb72226-ec05-4496-b97e-15555d6e1c40,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"This situation is clinically possible as airways can collapse or become blocked with a mucus plug. Without any ventilation the gas tensions inside the alveolus rapidly equilibrate with the returning venous blood, so alveolar gas tensions end up as a PO2 of 40 mmHg and a PCO2 of 45 mmHg. The venous gas tensions, never having been exposed to a ventilated alveolus, now circulate into the arterial system, and arterial PO2 becomes 40 mmHg and PCO2 becomes 45 mmHg there as well (figure 13.3).",True,Partial Pressures and V/Q,Figure 13.3,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.3.png,Figure 13.3: Partial pressures when V/Q = 0.
e532f18a-ba5e-4f35-8156-ac00b3e04e7e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"When Q = 0: Now let us go to the other extreme, where perfusion is zero and ventilation is normal (V/Q goes to infinity). Again, this can occur in reality should a pulmonary vessel become blocked by an embolus. In this scenario V/Q becomes infinity—anything divided by zero is infinity. With no perfusion, no gas exchange occurs in this alveolus, and as it is still being ventilated then the alveolar gas tensions equilibrate with the atmosphere (figure 13.4).",True,Partial Pressures and V/Q,Figure 13.4,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.4.png,Figure 13.4: Partial pressures when V/Q is infinite.
e532f18a-ba5e-4f35-8156-ac00b3e04e7e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"When Q = 0: Now let us go to the other extreme, where perfusion is zero and ventilation is normal (V/Q goes to infinity). Again, this can occur in reality should a pulmonary vessel become blocked by an embolus. In this scenario V/Q becomes infinity—anything divided by zero is infinity. With no perfusion, no gas exchange occurs in this alveolus, and as it is still being ventilated then the alveolar gas tensions equilibrate with the atmosphere (figure 13.4).",True,Partial Pressures and V/Q,Figure 13.4,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.4.png,Figure 13.4: Partial pressures when V/Q is infinite.
e532f18a-ba5e-4f35-8156-ac00b3e04e7e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"When Q = 0: Now let us go to the other extreme, where perfusion is zero and ventilation is normal (V/Q goes to infinity). Again, this can occur in reality should a pulmonary vessel become blocked by an embolus. In this scenario V/Q becomes infinity—anything divided by zero is infinity. With no perfusion, no gas exchange occurs in this alveolus, and as it is still being ventilated then the alveolar gas tensions equilibrate with the atmosphere (figure 13.4).",True,Partial Pressures and V/Q,Figure 13.4,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.4.png,Figure 13.4: Partial pressures when V/Q is infinite.
42bd6b84-3b74-4fad-ba58-3d4827e63798,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"So going from these extremes of V/Q as zero, passing through the ideal of V/Q of 1 to a V/Q of infinity, we get a range of alveolar gas tensions going from venous gas tensions when V/Q is zero to atmospheric gas tensions when V/Q is infinite.",True,Partial Pressures and V/Q,,,,
1170216f-9482-499d-bcd6-dcf2d081b697,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"This range of alveolar gas tensions is represented by the ventilation–perfusion line (figure 13.5). This graph takes a minute to come to grips with, so let us break it down. The axes of the graph show alveolar PO2 on the X and alveolar PCO2 on the Y. The plot shows the range of V/Q ratios we have just discussed, ranging from zero when there is perfusion but no ventilation, to infinity when there is ventilation but no perfusion. Looking at figure 13.5 more carefully will confirm our numbers. When ventilation and perfusion are present and V/Q is 1, then our alveolar PO2 is 100 mmHg, and the alveolar PCO2 is 40 mmHg—just as we have seen.",True,Partial Pressures and V/Q,Figure 13.5,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.5.png,Figure 13.5: Ventilation–perfusion line.
1170216f-9482-499d-bcd6-dcf2d081b697,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"This range of alveolar gas tensions is represented by the ventilation–perfusion line (figure 13.5). This graph takes a minute to come to grips with, so let us break it down. The axes of the graph show alveolar PO2 on the X and alveolar PCO2 on the Y. The plot shows the range of V/Q ratios we have just discussed, ranging from zero when there is perfusion but no ventilation, to infinity when there is ventilation but no perfusion. Looking at figure 13.5 more carefully will confirm our numbers. When ventilation and perfusion are present and V/Q is 1, then our alveolar PO2 is 100 mmHg, and the alveolar PCO2 is 40 mmHg—just as we have seen.",True,Partial Pressures and V/Q,Figure 13.5,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.5.png,Figure 13.5: Ventilation–perfusion line.
1170216f-9482-499d-bcd6-dcf2d081b697,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"This range of alveolar gas tensions is represented by the ventilation–perfusion line (figure 13.5). This graph takes a minute to come to grips with, so let us break it down. The axes of the graph show alveolar PO2 on the X and alveolar PCO2 on the Y. The plot shows the range of V/Q ratios we have just discussed, ranging from zero when there is perfusion but no ventilation, to infinity when there is ventilation but no perfusion. Looking at figure 13.5 more carefully will confirm our numbers. When ventilation and perfusion are present and V/Q is 1, then our alveolar PO2 is 100 mmHg, and the alveolar PCO2 is 40 mmHg—just as we have seen.",True,Partial Pressures and V/Q,Figure 13.5,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.5.png,Figure 13.5: Ventilation–perfusion line.
d113706c-fa40-4266-b922-ceede1721b41,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"If we stop ventilation and go to a V/Q of zero, we again see that the alveolar gas tensions become equal to venous values, with alveolar PO2 at 40 mmHg and PCO2 at 45 mmHg.",True,Partial Pressures and V/Q,,,,
91e8c626-cac0-4df3-a6fd-cc6c12b62c2d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"And finally, when we stop perfusion and V/Q becomes infinite, then alveolar PO2 becomes 150 mmHg and PCO2 becomes zero (i.e., equilibrates with the atmosphere).",True,Partial Pressures and V/Q,,,,
2f431234-f2e7-433b-b8fc-fbaf6308f5cf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,Summary,False,Summary,,,,
5a83599c-489e-47b3-9cd5-897b944ce3a3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"In summary, the ventilation–perfusion line show the effect of changing V/Q on alveolar gases. Reduce V/Q toward zero and the alveolar gas tensions tend toward venous gas tensions. Increase V/Q toward infinity and the alveolar gas tensions get closer to atmospheric partial pressures.",True,Summary,,,,
c4ee94d9-f44c-4c71-98b6-7a076fe70c2d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"The importance of understanding this becomes apparent when we see that V/Q changes across the structure of the lung, and if V/Q changes, then alveolar partial pressures change to.",True,Summary,,,,
1676ee36-ed2d-4335-8c9b-28211a03bcde,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,Let us look at the distribution of V/Q across the lung and why it changes from apex to base.,True,Summary,,,,
33016e3a-9bfe-46f0-97b4-e10c16090624,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,Distribution of V/Q,False,Distribution of V/Q,,,,
93de1bca-fcf9-46bd-9d6d-24bef5327ad4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"As you should understand, ventilation increases down the lung so is greatest at the base, and perfusion follows the same pattern—all due to the effects of gravity. But the increase in ventilation down the lung structure is not equal to the increase in perfusion, as can be seen in figure 13.6. You can see here that perfusion is higher than ventilation at the base; it falls off much more rapidly as the lung is ascended, so it ends up being lower than ventilation at the apex.",True,Distribution of V/Q,Figure 13.6,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
93de1bca-fcf9-46bd-9d6d-24bef5327ad4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"As you should understand, ventilation increases down the lung so is greatest at the base, and perfusion follows the same pattern—all due to the effects of gravity. But the increase in ventilation down the lung structure is not equal to the increase in perfusion, as can be seen in figure 13.6. You can see here that perfusion is higher than ventilation at the base; it falls off much more rapidly as the lung is ascended, so it ends up being lower than ventilation at the apex.",True,Distribution of V/Q,Figure 13.6,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
93de1bca-fcf9-46bd-9d6d-24bef5327ad4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"As you should understand, ventilation increases down the lung so is greatest at the base, and perfusion follows the same pattern—all due to the effects of gravity. But the increase in ventilation down the lung structure is not equal to the increase in perfusion, as can be seen in figure 13.6. You can see here that perfusion is higher than ventilation at the base; it falls off much more rapidly as the lung is ascended, so it ends up being lower than ventilation at the apex.",True,Distribution of V/Q,Figure 13.6,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
d82851ee-8a8d-4b08-8faa-c56dc7765004,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"This means there is a range of ventilation–perfusion ratios up the height of the lung (figure 13.6, maroon plot). At the base perfusion is higher than ventilation, so V/Q is less than 1, while toward the apex V/Q rises and becomes greater than 1. At about the level of the third rib, V/Q is perfect (yay!) as ventilation and perfusion are matched, seen here at the points the lines cross. This range of V/Q results in the previously mentioned whole lung average of 0.8.",True,Distribution of V/Q,Figure 13.6,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
d82851ee-8a8d-4b08-8faa-c56dc7765004,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"This means there is a range of ventilation–perfusion ratios up the height of the lung (figure 13.6, maroon plot). At the base perfusion is higher than ventilation, so V/Q is less than 1, while toward the apex V/Q rises and becomes greater than 1. At about the level of the third rib, V/Q is perfect (yay!) as ventilation and perfusion are matched, seen here at the points the lines cross. This range of V/Q results in the previously mentioned whole lung average of 0.8.",True,Distribution of V/Q,Figure 13.6,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
d82851ee-8a8d-4b08-8faa-c56dc7765004,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"This means there is a range of ventilation–perfusion ratios up the height of the lung (figure 13.6, maroon plot). At the base perfusion is higher than ventilation, so V/Q is less than 1, while toward the apex V/Q rises and becomes greater than 1. At about the level of the third rib, V/Q is perfect (yay!) as ventilation and perfusion are matched, seen here at the points the lines cross. This range of V/Q results in the previously mentioned whole lung average of 0.8.",True,Distribution of V/Q,Figure 13.6,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
026ca069-447f-41ba-8ab4-3fc62447c903,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,yay,False,yay,,,,
a009a3f9-5d01-4809-bed3-f83da5f48fca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"As you should appreciate from understanding the ventilation–perfusion line, this range of V/Q across the lung results in a range of alveolar gas partial pressures across the lung. The apical alveoli, being relatively overventilated (or underperfused, whichever way you would like to think about it), have a high V/Q and consequently have partial pressures closer to atmospheric partial pressures. On the other extreme, the basal alveoli are relatively underventilated (or overperfused, your choice) and so have a low V/Q, tending toward zero; thus their partial pressures are closer to venous values (figure 13.7).",True,yay,Figure 13.7,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.7.png,Figure 13.7: V/Q and alveolar gas distribution.
a009a3f9-5d01-4809-bed3-f83da5f48fca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"As you should appreciate from understanding the ventilation–perfusion line, this range of V/Q across the lung results in a range of alveolar gas partial pressures across the lung. The apical alveoli, being relatively overventilated (or underperfused, whichever way you would like to think about it), have a high V/Q and consequently have partial pressures closer to atmospheric partial pressures. On the other extreme, the basal alveoli are relatively underventilated (or overperfused, your choice) and so have a low V/Q, tending toward zero; thus their partial pressures are closer to venous values (figure 13.7).",True,yay,Figure 13.7,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.7.png,Figure 13.7: V/Q and alveolar gas distribution.
a009a3f9-5d01-4809-bed3-f83da5f48fca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"As you should appreciate from understanding the ventilation–perfusion line, this range of V/Q across the lung results in a range of alveolar gas partial pressures across the lung. The apical alveoli, being relatively overventilated (or underperfused, whichever way you would like to think about it), have a high V/Q and consequently have partial pressures closer to atmospheric partial pressures. On the other extreme, the basal alveoli are relatively underventilated (or overperfused, your choice) and so have a low V/Q, tending toward zero; thus their partial pressures are closer to venous values (figure 13.7).",True,yay,Figure 13.7,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.7.png,Figure 13.7: V/Q and alveolar gas distribution.
e2b1b912-2cbc-484c-ad37-64fd1d703560,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,overventilated,False,overventilated,,,,
0afbd6fe-8907-43c6-9197-f877555ba2fe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,overperfused,False,overperfused,,,,
6f56a143-905b-4dc9-9216-6d21cd3c93a5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"In between these two extremes is a progressive range, so what we see is that alveolar PO2 declines down the lung while alveolar PCO2 rises. As you might imagine, having a range of alveolar gas tensions down the lung has ramifications for gas exchange and particularly for oxygen saturation. This inequality in V/Q resulting in differences in alveolar PO2 is substantial enough to suppress arterial oxygen saturation—and contribute to your oxygen saturation meter never reading 100 percent. Let us see why.",True,overperfused,,,,
9dd1de21-7808-48ed-bd97-7c5fb6cad021,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"The difference in alveolar PO2 from apex to base is as high as 40 mmHg, as is reflected in this figure. The apical alveoli have a high PO2 (shown in figure 13.8 as 132 mmHg), primarily due to their poor perfusion and relatively high ventilation and thus high V/Q. This produces a high diffusion gradient from 132 mmHg in the apical alveoli, to 40 mmHg in the apical blood. Consequently, what blood does go to the apex becomes fully saturated before it heads back toward the left heart.",True,overperfused,Figure 13.8,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
9dd1de21-7808-48ed-bd97-7c5fb6cad021,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"The difference in alveolar PO2 from apex to base is as high as 40 mmHg, as is reflected in this figure. The apical alveoli have a high PO2 (shown in figure 13.8 as 132 mmHg), primarily due to their poor perfusion and relatively high ventilation and thus high V/Q. This produces a high diffusion gradient from 132 mmHg in the apical alveoli, to 40 mmHg in the apical blood. Consequently, what blood does go to the apex becomes fully saturated before it heads back toward the left heart.",True,overperfused,Figure 13.8,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
9dd1de21-7808-48ed-bd97-7c5fb6cad021,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"The difference in alveolar PO2 from apex to base is as high as 40 mmHg, as is reflected in this figure. The apical alveoli have a high PO2 (shown in figure 13.8 as 132 mmHg), primarily due to their poor perfusion and relatively high ventilation and thus high V/Q. This produces a high diffusion gradient from 132 mmHg in the apical alveoli, to 40 mmHg in the apical blood. Consequently, what blood does go to the apex becomes fully saturated before it heads back toward the left heart.",True,overperfused,Figure 13.8,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
ae556d42-532a-44ab-ab2f-d1ee6ae89c3e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"Down at the base, however, V/Q is low because of the high perfusion and relatively low ventilation. Consequently the PO2 in basal alveoli tend toward venous values, shown in figure 13.8 as 89 mmHg. This lower alveolar PO2 means a diminished diffusion gradient (from 89 in the alveoli to 40 mmHg in the blood), and combined with a shift down the hemoglobin saturation curve (more on this later), this means blood leaving the basal alveoli may not be completely saturated with oxygen.",True,overperfused,Figure 13.8,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
ae556d42-532a-44ab-ab2f-d1ee6ae89c3e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"Down at the base, however, V/Q is low because of the high perfusion and relatively low ventilation. Consequently the PO2 in basal alveoli tend toward venous values, shown in figure 13.8 as 89 mmHg. This lower alveolar PO2 means a diminished diffusion gradient (from 89 in the alveoli to 40 mmHg in the blood), and combined with a shift down the hemoglobin saturation curve (more on this later), this means blood leaving the basal alveoli may not be completely saturated with oxygen.",True,overperfused,Figure 13.8,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
ae556d42-532a-44ab-ab2f-d1ee6ae89c3e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"Down at the base, however, V/Q is low because of the high perfusion and relatively low ventilation. Consequently the PO2 in basal alveoli tend toward venous values, shown in figure 13.8 as 89 mmHg. This lower alveolar PO2 means a diminished diffusion gradient (from 89 in the alveoli to 40 mmHg in the blood), and combined with a shift down the hemoglobin saturation curve (more on this later), this means blood leaving the basal alveoli may not be completely saturated with oxygen.",True,overperfused,Figure 13.8,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
351e627e-cba1-478a-811d-737567f05112,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"When the blood from the apex and base mix on their journey back to the left heart, the outcome is that the combined oxygen saturation is less than 100 percent, about 97 percent. It is worth making perhaps an obvious but critical point here. The blood from the apex is exposed to a substantially higher PO2 and becomes 100 percent saturated (i.e., it cannot take on any more O2 as it is at its full oxygen carrying capacity). There is no way that it can pick up extra to compensate for the blood coming from basal alveoli, which are not at capacity.",True,overperfused,,,,
5be5b5c5-457e-4e84-8613-fe3faad97fcb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"The same is not true for CO2 though. Because of its high solubility, CO2 transport does not rely on a transporter protein like hemoglobin; the transfer of CO2 is really dependent on the diffusion gradient present. So at the apex the lower alveolar PCO2 (slightly less than 30 mmHg looking at our V/Q line) generates a larger diffusion gradient with venous blood, and more CO2 is transferred out the blood, meaning that it can compensate for the low diffusion gradient (perhaps only a few mmHg) that occurs between the alveoli and blood at the lung’s base.",True,overperfused,,,,
dc1fdc94-e3f3-43db-b999-11da3011b60e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,As a study exercise it may be worthwhile for you to go back to the ventilation–perfusion line and calculate the diffusion gradients for oxygen and carbon dioxide between the alveoli and venous blood at different heights in the lung. I urge you to come to grips with this concept as it is highly pertinent to respiratory disease and can explain clinical-related changes in blood gases.,True,overperfused,,,,
2973d3d8-1a98-47e0-916c-f587a76e59e3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"The take-home message, however, is that even the normal lung is not perfect and has an average V/Q ratio of 0.8, rather than the ideal of 1, and this slight matching of ventilation and perfusion contributes to the arterial saturation being slightly less than 100 percent, but has little effect on arterial CO2. If respiratory disease increases the mismatch, this effect on oxygen saturation can become more pronounced, but the lung has a defense mechanism for this.",True,overperfused,,,,
e12741f8-6b80-46a1-bd12-22376f0a1ef8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,Correcting V/Q Mismatches,False,Correcting V/Q Mismatches,,,,
3fc450ab-201a-473b-9a5d-a60637eeaf03,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"In an attempt to maintain V/Q close to 1 and prevent V/Q mismatching, the pulmonary vasculature has an unusual response to hypoxia. While the systemic vasculature responds to local hypoxia with a vasodilation to bring more blood to the area, the pulmonary vasculature constricts in the presence of low oxygen to shunt blood away from hypoxic regions.",True,Correcting V/Q Mismatches,,,,
669069be-d5d2-45f5-a336-0d7c66fb2903,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"Let us look at a common scenario that might occur in a patient with chronic bronchitis. Figure 13.9 represents two regions of the lung. One region becomes blocked by a mucus plug, and ventilation to that region goes to zero.",True,Correcting V/Q Mismatches,Figure 13.9,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.9.png,Figure 13.9: Correcting V/Q mismatches.
669069be-d5d2-45f5-a336-0d7c66fb2903,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"Let us look at a common scenario that might occur in a patient with chronic bronchitis. Figure 13.9 represents two regions of the lung. One region becomes blocked by a mucus plug, and ventilation to that region goes to zero.",True,Correcting V/Q Mismatches,Figure 13.9,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.9.png,Figure 13.9: Correcting V/Q mismatches.
669069be-d5d2-45f5-a336-0d7c66fb2903,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"Let us look at a common scenario that might occur in a patient with chronic bronchitis. Figure 13.9 represents two regions of the lung. One region becomes blocked by a mucus plug, and ventilation to that region goes to zero.",True,Correcting V/Q Mismatches,Figure 13.9,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.9.png,Figure 13.9: Correcting V/Q mismatches.
6b6c3efd-f977-46c6-91a7-1bb4e376b6f4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"The alveolar partial pressures will rapidly equilibrate to venous pressures, and desaturated blood goes back to the left heart from this region while the local region around this area becomes mildly hypoxic. The pulmonary vasculature responds to the hypoxia by vasoconstricting, reducing the perfusion to the unventilated region and helping to rematch the V/Q ratio in this region (i.e., low ventilation is matched with low perfusion). In common sense terms, there is no point sending pulmonary blood to an unventilated region, so the hypoxia-driven vasoconstriction prevents this from happening.",True,Correcting V/Q Mismatches,,,,
edab1de1-0a7e-471a-a799-35bd2ffca95b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"The distensibility of the pulmonary vasculature means that the blood is shunted to unconstricted vessels (i.e., those supplying ventilated regions). Thus the lung has its own inherent mechanism to optimize V/Q and promote the most effective gas exchange possible.",True,Correcting V/Q Mismatches,,,,
b5ecc9a6-3aa7-40de-8f3f-5fa2db658b06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"The unusual response of the pulmonary vasculature is demonstrated in figure 13.10, showing how as alveolar PO2 falls (as occurs with a decline in alveolar ventilation) then blood flow falls—and likewise, the more oxygen in the alveolus, the more pulmonary perfusion it receives.",True,Correcting V/Q Mismatches,Figure 13.10,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.10.png,Figure 13.10: Response of pulmonary vasculature to hypoxia.
b5ecc9a6-3aa7-40de-8f3f-5fa2db658b06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"The unusual response of the pulmonary vasculature is demonstrated in figure 13.10, showing how as alveolar PO2 falls (as occurs with a decline in alveolar ventilation) then blood flow falls—and likewise, the more oxygen in the alveolus, the more pulmonary perfusion it receives.",True,Correcting V/Q Mismatches,Figure 13.10,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.10.png,Figure 13.10: Response of pulmonary vasculature to hypoxia.
b5ecc9a6-3aa7-40de-8f3f-5fa2db658b06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"The unusual response of the pulmonary vasculature is demonstrated in figure 13.10, showing how as alveolar PO2 falls (as occurs with a decline in alveolar ventilation) then blood flow falls—and likewise, the more oxygen in the alveolus, the more pulmonary perfusion it receives.",True,Correcting V/Q Mismatches,Figure 13.10,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.10.png,Figure 13.10: Response of pulmonary vasculature to hypoxia.
6d7c4a75-0061-409a-b302-398d43925bec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"This effect is driven by a hypoxia-sensitive potassium channel found on the albeit sparse smooth muscle of the pulmonary arterioles. This channel is normally open and allows the exit of potassium, which in turn keeps the inside of the muscle cell polarized. When exposed to hypoxia the channel closes, and the outward potassium current stops, allowing the muscle cell’s membrane potential to rise and consequently depolarize to cause a contraction.",True,Correcting V/Q Mismatches,,,,
804c6df1-f651-46af-b8cb-39f0afc7afb9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"So to summarize, the ratio of ventilation and perfusion changes across the lung, and this affects the alveolar and consequently arterial gas tensions from those regions. While the lung does not reach the ideal V/Q ratio, it is capable of shunting pulmonary blood flow away from unventilated areas to optimize gas exchange.",True,Correcting V/Q Mismatches,,,,
d4edbe7d-1f54-4f5a-a37c-3e998da3c5b9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,Text,False,Text,,,,
7152b74f-4caf-4a6e-afc0-ab5acedce3f0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"Levitsky, Michael G. “Chapter 5: Ventilation–Perfusion Relationships.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
805686d7-4cb6-49c2-ad10-97ee8e85fea2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"West, John B. “Chapter 5: Ventilation–Perfusion Relationships—How Matching of Gas and Blood Determines Gas Exchange.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
da9e9548-498e-4dbf-afca-bb72882cfc75,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/#chapter-51-section-1,"Widdicombe, John G., and Andrew S. Davis. “Chapter 7.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
f6823036-b28b-4ca8-b40c-5e4b26e2f56d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"Let us start with a description of the ideal situation, where ventilation to alveoli is matched with the perfusion, then we will see how the lung does not quite achieve this.",True,Text,,,,
9c6c86f6-f0cd-461a-82fd-9e9630f8a665,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"This is what we would expect if the lung were perfect, with uniform distribution of ventilation and perfusion to all regions and a V/Q of 1 in all regions.",True,Text,,,,
5a0982c2-3786-4e4f-8855-96ea012ca31a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"The lung is not a perfect organ, however, and ventilation and perfusion are not equally distributed, and the lung as a whole only achieves an average V/Q of 0.8, which is close to our ideal of 1, but not quite there. Consequently, by the time the blood has passed the alveoli and regrouped in the pulmonary veins, the PO2 of the blood is less than alveolar. This alveolar–arterial PO2 difference is caused by the less-than-perfect matching of V and Q across the lung; but it is not all the lung’s fault, as venous blood that has been through the bronchial and a small section of the coronary circulation (and therefore is deoxygenated) is mixed into the vessels returning to the left heart, which brings down arterial saturation as well. The mixing-in of bronchial and coronary circulations and the less-than-ideal V/Q in the lung as a whole is the reason why your saturation monitors do not read 100 percent, but normal oxygen saturation is considered as 96–98 percent.",True,Text,,,,
7e75dd40-5945-42cf-8af8-32b9bebfd127,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,Partial Pressures and V/Q,False,Partial Pressures and V/Q,,,,
23b6bb33-4e09-4c5b-8349-53288689b054,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"When V and Q are matched (V/Q = 1): Atmospheric PO2 is diluted as it descends the airways to give an alveolar PO2 of 100 mmHg, and alveolar PCO2 is 40 mmHg. The blood returning from the tissue has a diminished PO2 of 40 mmHg and a raised PCO2 of 45 mmHg. As this blood passes the alveolus, oxygen moves into the bloodstream down its pressure gradient and CO2 moves into the alveolus down its pressure gradient. As ventilation and perfusion are matched then equilibrium is reached and the blood leaves with arterial gas tensions that are the same as alveolar tensions (figure 13.2).",True,Partial Pressures and V/Q,Figure 13.2,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.2-scaled.jpg,Figure 13.2: Partial pressures when V/Q = 1.
23b6bb33-4e09-4c5b-8349-53288689b054,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"When V and Q are matched (V/Q = 1): Atmospheric PO2 is diluted as it descends the airways to give an alveolar PO2 of 100 mmHg, and alveolar PCO2 is 40 mmHg. The blood returning from the tissue has a diminished PO2 of 40 mmHg and a raised PCO2 of 45 mmHg. As this blood passes the alveolus, oxygen moves into the bloodstream down its pressure gradient and CO2 moves into the alveolus down its pressure gradient. As ventilation and perfusion are matched then equilibrium is reached and the blood leaves with arterial gas tensions that are the same as alveolar tensions (figure 13.2).",True,Partial Pressures and V/Q,Figure 13.2,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.2-scaled.jpg,Figure 13.2: Partial pressures when V/Q = 1.
23b6bb33-4e09-4c5b-8349-53288689b054,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"When V and Q are matched (V/Q = 1): Atmospheric PO2 is diluted as it descends the airways to give an alveolar PO2 of 100 mmHg, and alveolar PCO2 is 40 mmHg. The blood returning from the tissue has a diminished PO2 of 40 mmHg and a raised PCO2 of 45 mmHg. As this blood passes the alveolus, oxygen moves into the bloodstream down its pressure gradient and CO2 moves into the alveolus down its pressure gradient. As ventilation and perfusion are matched then equilibrium is reached and the blood leaves with arterial gas tensions that are the same as alveolar tensions (figure 13.2).",True,Partial Pressures and V/Q,Figure 13.2,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.2-scaled.jpg,Figure 13.2: Partial pressures when V/Q = 1.
59547109-d528-4f6f-aeaa-f805dde4e86f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"When V = 0: Now let us look at another and extreme situation, where ventilation (V) is zero so our V/Q is zero (zero divided by anything is zero).",True,Partial Pressures and V/Q,,,,
764f60ae-2ab8-4ff9-948d-67a9836857e3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"This situation is clinically possible as airways can collapse or become blocked with a mucus plug. Without any ventilation the gas tensions inside the alveolus rapidly equilibrate with the returning venous blood, so alveolar gas tensions end up as a PO2 of 40 mmHg and a PCO2 of 45 mmHg. The venous gas tensions, never having been exposed to a ventilated alveolus, now circulate into the arterial system, and arterial PO2 becomes 40 mmHg and PCO2 becomes 45 mmHg there as well (figure 13.3).",True,Partial Pressures and V/Q,Figure 13.3,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.3.png,Figure 13.3: Partial pressures when V/Q = 0.
764f60ae-2ab8-4ff9-948d-67a9836857e3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"This situation is clinically possible as airways can collapse or become blocked with a mucus plug. Without any ventilation the gas tensions inside the alveolus rapidly equilibrate with the returning venous blood, so alveolar gas tensions end up as a PO2 of 40 mmHg and a PCO2 of 45 mmHg. The venous gas tensions, never having been exposed to a ventilated alveolus, now circulate into the arterial system, and arterial PO2 becomes 40 mmHg and PCO2 becomes 45 mmHg there as well (figure 13.3).",True,Partial Pressures and V/Q,Figure 13.3,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.3.png,Figure 13.3: Partial pressures when V/Q = 0.
764f60ae-2ab8-4ff9-948d-67a9836857e3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"This situation is clinically possible as airways can collapse or become blocked with a mucus plug. Without any ventilation the gas tensions inside the alveolus rapidly equilibrate with the returning venous blood, so alveolar gas tensions end up as a PO2 of 40 mmHg and a PCO2 of 45 mmHg. The venous gas tensions, never having been exposed to a ventilated alveolus, now circulate into the arterial system, and arterial PO2 becomes 40 mmHg and PCO2 becomes 45 mmHg there as well (figure 13.3).",True,Partial Pressures and V/Q,Figure 13.3,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.3.png,Figure 13.3: Partial pressures when V/Q = 0.
16a1a000-b685-4615-9ba6-b5cb4556960b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"When Q = 0: Now let us go to the other extreme, where perfusion is zero and ventilation is normal (V/Q goes to infinity). Again, this can occur in reality should a pulmonary vessel become blocked by an embolus. In this scenario V/Q becomes infinity—anything divided by zero is infinity. With no perfusion, no gas exchange occurs in this alveolus, and as it is still being ventilated then the alveolar gas tensions equilibrate with the atmosphere (figure 13.4).",True,Partial Pressures and V/Q,Figure 13.4,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.4.png,Figure 13.4: Partial pressures when V/Q is infinite.
16a1a000-b685-4615-9ba6-b5cb4556960b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"When Q = 0: Now let us go to the other extreme, where perfusion is zero and ventilation is normal (V/Q goes to infinity). Again, this can occur in reality should a pulmonary vessel become blocked by an embolus. In this scenario V/Q becomes infinity—anything divided by zero is infinity. With no perfusion, no gas exchange occurs in this alveolus, and as it is still being ventilated then the alveolar gas tensions equilibrate with the atmosphere (figure 13.4).",True,Partial Pressures and V/Q,Figure 13.4,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.4.png,Figure 13.4: Partial pressures when V/Q is infinite.
16a1a000-b685-4615-9ba6-b5cb4556960b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"When Q = 0: Now let us go to the other extreme, where perfusion is zero and ventilation is normal (V/Q goes to infinity). Again, this can occur in reality should a pulmonary vessel become blocked by an embolus. In this scenario V/Q becomes infinity—anything divided by zero is infinity. With no perfusion, no gas exchange occurs in this alveolus, and as it is still being ventilated then the alveolar gas tensions equilibrate with the atmosphere (figure 13.4).",True,Partial Pressures and V/Q,Figure 13.4,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.4.png,Figure 13.4: Partial pressures when V/Q is infinite.
2de7b6bc-91d6-4b27-861a-04feeb96b486,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"So going from these extremes of V/Q as zero, passing through the ideal of V/Q of 1 to a V/Q of infinity, we get a range of alveolar gas tensions going from venous gas tensions when V/Q is zero to atmospheric gas tensions when V/Q is infinite.",True,Partial Pressures and V/Q,,,,
fa67750a-bf94-4749-82f8-098fc3e28d27,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"This range of alveolar gas tensions is represented by the ventilation–perfusion line (figure 13.5). This graph takes a minute to come to grips with, so let us break it down. The axes of the graph show alveolar PO2 on the X and alveolar PCO2 on the Y. The plot shows the range of V/Q ratios we have just discussed, ranging from zero when there is perfusion but no ventilation, to infinity when there is ventilation but no perfusion. Looking at figure 13.5 more carefully will confirm our numbers. When ventilation and perfusion are present and V/Q is 1, then our alveolar PO2 is 100 mmHg, and the alveolar PCO2 is 40 mmHg—just as we have seen.",True,Partial Pressures and V/Q,Figure 13.5,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.5.png,Figure 13.5: Ventilation–perfusion line.
fa67750a-bf94-4749-82f8-098fc3e28d27,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"This range of alveolar gas tensions is represented by the ventilation–perfusion line (figure 13.5). This graph takes a minute to come to grips with, so let us break it down. The axes of the graph show alveolar PO2 on the X and alveolar PCO2 on the Y. The plot shows the range of V/Q ratios we have just discussed, ranging from zero when there is perfusion but no ventilation, to infinity when there is ventilation but no perfusion. Looking at figure 13.5 more carefully will confirm our numbers. When ventilation and perfusion are present and V/Q is 1, then our alveolar PO2 is 100 mmHg, and the alveolar PCO2 is 40 mmHg—just as we have seen.",True,Partial Pressures and V/Q,Figure 13.5,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.5.png,Figure 13.5: Ventilation–perfusion line.
fa67750a-bf94-4749-82f8-098fc3e28d27,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"This range of alveolar gas tensions is represented by the ventilation–perfusion line (figure 13.5). This graph takes a minute to come to grips with, so let us break it down. The axes of the graph show alveolar PO2 on the X and alveolar PCO2 on the Y. The plot shows the range of V/Q ratios we have just discussed, ranging from zero when there is perfusion but no ventilation, to infinity when there is ventilation but no perfusion. Looking at figure 13.5 more carefully will confirm our numbers. When ventilation and perfusion are present and V/Q is 1, then our alveolar PO2 is 100 mmHg, and the alveolar PCO2 is 40 mmHg—just as we have seen.",True,Partial Pressures and V/Q,Figure 13.5,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.5.png,Figure 13.5: Ventilation–perfusion line.
cd3546e2-b535-43f6-9d35-63f21602ce14,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"If we stop ventilation and go to a V/Q of zero, we again see that the alveolar gas tensions become equal to venous values, with alveolar PO2 at 40 mmHg and PCO2 at 45 mmHg.",True,Partial Pressures and V/Q,,,,
9adb37b7-743f-4bc4-aad2-a1c1da125564,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"And finally, when we stop perfusion and V/Q becomes infinite, then alveolar PO2 becomes 150 mmHg and PCO2 becomes zero (i.e., equilibrates with the atmosphere).",True,Partial Pressures and V/Q,,,,
8247a6b4-86c4-4cfd-8262-afd8d7814744,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,Summary,False,Summary,,,,
c82f7f8e-b1b6-4835-963a-a730a3ef39c6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"In summary, the ventilation–perfusion line show the effect of changing V/Q on alveolar gases. Reduce V/Q toward zero and the alveolar gas tensions tend toward venous gas tensions. Increase V/Q toward infinity and the alveolar gas tensions get closer to atmospheric partial pressures.",True,Summary,,,,
b67e5df2-991e-4564-ba32-e8a65a1c993c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"The importance of understanding this becomes apparent when we see that V/Q changes across the structure of the lung, and if V/Q changes, then alveolar partial pressures change to.",True,Summary,,,,
ea8404c7-6dbc-45aa-a875-85c2316160d7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,Let us look at the distribution of V/Q across the lung and why it changes from apex to base.,True,Summary,,,,
6c46e7af-612c-4750-9ed2-b3cfdd3ff2c5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,Distribution of V/Q,False,Distribution of V/Q,,,,
aa27645e-d896-4680-8902-383d3b8bf327,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"As you should understand, ventilation increases down the lung so is greatest at the base, and perfusion follows the same pattern—all due to the effects of gravity. But the increase in ventilation down the lung structure is not equal to the increase in perfusion, as can be seen in figure 13.6. You can see here that perfusion is higher than ventilation at the base; it falls off much more rapidly as the lung is ascended, so it ends up being lower than ventilation at the apex.",True,Distribution of V/Q,Figure 13.6,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
aa27645e-d896-4680-8902-383d3b8bf327,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"As you should understand, ventilation increases down the lung so is greatest at the base, and perfusion follows the same pattern—all due to the effects of gravity. But the increase in ventilation down the lung structure is not equal to the increase in perfusion, as can be seen in figure 13.6. You can see here that perfusion is higher than ventilation at the base; it falls off much more rapidly as the lung is ascended, so it ends up being lower than ventilation at the apex.",True,Distribution of V/Q,Figure 13.6,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
aa27645e-d896-4680-8902-383d3b8bf327,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"As you should understand, ventilation increases down the lung so is greatest at the base, and perfusion follows the same pattern—all due to the effects of gravity. But the increase in ventilation down the lung structure is not equal to the increase in perfusion, as can be seen in figure 13.6. You can see here that perfusion is higher than ventilation at the base; it falls off much more rapidly as the lung is ascended, so it ends up being lower than ventilation at the apex.",True,Distribution of V/Q,Figure 13.6,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
c5a7a778-cc65-4170-a531-09e81908cc50,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"This means there is a range of ventilation–perfusion ratios up the height of the lung (figure 13.6, maroon plot). At the base perfusion is higher than ventilation, so V/Q is less than 1, while toward the apex V/Q rises and becomes greater than 1. At about the level of the third rib, V/Q is perfect (yay!) as ventilation and perfusion are matched, seen here at the points the lines cross. This range of V/Q results in the previously mentioned whole lung average of 0.8.",True,Distribution of V/Q,Figure 13.6,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
c5a7a778-cc65-4170-a531-09e81908cc50,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"This means there is a range of ventilation–perfusion ratios up the height of the lung (figure 13.6, maroon plot). At the base perfusion is higher than ventilation, so V/Q is less than 1, while toward the apex V/Q rises and becomes greater than 1. At about the level of the third rib, V/Q is perfect (yay!) as ventilation and perfusion are matched, seen here at the points the lines cross. This range of V/Q results in the previously mentioned whole lung average of 0.8.",True,Distribution of V/Q,Figure 13.6,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
c5a7a778-cc65-4170-a531-09e81908cc50,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"This means there is a range of ventilation–perfusion ratios up the height of the lung (figure 13.6, maroon plot). At the base perfusion is higher than ventilation, so V/Q is less than 1, while toward the apex V/Q rises and becomes greater than 1. At about the level of the third rib, V/Q is perfect (yay!) as ventilation and perfusion are matched, seen here at the points the lines cross. This range of V/Q results in the previously mentioned whole lung average of 0.8.",True,Distribution of V/Q,Figure 13.6,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.6.png,"Figure 13.6: Ventilation, perfusion, and V/Q distributions."
ad0f4b3e-6206-4bb5-a4e2-b24fd88c71d0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,yay,False,yay,,,,
072c3adc-3356-4713-a81c-2272f23ae251,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"As you should appreciate from understanding the ventilation–perfusion line, this range of V/Q across the lung results in a range of alveolar gas partial pressures across the lung. The apical alveoli, being relatively overventilated (or underperfused, whichever way you would like to think about it), have a high V/Q and consequently have partial pressures closer to atmospheric partial pressures. On the other extreme, the basal alveoli are relatively underventilated (or overperfused, your choice) and so have a low V/Q, tending toward zero; thus their partial pressures are closer to venous values (figure 13.7).",True,yay,Figure 13.7,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.7.png,Figure 13.7: V/Q and alveolar gas distribution.
072c3adc-3356-4713-a81c-2272f23ae251,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"As you should appreciate from understanding the ventilation–perfusion line, this range of V/Q across the lung results in a range of alveolar gas partial pressures across the lung. The apical alveoli, being relatively overventilated (or underperfused, whichever way you would like to think about it), have a high V/Q and consequently have partial pressures closer to atmospheric partial pressures. On the other extreme, the basal alveoli are relatively underventilated (or overperfused, your choice) and so have a low V/Q, tending toward zero; thus their partial pressures are closer to venous values (figure 13.7).",True,yay,Figure 13.7,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.7.png,Figure 13.7: V/Q and alveolar gas distribution.
072c3adc-3356-4713-a81c-2272f23ae251,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"As you should appreciate from understanding the ventilation–perfusion line, this range of V/Q across the lung results in a range of alveolar gas partial pressures across the lung. The apical alveoli, being relatively overventilated (or underperfused, whichever way you would like to think about it), have a high V/Q and consequently have partial pressures closer to atmospheric partial pressures. On the other extreme, the basal alveoli are relatively underventilated (or overperfused, your choice) and so have a low V/Q, tending toward zero; thus their partial pressures are closer to venous values (figure 13.7).",True,yay,Figure 13.7,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.7.png,Figure 13.7: V/Q and alveolar gas distribution.
64ee551c-b8ce-495b-b649-66e2cb80297d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,overventilated,False,overventilated,,,,
eda039b0-075d-4998-84ed-7ec7f910e5bb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,overperfused,False,overperfused,,,,
59c64704-d145-40a9-afe0-b27d4fb130ae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"In between these two extremes is a progressive range, so what we see is that alveolar PO2 declines down the lung while alveolar PCO2 rises. As you might imagine, having a range of alveolar gas tensions down the lung has ramifications for gas exchange and particularly for oxygen saturation. This inequality in V/Q resulting in differences in alveolar PO2 is substantial enough to suppress arterial oxygen saturation—and contribute to your oxygen saturation meter never reading 100 percent. Let us see why.",True,overperfused,,,,
8774d232-d73a-4bfd-abe2-121b55f6fd62,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"The difference in alveolar PO2 from apex to base is as high as 40 mmHg, as is reflected in this figure. The apical alveoli have a high PO2 (shown in figure 13.8 as 132 mmHg), primarily due to their poor perfusion and relatively high ventilation and thus high V/Q. This produces a high diffusion gradient from 132 mmHg in the apical alveoli, to 40 mmHg in the apical blood. Consequently, what blood does go to the apex becomes fully saturated before it heads back toward the left heart.",True,overperfused,Figure 13.8,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
8774d232-d73a-4bfd-abe2-121b55f6fd62,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"The difference in alveolar PO2 from apex to base is as high as 40 mmHg, as is reflected in this figure. The apical alveoli have a high PO2 (shown in figure 13.8 as 132 mmHg), primarily due to their poor perfusion and relatively high ventilation and thus high V/Q. This produces a high diffusion gradient from 132 mmHg in the apical alveoli, to 40 mmHg in the apical blood. Consequently, what blood does go to the apex becomes fully saturated before it heads back toward the left heart.",True,overperfused,Figure 13.8,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
8774d232-d73a-4bfd-abe2-121b55f6fd62,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"The difference in alveolar PO2 from apex to base is as high as 40 mmHg, as is reflected in this figure. The apical alveoli have a high PO2 (shown in figure 13.8 as 132 mmHg), primarily due to their poor perfusion and relatively high ventilation and thus high V/Q. This produces a high diffusion gradient from 132 mmHg in the apical alveoli, to 40 mmHg in the apical blood. Consequently, what blood does go to the apex becomes fully saturated before it heads back toward the left heart.",True,overperfused,Figure 13.8,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
ccadc091-576f-49ed-993d-fa0348196370,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"Down at the base, however, V/Q is low because of the high perfusion and relatively low ventilation. Consequently the PO2 in basal alveoli tend toward venous values, shown in figure 13.8 as 89 mmHg. This lower alveolar PO2 means a diminished diffusion gradient (from 89 in the alveoli to 40 mmHg in the blood), and combined with a shift down the hemoglobin saturation curve (more on this later), this means blood leaving the basal alveoli may not be completely saturated with oxygen.",True,overperfused,Figure 13.8,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
ccadc091-576f-49ed-993d-fa0348196370,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"Down at the base, however, V/Q is low because of the high perfusion and relatively low ventilation. Consequently the PO2 in basal alveoli tend toward venous values, shown in figure 13.8 as 89 mmHg. This lower alveolar PO2 means a diminished diffusion gradient (from 89 in the alveoli to 40 mmHg in the blood), and combined with a shift down the hemoglobin saturation curve (more on this later), this means blood leaving the basal alveoli may not be completely saturated with oxygen.",True,overperfused,Figure 13.8,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
ccadc091-576f-49ed-993d-fa0348196370,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"Down at the base, however, V/Q is low because of the high perfusion and relatively low ventilation. Consequently the PO2 in basal alveoli tend toward venous values, shown in figure 13.8 as 89 mmHg. This lower alveolar PO2 means a diminished diffusion gradient (from 89 in the alveoli to 40 mmHg in the blood), and combined with a shift down the hemoglobin saturation curve (more on this later), this means blood leaving the basal alveoli may not be completely saturated with oxygen.",True,overperfused,Figure 13.8,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.8.png,Figure 13.8: Consequences of V/Q nonuniformity on arterial PO2.
9eaa7b9e-313b-4046-ae92-8731d0564334,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"When the blood from the apex and base mix on their journey back to the left heart, the outcome is that the combined oxygen saturation is less than 100 percent, about 97 percent. It is worth making perhaps an obvious but critical point here. The blood from the apex is exposed to a substantially higher PO2 and becomes 100 percent saturated (i.e., it cannot take on any more O2 as it is at its full oxygen carrying capacity). There is no way that it can pick up extra to compensate for the blood coming from basal alveoli, which are not at capacity.",True,overperfused,,,,
aaf0e787-e829-40b5-b56c-864f44fd31f8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"The same is not true for CO2 though. Because of its high solubility, CO2 transport does not rely on a transporter protein like hemoglobin; the transfer of CO2 is really dependent on the diffusion gradient present. So at the apex the lower alveolar PCO2 (slightly less than 30 mmHg looking at our V/Q line) generates a larger diffusion gradient with venous blood, and more CO2 is transferred out the blood, meaning that it can compensate for the low diffusion gradient (perhaps only a few mmHg) that occurs between the alveoli and blood at the lung’s base.",True,overperfused,,,,
e5f495e5-b5d9-4608-9c6a-70e5941d513c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,As a study exercise it may be worthwhile for you to go back to the ventilation–perfusion line and calculate the diffusion gradients for oxygen and carbon dioxide between the alveoli and venous blood at different heights in the lung. I urge you to come to grips with this concept as it is highly pertinent to respiratory disease and can explain clinical-related changes in blood gases.,True,overperfused,,,,
bb6c7586-cf43-4f90-a25e-39aafc8e1188,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"The take-home message, however, is that even the normal lung is not perfect and has an average V/Q ratio of 0.8, rather than the ideal of 1, and this slight matching of ventilation and perfusion contributes to the arterial saturation being slightly less than 100 percent, but has little effect on arterial CO2. If respiratory disease increases the mismatch, this effect on oxygen saturation can become more pronounced, but the lung has a defense mechanism for this.",True,overperfused,,,,
19b4552b-afc8-40ee-b0fc-9c70d4857271,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,Correcting V/Q Mismatches,False,Correcting V/Q Mismatches,,,,
df5e209e-0a53-4203-8c49-c4fa7660a219,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"In an attempt to maintain V/Q close to 1 and prevent V/Q mismatching, the pulmonary vasculature has an unusual response to hypoxia. While the systemic vasculature responds to local hypoxia with a vasodilation to bring more blood to the area, the pulmonary vasculature constricts in the presence of low oxygen to shunt blood away from hypoxic regions.",True,Correcting V/Q Mismatches,,,,
a9a93d3f-15e7-433f-8ad2-1bfdbbbb617d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"Let us look at a common scenario that might occur in a patient with chronic bronchitis. Figure 13.9 represents two regions of the lung. One region becomes blocked by a mucus plug, and ventilation to that region goes to zero.",True,Correcting V/Q Mismatches,Figure 13.9,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.9.png,Figure 13.9: Correcting V/Q mismatches.
a9a93d3f-15e7-433f-8ad2-1bfdbbbb617d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"Let us look at a common scenario that might occur in a patient with chronic bronchitis. Figure 13.9 represents two regions of the lung. One region becomes blocked by a mucus plug, and ventilation to that region goes to zero.",True,Correcting V/Q Mismatches,Figure 13.9,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.9.png,Figure 13.9: Correcting V/Q mismatches.
a9a93d3f-15e7-433f-8ad2-1bfdbbbb617d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"Let us look at a common scenario that might occur in a patient with chronic bronchitis. Figure 13.9 represents two regions of the lung. One region becomes blocked by a mucus plug, and ventilation to that region goes to zero.",True,Correcting V/Q Mismatches,Figure 13.9,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.9.png,Figure 13.9: Correcting V/Q mismatches.
71b7f775-99bb-4d56-801e-48562d196006,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"The alveolar partial pressures will rapidly equilibrate to venous pressures, and desaturated blood goes back to the left heart from this region while the local region around this area becomes mildly hypoxic. The pulmonary vasculature responds to the hypoxia by vasoconstricting, reducing the perfusion to the unventilated region and helping to rematch the V/Q ratio in this region (i.e., low ventilation is matched with low perfusion). In common sense terms, there is no point sending pulmonary blood to an unventilated region, so the hypoxia-driven vasoconstriction prevents this from happening.",True,Correcting V/Q Mismatches,,,,
b3505987-76f4-4df9-b248-a82e56fae4bb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"The distensibility of the pulmonary vasculature means that the blood is shunted to unconstricted vessels (i.e., those supplying ventilated regions). Thus the lung has its own inherent mechanism to optimize V/Q and promote the most effective gas exchange possible.",True,Correcting V/Q Mismatches,,,,
f33f175e-a096-4e11-b1ea-5512d7ae1654,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"The unusual response of the pulmonary vasculature is demonstrated in figure 13.10, showing how as alveolar PO2 falls (as occurs with a decline in alveolar ventilation) then blood flow falls—and likewise, the more oxygen in the alveolus, the more pulmonary perfusion it receives.",True,Correcting V/Q Mismatches,Figure 13.10,Distribution of V/Q,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.10.png,Figure 13.10: Response of pulmonary vasculature to hypoxia.
f33f175e-a096-4e11-b1ea-5512d7ae1654,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"The unusual response of the pulmonary vasculature is demonstrated in figure 13.10, showing how as alveolar PO2 falls (as occurs with a decline in alveolar ventilation) then blood flow falls—and likewise, the more oxygen in the alveolus, the more pulmonary perfusion it receives.",True,Correcting V/Q Mismatches,Figure 13.10,Ventilation and Perfusion in the Normal Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.10.png,Figure 13.10: Response of pulmonary vasculature to hypoxia.
f33f175e-a096-4e11-b1ea-5512d7ae1654,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"The unusual response of the pulmonary vasculature is demonstrated in figure 13.10, showing how as alveolar PO2 falls (as occurs with a decline in alveolar ventilation) then blood flow falls—and likewise, the more oxygen in the alveolus, the more pulmonary perfusion it receives.",True,Correcting V/Q Mismatches,Figure 13.10,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/13.10.png,Figure 13.10: Response of pulmonary vasculature to hypoxia.
39f38eda-2cd7-48c2-a3c6-11f27557bc7b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"This effect is driven by a hypoxia-sensitive potassium channel found on the albeit sparse smooth muscle of the pulmonary arterioles. This channel is normally open and allows the exit of potassium, which in turn keeps the inside of the muscle cell polarized. When exposed to hypoxia the channel closes, and the outward potassium current stops, allowing the muscle cell’s membrane potential to rise and consequently depolarize to cause a contraction.",True,Correcting V/Q Mismatches,,,,
1b2c2f24-02a7-4434-add9-71cb3b362136,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"So to summarize, the ratio of ventilation and perfusion changes across the lung, and this affects the alveolar and consequently arterial gas tensions from those regions. While the lung does not reach the ideal V/Q ratio, it is capable of shunting pulmonary blood flow away from unventilated areas to optimize gas exchange.",True,Correcting V/Q Mismatches,,,,
a142af58-292d-4366-a64d-c420aeff0556,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,Text,False,Text,,,,
a63cd382-f964-42bf-9e94-c976f07b6ab5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"Levitsky, Michael G. “Chapter 5: Ventilation–Perfusion Relationships.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
40947d5e-b13b-4c2c-b62c-2e44c85ee168,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"West, John B. “Chapter 5: Ventilation–Perfusion Relationships—How Matching of Gas and Blood Determines Gas Exchange.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
40c52c43-6692-415e-b048-8080678247b2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,13. Ventilation and Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/ventilation-and-perfusion/,"Widdicombe, John G., and Andrew S. Davis. “Chapter 7.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
5ee0f2e6-eb61-4d12-a78b-a5732f027f84,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,CO₂ and pH,False,CO₂ and pH,,,,
ea2fb480-27e3-4171-a770-1b37db5c154e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,We will start by revisiting the equation dealt with in the previous chapter in the context of four different clinical scenarios.,True,CO₂ and pH,,,,
16446bf3-460e-4969-b016-96c12cf45a27,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"Case #1, normal: In the normal situation an increase in tissue metabolism leads to a rise in arterial CO2, pushing the equation to the right and causing a rise in hydrogen ion concentration and a consequent fall in pH. Both the rise in CO2 and fall in pH stimulate breathing. This increase in alveolar ventilation leads to a fall in arterial CO2, pushing the equation back left and lowering hydrogen ions back to normal.",True,CO₂ and pH,,,,
fdc2ed6d-8799-410e-a703-6503d5741b98,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.1,True,CO₂ and pH,,,,
140bedfa-4f7f-4a6e-bb0b-62c2b3339317,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],False,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
db23bf0b-5b23-44b6-9224-f9cbe64672a2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"Case #2, metabolic acidosis: CO2 is by no means the only source of hydrogen ions in the system. Most metabolic pathways result in acidic by-products, and the pulmonary, renal, and buffering systems are generally battling to raise blood and tissue pH back from their tendency to turn acidic. The rise in hydrogen ions resulting from metabolic processes is referred to as metabolic acidosis. The fall in pH stimulates an increase in respiration, which in turn causes a fall in CO2, and the lower CO2 drives the equation to the left, reducing the number of H+ and thereby raising pH back to normal. Here the pulmonary system has compensated for a metabolic process, and this is referred to as respiratory compensation of metabolic acidosis. The patient may now have a normal blood pH, but the CO2 will be low. In summary, all the pulmonary system has done is get rid of one source of hydrogen ions (carbonic acid derived from dissolved CO2) to compensate for another source of hydrogen ions it cannot do anything about (most metabolically driven acids are nonvolatile (i.e., do not vaporize into a gas the lungs can get rid of)).",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
77c2cd90-c65f-4988-81d6-8df953baee37,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"The advantage of the pulmonary system being involved in pH regulation is that it is quick—a few larger breaths and arterial PCO2 can be dropped significantly. So the pulmonary system is adept at minute-by-minute (or breath-by-breath) regulation of pH that copes admirably with short-term changes in pH. It is worth noting here that metabolic alkalosis can be reversed by reducing or even stopping breathing, allowing CO2 to accumulate in the arterial blood and lowering pH back to normal.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
6ec8ba64-b3ae-4b7f-9a63-bd327d915ad9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"The disadvantage to using the pulmonary system for compensation is that it can only mediate its effect via CO2. So any metabolic acids are eventually dealt with by the renal system, which, although much slower, is capable of excreting any nonvolatile metabolic acids. So through a combination of rapid pulmonary CO2 expulsion and slower but more versatile renal function, pH is normally maintained within a tight range even in the face of large metabolic changes. The kidney also has the advantage of being able to modify bicarbonate levels, which we will see the importance of when we look at the buffering systems in a moment.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
d1e8a073-5819-4d14-9074-f6714dad77f8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"It is worth noting here, especially for the chemists and biochemists among you, that although equation 12.1 is a reversible reaction, it is open at both ends—the lung being able to expel or retain CO2 at one end and the kidneys being able to retain or expel hydrogen ions and bicarbonate at the other.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
35815c54-9b81-433e-a563-dbe456ff07e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"Case #3, respiratory acidosis: Given its capability to influence pH, failure of the lung to expel an appropriate amount of CO2 can lead to deviations in pH. Let us take a case of severe lung disease, say COPD, for example. The disease has diminished the ability of the lung to expel CO2, so arterial PCO2 rises, pushing the equation to the right and causing a fall in pH, referred to as respiratory acidosis. This acid must be immediately buffered until kidney function can be modified to begin secreting the excess hydrogen ions and even produce more bicarbonate to replenish the buffering system, a process referred to as metabolic compensation of respiratory acidosis.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
e8008f82-c1bf-49b5-baaa-22b25e12ee7f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"Case #4, respiratory alkalosis: Likewise, if ventilation is inappropriately high with respect to CO2 production, such as during a period of hyperventilation, then too much CO2 will be lost and pH will fall. The alkalosis must be immediately buffered to avoid deleterious effects. Over the longer term the kidney can lower the raised pH by reabsorbing hydrogen ions and even excreting bicarbonate buffer—again this is termed metabolic compensation—but this time for an alkalosis caused by an inappropriate respiratory response.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
0f163346-458b-45a9-a65b-95c60bc575f7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Physiological Buffers,False,Physiological Buffers,,,,
f72b4585-52c0-47fd-b96e-a0b5a1b90050,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"Although the lung’s ability to expel CO2 and the kidney’s ability to excrete or absorb hydrogen ions allow close regulation of pH, their responses alone are not sufficient to prevent immediate local changes in pH at the tissue. This is the role of the buffering systems.",True,Physiological Buffers,,,,
26fd6b87-32ee-4b2c-905a-70eb6d98a77e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"Buffering systems are chemicals within tissue and the blood that have the ability to absorb either hydrogen ions and/or hydroxyl ions. Once these ions are removed from solution (albeit temporarily) then their effect on pH is diminished. We will deal with buffers in the context of acids, as this is the most common physiological situation.",True,Physiological Buffers,,,,
23345a9c-842f-4ed1-9cba-d40edcb25547,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"If you need an analogy for the function of buffers, imagine them as a chemical mop—they soak up the hydrogen ions and stop them from making a cellular mess, but the hydrogen ions, although contained, remain in the system. It is the role of the lungs and kidneys to “rinse the mop” and get rid of the hydrogen ions from the system.",True,Physiological Buffers,,,,
9d19f602-f3c7-4945-9ebb-5d0a31d36214,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,There are three major chemical buffering groups in the body:,False,There are three major chemical buffering groups in the body:,,,,
c8b8ae17-d07a-493a-8cd3-fde32c396473,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,We will deal with the bicarbonate system as it involves the respiratory system and is also the major extracellular buffer.,True,There are three major chemical buffering groups in the body:,,,,
087c802c-0b68-42ec-91de-d6259e279fe8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"Bicarbonate buffering: A buffering system consists of a weak base capable of absorbing a strong acid and a weak acid capable of absorbing a strong base. As such, the bicarbonate system involves two components: sodium bicarbonate (a weak base) and carbonic acid (a weak acid). Let us look at how it works and put it in the context of the lungs.",True,There are three major chemical buffering groups in the body:,,,,
47bf8a28-4a36-4e0e-bda2-f27a32c33c45,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"First let us see how a weak acid (carbonic acid) deals with a strong base, in this example, sodium hydroxide (equation 12.2).",True,There are three major chemical buffering groups in the body:,,,,
66792690-dd0a-4e83-9a46-88c6905bf79a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Buffering a strong base using a weak acid:,False,Buffering a strong base using a weak acid:,,,,
fb3546a9-0983-4009-8e9d-b3e78e90523c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.2,True,Buffering a strong base using a weak acid:,,,,
da34b74f-1cae-45b9-8179-858e0495bf64,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]NaOH = \color{red}{H_2CO_3}[/latex],False,[latex]NaOH = \color{red}{H_2CO_3}[/latex],,,,
e1ad139f-7978-4608-af1b-7556856d401e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Sodium hydroxide is a strong base as it rapidly dissociates into a hydroxyl ion and a sodium ion.,True,[latex]NaOH = \color{red}{H_2CO_3}[/latex],,,,
42d94e92-061d-4871-904d-04f77c63046d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.3,True,[latex]NaOH = \color{red}{H_2CO_3}[/latex],,,,
1add7b6c-2aa9-48be-aee9-c6ebabc0fb16,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + \color{red}{H_2CO_3}[/latex],False,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + \color{red}{H_2CO_3}[/latex],,,,
4f3f5a69-ba8f-4549-bab4-292beee0959b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,The hydroxyl ion is the potential threat to physiological function so must be buffered. This is achieved by the carbonic acid dissociating into a hydrogen ion and bicarbonate (a process you are familiar with).,True,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + \color{red}{H_2CO_3}[/latex],,,,
ae4e6579-5e24-4f67-9987-4717f457a4fe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,These dissociated ions now bind to form new partnerships as water and sodium hydroxide (a weak base) (equation 12.4).,True,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + \color{red}{H_2CO_3}[/latex],,,,
d8b408f0-bc3e-4c6b-89dc-dd5e878b648c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.4,True,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + \color{red}{H_2CO_3}[/latex],,,,
ec7e0044-1451-48e5-b8d5-d7b0058d9a1b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + {{HCO_{3-}}\atop{{H}^{+}}} \rightarrow H_2O + \color{blue}{NaHCO_3}[/latex],False,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + {{HCO_{3-}}\atop{{H}^{+}}} \rightarrow H_2O + \color{blue}{NaHCO_3}[/latex],,,,
9a350d0c-5c12-4a60-acb7-3a67266b34f6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"So there are a couple of things to notice here beyond watching the ions move and form new components. First, the buffering process has taken a situation with the threat from a strong base (NaOH) and toned it down to a situation with a weak base (NaHCO3); the problem has not gone away, it has just been reduced (or buffered). Second, you will see that both of the components of the bicarbonate system, carbonic acid and sodium bicarbonate, appear in the equation—we have just shifted from one to the other.",True,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + {{HCO_{3-}}\atop{{H}^{+}}} \rightarrow H_2O + \color{blue}{NaHCO_3}[/latex],,,,
878bc0ce-7107-4a1f-a019-df3dfb03e34b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Let us look at the opposite situation to see what happens when the buffering system is faced with a strong acid. This time a strong acid (hydrochloric acid) is faced with our weak base (sodium bicarbonate) (equation 12.5).,True,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + {{HCO_{3-}}\atop{{H}^{+}}} \rightarrow H_2O + \color{blue}{NaHCO_3}[/latex],,,,
06fefffb-513c-4917-add7-d5e7fc7b00f6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Buffering a strong acid using a weak base:,False,Buffering a strong acid using a weak base:,,,,
2063bd6a-3edb-41e1-a16e-ef606250eee3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.5,True,Buffering a strong acid using a weak base:,,,,
e10f18a4-1d88-48b0-895a-bbcfc6745904,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]HCl + \color{blue}{NaHCO_3}[/latex],False,[latex]HCl + \color{blue}{NaHCO_3}[/latex],,,,
db76f4fe-e2d4-4d0f-aaf5-6965c23db3c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,The hydrochloric acid rapidly dissociates into a hydrogen ion and a chloride ion. The hydrogen ion now threatens physiological function and must be buffered.,True,[latex]HCl + \color{blue}{NaHCO_3}[/latex],,,,
1eb1aeae-594e-4ea9-88f7-bf0383796b62,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"Our weak base dissociates into sodium and bicarbonate ions. Again our ions recombine, this time to produce harmless sodium chloride and carbonic acid (equation 12.6).",True,[latex]HCl + \color{blue}{NaHCO_3}[/latex],,,,
ebc2054b-30a6-4459-91da-c8118b19aa8f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.6,True,[latex]HCl + \color{blue}{NaHCO_3}[/latex],,,,
822cec6f-4092-4f02-85b7-5dc8d937dc8b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],False,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
f1801785-6c58-4deb-a6e9-aaf2058defcf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"Notice again we have reduced but not removed the threat as we have gone from the presence of a strong acid to a weak one. Also notice that our two components in the bicarbonate system appear in the equation, and we have switched from one to the other. This should now make you realize that these two components are part of a reversible equation, and this reversible equation, even after the addition of sodium to one end, should look rather familiar (equation 12.7).",True,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
1f5c6336-a2f1-4085-85fc-3a8130d66321,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.7,True,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
adb8de3f-e965-4d79-a6ba-0cea0eccc889,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]CO_2 + H_2O \leftrightarrow {\color{red}{H_2CO_3}} \leftrightarrow H^+ + HCO_{3-} + Na^+ \leftrightarrow \color{blue}{NaHCO_3}[/latex],True,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
5e09f7f8-0d8f-4c2e-bdec-e19540e63114,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,As CO2 is at one end of the equation you should appreciate how alveolar ventilation can influence the bicarbonate buffering system.,True,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
0896e08a-3c5a-4299-9cee-dcfa6cd5fa6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"Because of their critical role in maintaining blood pH, bicarbonate ions are routinely measured along with arterial blood gases. Knowing what the blood pH, arterial CO2, and bicarbonate levels are provides a very powerful and commonly used diagnostic measure allowing us not only to determine the pH status of the patient, but also the source of the problem and whether the renal or pulmonary systems are achieving compensation. Because of its power and common use, we are going to go through some fundamentals, and I am afraid that means looking at the bane of many a medical student: the Henderson–Hasselbalch equation. For those with a background in chemistry you might skip the next section, but for the rest of us, we are going to go through this step-by-step.",True,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
21700396-0409-48d1-8732-c9cdc5a0032b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,The Henderson–Hasselbalch Equation,False,The Henderson–Hasselbalch Equation,,,,
81b98d6e-3e75-4f0c-a0ac-278ce9a2df5c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"What we will see is how the balance of bicarbonate and hydrogen ions determines pH, and how both of these ions can be influenced by the kidneys and lungs to keep pH constant.",True,The Henderson–Hasselbalch Equation,,,,
760a718a-a216-4a37-8c6f-f0f1b36a2fa5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"First, we will take the central and most important part of the infamous equation, discarding the more innocuous ends.",True,The Henderson–Hasselbalch Equation,,,,
0e6291a7-0d8a-4714-91b8-042149345179,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.8,True,The Henderson–Hasselbalch Equation,,,,
36c2b81c-38c5-4538-b1f8-1ffad768759d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]H_2CO_3 \leftrightarrow H^+ + HCO_{3-}[/latex],False,[latex]H_2CO_3 \leftrightarrow H^+ + HCO_{3-}[/latex],,,,
52b0910e-66e7-4ea7-b808-7bf235ca5f09,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"This central portion describes the dissociation of carbonic acid into hydrogen and bicarbonate ions. But because carbonic acid is a weak acid, this dissociation is incomplete—some carbonic acid staying whole, some dissociating into the ions. The level of dissociation is described by the dissociation constant (K’), which really is the ratio of the concentrations of dissociated components to carbonic acid (equation 12.9).",True,[latex]H_2CO_3 \leftrightarrow H^+ + HCO_{3-}[/latex],,,,
1fb66582-ac9a-4976-adee-7dc6671c87ff,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.9,True,[latex]H_2CO_3 \leftrightarrow H^+ + HCO_{3-}[/latex],,,,
b358a530-a2bb-4531-a5a2-0d48a1818be3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]K' = \displaystyle\frac{{H}^{+} \times {HCO}_{3}-}{H_2CO_3}[/latex],False,[latex]K' = \displaystyle\frac{{H}^{+} \times {HCO}_{3}-}{H_2CO_3}[/latex],,,,
79c07495-44ad-4277-a808-17d821c6fd99,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"Because we are interested in calculating the pH, however, we are more interested in the amount of hydrogen ions, so rearranging this equation for hydrogen ion concentration we see the hydrogen ion concentration is the dissociation constant, multiplied by the ratio of carbonic acid and bicarbonate (equation 12.10).",True,[latex]K' = \displaystyle\frac{{H}^{+} \times {HCO}_{3}-}{H_2CO_3}[/latex],,,,
2f9e7dda-eeab-4d6a-9d3f-2ce41e59725e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.10,True,[latex]K' = \displaystyle\frac{{H}^{+} \times {HCO}_{3}-}{H_2CO_3}[/latex],,,,
9bfa7b78-9d1f-4cf8-9d9d-2381ed46a6c5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]H^+ = K' \times \displaystyle\frac{H_2CO_3}{HCO_3-}[/latex],False,[latex]H^+ = K' \times \displaystyle\frac{H_2CO_3}{HCO_3-}[/latex],,,,
882d5f35-6e05-4327-a5a9-f749b464cacd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"This equation theoretically would allow us to now determine hydrogen concentration and therefore pH, but there are some practical problems for us, the first of which is that the instability of carbonic acid means we cannot measure its concentration. So we have to use a proxy measure. The amount of carbonic acid is determined by the amount of carbon dioxide, as can be seen in the equation that is so familiar to you—the greater the amount of CO2, the more carbonic acid.",True,[latex]H^+ = K' \times \displaystyle\frac{H_2CO_3}{HCO_3-}[/latex],,,,
7a32bc29-717f-41f0-b1e0-869a9ea58d5a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.11,True,[latex]H^+ = K' \times \displaystyle\frac{H_2CO_3}{HCO_3-}[/latex],,,,
6e22a0cd-57ca-4602-ad2b-bdcdcfb712f3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],False,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
9cab90f6-802a-4357-8093-bbe7a798e746,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"So after accounting for the dissociation constant of carbonic acid and CO2 and water, we can simply replace carbonic acid concentration with concentration of CO2 (equation 12.12).",True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
73357170-0c41-4678-be54-1f9ce98a2ba6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.12,True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
e8ab1dfb-39f6-4f0e-b312-4cb7578c5aa2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]H^+ = K' \times \displaystyle\frac{CO_2}{HCO_3}[/latex],False,[latex]H^+ = K' \times \displaystyle\frac{CO_2}{HCO_3}[/latex],,,,
59a53658-cafa-4506-b401-90cf7fa4e992,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"We then bump into our next practical problem: our equation now has CO2 concentration in it, but clinically we do not measure CO2 as a concentration (as in mmols), but as a partial pressure. So our next and nearly final step is to convert CO2 concentration to CO2 partial pressure, and we do this by multiplying the partial pressure (our measured value) by the solubility coefficient of carbon dioxide, which happens to be 0.03 mmol/mmHg. Our equation thus now can be completed using our adjusted PCO2 (equation 12.13).",True,[latex]H^+ = K' \times \displaystyle\frac{CO_2}{HCO_3}[/latex],,,,
e3677c67-66a7-48c0-bfc3-ec4a981f8ba3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,mmols,False,mmols,,,,
5fb23906-ec05-4145-9fb9-c4f11c07fff7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.13,True,mmols,,,,
c999d1c1-a354-40fb-b948-062118219ced,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]H^+ = K' \times \displaystyle\frac{0.03 \times PCO_2}{HCO_3-}[/latex],True,mmols,,,,
f01aca0b-94fd-463c-9c40-200c25366d18,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"Our equation as it is now allows us to calculate hydrogen ion concentration, but we need pH, so we have to make a conversion. Because pH is the negative logarithm of hydrogen concentration, we express everything in the negative log form. And because the negative log of the dissociation constant is referred to as pK, then we can simplify our equation one more step (equation 12.14).",True,mmols,,,,
141e4cc0-2e0f-4828-bcdb-f9f036ce8025,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.14,True,mmols,,,,
216a3094-2d61-4371-bf6e-103ac215c266,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]pH = pK - log \displaystyle\frac{0.03 \times PCO_2}{HCO_3-}[/latex],True,mmols,,,,
2bfd10e7-0293-44d7-ac18-adc347b19bf0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"To make our equation simple to use, we now get rid of the negative log, and so get the following (equation 12.15):",True,mmols,,,,
f11ae011-4301-4ba2-8d2b-90254aa2216f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.15,True,mmols,,,,
19b76e70-9f12-4e25-88c0-d410b90fcfc9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]pH = pK + log \displaystyle\frac{HCO_3-}{0.03 \times PCO_2}[/latex],True,mmols,,,,
3797eedb-d09c-4039-a6cc-625e57295f26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"We know that the pK of the bicarbonate system happens to be 6.1, so substituting this into the equation we end up with the Henderson–Hasselbalch equation (equation 12.16).",True,mmols,,,,
698b5c20-1a0f-4f23-a5f6-009e22670511,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Let us put this in context.,False,Let us put this in context.,,,,
374bd71e-dd8c-4003-b290-defe7784b4a4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"First, the equation shows that if CO2 rises then pH falls, and because CO2 is under the influence of alveolar ventilation, this explains how the alveolar ventilation can now control pH. It also shows that if bicarbonate increases then pH increases, and equally if bicarbonate falls then pH falls. Because the bicarbonate concentration can be modified either way by the kidneys, the equation also shows how the kidneys can modify pH (equation 12.16).",True,Let us put this in context.,,,,
c957205f-7a9a-4194-9e95-686b2e6ca388,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.16,True,Let us put this in context.,,,,
15e7940c-b483-474e-97bf-32f14968cbee,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Role of kidneys (numerator) / Role of lungs (denominator),False,Role of kidneys (numerator) / Role of lungs (denominator),,,,
534628eb-7f64-4af9-936f-53fa3556ec28,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]pH = 6.1 + log \displaystyle\frac{HCO_3-}{0.03 \times PCO_2}[/latex],True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
7231703f-c12d-40db-a20b-d4f56c76d129,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"The involvement of these two major physiological systems in this equation make the bicarbonate system a very powerful buffer, particularly when considering that there is an unlimited source of CO2 and therefore bicarbonate supplied by the metabolism.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
eba6def9-d3b1-42ff-988e-505a304594b8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"But more importantly it shows that pH is actually determined by the ratio of bicarbonate and CO2 and that both are equally important. This fact is critical to appreciate as it forms the basis of understanding the compensation mechanisms we dealt with earlier. This is why I put you through this derivation. So for example, if a rise in CO2 (such as in lung disease) is accompanied by an equal rise in bicarbonate (generated by the kidney), then the ratio between the two remains the same and therefore pH remains the same. Likewise, if during a fall in CO2 the kidneys excrete bicarbonate, then pH can be kept constant. So before we finish, let us show you that the equation actually works by plugging in some numbers.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
623e363a-f06c-41a1-9e07-3e6021a946c4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"Example #1: Let us start with normal values, a PCO2 of 40 mmHg and a bicarbonate of 24, and plug these into the equation. This comes to 6.1 plus the log of 20, which is 6.1 plus 1.3, or 7.4 (i.e., normal arterial pH).",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
292a3a0b-56ea-4fc7-b1e6-037b80f9073c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.17,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
4c240ea9-ce0f-437e-ae45-67be7bc2935e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]pH = 6.1 + log \displaystyle\frac{24}{(0.03 \times 40)} = 6.1 + log(20) = 6.1 + 1.3 = 7.4[/latex],True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
05de98cb-e574-4d49-8bb8-febbd72b82a9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"Example #2: Now let us look at a case of acute lung failure that has caused a rise in arterial PCO2, but has not persisted long enough for the kidney to respond and compensate. PCO2 has risen to 50 mmHg, and bicarbonate has not changed. Our calculation now goes to 6.1 plus the log of 16, which is 6.1 plus 1.2, and pH has fallen to 7.3.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
4f9ee187-3846-4527-b265-95d683d74cba,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.18,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
e535cbc4-78e5-40b0-9939-1f4f5aae5327,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]pH = 6.1 + log \displaystyle\frac{24}{(0.03 \times 50)} = 6.1 + log(16) = 6.1 + 1.2 = 7.3[/latex],True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
8b40b76c-60f6-4500-8590-209c9ece66cc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"We now have three numbers that can give a meaningful clinical interpretation. The low pH indicates the patient is in acidosis. The raised PCO2 suggests that this is respiratory acidosis, and the unchanged bicarbonate suggests no metabolic compensation has taken place.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
4847b373-58a8-45de-bfd3-46682622abae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"Example #3: Now let us return to our patient thirty-six hours later when we have given the kidney a chance to respond. The patient’s PCO2 remains at 50 because of the persistent lung problem, but the kidney has raised the bicarbonate to 30. Now our equation becomes 6.1 plus the log of 20, or 6.1 plus 1.3, and pH is 7.4—apparently normal.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
f804c3e7-30d1-4ff6-9344-fcbefcaee359,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Equation 12.19,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
86bd34ca-e88b-4435-8806-83fa52171c85,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,[latex]pH = 6.1 + log \displaystyle\frac{30}{(0.03 \times 50)} = 6.1 + log(20) = 6.1 + 1.3 = 7.4[/latex],True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
7926b4fc-57c6-4f45-9af9-cba923d699fc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,But when we look at all three numbers we see that the patient is far from normal: the pH is okay only because the kidneys have raised bicarbonate to match the raised CO2 and keep the ratio the same. So we now have a respiratory acidosis with metabolic compensation.,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
6b5a5342-02e1-4bb5-85a8-00574d1627f8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,Summary,False,Summary,,,,
d40c9d57-bc43-4fb6-9f0e-e3553ce1f145,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-4,"So although it has been a long journey through this chapter you should now be able to interpret blood gas values to determine whether a patient is in acidosis or alkalosis and whether or not compensation is present. I strongly recommend writing the Henderson–Hasselbalch equation as a formula in Excel so that you can plug in CO2 and bicarbonate values and see what happens to pH. By repeatedly interpreting blood gas values and pH, determining the status of a patient will rapidly become second nature.",True,Summary,,,,
7a9910b7-7d7b-45a9-9e2e-192897fb2049,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,CO₂ and pH,False,CO₂ and pH,,,,
7635e9d4-5cc3-4b12-936c-bae92ddefa38,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,We will start by revisiting the equation dealt with in the previous chapter in the context of four different clinical scenarios.,True,CO₂ and pH,,,,
eded4583-1e82-492b-a163-40018ccc7f90,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"Case #1, normal: In the normal situation an increase in tissue metabolism leads to a rise in arterial CO2, pushing the equation to the right and causing a rise in hydrogen ion concentration and a consequent fall in pH. Both the rise in CO2 and fall in pH stimulate breathing. This increase in alveolar ventilation leads to a fall in arterial CO2, pushing the equation back left and lowering hydrogen ions back to normal.",True,CO₂ and pH,,,,
b40b961a-9248-4e05-b7eb-648852a076f3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.1,True,CO₂ and pH,,,,
8fa02f4c-d11e-4c70-ac12-97b2dbc4a115,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],False,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
68e4b411-f278-47d9-9357-6e69707f255b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"Case #2, metabolic acidosis: CO2 is by no means the only source of hydrogen ions in the system. Most metabolic pathways result in acidic by-products, and the pulmonary, renal, and buffering systems are generally battling to raise blood and tissue pH back from their tendency to turn acidic. The rise in hydrogen ions resulting from metabolic processes is referred to as metabolic acidosis. The fall in pH stimulates an increase in respiration, which in turn causes a fall in CO2, and the lower CO2 drives the equation to the left, reducing the number of H+ and thereby raising pH back to normal. Here the pulmonary system has compensated for a metabolic process, and this is referred to as respiratory compensation of metabolic acidosis. The patient may now have a normal blood pH, but the CO2 will be low. In summary, all the pulmonary system has done is get rid of one source of hydrogen ions (carbonic acid derived from dissolved CO2) to compensate for another source of hydrogen ions it cannot do anything about (most metabolically driven acids are nonvolatile (i.e., do not vaporize into a gas the lungs can get rid of)).",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
26e26c8c-6f26-413b-8752-8905f5259556,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"The advantage of the pulmonary system being involved in pH regulation is that it is quick—a few larger breaths and arterial PCO2 can be dropped significantly. So the pulmonary system is adept at minute-by-minute (or breath-by-breath) regulation of pH that copes admirably with short-term changes in pH. It is worth noting here that metabolic alkalosis can be reversed by reducing or even stopping breathing, allowing CO2 to accumulate in the arterial blood and lowering pH back to normal.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
684c86b4-2283-499a-b4f1-c504aa8fd547,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"The disadvantage to using the pulmonary system for compensation is that it can only mediate its effect via CO2. So any metabolic acids are eventually dealt with by the renal system, which, although much slower, is capable of excreting any nonvolatile metabolic acids. So through a combination of rapid pulmonary CO2 expulsion and slower but more versatile renal function, pH is normally maintained within a tight range even in the face of large metabolic changes. The kidney also has the advantage of being able to modify bicarbonate levels, which we will see the importance of when we look at the buffering systems in a moment.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
ade91fd7-f444-4f3e-8fd7-2f56a6ef05b2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"It is worth noting here, especially for the chemists and biochemists among you, that although equation 12.1 is a reversible reaction, it is open at both ends—the lung being able to expel or retain CO2 at one end and the kidneys being able to retain or expel hydrogen ions and bicarbonate at the other.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
636eab4b-8ad6-48b1-94b0-59525908a8cc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"Case #3, respiratory acidosis: Given its capability to influence pH, failure of the lung to expel an appropriate amount of CO2 can lead to deviations in pH. Let us take a case of severe lung disease, say COPD, for example. The disease has diminished the ability of the lung to expel CO2, so arterial PCO2 rises, pushing the equation to the right and causing a fall in pH, referred to as respiratory acidosis. This acid must be immediately buffered until kidney function can be modified to begin secreting the excess hydrogen ions and even produce more bicarbonate to replenish the buffering system, a process referred to as metabolic compensation of respiratory acidosis.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
65f66fbe-bcca-4847-b1a3-330998c05b6f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"Case #4, respiratory alkalosis: Likewise, if ventilation is inappropriately high with respect to CO2 production, such as during a period of hyperventilation, then too much CO2 will be lost and pH will fall. The alkalosis must be immediately buffered to avoid deleterious effects. Over the longer term the kidney can lower the raised pH by reabsorbing hydrogen ions and even excreting bicarbonate buffer—again this is termed metabolic compensation—but this time for an alkalosis caused by an inappropriate respiratory response.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
073fe4eb-e88f-4517-8de9-e683630307cc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Physiological Buffers,False,Physiological Buffers,,,,
48b40028-130c-430c-ac4a-8a9706f247fe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"Although the lung’s ability to expel CO2 and the kidney’s ability to excrete or absorb hydrogen ions allow close regulation of pH, their responses alone are not sufficient to prevent immediate local changes in pH at the tissue. This is the role of the buffering systems.",True,Physiological Buffers,,,,
102c38ab-0ffa-423d-95a2-bc551b7d1d16,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"Buffering systems are chemicals within tissue and the blood that have the ability to absorb either hydrogen ions and/or hydroxyl ions. Once these ions are removed from solution (albeit temporarily) then their effect on pH is diminished. We will deal with buffers in the context of acids, as this is the most common physiological situation.",True,Physiological Buffers,,,,
9af4c3ec-e128-408f-8c54-957c7a7cf432,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"If you need an analogy for the function of buffers, imagine them as a chemical mop—they soak up the hydrogen ions and stop them from making a cellular mess, but the hydrogen ions, although contained, remain in the system. It is the role of the lungs and kidneys to “rinse the mop” and get rid of the hydrogen ions from the system.",True,Physiological Buffers,,,,
a6da1bd0-2e87-4d6a-aa92-485e39314756,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,There are three major chemical buffering groups in the body:,False,There are three major chemical buffering groups in the body:,,,,
6bf051e4-6a9a-470b-afc9-4e109edc7722,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,We will deal with the bicarbonate system as it involves the respiratory system and is also the major extracellular buffer.,True,There are three major chemical buffering groups in the body:,,,,
75c70bd2-ba0a-4e50-b527-e0c6149ef471,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"Bicarbonate buffering: A buffering system consists of a weak base capable of absorbing a strong acid and a weak acid capable of absorbing a strong base. As such, the bicarbonate system involves two components: sodium bicarbonate (a weak base) and carbonic acid (a weak acid). Let us look at how it works and put it in the context of the lungs.",True,There are three major chemical buffering groups in the body:,,,,
f4c290a6-f6d6-4753-b1b3-050de92a44e9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"First let us see how a weak acid (carbonic acid) deals with a strong base, in this example, sodium hydroxide (equation 12.2).",True,There are three major chemical buffering groups in the body:,,,,
f5d32cd1-0977-4ef4-b318-edab1e1bc74e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Buffering a strong base using a weak acid:,False,Buffering a strong base using a weak acid:,,,,
b3ec763b-98cb-461f-8c11-8d6362044001,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.2,True,Buffering a strong base using a weak acid:,,,,
2b3a4025-1d0b-4923-a73a-f2715a4cb674,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]NaOH = \color{red}{H_2CO_3}[/latex],False,[latex]NaOH = \color{red}{H_2CO_3}[/latex],,,,
559acb45-25ea-4de6-96d3-6c3401831c26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Sodium hydroxide is a strong base as it rapidly dissociates into a hydroxyl ion and a sodium ion.,True,[latex]NaOH = \color{red}{H_2CO_3}[/latex],,,,
dbfe099a-3fc3-4dbb-b5dc-0965dee90337,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.3,True,[latex]NaOH = \color{red}{H_2CO_3}[/latex],,,,
ab60ecd1-1d3b-4d38-8425-9bcb1dc35825,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + \color{red}{H_2CO_3}[/latex],False,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + \color{red}{H_2CO_3}[/latex],,,,
bffc1ad9-52a7-49b5-bda2-01c5d8b89a19,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,The hydroxyl ion is the potential threat to physiological function so must be buffered. This is achieved by the carbonic acid dissociating into a hydrogen ion and bicarbonate (a process you are familiar with).,True,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + \color{red}{H_2CO_3}[/latex],,,,
c6909dd5-aa7d-4d0a-af3b-f0284b24290c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,These dissociated ions now bind to form new partnerships as water and sodium hydroxide (a weak base) (equation 12.4).,True,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + \color{red}{H_2CO_3}[/latex],,,,
90e968bf-93ce-458e-9726-8a494986ca64,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.4,True,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + \color{red}{H_2CO_3}[/latex],,,,
38a527e8-8633-4a1c-8514-1fe33f894ac2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + {{HCO_{3-}}\atop{{H}^{+}}} \rightarrow H_2O + \color{blue}{NaHCO_3}[/latex],False,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + {{HCO_{3-}}\atop{{H}^{+}}} \rightarrow H_2O + \color{blue}{NaHCO_3}[/latex],,,,
4e658abf-28ec-4b83-8004-94b7ebcdad57,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"So there are a couple of things to notice here beyond watching the ions move and form new components. First, the buffering process has taken a situation with the threat from a strong base (NaOH) and toned it down to a situation with a weak base (NaHCO3); the problem has not gone away, it has just been reduced (or buffered). Second, you will see that both of the components of the bicarbonate system, carbonic acid and sodium bicarbonate, appear in the equation—we have just shifted from one to the other.",True,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + {{HCO_{3-}}\atop{{H}^{+}}} \rightarrow H_2O + \color{blue}{NaHCO_3}[/latex],,,,
f589b692-3f6f-4f69-a4df-1dfd015d21d0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Let us look at the opposite situation to see what happens when the buffering system is faced with a strong acid. This time a strong acid (hydrochloric acid) is faced with our weak base (sodium bicarbonate) (equation 12.5).,True,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + {{HCO_{3-}}\atop{{H}^{+}}} \rightarrow H_2O + \color{blue}{NaHCO_3}[/latex],,,,
66541182-4aa2-440c-bad0-32e94421ca4d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Buffering a strong acid using a weak base:,False,Buffering a strong acid using a weak base:,,,,
c1db143b-2499-448a-9b96-ef426c060f7d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.5,True,Buffering a strong acid using a weak base:,,,,
bfb39b91-d67c-473b-9163-756c3ebb25d0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]HCl + \color{blue}{NaHCO_3}[/latex],False,[latex]HCl + \color{blue}{NaHCO_3}[/latex],,,,
8e64c046-0269-4c67-a2b0-185a12e17afc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,The hydrochloric acid rapidly dissociates into a hydrogen ion and a chloride ion. The hydrogen ion now threatens physiological function and must be buffered.,True,[latex]HCl + \color{blue}{NaHCO_3}[/latex],,,,
88dad615-eef3-47ef-b00d-474503e6a40d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"Our weak base dissociates into sodium and bicarbonate ions. Again our ions recombine, this time to produce harmless sodium chloride and carbonic acid (equation 12.6).",True,[latex]HCl + \color{blue}{NaHCO_3}[/latex],,,,
f7b482c9-74b1-420b-a456-a1ea79a53e8c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.6,True,[latex]HCl + \color{blue}{NaHCO_3}[/latex],,,,
c1c13c6f-09cd-4dba-9502-996a3c9bdef1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],False,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
6ef50c9e-ced8-42e6-a30c-4ee3278b4c93,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"Notice again we have reduced but not removed the threat as we have gone from the presence of a strong acid to a weak one. Also notice that our two components in the bicarbonate system appear in the equation, and we have switched from one to the other. This should now make you realize that these two components are part of a reversible equation, and this reversible equation, even after the addition of sodium to one end, should look rather familiar (equation 12.7).",True,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
1177be82-7fd5-43eb-bb2e-747c9398c6f3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.7,True,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
d5579bfa-129c-40b6-aefb-7ef34035add7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]CO_2 + H_2O \leftrightarrow {\color{red}{H_2CO_3}} \leftrightarrow H^+ + HCO_{3-} + Na^+ \leftrightarrow \color{blue}{NaHCO_3}[/latex],True,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
9041f83b-7bc4-462d-8954-331d4966756a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,As CO2 is at one end of the equation you should appreciate how alveolar ventilation can influence the bicarbonate buffering system.,True,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
3edc9ec4-52e1-441e-99f1-fc8dbd46c36d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"Because of their critical role in maintaining blood pH, bicarbonate ions are routinely measured along with arterial blood gases. Knowing what the blood pH, arterial CO2, and bicarbonate levels are provides a very powerful and commonly used diagnostic measure allowing us not only to determine the pH status of the patient, but also the source of the problem and whether the renal or pulmonary systems are achieving compensation. Because of its power and common use, we are going to go through some fundamentals, and I am afraid that means looking at the bane of many a medical student: the Henderson–Hasselbalch equation. For those with a background in chemistry you might skip the next section, but for the rest of us, we are going to go through this step-by-step.",True,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
959108bc-f443-4eae-93a6-4148f5943963,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,The Henderson–Hasselbalch Equation,False,The Henderson–Hasselbalch Equation,,,,
ab9ce5bb-4478-4c7e-b8a3-c47e0ebeece1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"What we will see is how the balance of bicarbonate and hydrogen ions determines pH, and how both of these ions can be influenced by the kidneys and lungs to keep pH constant.",True,The Henderson–Hasselbalch Equation,,,,
3c346865-52cb-48c1-9a3a-52ba8fe159df,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"First, we will take the central and most important part of the infamous equation, discarding the more innocuous ends.",True,The Henderson–Hasselbalch Equation,,,,
da746a78-44fc-46d3-ba1b-f1eaf1651a83,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.8,True,The Henderson–Hasselbalch Equation,,,,
605c06c5-dce1-4fb6-a8aa-188075eec0da,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]H_2CO_3 \leftrightarrow H^+ + HCO_{3-}[/latex],False,[latex]H_2CO_3 \leftrightarrow H^+ + HCO_{3-}[/latex],,,,
6a592c4f-79cc-43c7-8c0d-d37df1e949ef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"This central portion describes the dissociation of carbonic acid into hydrogen and bicarbonate ions. But because carbonic acid is a weak acid, this dissociation is incomplete—some carbonic acid staying whole, some dissociating into the ions. The level of dissociation is described by the dissociation constant (K’), which really is the ratio of the concentrations of dissociated components to carbonic acid (equation 12.9).",True,[latex]H_2CO_3 \leftrightarrow H^+ + HCO_{3-}[/latex],,,,
dfe568c1-8b86-4c69-8161-8ead814b81d5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.9,True,[latex]H_2CO_3 \leftrightarrow H^+ + HCO_{3-}[/latex],,,,
464b6f62-800b-410d-b51e-cfb2bf80e528,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]K' = \displaystyle\frac{{H}^{+} \times {HCO}_{3}-}{H_2CO_3}[/latex],False,[latex]K' = \displaystyle\frac{{H}^{+} \times {HCO}_{3}-}{H_2CO_3}[/latex],,,,
42ad8d3f-6edd-496c-9916-e77a131ecc85,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"Because we are interested in calculating the pH, however, we are more interested in the amount of hydrogen ions, so rearranging this equation for hydrogen ion concentration we see the hydrogen ion concentration is the dissociation constant, multiplied by the ratio of carbonic acid and bicarbonate (equation 12.10).",True,[latex]K' = \displaystyle\frac{{H}^{+} \times {HCO}_{3}-}{H_2CO_3}[/latex],,,,
5ffe9ac8-3a2d-418a-8d40-555c55ef427d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.10,True,[latex]K' = \displaystyle\frac{{H}^{+} \times {HCO}_{3}-}{H_2CO_3}[/latex],,,,
5e3b025b-17d3-46ec-a290-f5c4af40565c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]H^+ = K' \times \displaystyle\frac{H_2CO_3}{HCO_3-}[/latex],False,[latex]H^+ = K' \times \displaystyle\frac{H_2CO_3}{HCO_3-}[/latex],,,,
612a79bb-942e-457c-8251-88135a0b62d2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"This equation theoretically would allow us to now determine hydrogen concentration and therefore pH, but there are some practical problems for us, the first of which is that the instability of carbonic acid means we cannot measure its concentration. So we have to use a proxy measure. The amount of carbonic acid is determined by the amount of carbon dioxide, as can be seen in the equation that is so familiar to you—the greater the amount of CO2, the more carbonic acid.",True,[latex]H^+ = K' \times \displaystyle\frac{H_2CO_3}{HCO_3-}[/latex],,,,
b1d7f0d8-ffd2-4254-8734-85adc62c3101,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.11,True,[latex]H^+ = K' \times \displaystyle\frac{H_2CO_3}{HCO_3-}[/latex],,,,
f619004b-e1c3-4587-9201-c02bbb52cc00,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],False,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
0eaad187-acd4-4ea7-ace1-7b0fbf64e606,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"So after accounting for the dissociation constant of carbonic acid and CO2 and water, we can simply replace carbonic acid concentration with concentration of CO2 (equation 12.12).",True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
ec19df2c-54c2-4d18-a4fe-ffec4226d0ff,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.12,True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
1a156f7e-ef74-43ad-9336-6dcb35433b27,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]H^+ = K' \times \displaystyle\frac{CO_2}{HCO_3}[/latex],False,[latex]H^+ = K' \times \displaystyle\frac{CO_2}{HCO_3}[/latex],,,,
a95b914d-80f3-43ff-8773-7c934e8b6333,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"We then bump into our next practical problem: our equation now has CO2 concentration in it, but clinically we do not measure CO2 as a concentration (as in mmols), but as a partial pressure. So our next and nearly final step is to convert CO2 concentration to CO2 partial pressure, and we do this by multiplying the partial pressure (our measured value) by the solubility coefficient of carbon dioxide, which happens to be 0.03 mmol/mmHg. Our equation thus now can be completed using our adjusted PCO2 (equation 12.13).",True,[latex]H^+ = K' \times \displaystyle\frac{CO_2}{HCO_3}[/latex],,,,
8d7d4d0f-8ebb-456f-bbc8-e77403ad6513,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,mmols,False,mmols,,,,
989b3321-913d-4540-a437-06f907909442,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.13,True,mmols,,,,
f26bd324-3401-4182-b521-a870713b8675,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]H^+ = K' \times \displaystyle\frac{0.03 \times PCO_2}{HCO_3-}[/latex],True,mmols,,,,
c392a457-4f67-4903-a7fe-1931fd990ca6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"Our equation as it is now allows us to calculate hydrogen ion concentration, but we need pH, so we have to make a conversion. Because pH is the negative logarithm of hydrogen concentration, we express everything in the negative log form. And because the negative log of the dissociation constant is referred to as pK, then we can simplify our equation one more step (equation 12.14).",True,mmols,,,,
4bfd8f72-b4d5-4308-8d02-2a2a9a8e0dbe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.14,True,mmols,,,,
4f8b4508-c479-4e6c-b0c3-f72db03dff22,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]pH = pK - log \displaystyle\frac{0.03 \times PCO_2}{HCO_3-}[/latex],True,mmols,,,,
aaf7bba9-6582-40b7-9cda-50845bb60846,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"To make our equation simple to use, we now get rid of the negative log, and so get the following (equation 12.15):",True,mmols,,,,
2828230d-9573-4e64-b61d-f7f8384cac32,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.15,True,mmols,,,,
52b3a75d-c309-44c9-8447-838fdbe070f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]pH = pK + log \displaystyle\frac{HCO_3-}{0.03 \times PCO_2}[/latex],True,mmols,,,,
6b42f666-b6cf-4e12-a8ed-415c4d065a25,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"We know that the pK of the bicarbonate system happens to be 6.1, so substituting this into the equation we end up with the Henderson–Hasselbalch equation (equation 12.16).",True,mmols,,,,
fa168222-b6a1-494a-a692-c7fbbb93a8bf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Let us put this in context.,False,Let us put this in context.,,,,
543ceafc-0d1d-4de0-a808-c372a92b7ca3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"First, the equation shows that if CO2 rises then pH falls, and because CO2 is under the influence of alveolar ventilation, this explains how the alveolar ventilation can now control pH. It also shows that if bicarbonate increases then pH increases, and equally if bicarbonate falls then pH falls. Because the bicarbonate concentration can be modified either way by the kidneys, the equation also shows how the kidneys can modify pH (equation 12.16).",True,Let us put this in context.,,,,
6fd0db2a-8198-4cdf-bde5-159e333e4469,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.16,True,Let us put this in context.,,,,
02c6231d-d6d9-41e0-8129-cf24ae10dbbd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Role of kidneys (numerator) / Role of lungs (denominator),False,Role of kidneys (numerator) / Role of lungs (denominator),,,,
fac7d80b-ac5a-43f6-bcfc-2b0a82f6186f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]pH = 6.1 + log \displaystyle\frac{HCO_3-}{0.03 \times PCO_2}[/latex],True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
9584c329-3cd3-4aa6-aa1a-2a681f2df73f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"The involvement of these two major physiological systems in this equation make the bicarbonate system a very powerful buffer, particularly when considering that there is an unlimited source of CO2 and therefore bicarbonate supplied by the metabolism.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
288e0c93-2d28-4a48-818a-958878e53d12,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"But more importantly it shows that pH is actually determined by the ratio of bicarbonate and CO2 and that both are equally important. This fact is critical to appreciate as it forms the basis of understanding the compensation mechanisms we dealt with earlier. This is why I put you through this derivation. So for example, if a rise in CO2 (such as in lung disease) is accompanied by an equal rise in bicarbonate (generated by the kidney), then the ratio between the two remains the same and therefore pH remains the same. Likewise, if during a fall in CO2 the kidneys excrete bicarbonate, then pH can be kept constant. So before we finish, let us show you that the equation actually works by plugging in some numbers.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
9d8fc5aa-5d29-4e97-9219-d81709f58822,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"Example #1: Let us start with normal values, a PCO2 of 40 mmHg and a bicarbonate of 24, and plug these into the equation. This comes to 6.1 plus the log of 20, which is 6.1 plus 1.3, or 7.4 (i.e., normal arterial pH).",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
98f3dbe9-a97b-4005-8550-ea186c8599da,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.17,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
041b11d4-094c-48ba-9336-4966ebe60a79,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]pH = 6.1 + log \displaystyle\frac{24}{(0.03 \times 40)} = 6.1 + log(20) = 6.1 + 1.3 = 7.4[/latex],True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
9eedf056-94a6-4a99-a705-46f744839d29,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"Example #2: Now let us look at a case of acute lung failure that has caused a rise in arterial PCO2, but has not persisted long enough for the kidney to respond and compensate. PCO2 has risen to 50 mmHg, and bicarbonate has not changed. Our calculation now goes to 6.1 plus the log of 16, which is 6.1 plus 1.2, and pH has fallen to 7.3.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
cb8a5393-8fc2-472f-9917-f784db70d481,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.18,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
565a5970-f6fe-479c-838e-c695bc5c0d07,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]pH = 6.1 + log \displaystyle\frac{24}{(0.03 \times 50)} = 6.1 + log(16) = 6.1 + 1.2 = 7.3[/latex],True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
7c229ba9-8e4a-46b5-af41-2414620080e9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"We now have three numbers that can give a meaningful clinical interpretation. The low pH indicates the patient is in acidosis. The raised PCO2 suggests that this is respiratory acidosis, and the unchanged bicarbonate suggests no metabolic compensation has taken place.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
0829674d-4f3d-46e2-8308-554c51b7bdd3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"Example #3: Now let us return to our patient thirty-six hours later when we have given the kidney a chance to respond. The patient’s PCO2 remains at 50 because of the persistent lung problem, but the kidney has raised the bicarbonate to 30. Now our equation becomes 6.1 plus the log of 20, or 6.1 plus 1.3, and pH is 7.4—apparently normal.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
e4e6f47f-32c4-4e08-a5e0-5f38716ac585,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Equation 12.19,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
d915b3e8-ec83-46ed-b5d0-bc6365c4ad78,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,[latex]pH = 6.1 + log \displaystyle\frac{30}{(0.03 \times 50)} = 6.1 + log(20) = 6.1 + 1.3 = 7.4[/latex],True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
1ecaa722-687e-4925-8dac-44119c55bb03,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,But when we look at all three numbers we see that the patient is far from normal: the pH is okay only because the kidneys have raised bicarbonate to match the raised CO2 and keep the ratio the same. So we now have a respiratory acidosis with metabolic compensation.,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
e6e09160-f689-49f5-9215-c8d86278f8f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,Summary,False,Summary,,,,
3594e333-da78-4d35-b181-e81d28562eba,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Henderson–Hasselbalch Equation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-3,"So although it has been a long journey through this chapter you should now be able to interpret blood gas values to determine whether a patient is in acidosis or alkalosis and whether or not compensation is present. I strongly recommend writing the Henderson–Hasselbalch equation as a formula in Excel so that you can plug in CO2 and bicarbonate values and see what happens to pH. By repeatedly interpreting blood gas values and pH, determining the status of a patient will rapidly become second nature.",True,Summary,,,,
2a0eceeb-4a4e-42a5-a545-36b64178b02c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,CO₂ and pH,False,CO₂ and pH,,,,
161757a1-7a8a-4bf5-a2ee-421b75d2687d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,We will start by revisiting the equation dealt with in the previous chapter in the context of four different clinical scenarios.,True,CO₂ and pH,,,,
d6c923a1-ef4a-472d-aff9-f73533127f92,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"Case #1, normal: In the normal situation an increase in tissue metabolism leads to a rise in arterial CO2, pushing the equation to the right and causing a rise in hydrogen ion concentration and a consequent fall in pH. Both the rise in CO2 and fall in pH stimulate breathing. This increase in alveolar ventilation leads to a fall in arterial CO2, pushing the equation back left and lowering hydrogen ions back to normal.",True,CO₂ and pH,,,,
2a3964be-e780-4a53-a695-21f408cd84f7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.1,True,CO₂ and pH,,,,
ebfe9e4c-b285-48d5-a3f0-d0941d088387,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,CO2+H2O⇔H2CO3⇔H++HCO−3,False,CO2+H2O⇔H2CO3⇔H++HCO−3,,,,
6afb88c5-6205-49cc-b4ce-494943dea979,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,C,False,C,,,,
f646c288-364a-4f40-9ebd-a5bb0ab1f6fe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,O2,False,O2,,,,
7a786602-a217-4e86-b6ac-e1db1463c16d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,O,False,O,,,,
30dd752b-9620-487e-bbbf-becb76d589cd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,2,False,2,,,,
a9bee480-863d-4bfc-b783-5e876d5de499,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,+,False,+,,,,
ba294884-fc12-42e1-b8a6-13dfc4ecfd8c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,H2,False,H2,,,,
d79dab69-7d99-4709-8ef9-d1fbd3610bf5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,H,False,H,,,,
b114d319-8b95-4dd9-ba0e-8c1d889ad835,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,⇔,False,⇔,,,,
0212cc1a-7925-4685-b325-c3de0f2ea69a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,O3,False,O3,,,,
05c2e4cb-8705-4eca-8a7b-74825c39632b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,3,False,3,,,,
a77e2df0-9147-488a-98d7-1ae6175e6b55,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,H+,False,H+,,,,
dcac99e2-6a30-4711-bf62-9ddfc5d0c1fa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,O−3,False,O−3,,,,
957058a7-79c9-4e7a-9071-61939d1c36fc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,−3,False,−3,,,,
3ebda612-6208-42b6-9b3d-abdad0c64a01,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,−,False,−,,,,
8267944c-a45f-4e23-b61b-101adab95051,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"Case #2, metabolic acidosis: CO2 is by no means the only source of hydrogen ions in the system. Most metabolic pathways result in acidic by-products, and the pulmonary, renal, and buffering systems are generally battling to raise blood and tissue pH back from their tendency to turn acidic. The rise in hydrogen ions resulting from metabolic processes is referred to as metabolic acidosis. The fall in pH stimulates an increase in respiration, which in turn causes a fall in CO2, and the lower CO2 drives the equation to the left, reducing the number of H+ and thereby raising pH back to normal. Here the pulmonary system has compensated for a metabolic process, and this is referred to as respiratory compensation of metabolic acidosis. The patient may now have a normal blood pH, but the CO2 will be low. In summary, all the pulmonary system has done is get rid of one source of hydrogen ions (carbonic acid derived from dissolved CO2) to compensate for another source of hydrogen ions it cannot do anything about (most metabolically driven acids are nonvolatile (i.e., do not vaporize into a gas the lungs can get rid of)).",True,−,,,,
c0203243-c202-42c2-acaa-d89cd8086f1a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"The advantage of the pulmonary system being involved in pH regulation is that it is quick—a few larger breaths and arterial PCO2 can be dropped significantly. So the pulmonary system is adept at minute-by-minute (or breath-by-breath) regulation of pH that copes admirably with short-term changes in pH. It is worth noting here that metabolic alkalosis can be reversed by reducing or even stopping breathing, allowing CO2 to accumulate in the arterial blood and lowering pH back to normal.",True,−,,,,
8e165cef-e7ea-418c-aaed-e77a20568c38,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"The disadvantage to using the pulmonary system for compensation is that it can only mediate its effect via CO2. So any metabolic acids are eventually dealt with by the renal system, which, although much slower, is capable of excreting any nonvolatile metabolic acids. So through a combination of rapid pulmonary CO2 expulsion and slower but more versatile renal function, pH is normally maintained within a tight range even in the face of large metabolic changes. The kidney also has the advantage of being able to modify bicarbonate levels, which we will see the importance of when we look at the buffering systems in a moment.",True,−,,,,
2e6f4e38-c2a1-4d8d-9eba-09828bd2642a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"It is worth noting here, especially for the chemists and biochemists among you, that although equation 12.1 is a reversible reaction, it is open at both ends—the lung being able to expel or retain CO2 at one end and the kidneys being able to retain or expel hydrogen ions and bicarbonate at the other.",True,−,,,,
42d79c3f-3a63-43aa-ba2e-725f2ccd0c91,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"Case #3, respiratory acidosis: Given its capability to influence pH, failure of the lung to expel an appropriate amount of CO2 can lead to deviations in pH. Let us take a case of severe lung disease, say COPD, for example. The disease has diminished the ability of the lung to expel CO2, so arterial PCO2 rises, pushing the equation to the right and causing a fall in pH, referred to as respiratory acidosis. This acid must be immediately buffered until kidney function can be modified to begin secreting the excess hydrogen ions and even produce more bicarbonate to replenish the buffering system, a process referred to as metabolic compensation of respiratory acidosis.",True,−,,,,
a7052e76-7a9d-488b-80d3-3b3cacb1e718,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"Case #4, respiratory alkalosis: Likewise, if ventilation is inappropriately high with respect to CO2 production, such as during a period of hyperventilation, then too much CO2 will be lost and pH will fall. The alkalosis must be immediately buffered to avoid deleterious effects. Over the longer term the kidney can lower the raised pH by reabsorbing hydrogen ions and even excreting bicarbonate buffer—again this is termed metabolic compensation—but this time for an alkalosis caused by an inappropriate respiratory response.",True,−,,,,
0658d98f-54df-4361-b506-1f11b52a26dc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Physiological Buffers,False,Physiological Buffers,,,,
7a729365-4994-45af-b166-a0d7232302f1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"Although the lung’s ability to expel CO2 and the kidney’s ability to excrete or absorb hydrogen ions allow close regulation of pH, their responses alone are not sufficient to prevent immediate local changes in pH at the tissue. This is the role of the buffering systems.",True,Physiological Buffers,,,,
0e2bb7c8-0a6a-4d6a-b5c8-4b9d3072a95b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"Buffering systems are chemicals within tissue and the blood that have the ability to absorb either hydrogen ions and/or hydroxyl ions. Once these ions are removed from solution (albeit temporarily) then their effect on pH is diminished. We will deal with buffers in the context of acids, as this is the most common physiological situation.",True,Physiological Buffers,,,,
af89851f-1e63-4b76-b03f-3de036988216,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"If you need an analogy for the function of buffers, imagine them as a chemical mop—they soak up the hydrogen ions and stop them from making a cellular mess, but the hydrogen ions, although contained, remain in the system. It is the role of the lungs and kidneys to “rinse the mop” and get rid of the hydrogen ions from the system.",True,Physiological Buffers,,,,
f77d17b3-5e74-44e5-a58d-081f80516d91,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,There are three major chemical buffering groups in the body:,False,There are three major chemical buffering groups in the body:,,,,
1f642023-049e-4777-9c2d-344a1f7c4334,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,We will deal with the bicarbonate system as it involves the respiratory system and is also the major extracellular buffer.,True,There are three major chemical buffering groups in the body:,,,,
bc08831e-cf05-42f8-afa3-b30f4ee62de7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"Bicarbonate buffering: A buffering system consists of a weak base capable of absorbing a strong acid and a weak acid capable of absorbing a strong base. As such, the bicarbonate system involves two components: sodium bicarbonate (a weak base) and carbonic acid (a weak acid). Let us look at how it works and put it in the context of the lungs.",True,There are three major chemical buffering groups in the body:,,,,
53a389de-b0fc-4123-a04d-179db95885c3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"First let us see how a weak acid (carbonic acid) deals with a strong base, in this example, sodium hydroxide (equation 12.2).",True,There are three major chemical buffering groups in the body:,,,,
55702dd9-f654-42bf-8b5e-ce45f74f3be5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Buffering a strong base using a weak acid:,False,Buffering a strong base using a weak acid:,,,,
ac2321aa-4c4d-423e-a81b-4b54db278775,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.2,True,Buffering a strong base using a weak acid:,,,,
323a77c4-0415-4239-857e-96e381bc2e22,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,NaOH=H2CO3,False,NaOH=H2CO3,,,,
3b262001-f7ee-4007-a370-d3c0633d5079,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,N,False,N,,,,
47e1a489-7810-417a-8e14-9d28d4528324,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,a,False,a,,,,
fb9f0133-72a0-418b-883d-bb4902a66601,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,=,False,=,,,,
041df9f6-c9b7-4ff2-b2d7-667fa21a0536,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,H2CO3,False,H2CO3,,,,
b7731370-6e90-4164-aad7-bac97dd23a84,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Sodium hydroxide is a strong base as it rapidly dissociates into a hydroxyl ion and a sodium ion.,True,H2CO3,,,,
0d294464-f897-4b1e-9065-e4576a1c50ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.3,True,H2CO3,,,,
ce5ccda8-2f24-455a-aa9f-066c950a708f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Na+OH−+H2CO3,False,Na+OH−+H2CO3,,,,
0e701d96-df01-4d70-a6ea-c9a1f3005616,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Na+OH−,False,Na+OH−,,,,
ecc6cc92-eb04-451e-94f5-b10e1d8cc517,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Na+,False,Na+,,,,
b18c9d07-8964-4219-954b-aa097996611b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,a+,False,a+,,,,
827ea1ee-9009-4f86-812d-66e5c9332109,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,OH−,False,OH−,,,,
931e55c5-75ea-4629-99f3-77e71b6326a1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,OH,False,OH,,,,
0f3871a7-5426-478e-a0d9-5d61ac54935e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,The hydroxyl ion is the potential threat to physiological function so must be buffered. This is achieved by the carbonic acid dissociating into a hydrogen ion and bicarbonate (a process you are familiar with).,True,OH,,,,
fd5b5f35-a566-4992-8dfe-27b01aacb8c6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,These dissociated ions now bind to form new partnerships as water and sodium hydroxide (a weak base) (equation 12.4).,True,OH,,,,
c588dfe3-5506-451e-812c-8737f50b01e9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.4,True,OH,,,,
1403d761-e34c-4fc5-9b76-a0a88ea1d830,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Na+OH−+HCO3−H+→H2O+NaHCO3,False,Na+OH−+HCO3−H+→H2O+NaHCO3,,,,
9010f0e0-fd88-4e22-9fb0-493ae6d79022,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,HCO3−H+,False,HCO3−H+,,,,
f96a7e23-59e6-44bc-b024-62a06514cf92,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,HCO3−,False,HCO3−,,,,
093157ce-1d96-4198-b6d6-71d2d8759849,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,O3−,False,O3−,,,,
c6626eb3-af85-4eb0-ab80-0acfa1ff5fff,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,3−,False,3−,,,,
4cb4237b-73ea-4b83-b1c0-3b24407f0c8f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,→,False,→,,,,
5414444f-35a7-4a89-8827-d648cd75c6b2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,NaHCO3,False,NaHCO3,,,,
f8fa61a7-dfb6-47dd-aae8-1ab08f9c562b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"So there are a couple of things to notice here beyond watching the ions move and form new components. First, the buffering process has taken a situation with the threat from a strong base (NaOH) and toned it down to a situation with a weak base (NaHCO3); the problem has not gone away, it has just been reduced (or buffered). Second, you will see that both of the components of the bicarbonate system, carbonic acid and sodium bicarbonate, appear in the equation—we have just shifted from one to the other.",True,NaHCO3,,,,
9f07875b-4f6e-4cca-b5d1-e86f67e4f0ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Let us look at the opposite situation to see what happens when the buffering system is faced with a strong acid. This time a strong acid (hydrochloric acid) is faced with our weak base (sodium bicarbonate) (equation 12.5).,True,NaHCO3,,,,
e353d4ea-5103-4c39-aba7-e4f52c8ca2aa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Buffering a strong acid using a weak base:,False,Buffering a strong acid using a weak base:,,,,
b2b446f5-1663-4765-a340-05ff09fb8381,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.5,True,Buffering a strong acid using a weak base:,,,,
4ede2123-2fe6-4b04-8dd7-cd6f58a6136a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,HCl+NaHCO3,False,HCl+NaHCO3,,,,
372fc6fe-e6c0-46df-bb0d-c04c02428e30,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,l,False,l,,,,
3f1b3ee9-2f1c-4006-a7cd-86fddd046793,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,The hydrochloric acid rapidly dissociates into a hydrogen ion and a chloride ion. The hydrogen ion now threatens physiological function and must be buffered.,True,l,,,,
3eeb1c85-3d81-417a-8657-7bfa54c4251f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"Our weak base dissociates into sodium and bicarbonate ions. Again our ions recombine, this time to produce harmless sodium chloride and carbonic acid (equation 12.6).",True,l,,,,
267c2bea-4dd8-403f-9fae-4257e72dcb38,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.6,True,l,,,,
5512bf08-739b-4a05-851b-7ea9461bea55,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,H+Cl−+HCO3−Na+→NaCl+H2CO3,False,H+Cl−+HCO3−Na+→NaCl+H2CO3,,,,
efbb097e-a645-4e2a-92ee-54e98c9ca10b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,H+Cl−,False,H+Cl−,,,,
a7f0bd88-c958-47b2-87ad-5a1abbb2fbf9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Cl−,False,Cl−,,,,
86c456b0-c634-416a-b72b-89e068c0c485,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Cl,False,Cl,,,,
43dfb1c3-1db6-42e9-9c2e-a8b61da64c9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,HCO3−Na+,False,HCO3−Na+,,,,
9cb0f9b5-8f5f-471b-a2cc-007fe3beb025,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Na,False,Na,,,,
1df2fd14-0cf1-4a19-966a-28f815a088ca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"Notice again we have reduced but not removed the threat as we have gone from the presence of a strong acid to a weak one. Also notice that our two components in the bicarbonate system appear in the equation, and we have switched from one to the other. This should now make you realize that these two components are part of a reversible equation, and this reversible equation, even after the addition of sodium to one end, should look rather familiar (equation 12.7).",True,Na,,,,
5f39b870-ee32-4d6e-bf09-c18cf342e130,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.7,True,Na,,,,
003facc0-6a22-461c-9480-ea7b7669a46c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,CO2+H2O↔H2CO3↔H++HCO3−+Na+↔NaHCO3,False,CO2+H2O↔H2CO3↔H++HCO3−+Na+↔NaHCO3,,,,
ab6d0942-bcaa-4b98-8433-6a7445d2e14e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,↔,False,↔,,,,
2b6e1e15-eb5a-4e64-9605-bb130ce545cf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,As CO2 is at one end of the equation you should appreciate how alveolar ventilation can influence the bicarbonate buffering system.,True,↔,,,,
279767a5-f9b2-43e3-b1ff-009aa4acc170,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"Because of their critical role in maintaining blood pH, bicarbonate ions are routinely measured along with arterial blood gases. Knowing what the blood pH, arterial CO2, and bicarbonate levels are provides a very powerful and commonly used diagnostic measure allowing us not only to determine the pH status of the patient, but also the source of the problem and whether the renal or pulmonary systems are achieving compensation. Because of its power and common use, we are going to go through some fundamentals, and I am afraid that means looking at the bane of many a medical student: the Henderson–Hasselbalch equation. For those with a background in chemistry you might skip the next section, but for the rest of us, we are going to go through this step-by-step.",True,↔,,,,
26e2e49b-e378-4a29-85c9-b663d321dbfd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,The Henderson–Hasselbalch Equation,False,The Henderson–Hasselbalch Equation,,,,
78601e7b-083c-457d-814e-4448cddf853e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"What we will see is how the balance of bicarbonate and hydrogen ions determines pH, and how both of these ions can be influenced by the kidneys and lungs to keep pH constant.",True,The Henderson–Hasselbalch Equation,,,,
b711aa13-02c7-4fe3-8569-f26f27ea87a0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"First, we will take the central and most important part of the infamous equation, discarding the more innocuous ends.",True,The Henderson–Hasselbalch Equation,,,,
bc2d624c-d883-4dbc-a756-7e6d379f8c3d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.8,True,The Henderson–Hasselbalch Equation,,,,
96f7580d-b019-43e7-a26b-0b09338df38b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,H2CO3↔H++HCO3−,False,H2CO3↔H++HCO3−,,,,
44615fe5-0208-4dd5-af2d-f0a6814469f6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"This central portion describes the dissociation of carbonic acid into hydrogen and bicarbonate ions. But because carbonic acid is a weak acid, this dissociation is incomplete—some carbonic acid staying whole, some dissociating into the ions. The level of dissociation is described by the dissociation constant (K’), which really is the ratio of the concentrations of dissociated components to carbonic acid (equation 12.9).",True,H2CO3↔H++HCO3−,,,,
6d2386be-d858-4184-a541-6a9b948647ae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.9,True,H2CO3↔H++HCO3−,,,,
1643fafe-702b-49b9-ae0f-6b42b80ff2bd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,K′=H+×HCO3−H2CO3,False,K′=H+×HCO3−H2CO3,,,,
fb2cef64-cb7f-4c57-8dc6-60459cc33498,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,K′,False,K′,,,,
557b07cb-4132-4b35-a786-403d1fa65ac2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,K,False,K,,,,
b45c7c1c-a960-4bf9-b6c9-1c83e89338a5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,′,False,′,,,,
95d959a6-1b6a-45f2-8d82-be9e662baaa3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,H+×HCO3−H2CO3,False,H+×HCO3−H2CO3,,,,
67d26654-a446-4a91-a622-c158f3836cd2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,H+×HCO3−,False,H+×HCO3−,,,,
c74afed3-fc10-46c4-a55a-cdc2b5a2faf2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,×,False,×,,,,
41d625c2-8c5c-45ca-a735-5e580f26e6c6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,HCO3,False,HCO3,,,,
1c17bdc7-e42d-4186-a47d-a296812b613d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,HCO,False,HCO,,,,
9467cd32-a856-4951-a678-988c8bf248ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"Because we are interested in calculating the pH, however, we are more interested in the amount of hydrogen ions, so rearranging this equation for hydrogen ion concentration we see the hydrogen ion concentration is the dissociation constant, multiplied by the ratio of carbonic acid and bicarbonate (equation 12.10).",True,HCO,,,,
c81d8ac8-9043-4313-83f8-5ce2a9ed71a7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.10,True,HCO,,,,
05cc8475-a587-4a74-853c-7979c3853290,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,H+=K′×H2CO3HCO3−,False,H+=K′×H2CO3HCO3−,,,,
20d5e889-03e5-4952-bb74-cfb262d31527,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,H2CO3HCO3−,False,H2CO3HCO3−,,,,
627fe094-070f-404a-ba8a-1b046326fb33,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"This equation theoretically would allow us to now determine hydrogen concentration and therefore pH, but there are some practical problems for us, the first of which is that the instability of carbonic acid means we cannot measure its concentration. So we have to use a proxy measure. The amount of carbonic acid is determined by the amount of carbon dioxide, as can be seen in the equation that is so familiar to you—the greater the amount of CO2, the more carbonic acid.",True,H2CO3HCO3−,,,,
5d2363e6-2070-46c2-bb1f-a275d6a37be7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.11,True,H2CO3HCO3−,,,,
79805d7a-8695-49b2-afc6-dcf4d1cec9b5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,CO2+H2O↔H2CO3↔H++HCO3−,False,CO2+H2O↔H2CO3↔H++HCO3−,,,,
fa7e2e71-f7d4-46b6-acd9-0da0c77c838b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"So after accounting for the dissociation constant of carbonic acid and CO2 and water, we can simply replace carbonic acid concentration with concentration of CO2 (equation 12.12).",True,CO2+H2O↔H2CO3↔H++HCO3−,,,,
2b500289-eb6d-4827-8de6-d5dc26bc507d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.12,True,CO2+H2O↔H2CO3↔H++HCO3−,,,,
12260132-35be-4ef4-ad9c-b4ec0092ba61,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,H+=K′×CO2HCO3,False,H+=K′×CO2HCO3,,,,
ce9870a2-24a4-4666-90cf-fcb1100973bc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,CO2HCO3,False,CO2HCO3,,,,
77bc8cf5-1835-4a57-b8d7-56a18d292984,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,CO2,False,CO2,,,,
248c5eb2-6525-4e7d-ae94-5ceebd2c0d12,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"We then bump into our next practical problem: our equation now has CO2 concentration in it, but clinically we do not measure CO2 as a concentration (as in mmols), but as a partial pressure. So our next and nearly final step is to convert CO2 concentration to CO2 partial pressure, and we do this by multiplying the partial pressure (our measured value) by the solubility coefficient of carbon dioxide, which happens to be 0.03 mmol/mmHg. Our equation thus now can be completed using our adjusted PCO2 (equation 12.13).",True,CO2,,,,
713bc452-b1ec-4baa-bf37-174c502008e4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,mmols,False,mmols,,,,
73c29c5c-d8c9-427f-aa26-a0740c9b29a8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.13,True,mmols,,,,
e82a61a5-e5c5-483d-924a-4ac5dafa4cb7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,H+=K′×0.03×PCO2HCO3−,True,mmols,,,,
3706f7af-3861-4a03-8216-2ad249cd8ff0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,0.03×PCO2HCO3−,True,mmols,,,,
ef98bd66-f9b0-4324-a4ce-b4b086292b6f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,0.03×PCO2,True,mmols,,,,
4be474bd-b88e-4780-ad20-7e277ccd2627,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,0.03,True,mmols,,,,
6ae83798-7c93-4a9b-bdfd-103ae47d85e8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,P,False,P,,,,
216d98f4-c130-40fc-aa3e-b90b6f2d933d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"Our equation as it is now allows us to calculate hydrogen ion concentration, but we need pH, so we have to make a conversion. Because pH is the negative logarithm of hydrogen concentration, we express everything in the negative log form. And because the negative log of the dissociation constant is referred to as pK, then we can simplify our equation one more step (equation 12.14).",True,P,,,,
b14b5f71-6bbf-4a67-94bb-a0fc43e9781f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.14,True,P,,,,
7b7262cf-655e-4df9-a510-3d303f3af6b4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,pH=pK−log0.03×PCO2HCO3−,True,P,,,,
b810a656-3406-4323-b10b-cdf9617d6c80,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,p,False,p,,,,
43857add-f508-45d8-a4d8-397ce5bcb6d8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,o,False,o,,,,
fbaf64b0-ab9a-400b-919e-fed4421bf4ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,g,False,g,,,,
8de75fae-394f-4449-9d30-51cb89f2e44f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"To make our equation simple to use, we now get rid of the negative log, and so get the following (equation 12.15):",True,g,,,,
93df939a-5f33-4c78-b1fe-9188bfc9ee89,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.15,True,g,,,,
f9c9695b-fb6b-4941-bd36-de97e862f136,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,pH=pK+logHCO3−0.03×PCO2,True,g,,,,
a869269b-a999-4192-8dc9-82b12a7ba6a6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,HCO3−0.03×PCO2,True,g,,,,
e01ef9b2-3e87-47eb-9137-07b9f1dbe4f2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"We know that the pK of the bicarbonate system happens to be 6.1, so substituting this into the equation we end up with the Henderson–Hasselbalch equation (equation 12.16).",True,g,,,,
cfb4c359-a2dd-4426-b29c-46eb0636076d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Let us put this in context.,False,Let us put this in context.,,,,
35a53b7f-e308-48f6-88b5-681d34ab54f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"First, the equation shows that if CO2 rises then pH falls, and because CO2 is under the influence of alveolar ventilation, this explains how the alveolar ventilation can now control pH. It also shows that if bicarbonate increases then pH increases, and equally if bicarbonate falls then pH falls. Because the bicarbonate concentration can be modified either way by the kidneys, the equation also shows how the kidneys can modify pH (equation 12.16).",True,Let us put this in context.,,,,
ecd0c696-76ae-45be-8532-fbad0c798236,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.16,True,Let us put this in context.,,,,
8f0e65c7-2887-4c65-acad-f288970f9a05,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Role of kidneys (numerator) / Role of lungs (denominator),False,Role of kidneys (numerator) / Role of lungs (denominator),,,,
6ddbaaf9-7a2a-4b9b-8d74-b774941c7136,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,pH=6.1+logHCO3−0.03×PCO2,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
55f3492c-55b5-44d4-ad06-036d952ff6e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,6.1,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
8255cacb-bb4a-4297-9f2a-a34296125305,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"The involvement of these two major physiological systems in this equation make the bicarbonate system a very powerful buffer, particularly when considering that there is an unlimited source of CO2 and therefore bicarbonate supplied by the metabolism.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
0cbefab7-0b88-49cc-b6c8-b1b8245de48c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"But more importantly it shows that pH is actually determined by the ratio of bicarbonate and CO2 and that both are equally important. This fact is critical to appreciate as it forms the basis of understanding the compensation mechanisms we dealt with earlier. This is why I put you through this derivation. So for example, if a rise in CO2 (such as in lung disease) is accompanied by an equal rise in bicarbonate (generated by the kidney), then the ratio between the two remains the same and therefore pH remains the same. Likewise, if during a fall in CO2 the kidneys excrete bicarbonate, then pH can be kept constant. So before we finish, let us show you that the equation actually works by plugging in some numbers.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
d0f4b4b9-b616-4688-9b5b-f665c550ca0e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"Example #1: Let us start with normal values, a PCO2 of 40 mmHg and a bicarbonate of 24, and plug these into the equation. This comes to 6.1 plus the log of 20, which is 6.1 plus 1.3, or 7.4 (i.e., normal arterial pH).",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
4b145eef-373f-4e65-b38c-e80bae039fc3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.17,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
b8954cf1-75b5-4256-9528-49af358c6e3d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,pH=6.1+log24(0.03×40)=6.1+log(20)=6.1+1.3=7.4,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
1ce19981-006a-4f64-97c8-50dc2200621c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,24(0.03×40)=6.1+log(20)=6.1+1.3=7.4,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
a50c81b1-4a7f-47be-baa9-fa3da579493a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,24(0.03×40),True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
43a6ca03-aecc-42da-88d9-7317341b15da,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,24,False,24,,,,
708c86ec-800a-44e5-aef2-8f0148e50215,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,(0.03×40),True,24,,,,
a8be38ca-43ca-4075-95f4-3836892dcfd8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,(,False,(,,,,
844fc6ce-2e1b-4f21-85f7-a118b92346d3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,40,False,40,,,,
c62dc537-32ac-495a-87fd-5bf81eb0ca51,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,),False,),,,,
7df02790-098b-4f27-8ed8-fd043211e22b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,20,False,20,,,,
d4014eb0-33ed-48d6-bbef-e19beaf2f4c0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,1.3,True,20,,,,
f68310d5-2dbe-469d-8a0e-847c99ecfd27,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,7.4,True,20,,,,
9f0c586f-2ede-469e-9830-e374002795cb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"Example #2: Now let us look at a case of acute lung failure that has caused a rise in arterial PCO2, but has not persisted long enough for the kidney to respond and compensate. PCO2 has risen to 50 mmHg, and bicarbonate has not changed. Our calculation now goes to 6.1 plus the log of 16, which is 6.1 plus 1.2, and pH has fallen to 7.3.",True,20,,,,
fe813cd8-8179-47e5-bcf8-9119fb137f16,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.18,True,20,,,,
4385d215-fc84-4427-bcce-26cf8e7c8143,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,pH=6.1+log24(0.03×50)=6.1+log(16)=6.1+1.2=7.3,True,20,,,,
132ce581-bc38-4038-a3fe-51470dad698b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,24(0.03×50)=6.1+log(16)=6.1+1.2=7.3,True,20,,,,
5633a829-9b2f-4382-a22a-8bd3b01dacef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,24(0.03×50),True,20,,,,
d7fa266f-a818-4027-98fd-e173f1de9787,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,(0.03×50),True,20,,,,
02a0498d-dd93-4b1a-a18d-cb35608ad8df,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,50,False,50,,,,
c0a5fa82-b26a-40f6-9ec2-0ff40398bb3b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,16,False,16,,,,
04d9fa4f-c088-4e9c-8c66-41689fd640a9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,1.2,True,16,,,,
71fd15d4-890b-4da9-873c-7c200bd81a65,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,7.3,True,16,,,,
87cb3580-6f30-4cb9-9cb6-b2dd4adc8674,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"We now have three numbers that can give a meaningful clinical interpretation. The low pH indicates the patient is in acidosis. The raised PCO2 suggests that this is respiratory acidosis, and the unchanged bicarbonate suggests no metabolic compensation has taken place.",True,16,,,,
666fa5d6-18dc-47f6-8b75-47d4a145bfbe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"Example #3: Now let us return to our patient thirty-six hours later when we have given the kidney a chance to respond. The patient’s PCO2 remains at 50 because of the persistent lung problem, but the kidney has raised the bicarbonate to 30. Now our equation becomes 6.1 plus the log of 20, or 6.1 plus 1.3, and pH is 7.4—apparently normal.",True,16,,,,
d9d1e242-0fa7-4b5a-9008-63806ecc1b51,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Equation 12.19,True,16,,,,
9665794a-c243-4bbc-bdbc-eb738773735b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,pH=6.1+log30(0.03×50)=6.1+log(20)=6.1+1.3=7.4,True,16,,,,
1b9cb9c6-b06e-41ce-a263-2ec6ffa6ab3b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,30(0.03×50)=6.1+log(20)=6.1+1.3=7.4,True,16,,,,
4809f530-daa0-49a3-83c0-f1a87d50fdca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,30(0.03×50),True,16,,,,
2a9be877-b1fa-4561-9574-0e61464ed6d5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,30,False,30,,,,
2ef7a56f-14f8-44da-8afd-2bdb7a40c431,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,But when we look at all three numbers we see that the patient is far from normal: the pH is okay only because the kidneys have raised bicarbonate to match the raised CO2 and keep the ratio the same. So we now have a respiratory acidosis with metabolic compensation.,True,30,,,,
9cd5692c-0ec7-4108-96a4-d9e51fa19700,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,Summary,False,Summary,,,,
592b5824-00df-4ec6-be47-e131b659f38f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Buffers,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-2,"So although it has been a long journey through this chapter you should now be able to interpret blood gas values to determine whether a patient is in acidosis or alkalosis and whether or not compensation is present. I strongly recommend writing the Henderson–Hasselbalch equation as a formula in Excel so that you can plug in CO2 and bicarbonate values and see what happens to pH. By repeatedly interpreting blood gas values and pH, determining the status of a patient will rapidly become second nature.",True,Summary,,,,
01d72131-9f9c-476e-a5c4-b19d9c7a0b29,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,CO₂ and pH,False,CO₂ and pH,,,,
cee61b8a-6be3-4066-ae97-12f7d91ab18e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,We will start by revisiting the equation dealt with in the previous chapter in the context of four different clinical scenarios.,True,CO₂ and pH,,,,
6194e10b-3be4-4a33-bccc-4a586f1f4411,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"Case #1, normal: In the normal situation an increase in tissue metabolism leads to a rise in arterial CO2, pushing the equation to the right and causing a rise in hydrogen ion concentration and a consequent fall in pH. Both the rise in CO2 and fall in pH stimulate breathing. This increase in alveolar ventilation leads to a fall in arterial CO2, pushing the equation back left and lowering hydrogen ions back to normal.",True,CO₂ and pH,,,,
72d71673-a604-4a5d-8a08-2c4df17eec1a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.1,True,CO₂ and pH,,,,
57de4619-7e3c-45fc-b703-7595de671e8f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,CO2+H2O⇔H2CO3⇔H++HCO−3CO2+H2O⇔H2CO3⇔H++HCO−3,False,CO2+H2O⇔H2CO3⇔H++HCO−3CO2+H2O⇔H2CO3⇔H++HCO−3,,,,
43616880-ab5b-4fd4-85da-8e084b7d8e97,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,CO2+H2O⇔H2CO3⇔H++HCO−3,False,CO2+H2O⇔H2CO3⇔H++HCO−3,,,,
13ff9e94-400b-439e-9941-66656e635c94,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,C,False,C,,,,
a49f7320-b2eb-45b8-87bf-86c47f4afe28,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,O2,False,O2,,,,
23480c48-54a6-4a21-a98f-2047ec9c1f4a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,O,False,O,,,,
00cd2b11-7d3c-4273-bd02-5d080903fa57,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,2,False,2,,,,
8fd913dd-5d2f-4709-a1b3-3574427856aa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,+,False,+,,,,
7c8df3aa-a3c2-4257-aa5d-8edc6e851ee6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,H2,False,H2,,,,
be04e83b-6eb0-48c1-883a-104fb46afa33,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,H,False,H,,,,
bc9e3e73-e639-4052-a730-5676169dff72,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,⇔,False,⇔,,,,
fb4057f1-b1f4-4ad6-b63e-1aaf4851368f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,O3,False,O3,,,,
62c97042-bb76-4073-86dd-64c4c7b28231,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,3,False,3,,,,
390be26e-45a0-4cd0-8d73-656199ddf48e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,H+,False,H+,,,,
dfb7b4d5-aa15-4cf7-a3dd-7209f5a15bf8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,O−3,False,O−3,,,,
b6f311e7-70f3-4187-918a-e404148f316d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,−3,False,−3,,,,
d5b1acc9-4628-4aa5-b999-6c2e6a625777,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,−,False,−,,,,
d3e44736-6f73-4d96-a5d1-3da20b37bf32,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"Case #2, metabolic acidosis: CO2 is by no means the only source of hydrogen ions in the system. Most metabolic pathways result in acidic by-products, and the pulmonary, renal, and buffering systems are generally battling to raise blood and tissue pH back from their tendency to turn acidic. The rise in hydrogen ions resulting from metabolic processes is referred to as metabolic acidosis. The fall in pH stimulates an increase in respiration, which in turn causes a fall in CO2, and the lower CO2 drives the equation to the left, reducing the number of H+ and thereby raising pH back to normal. Here the pulmonary system has compensated for a metabolic process, and this is referred to as respiratory compensation of metabolic acidosis. The patient may now have a normal blood pH, but the CO2 will be low. In summary, all the pulmonary system has done is get rid of one source of hydrogen ions (carbonic acid derived from dissolved CO2) to compensate for another source of hydrogen ions it cannot do anything about (most metabolically driven acids are nonvolatile (i.e., do not vaporize into a gas the lungs can get rid of)).",True,−,,,,
9bd25a75-9197-4957-b879-643bed7bd1b5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"The advantage of the pulmonary system being involved in pH regulation is that it is quick—a few larger breaths and arterial PCO2 can be dropped significantly. So the pulmonary system is adept at minute-by-minute (or breath-by-breath) regulation of pH that copes admirably with short-term changes in pH. It is worth noting here that metabolic alkalosis can be reversed by reducing or even stopping breathing, allowing CO2 to accumulate in the arterial blood and lowering pH back to normal.",True,−,,,,
ef2e9566-957d-4ccb-bcd8-84e787eab7c7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"The disadvantage to using the pulmonary system for compensation is that it can only mediate its effect via CO2. So any metabolic acids are eventually dealt with by the renal system, which, although much slower, is capable of excreting any nonvolatile metabolic acids. So through a combination of rapid pulmonary CO2 expulsion and slower but more versatile renal function, pH is normally maintained within a tight range even in the face of large metabolic changes. The kidney also has the advantage of being able to modify bicarbonate levels, which we will see the importance of when we look at the buffering systems in a moment.",True,−,,,,
0ec1e6ec-373d-41e0-99c9-19cc936038c3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"It is worth noting here, especially for the chemists and biochemists among you, that although equation 12.1 is a reversible reaction, it is open at both ends—the lung being able to expel or retain CO2 at one end and the kidneys being able to retain or expel hydrogen ions and bicarbonate at the other.",True,−,,,,
2cdf75cb-5dce-4a89-a1bf-43027e74f809,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"Case #3, respiratory acidosis: Given its capability to influence pH, failure of the lung to expel an appropriate amount of CO2 can lead to deviations in pH. Let us take a case of severe lung disease, say COPD, for example. The disease has diminished the ability of the lung to expel CO2, so arterial PCO2 rises, pushing the equation to the right and causing a fall in pH, referred to as respiratory acidosis. This acid must be immediately buffered until kidney function can be modified to begin secreting the excess hydrogen ions and even produce more bicarbonate to replenish the buffering system, a process referred to as metabolic compensation of respiratory acidosis.",True,−,,,,
00528dc5-2118-4e69-98ec-a08d29a3051f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"Case #4, respiratory alkalosis: Likewise, if ventilation is inappropriately high with respect to CO2 production, such as during a period of hyperventilation, then too much CO2 will be lost and pH will fall. The alkalosis must be immediately buffered to avoid deleterious effects. Over the longer term the kidney can lower the raised pH by reabsorbing hydrogen ions and even excreting bicarbonate buffer—again this is termed metabolic compensation—but this time for an alkalosis caused by an inappropriate respiratory response.",True,−,,,,
f09d44e8-5e38-419a-a62c-f61ed6f30d8c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Physiological Buffers,False,Physiological Buffers,,,,
7e8046bb-19b3-4d31-a3ab-3bb6ee4f776e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"Although the lung’s ability to expel CO2 and the kidney’s ability to excrete or absorb hydrogen ions allow close regulation of pH, their responses alone are not sufficient to prevent immediate local changes in pH at the tissue. This is the role of the buffering systems.",True,Physiological Buffers,,,,
22e7a5e8-cd84-4ec1-80ef-9662b8aaf867,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"Buffering systems are chemicals within tissue and the blood that have the ability to absorb either hydrogen ions and/or hydroxyl ions. Once these ions are removed from solution (albeit temporarily) then their effect on pH is diminished. We will deal with buffers in the context of acids, as this is the most common physiological situation.",True,Physiological Buffers,,,,
c3420277-62e6-46b1-9efe-97d27839e508,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"If you need an analogy for the function of buffers, imagine them as a chemical mop—they soak up the hydrogen ions and stop them from making a cellular mess, but the hydrogen ions, although contained, remain in the system. It is the role of the lungs and kidneys to “rinse the mop” and get rid of the hydrogen ions from the system.",True,Physiological Buffers,,,,
e8f0c9d3-aa4e-4180-a5f9-345fb297cf86,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,There are three major chemical buffering groups in the body:,False,There are three major chemical buffering groups in the body:,,,,
be6e0ff7-dbce-4431-bb11-76e459f25fd4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,We will deal with the bicarbonate system as it involves the respiratory system and is also the major extracellular buffer.,True,There are three major chemical buffering groups in the body:,,,,
3521c1c7-bc04-4937-b026-0cdbb66ed63f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"Bicarbonate buffering: A buffering system consists of a weak base capable of absorbing a strong acid and a weak acid capable of absorbing a strong base. As such, the bicarbonate system involves two components: sodium bicarbonate (a weak base) and carbonic acid (a weak acid). Let us look at how it works and put it in the context of the lungs.",True,There are three major chemical buffering groups in the body:,,,,
6ec5b5e3-d23a-41b3-90b3-2f85b48a29dc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"First let us see how a weak acid (carbonic acid) deals with a strong base, in this example, sodium hydroxide (equation 12.2).",True,There are three major chemical buffering groups in the body:,,,,
49dfb3d1-d1b0-47eb-9f63-8f6dacd6d5df,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Buffering a strong base using a weak acid:,False,Buffering a strong base using a weak acid:,,,,
b7ebfecd-a0ef-4964-bfb8-5695eb050da3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.2,True,Buffering a strong base using a weak acid:,,,,
a58791f1-5daf-45e0-8971-8be6830c4b3a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,NaOH=H2CO3NaOH=H2CO3,False,NaOH=H2CO3NaOH=H2CO3,,,,
e6261efb-366e-48b9-b4c7-0931416eaefe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,NaOH=H2CO3,False,NaOH=H2CO3,,,,
1941b88e-60a7-4c99-81ab-d57a2ebc95bb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,N,False,N,,,,
a3e2405e-6848-420e-9b66-651a5134d132,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,a,False,a,,,,
503a4ad8-dcc0-4ca7-9ef0-b2097b4ef8d2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,=,False,=,,,,
e7be1b97-70ae-47a2-9d3b-435ce9dd918b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,H2CO3,False,H2CO3,,,,
761af85e-af1e-4b7a-b5f9-46dd6fe9e2f2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Sodium hydroxide is a strong base as it rapidly dissociates into a hydroxyl ion and a sodium ion.,True,H2CO3,,,,
17a70f51-2dd2-4977-9574-a0f569179e5f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.3,True,H2CO3,,,,
7584b5af-9d68-48cd-af6f-291c9fa20e62,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Na+OH−+H2CO3,False,Na+OH−+H2CO3,,,,
b72b8054-eb50-4106-90fe-01144a10cb42,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Na+OH−,False,Na+OH−,,,,
d60dc7b9-866e-427c-b668-690792c85c28,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Na+,False,Na+,,,,
5593e977-dca1-4d7c-9804-4246b319ba2f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,a+,False,a+,,,,
b7ababc3-b30c-44bb-bad0-68fb81dfc7a8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,OH−,False,OH−,,,,
dbee4403-1f0d-47f2-967f-89236fcf129e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,OH,False,OH,,,,
3d2ce167-dbf7-4a55-b376-26da2a36639a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,The hydroxyl ion is the potential threat to physiological function so must be buffered. This is achieved by the carbonic acid dissociating into a hydrogen ion and bicarbonate (a process you are familiar with).,True,OH,,,,
17435a1a-79a0-43d9-85df-fc64ab3fabf4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,These dissociated ions now bind to form new partnerships as water and sodium hydroxide (a weak base) (equation 12.4).,True,OH,,,,
badbd671-9475-4c13-b693-d863f0fa7417,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.4,True,OH,,,,
c439c619-ddd3-419a-bb20-ee70c4b30208,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Na+OH−+HCO3−H+→H2O+NaHCO3,False,Na+OH−+HCO3−H+→H2O+NaHCO3,,,,
2ecc8db4-be2f-4e47-b37c-a1ee5a34040d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,HCO3−H+,False,HCO3−H+,,,,
0f71c3d6-3d5a-4159-bf2e-32236794cb25,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,HCO3−,False,HCO3−,,,,
5c6095ab-9f18-43e6-8da6-fc30343b998d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,O3−,False,O3−,,,,
5377c697-25f0-4278-bfc2-d54798adbdd5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,3−,False,3−,,,,
cd5ace70-8d54-42ae-b0e5-38664071fe96,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,→,False,→,,,,
bcff633f-04d0-49c1-8be8-90b019ee0675,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,NaHCO3,False,NaHCO3,,,,
87c394d8-042d-4f02-b469-ef79ae05c96e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"So there are a couple of things to notice here beyond watching the ions move and form new components. First, the buffering process has taken a situation with the threat from a strong base (NaOH) and toned it down to a situation with a weak base (NaHCO3); the problem has not gone away, it has just been reduced (or buffered). Second, you will see that both of the components of the bicarbonate system, carbonic acid and sodium bicarbonate, appear in the equation—we have just shifted from one to the other.",True,NaHCO3,,,,
a253a318-21c6-4fba-96a6-cd2610f98d26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Let us look at the opposite situation to see what happens when the buffering system is faced with a strong acid. This time a strong acid (hydrochloric acid) is faced with our weak base (sodium bicarbonate) (equation 12.5).,True,NaHCO3,,,,
255ef07b-4856-4342-8156-bc24b9239ea7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Buffering a strong acid using a weak base:,False,Buffering a strong acid using a weak base:,,,,
3d2418ea-7102-445b-b593-cc36afcbd97f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.5,True,Buffering a strong acid using a weak base:,,,,
064221f2-fbf3-4c29-82dc-294ff1543a0d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,HCl+NaHCO3,False,HCl+NaHCO3,,,,
c479a2a4-b78e-4171-a840-67f918b535f6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,l,False,l,,,,
a238666f-1912-4a77-9f9d-69a80061b2cf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,The hydrochloric acid rapidly dissociates into a hydrogen ion and a chloride ion. The hydrogen ion now threatens physiological function and must be buffered.,True,l,,,,
b8ca94aa-0f0f-450d-aa7e-5536f9eb604b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"Our weak base dissociates into sodium and bicarbonate ions. Again our ions recombine, this time to produce harmless sodium chloride and carbonic acid (equation 12.6).",True,l,,,,
e7e67bc4-3ef0-41fc-97b4-ad80bfa4b383,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.6,True,l,,,,
16865d18-09b7-4940-baf3-97a1f0186987,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,H+Cl−+HCO3−Na+→NaCl+H2CO3,False,H+Cl−+HCO3−Na+→NaCl+H2CO3,,,,
dbe0f512-2b69-42a3-8cc0-2b5f69fc8d14,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,H+Cl−,False,H+Cl−,,,,
da5c165b-7c36-4747-964f-f778485c7cab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Cl−,False,Cl−,,,,
3083e91f-d804-4048-a6ac-09ac13f2a8ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Cl,False,Cl,,,,
9ca4eac8-193f-448c-bdb8-d274cffb3d76,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,HCO3−Na+,False,HCO3−Na+,,,,
5aa25c22-e61c-4a6a-8142-0f6e921ba28b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Na,False,Na,,,,
856d9a24-ec11-468c-916e-0e2f291ff5e8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"Notice again we have reduced but not removed the threat as we have gone from the presence of a strong acid to a weak one. Also notice that our two components in the bicarbonate system appear in the equation, and we have switched from one to the other. This should now make you realize that these two components are part of a reversible equation, and this reversible equation, even after the addition of sodium to one end, should look rather familiar (equation 12.7).",True,Na,,,,
8cb1c9f3-cca1-46af-a07a-d85b430ce730,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.7,True,Na,,,,
9a6af37a-086c-491c-98a7-754d7cd786f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,CO2+H2O↔H2CO3↔H++HCO3−+Na+↔NaHCO3,False,CO2+H2O↔H2CO3↔H++HCO3−+Na+↔NaHCO3,,,,
8f1d8e69-3ece-4ed8-aa60-ebab07a9c89e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,↔,False,↔,,,,
c6292194-7b1c-4540-bd91-022e731383ef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,As CO2 is at one end of the equation you should appreciate how alveolar ventilation can influence the bicarbonate buffering system.,True,↔,,,,
598f7f2c-851a-4153-a0dc-ff2c14f506ec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"Because of their critical role in maintaining blood pH, bicarbonate ions are routinely measured along with arterial blood gases. Knowing what the blood pH, arterial CO2, and bicarbonate levels are provides a very powerful and commonly used diagnostic measure allowing us not only to determine the pH status of the patient, but also the source of the problem and whether the renal or pulmonary systems are achieving compensation. Because of its power and common use, we are going to go through some fundamentals, and I am afraid that means looking at the bane of many a medical student: the Henderson–Hasselbalch equation. For those with a background in chemistry you might skip the next section, but for the rest of us, we are going to go through this step-by-step.",True,↔,,,,
6486a92d-8579-4bb6-b9bd-500d533d4b6b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,The Henderson–Hasselbalch Equation,False,The Henderson–Hasselbalch Equation,,,,
54d646f3-7c95-4bfa-b465-8285734b9646,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"What we will see is how the balance of bicarbonate and hydrogen ions determines pH, and how both of these ions can be influenced by the kidneys and lungs to keep pH constant.",True,The Henderson–Hasselbalch Equation,,,,
a9e4e420-0387-4cc0-af75-08e827a4dde0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"First, we will take the central and most important part of the infamous equation, discarding the more innocuous ends.",True,The Henderson–Hasselbalch Equation,,,,
29e0793a-a10d-44de-815d-a2edb447fc49,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.8,True,The Henderson–Hasselbalch Equation,,,,
01b33c46-72a3-4ae7-ac81-cc69696c9c13,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,H2CO3↔H++HCO3−,False,H2CO3↔H++HCO3−,,,,
43af23ec-5e69-4d87-81d6-d3e0566f69f4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"This central portion describes the dissociation of carbonic acid into hydrogen and bicarbonate ions. But because carbonic acid is a weak acid, this dissociation is incomplete—some carbonic acid staying whole, some dissociating into the ions. The level of dissociation is described by the dissociation constant (K’), which really is the ratio of the concentrations of dissociated components to carbonic acid (equation 12.9).",True,H2CO3↔H++HCO3−,,,,
30166b93-9515-4d6b-ad11-e91d0aa9f1b9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.9,True,H2CO3↔H++HCO3−,,,,
fd1d3f05-4092-494f-92fe-8e684c8a7171,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,K′=H+×HCO3−H2CO3,False,K′=H+×HCO3−H2CO3,,,,
bcacbb8f-7d9d-4e16-b738-6ccf5bd30b27,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,K′,False,K′,,,,
dc71946e-c4ad-4e05-82f9-499a9feb729c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,K,False,K,,,,
75a6daa4-46ce-4274-a0e1-4104000ae197,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,′,False,′,,,,
2ef4c722-55d9-4545-afeb-4e0a664835fd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,H+×HCO3−H2CO3,False,H+×HCO3−H2CO3,,,,
d1aeba9d-ec04-40b7-9de6-f95ae443aa73,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,H+×HCO3−,False,H+×HCO3−,,,,
ae23ca01-034d-4fde-95e6-d94a57468e94,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,×,False,×,,,,
113670a4-109f-4413-89ab-9a3e42f2405b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,HCO3,False,HCO3,,,,
d8f98f21-5497-467f-befc-c6ad6ccc358c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,HCO,False,HCO,,,,
27523ed2-99e4-40f5-8341-79248084d580,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"Because we are interested in calculating the pH, however, we are more interested in the amount of hydrogen ions, so rearranging this equation for hydrogen ion concentration we see the hydrogen ion concentration is the dissociation constant, multiplied by the ratio of carbonic acid and bicarbonate (equation 12.10).",True,HCO,,,,
6268b1c2-4f97-4d90-9637-7adcd12fe2d8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.10,True,HCO,,,,
6698e83d-da90-4d6f-95b2-953bf163b2fc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,H+=K′×H2CO3HCO3−,False,H+=K′×H2CO3HCO3−,,,,
b1464a17-6d9d-4264-b18d-7601db223947,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,H2CO3HCO3−,False,H2CO3HCO3−,,,,
fa7fce85-5c45-4ed3-886a-6a8f1a919af3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"This equation theoretically would allow us to now determine hydrogen concentration and therefore pH, but there are some practical problems for us, the first of which is that the instability of carbonic acid means we cannot measure its concentration. So we have to use a proxy measure. The amount of carbonic acid is determined by the amount of carbon dioxide, as can be seen in the equation that is so familiar to you—the greater the amount of CO2, the more carbonic acid.",True,H2CO3HCO3−,,,,
2c97e7d3-79b8-40a5-adc6-a615f152ad33,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.11,True,H2CO3HCO3−,,,,
44a448fe-f8e1-471d-8677-b502cb8dbca8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,CO2+H2O↔H2CO3↔H++HCO3−,False,CO2+H2O↔H2CO3↔H++HCO3−,,,,
b3fa0fd4-48f7-4588-9a32-764a42241e6f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"So after accounting for the dissociation constant of carbonic acid and CO2 and water, we can simply replace carbonic acid concentration with concentration of CO2 (equation 12.12).",True,CO2+H2O↔H2CO3↔H++HCO3−,,,,
60ccfa41-88be-446b-8bdf-0de6880f788f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.12,True,CO2+H2O↔H2CO3↔H++HCO3−,,,,
2fc3279f-66c8-4af0-8f8c-9ff1544eaf56,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,H+=K′×CO2HCO3,False,H+=K′×CO2HCO3,,,,
0fea6c50-01e8-41ee-8c45-1678a6247749,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,CO2HCO3,False,CO2HCO3,,,,
db5c43cc-b3da-41ff-be03-ba683149178d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,CO2,False,CO2,,,,
eed3899d-59e9-44f0-862e-0427d0e33e1b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"We then bump into our next practical problem: our equation now has CO2 concentration in it, but clinically we do not measure CO2 as a concentration (as in mmols), but as a partial pressure. So our next and nearly final step is to convert CO2 concentration to CO2 partial pressure, and we do this by multiplying the partial pressure (our measured value) by the solubility coefficient of carbon dioxide, which happens to be 0.03 mmol/mmHg. Our equation thus now can be completed using our adjusted PCO2 (equation 12.13).",True,CO2,,,,
30c5d527-42b5-4782-888a-dbdc8a2b7034,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,mmols,False,mmols,,,,
93b092d9-98d2-472c-b0b4-8ae3f4eb4dfa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.13,True,mmols,,,,
0348aae2-7f69-4ed1-bb10-105756413efa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,H+=K′×0.03×PCO2HCO3−,True,mmols,,,,
0e5fb13f-f591-4662-bdbc-65293783224f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,0.03×PCO2HCO3−,True,mmols,,,,
9ee96d3a-830a-4f4a-980b-e3c9181b2324,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,0.03×PCO2,True,mmols,,,,
9ac028f9-27ac-4b9f-98a0-6af56ecee0bf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,0.03,True,mmols,,,,
1bf6f9be-46f7-43c7-b10b-e23f073303ee,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,P,False,P,,,,
afe9aaa2-b196-4d93-857a-28470b8a12a6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"Our equation as it is now allows us to calculate hydrogen ion concentration, but we need pH, so we have to make a conversion. Because pH is the negative logarithm of hydrogen concentration, we express everything in the negative log form. And because the negative log of the dissociation constant is referred to as pK, then we can simplify our equation one more step (equation 12.14).",True,P,,,,
5b15a5db-6392-420d-8d17-121573e104e1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.14,True,P,,,,
98da1ea8-db96-4ce5-a11f-14e2ffc40f95,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,pH=pK−log0.03×PCO2HCO3−,True,P,,,,
34df23b1-8aea-4425-b71a-fdd72ad7f655,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,p,False,p,,,,
60b67858-2d34-4055-be1c-7b6342df1ba4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,o,False,o,,,,
b2078612-f833-413a-a147-ec16f0570360,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,g,False,g,,,,
db57e823-b4a1-491c-b9ae-6f49adac6901,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"To make our equation simple to use, we now get rid of the negative log, and so get the following (equation 12.15):",True,g,,,,
7717b004-092a-4081-b2d2-0d0f9169d963,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.15,True,g,,,,
33b72e09-2266-4ffe-bd7d-05dc8caf5241,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,pH=pK+logHCO3−0.03×PCO2,True,g,,,,
995ed153-6558-48c2-9867-d685f544bea2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,HCO3−0.03×PCO2,True,g,,,,
329efb0b-2b24-4593-9965-3acfd21ed61b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"We know that the pK of the bicarbonate system happens to be 6.1, so substituting this into the equation we end up with the Henderson–Hasselbalch equation (equation 12.16).",True,g,,,,
05f58f2a-4be6-4caa-bc36-f85064e1d086,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Let us put this in context.,False,Let us put this in context.,,,,
347cce12-301b-4345-9908-2b82c70005d2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"First, the equation shows that if CO2 rises then pH falls, and because CO2 is under the influence of alveolar ventilation, this explains how the alveolar ventilation can now control pH. It also shows that if bicarbonate increases then pH increases, and equally if bicarbonate falls then pH falls. Because the bicarbonate concentration can be modified either way by the kidneys, the equation also shows how the kidneys can modify pH (equation 12.16).",True,Let us put this in context.,,,,
ef54dd93-6f4a-4b46-ba8c-fd8f8cdaba83,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.16,True,Let us put this in context.,,,,
785eaae9-e4bf-42dc-ad87-57eb550bd185,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Role of kidneys (numerator) / Role of lungs (denominator),False,Role of kidneys (numerator) / Role of lungs (denominator),,,,
ce06c6e7-2a4f-466b-a4df-61f2d9c2817b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,pH=6.1+logHCO3−0.03×PCO2,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
644e2f23-9895-4d96-854f-8a49a41a1ffd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,6.1,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
71060403-5e4c-4243-a727-78b3ea137153,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"The involvement of these two major physiological systems in this equation make the bicarbonate system a very powerful buffer, particularly when considering that there is an unlimited source of CO2 and therefore bicarbonate supplied by the metabolism.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
2bdb79f1-362e-4d8d-9096-cadba03c92d1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"But more importantly it shows that pH is actually determined by the ratio of bicarbonate and CO2 and that both are equally important. This fact is critical to appreciate as it forms the basis of understanding the compensation mechanisms we dealt with earlier. This is why I put you through this derivation. So for example, if a rise in CO2 (such as in lung disease) is accompanied by an equal rise in bicarbonate (generated by the kidney), then the ratio between the two remains the same and therefore pH remains the same. Likewise, if during a fall in CO2 the kidneys excrete bicarbonate, then pH can be kept constant. So before we finish, let us show you that the equation actually works by plugging in some numbers.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
3d4d615a-a0ac-49e5-ba63-8f60a68e3d2e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"Example #1: Let us start with normal values, a PCO2 of 40 mmHg and a bicarbonate of 24, and plug these into the equation. This comes to 6.1 plus the log of 20, which is 6.1 plus 1.3, or 7.4 (i.e., normal arterial pH).",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
d93f7b97-9285-4a7f-b542-86e4ad7cc952,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.17,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
e90a343a-8228-4593-80d5-a0cfc9f1abfe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,pH=6.1+log24(0.03×40)=6.1+log(20)=6.1+1.3=7.4,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
3895d603-1793-475a-983a-0fcff7ed30d1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,24(0.03×40)=6.1+log(20)=6.1+1.3=7.4,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
8b224997-a52c-4231-9c07-3371350abc81,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,24(0.03×40),True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
471555a4-5457-48f0-b799-4478254926c1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,24,False,24,,,,
76aabc0e-96dd-4e18-aad6-d11428ae819d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,(0.03×40),True,24,,,,
8420f949-3017-4568-aef5-724b851da45d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,(,False,(,,,,
dcc04634-2b72-4dab-a86a-456182c3c8ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,40,False,40,,,,
879db602-29ac-4ad2-918f-86ca47f03925,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,),False,),,,,
3add0cd9-ca76-4a1d-b814-0b90669ce3a5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,20,False,20,,,,
57cfc639-85fc-4050-a7b0-a1ad24fe90f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,1.3,True,20,,,,
1a15e0cb-96c4-4a96-83df-5cff25d9c803,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,7.4,True,20,,,,
3c76a4c3-8089-4b00-95b0-06d4330b25af,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"Example #2: Now let us look at a case of acute lung failure that has caused a rise in arterial PCO2, but has not persisted long enough for the kidney to respond and compensate. PCO2 has risen to 50 mmHg, and bicarbonate has not changed. Our calculation now goes to 6.1 plus the log of 16, which is 6.1 plus 1.2, and pH has fallen to 7.3.",True,20,,,,
543ee40a-17c5-43f8-8802-8ac1cfbf1898,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.18,True,20,,,,
3fe5c6a1-e467-4f0c-85b8-ca1a7d908628,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,pH=6.1+log24(0.03×50)=6.1+log(16)=6.1+1.2=7.3,True,20,,,,
ace5de69-3549-4a27-b280-a10c83ec3fcc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,24(0.03×50)=6.1+log(16)=6.1+1.2=7.3,True,20,,,,
56dea4f6-f8d7-423a-8173-7a6a768bcb9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,24(0.03×50),True,20,,,,
bd235d62-c717-4ddf-b128-dbd4b2a2d26d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,(0.03×50),True,20,,,,
9b3607b3-a7a8-4c41-a9a7-b0d3844a21a8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,50,False,50,,,,
edc02114-f9ed-4bd9-9053-9f8de6a5db73,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,16,False,16,,,,
94b6961a-7c01-404c-b1c3-c79d27613383,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,1.2,True,16,,,,
f83366f9-6ec7-4995-a4b2-9a34798795d0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,7.3,True,16,,,,
c3ef8464-fdf9-446d-8dee-f9425e1f82bd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"We now have three numbers that can give a meaningful clinical interpretation. The low pH indicates the patient is in acidosis. The raised PCO2 suggests that this is respiratory acidosis, and the unchanged bicarbonate suggests no metabolic compensation has taken place.",True,16,,,,
dfefa465-2609-41db-9501-f0367f9af183,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"Example #3: Now let us return to our patient thirty-six hours later when we have given the kidney a chance to respond. The patient’s PCO2 remains at 50 because of the persistent lung problem, but the kidney has raised the bicarbonate to 30. Now our equation becomes 6.1 plus the log of 20, or 6.1 plus 1.3, and pH is 7.4—apparently normal.",True,16,,,,
d0f83bdf-4933-4c9e-b407-1fd4e2a94f71,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Equation 12.19,True,16,,,,
a4bdd6c4-0be6-4cbd-bae3-97035f54fb8b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,pH=6.1+log30(0.03×50)=6.1+log(20)=6.1+1.3=7.4,True,16,,,,
99ef411e-e8c9-4df7-a72b-1ba62700c2b6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,30(0.03×50)=6.1+log(20)=6.1+1.3=7.4,True,16,,,,
73c42810-c241-445c-b67f-066b14cf6e11,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,30(0.03×50),True,16,,,,
abdd7511-cf07-48a2-9fa7-8bea916af03c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,30,False,30,,,,
d3d07e5c-8cee-4be3-b78c-18810e1e6f13,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,But when we look at all three numbers we see that the patient is far from normal: the pH is okay only because the kidneys have raised bicarbonate to match the raised CO2 and keep the ratio the same. So we now have a respiratory acidosis with metabolic compensation.,True,30,,,,
006a3412-21bc-4569-b8b0-817ec31e7187,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,Summary,False,Summary,,,,
02a6ab97-123a-4459-b1bc-d25a5efba12b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Alveolar Ventilation and Arterial pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/#chapter-49-section-1,"So although it has been a long journey through this chapter you should now be able to interpret blood gas values to determine whether a patient is in acidosis or alkalosis and whether or not compensation is present. I strongly recommend writing the Henderson–Hasselbalch equation as a formula in Excel so that you can plug in CO2 and bicarbonate values and see what happens to pH. By repeatedly interpreting blood gas values and pH, determining the status of a patient will rapidly become second nature.",True,Summary,,,,
0c32d9c0-5de0-491a-af61-bbd87b8ff60f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,CO₂ and pH,False,CO₂ and pH,,,,
517a000b-299f-47c2-9f5f-d97d64e9167b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,We will start by revisiting the equation dealt with in the previous chapter in the context of four different clinical scenarios.,True,CO₂ and pH,,,,
6705fd16-c42c-4d5e-aad2-0dcec514d3ef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"Case #1, normal: In the normal situation an increase in tissue metabolism leads to a rise in arterial CO2, pushing the equation to the right and causing a rise in hydrogen ion concentration and a consequent fall in pH. Both the rise in CO2 and fall in pH stimulate breathing. This increase in alveolar ventilation leads to a fall in arterial CO2, pushing the equation back left and lowering hydrogen ions back to normal.",True,CO₂ and pH,,,,
d227b2ac-98ea-4abc-bc12-e44360fb73e3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.1,True,CO₂ and pH,,,,
1ff761fc-8da7-4d78-a371-03547fd30789,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],False,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
b2bf50b5-027f-462a-9ea1-679511a15d17,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"Case #2, metabolic acidosis: CO2 is by no means the only source of hydrogen ions in the system. Most metabolic pathways result in acidic by-products, and the pulmonary, renal, and buffering systems are generally battling to raise blood and tissue pH back from their tendency to turn acidic. The rise in hydrogen ions resulting from metabolic processes is referred to as metabolic acidosis. The fall in pH stimulates an increase in respiration, which in turn causes a fall in CO2, and the lower CO2 drives the equation to the left, reducing the number of H+ and thereby raising pH back to normal. Here the pulmonary system has compensated for a metabolic process, and this is referred to as respiratory compensation of metabolic acidosis. The patient may now have a normal blood pH, but the CO2 will be low. In summary, all the pulmonary system has done is get rid of one source of hydrogen ions (carbonic acid derived from dissolved CO2) to compensate for another source of hydrogen ions it cannot do anything about (most metabolically driven acids are nonvolatile (i.e., do not vaporize into a gas the lungs can get rid of)).",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
7b92403d-e87f-4919-a125-3129f3001233,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"The advantage of the pulmonary system being involved in pH regulation is that it is quick—a few larger breaths and arterial PCO2 can be dropped significantly. So the pulmonary system is adept at minute-by-minute (or breath-by-breath) regulation of pH that copes admirably with short-term changes in pH. It is worth noting here that metabolic alkalosis can be reversed by reducing or even stopping breathing, allowing CO2 to accumulate in the arterial blood and lowering pH back to normal.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
8b749f70-7534-4425-a4d9-22cdcb14a943,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"The disadvantage to using the pulmonary system for compensation is that it can only mediate its effect via CO2. So any metabolic acids are eventually dealt with by the renal system, which, although much slower, is capable of excreting any nonvolatile metabolic acids. So through a combination of rapid pulmonary CO2 expulsion and slower but more versatile renal function, pH is normally maintained within a tight range even in the face of large metabolic changes. The kidney also has the advantage of being able to modify bicarbonate levels, which we will see the importance of when we look at the buffering systems in a moment.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
7c71ac9a-9e51-4418-bc70-1fe2d5efb5d3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"It is worth noting here, especially for the chemists and biochemists among you, that although equation 12.1 is a reversible reaction, it is open at both ends—the lung being able to expel or retain CO2 at one end and the kidneys being able to retain or expel hydrogen ions and bicarbonate at the other.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
821409dc-79ba-40d4-a68c-7994a7f656dc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"Case #3, respiratory acidosis: Given its capability to influence pH, failure of the lung to expel an appropriate amount of CO2 can lead to deviations in pH. Let us take a case of severe lung disease, say COPD, for example. The disease has diminished the ability of the lung to expel CO2, so arterial PCO2 rises, pushing the equation to the right and causing a fall in pH, referred to as respiratory acidosis. This acid must be immediately buffered until kidney function can be modified to begin secreting the excess hydrogen ions and even produce more bicarbonate to replenish the buffering system, a process referred to as metabolic compensation of respiratory acidosis.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
f46a5c1d-1162-4ff9-9765-773b83148822,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"Case #4, respiratory alkalosis: Likewise, if ventilation is inappropriately high with respect to CO2 production, such as during a period of hyperventilation, then too much CO2 will be lost and pH will fall. The alkalosis must be immediately buffered to avoid deleterious effects. Over the longer term the kidney can lower the raised pH by reabsorbing hydrogen ions and even excreting bicarbonate buffer—again this is termed metabolic compensation—but this time for an alkalosis caused by an inappropriate respiratory response.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
37da14ca-0925-42c5-bdee-1a2d10524305,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Physiological Buffers,False,Physiological Buffers,,,,
d4e41e57-e39b-421c-af54-3f314f4742d2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"Although the lung’s ability to expel CO2 and the kidney’s ability to excrete or absorb hydrogen ions allow close regulation of pH, their responses alone are not sufficient to prevent immediate local changes in pH at the tissue. This is the role of the buffering systems.",True,Physiological Buffers,,,,
edf22b8a-49b3-49fc-925d-962b0083aceb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"Buffering systems are chemicals within tissue and the blood that have the ability to absorb either hydrogen ions and/or hydroxyl ions. Once these ions are removed from solution (albeit temporarily) then their effect on pH is diminished. We will deal with buffers in the context of acids, as this is the most common physiological situation.",True,Physiological Buffers,,,,
a63060d0-eb94-4129-820f-85fd7a8ec5c5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"If you need an analogy for the function of buffers, imagine them as a chemical mop—they soak up the hydrogen ions and stop them from making a cellular mess, but the hydrogen ions, although contained, remain in the system. It is the role of the lungs and kidneys to “rinse the mop” and get rid of the hydrogen ions from the system.",True,Physiological Buffers,,,,
2e8d9d95-9245-40a2-afbc-b292e65b3016,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,There are three major chemical buffering groups in the body:,False,There are three major chemical buffering groups in the body:,,,,
b7422e1a-2a89-42a0-951d-6486b215fd3a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,We will deal with the bicarbonate system as it involves the respiratory system and is also the major extracellular buffer.,True,There are three major chemical buffering groups in the body:,,,,
a056706a-ccd7-4c03-be2f-7be7e9dd2a63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"Bicarbonate buffering: A buffering system consists of a weak base capable of absorbing a strong acid and a weak acid capable of absorbing a strong base. As such, the bicarbonate system involves two components: sodium bicarbonate (a weak base) and carbonic acid (a weak acid). Let us look at how it works and put it in the context of the lungs.",True,There are three major chemical buffering groups in the body:,,,,
a5abef6d-77e9-4c55-a599-bb3ca5dfebbc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"First let us see how a weak acid (carbonic acid) deals with a strong base, in this example, sodium hydroxide (equation 12.2).",True,There are three major chemical buffering groups in the body:,,,,
19f6fd1f-60ca-4e07-9c03-2abf1c83b00d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Buffering a strong base using a weak acid:,False,Buffering a strong base using a weak acid:,,,,
9543c163-b1ba-497f-ad36-a6b6147db467,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.2,True,Buffering a strong base using a weak acid:,,,,
d92c991f-d033-4070-94b6-66605b42104e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]NaOH = \color{red}{H_2CO_3}[/latex],False,[latex]NaOH = \color{red}{H_2CO_3}[/latex],,,,
de1c81e4-3a9e-414a-a624-599bcf149fb2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Sodium hydroxide is a strong base as it rapidly dissociates into a hydroxyl ion and a sodium ion.,True,[latex]NaOH = \color{red}{H_2CO_3}[/latex],,,,
e84465c2-c999-485f-be97-8a9e954a8b8b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.3,True,[latex]NaOH = \color{red}{H_2CO_3}[/latex],,,,
ae0937aa-b7a9-472d-a6a0-41fc25901e34,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + \color{red}{H_2CO_3}[/latex],False,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + \color{red}{H_2CO_3}[/latex],,,,
37022931-4553-43b9-ad70-1fc83c892ae7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,The hydroxyl ion is the potential threat to physiological function so must be buffered. This is achieved by the carbonic acid dissociating into a hydrogen ion and bicarbonate (a process you are familiar with).,True,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + \color{red}{H_2CO_3}[/latex],,,,
83d308a3-8c0a-4d21-964a-66b8f6c08edd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,These dissociated ions now bind to form new partnerships as water and sodium hydroxide (a weak base) (equation 12.4).,True,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + \color{red}{H_2CO_3}[/latex],,,,
ece48077-c412-415c-9f8f-fb103ef74a63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.4,True,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + \color{red}{H_2CO_3}[/latex],,,,
a4ef35c8-1080-480b-b336-bab7be539e5a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + {{HCO_{3-}}\atop{{H}^{+}}} \rightarrow H_2O + \color{blue}{NaHCO_3}[/latex],False,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + {{HCO_{3-}}\atop{{H}^{+}}} \rightarrow H_2O + \color{blue}{NaHCO_3}[/latex],,,,
87cf568e-c41b-4cfb-a38d-249a4def9982,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"So there are a couple of things to notice here beyond watching the ions move and form new components. First, the buffering process has taken a situation with the threat from a strong base (NaOH) and toned it down to a situation with a weak base (NaHCO3); the problem has not gone away, it has just been reduced (or buffered). Second, you will see that both of the components of the bicarbonate system, carbonic acid and sodium bicarbonate, appear in the equation—we have just shifted from one to the other.",True,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + {{HCO_{3-}}\atop{{H}^{+}}} \rightarrow H_2O + \color{blue}{NaHCO_3}[/latex],,,,
1acd26af-0fb3-4690-ba6f-6e647326d30d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Let us look at the opposite situation to see what happens when the buffering system is faced with a strong acid. This time a strong acid (hydrochloric acid) is faced with our weak base (sodium bicarbonate) (equation 12.5).,True,[latex]{{Na^{+}}\atop{\color{red}{OH}^{-}}} + {{HCO_{3-}}\atop{{H}^{+}}} \rightarrow H_2O + \color{blue}{NaHCO_3}[/latex],,,,
bb1db1b4-54b7-4865-a9dd-28c037cf985a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Buffering a strong acid using a weak base:,False,Buffering a strong acid using a weak base:,,,,
481a8a82-8c93-482c-9f79-06c641322135,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.5,True,Buffering a strong acid using a weak base:,,,,
2dccfae6-65d7-4557-b856-0c2dbf0a03ce,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]HCl + \color{blue}{NaHCO_3}[/latex],False,[latex]HCl + \color{blue}{NaHCO_3}[/latex],,,,
bea92137-918f-4ef8-b863-c7963ce1f333,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,The hydrochloric acid rapidly dissociates into a hydrogen ion and a chloride ion. The hydrogen ion now threatens physiological function and must be buffered.,True,[latex]HCl + \color{blue}{NaHCO_3}[/latex],,,,
861f31fe-7ae4-42eb-a4db-01ffb1933779,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"Our weak base dissociates into sodium and bicarbonate ions. Again our ions recombine, this time to produce harmless sodium chloride and carbonic acid (equation 12.6).",True,[latex]HCl + \color{blue}{NaHCO_3}[/latex],,,,
4c37a686-6340-4c05-9fe9-18dff0a48b1a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.6,True,[latex]HCl + \color{blue}{NaHCO_3}[/latex],,,,
2e93e6e4-89c9-4c7d-a57a-195ea1189da0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],False,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
af9e555b-4e53-49a0-98f1-a8a3e62dd348,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"Notice again we have reduced but not removed the threat as we have gone from the presence of a strong acid to a weak one. Also notice that our two components in the bicarbonate system appear in the equation, and we have switched from one to the other. This should now make you realize that these two components are part of a reversible equation, and this reversible equation, even after the addition of sodium to one end, should look rather familiar (equation 12.7).",True,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
a7834ffa-1cb9-4efe-8d89-ef7bd8c996c0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.7,True,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
ca95b4ce-4544-4bd3-ab18-36336ff03696,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]CO_2 + H_2O \leftrightarrow {\color{red}{H_2CO_3}} \leftrightarrow H^+ + HCO_{3-} + Na^+ \leftrightarrow \color{blue}{NaHCO_3}[/latex],True,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
f88e48c9-bce6-4ed0-aafb-133a30011ada,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,As CO2 is at one end of the equation you should appreciate how alveolar ventilation can influence the bicarbonate buffering system.,True,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
c8eb62da-47aa-44aa-ad1a-aa413f6e7090,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"Because of their critical role in maintaining blood pH, bicarbonate ions are routinely measured along with arterial blood gases. Knowing what the blood pH, arterial CO2, and bicarbonate levels are provides a very powerful and commonly used diagnostic measure allowing us not only to determine the pH status of the patient, but also the source of the problem and whether the renal or pulmonary systems are achieving compensation. Because of its power and common use, we are going to go through some fundamentals, and I am afraid that means looking at the bane of many a medical student: the Henderson–Hasselbalch equation. For those with a background in chemistry you might skip the next section, but for the rest of us, we are going to go through this step-by-step.",True,[latex]{{\color{red}{H}^{+}}\atop{{Cl}^{-}}} + {{HCO_{3-}}\atop{{Na}^{+}}} \rightarrow NaCl + \color{red}{H_2CO_3}[/latex],,,,
22964ad7-1987-4e51-be58-a5593842c9c2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,The Henderson–Hasselbalch Equation,False,The Henderson–Hasselbalch Equation,,,,
0ee3ff45-1fa0-44af-bb96-442b3f9687b4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"What we will see is how the balance of bicarbonate and hydrogen ions determines pH, and how both of these ions can be influenced by the kidneys and lungs to keep pH constant.",True,The Henderson–Hasselbalch Equation,,,,
f696e4ea-a827-475e-abe1-e147d18f4e8b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"First, we will take the central and most important part of the infamous equation, discarding the more innocuous ends.",True,The Henderson–Hasselbalch Equation,,,,
97bccf91-6fff-478e-93a1-a5e697705c27,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.8,True,The Henderson–Hasselbalch Equation,,,,
d9b9b4d0-a7ce-4794-8291-c928cf247169,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]H_2CO_3 \leftrightarrow H^+ + HCO_{3-}[/latex],False,[latex]H_2CO_3 \leftrightarrow H^+ + HCO_{3-}[/latex],,,,
86ca2649-b75c-46f9-92be-56fa8f54aa95,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"This central portion describes the dissociation of carbonic acid into hydrogen and bicarbonate ions. But because carbonic acid is a weak acid, this dissociation is incomplete—some carbonic acid staying whole, some dissociating into the ions. The level of dissociation is described by the dissociation constant (K’), which really is the ratio of the concentrations of dissociated components to carbonic acid (equation 12.9).",True,[latex]H_2CO_3 \leftrightarrow H^+ + HCO_{3-}[/latex],,,,
d3a6d4c8-1227-4c4e-8f32-76b403c2231d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.9,True,[latex]H_2CO_3 \leftrightarrow H^+ + HCO_{3-}[/latex],,,,
5438f44a-451d-455d-80fd-60203589f6dd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]K' = \displaystyle\frac{{H}^{+} \times {HCO}_{3}-}{H_2CO_3}[/latex],False,[latex]K' = \displaystyle\frac{{H}^{+} \times {HCO}_{3}-}{H_2CO_3}[/latex],,,,
ae3bdcdc-47c4-4fee-8492-ad0e7c778a4b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"Because we are interested in calculating the pH, however, we are more interested in the amount of hydrogen ions, so rearranging this equation for hydrogen ion concentration we see the hydrogen ion concentration is the dissociation constant, multiplied by the ratio of carbonic acid and bicarbonate (equation 12.10).",True,[latex]K' = \displaystyle\frac{{H}^{+} \times {HCO}_{3}-}{H_2CO_3}[/latex],,,,
34ecdb1e-7908-4763-8107-ea1c067a5934,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.10,True,[latex]K' = \displaystyle\frac{{H}^{+} \times {HCO}_{3}-}{H_2CO_3}[/latex],,,,
f6af71bf-f134-40db-9b6f-a610cf0348b9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]H^+ = K' \times \displaystyle\frac{H_2CO_3}{HCO_3-}[/latex],False,[latex]H^+ = K' \times \displaystyle\frac{H_2CO_3}{HCO_3-}[/latex],,,,
a06c7dd8-82c8-4391-af6f-1c20b3b96c33,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"This equation theoretically would allow us to now determine hydrogen concentration and therefore pH, but there are some practical problems for us, the first of which is that the instability of carbonic acid means we cannot measure its concentration. So we have to use a proxy measure. The amount of carbonic acid is determined by the amount of carbon dioxide, as can be seen in the equation that is so familiar to you—the greater the amount of CO2, the more carbonic acid.",True,[latex]H^+ = K' \times \displaystyle\frac{H_2CO_3}{HCO_3-}[/latex],,,,
a19f3b8a-35c0-4b63-8705-a4e42217270b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.11,True,[latex]H^+ = K' \times \displaystyle\frac{H_2CO_3}{HCO_3-}[/latex],,,,
9f4ebcb2-61ac-491f-a344-fb698cc5fe4e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],False,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
73fd7017-c2d1-4767-97f2-bd984a31077b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"So after accounting for the dissociation constant of carbonic acid and CO2 and water, we can simply replace carbonic acid concentration with concentration of CO2 (equation 12.12).",True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
0b642974-ab20-44e5-a178-c0f123a08c27,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.12,True,[latex]CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3-[/latex],,,,
4ee94d9e-90b4-447d-8fb4-3f5eb652186d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]H^+ = K' \times \displaystyle\frac{CO_2}{HCO_3}[/latex],False,[latex]H^+ = K' \times \displaystyle\frac{CO_2}{HCO_3}[/latex],,,,
4f64cf52-2d1d-4895-9d33-57b9334e380a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"We then bump into our next practical problem: our equation now has CO2 concentration in it, but clinically we do not measure CO2 as a concentration (as in mmols), but as a partial pressure. So our next and nearly final step is to convert CO2 concentration to CO2 partial pressure, and we do this by multiplying the partial pressure (our measured value) by the solubility coefficient of carbon dioxide, which happens to be 0.03 mmol/mmHg. Our equation thus now can be completed using our adjusted PCO2 (equation 12.13).",True,[latex]H^+ = K' \times \displaystyle\frac{CO_2}{HCO_3}[/latex],,,,
5b96b63d-6b0c-4f6d-a9bc-64a046332989,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,mmols,False,mmols,,,,
b5cb916a-834d-4440-a328-88225ad4fc2f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.13,True,mmols,,,,
b059015d-cb6e-4a83-ad5c-fa1ac1c78e46,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]H^+ = K' \times \displaystyle\frac{0.03 \times PCO_2}{HCO_3-}[/latex],True,mmols,,,,
b8e2f1b1-60c0-41c6-8981-7e86c66d8c09,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"Our equation as it is now allows us to calculate hydrogen ion concentration, but we need pH, so we have to make a conversion. Because pH is the negative logarithm of hydrogen concentration, we express everything in the negative log form. And because the negative log of the dissociation constant is referred to as pK, then we can simplify our equation one more step (equation 12.14).",True,mmols,,,,
0bd0c892-3160-44d6-8297-c32011910844,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.14,True,mmols,,,,
68a46e13-4380-4e2e-a1a8-ee172a867ac3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]pH = pK - log \displaystyle\frac{0.03 \times PCO_2}{HCO_3-}[/latex],True,mmols,,,,
08ce7ce0-1377-4e90-bd86-97fb61b480eb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"To make our equation simple to use, we now get rid of the negative log, and so get the following (equation 12.15):",True,mmols,,,,
36277ff2-4373-436f-b46c-26f5836f07da,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.15,True,mmols,,,,
ddd6f468-ea5e-4e50-8742-2360f098ce04,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]pH = pK + log \displaystyle\frac{HCO_3-}{0.03 \times PCO_2}[/latex],True,mmols,,,,
76a21b69-341c-4499-b167-3bc4abfe4681,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"We know that the pK of the bicarbonate system happens to be 6.1, so substituting this into the equation we end up with the Henderson–Hasselbalch equation (equation 12.16).",True,mmols,,,,
637f3ada-101f-4a4d-ba6d-db0f1d9405f2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Let us put this in context.,False,Let us put this in context.,,,,
3f5b92ec-35b6-485c-babc-63f419353d20,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"First, the equation shows that if CO2 rises then pH falls, and because CO2 is under the influence of alveolar ventilation, this explains how the alveolar ventilation can now control pH. It also shows that if bicarbonate increases then pH increases, and equally if bicarbonate falls then pH falls. Because the bicarbonate concentration can be modified either way by the kidneys, the equation also shows how the kidneys can modify pH (equation 12.16).",True,Let us put this in context.,,,,
edab865c-cf95-4376-9688-cb07a7e175f1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.16,True,Let us put this in context.,,,,
53bbd233-f5c6-4c05-ab27-545c96e57df4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Role of kidneys (numerator) / Role of lungs (denominator),False,Role of kidneys (numerator) / Role of lungs (denominator),,,,
737f1759-5373-4f53-9206-1eb4acd6db38,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]pH = 6.1 + log \displaystyle\frac{HCO_3-}{0.03 \times PCO_2}[/latex],True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
4e9525b4-449a-4af8-bc30-082bddc94308,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"The involvement of these two major physiological systems in this equation make the bicarbonate system a very powerful buffer, particularly when considering that there is an unlimited source of CO2 and therefore bicarbonate supplied by the metabolism.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
c9da24da-bd69-4454-bf49-a72029450013,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"But more importantly it shows that pH is actually determined by the ratio of bicarbonate and CO2 and that both are equally important. This fact is critical to appreciate as it forms the basis of understanding the compensation mechanisms we dealt with earlier. This is why I put you through this derivation. So for example, if a rise in CO2 (such as in lung disease) is accompanied by an equal rise in bicarbonate (generated by the kidney), then the ratio between the two remains the same and therefore pH remains the same. Likewise, if during a fall in CO2 the kidneys excrete bicarbonate, then pH can be kept constant. So before we finish, let us show you that the equation actually works by plugging in some numbers.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
1056b574-02fa-45e9-aaa8-cb311be41559,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"Example #1: Let us start with normal values, a PCO2 of 40 mmHg and a bicarbonate of 24, and plug these into the equation. This comes to 6.1 plus the log of 20, which is 6.1 plus 1.3, or 7.4 (i.e., normal arterial pH).",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
c8122fb1-b78d-452a-bf9b-332940424380,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.17,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
27e52df5-ba53-4fef-a4bf-6ccc73465e49,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]pH = 6.1 + log \displaystyle\frac{24}{(0.03 \times 40)} = 6.1 + log(20) = 6.1 + 1.3 = 7.4[/latex],True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
1b7b3d62-2842-477c-8d1f-27417a209ea3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"Example #2: Now let us look at a case of acute lung failure that has caused a rise in arterial PCO2, but has not persisted long enough for the kidney to respond and compensate. PCO2 has risen to 50 mmHg, and bicarbonate has not changed. Our calculation now goes to 6.1 plus the log of 16, which is 6.1 plus 1.2, and pH has fallen to 7.3.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
15afc785-3664-4006-9f73-537614135589,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.18,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
c4f69f3a-5cdf-4bcb-9823-0246ab2c9dce,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]pH = 6.1 + log \displaystyle\frac{24}{(0.03 \times 50)} = 6.1 + log(16) = 6.1 + 1.2 = 7.3[/latex],True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
08474891-2ebe-4ff6-99b7-ba8bc322a715,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"We now have three numbers that can give a meaningful clinical interpretation. The low pH indicates the patient is in acidosis. The raised PCO2 suggests that this is respiratory acidosis, and the unchanged bicarbonate suggests no metabolic compensation has taken place.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
715f41c6-1c65-4e44-a5fb-8ebf6ae4ae83,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"Example #3: Now let us return to our patient thirty-six hours later when we have given the kidney a chance to respond. The patient’s PCO2 remains at 50 because of the persistent lung problem, but the kidney has raised the bicarbonate to 30. Now our equation becomes 6.1 plus the log of 20, or 6.1 plus 1.3, and pH is 7.4—apparently normal.",True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
5fa494ee-c813-4a7a-9403-936e39f476b3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Equation 12.19,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
d4580748-b0e9-456a-a621-65c61ac2cdc0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,[latex]pH = 6.1 + log \displaystyle\frac{30}{(0.03 \times 50)} = 6.1 + log(20) = 6.1 + 1.3 = 7.4[/latex],True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
031849bc-85ba-4fad-86ce-96bf52ebd0ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,But when we look at all three numbers we see that the patient is far from normal: the pH is okay only because the kidneys have raised bicarbonate to match the raised CO2 and keep the ratio the same. So we now have a respiratory acidosis with metabolic compensation.,True,Role of kidneys (numerator) / Role of lungs (denominator),,,,
b39b81c9-bb8a-4f68-ad4e-414077c131ed,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,Summary,False,Summary,,,,
d90c9148-4783-4567-96bd-9a1587eeb64e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,12. Alkalosis and Acidosis,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/alkalosis-and-acidosis/,"So although it has been a long journey through this chapter you should now be able to interpret blood gas values to determine whether a patient is in acidosis or alkalosis and whether or not compensation is present. I strongly recommend writing the Henderson–Hasselbalch equation as a formula in Excel so that you can plug in CO2 and bicarbonate values and see what happens to pH. By repeatedly interpreting blood gas values and pH, determining the status of a patient will rapidly become second nature.",True,Summary,,,,
40fb1d75-909e-4706-94bf-a755b197701e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,"The reason control of arterial CO2 is so critical is that it influences arterial pH. Too much CO2 in the blood and acidosis arises, while too little raises pH to produce an alkalosis. Any deviation from a set point pH of around 7.4 can be highly dangerous as changes in pH rapidly generate changes in protein shape and function. As enzymes, membrane transporters, channels, and more start to lose function, then cellular and systemic function rapidly deteriorates. With its high metabolic rate and critical need to maintain control over its membrane potential, the nervous system is usually the first to suffer when pH changes.",True,Summary,,,,
ab1f69bb-3518-440c-be06-d94cfd9339df,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,"So we now need to look at the relationships between CO2, arterial pH, and alveolar ventilation. Before starting this chapter you should be completely happy that you have an understanding of pH and what constitutes a weak or a strong acid and reversible reactions.",True,Summary,,,,
444c6908-4fdf-4e77-a8a1-725ea0d3fc03,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,"Active cells produce CO2 through their anerobic and aerobic metabolic pathways. This CO2 rapidly combines with water in the cytoplasm or plasma to produce carbonic acid. Carbonic acid is a weak acid, meaning that some but not all of it dissociates onto a hydrogen ion and bicarbonate ion. Both these molecules are critical players in the maintenance of pH, and this equation explains why CO2 influences arterial pH.",True,Summary,,,,
2f97cccc-a65a-4109-9659-c9222c851228,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,Equation 11.1,True,Summary,,,,
ed125284-bbf0-4fae-915d-175fbb54f480,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],False,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
6798f346-3c4c-4f92-b7fd-0403b6a90749,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,"It is well worth committing this equation to memory and ensuring you have a good understanding of it as it is not only crucial in pulmonary pH regulation, but you will also see this equation again in renal physiology, gastrointestinal physiology, and other systems. I would argue that this is the most important equation in physiology. But let us look at it in terms of respiratory gases and the pulmonary system.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
4d741c84-caf4-456b-9b55-2651796fe020,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,"It is critical to understand that this equation is reversible, so it really describes a balance. If CO2 at the tissue rises, the reaction is driven to the right, and consequently the amount of hydrogen ion is increased and pH falls. Conversely, if CO2 falls, then the reaction is driven to the left, so hydrogen ion concentration falls and pH rises. Because the lung has the ability to control the expulsion rate of CO2 from blood, the lung also has the ability to influence pH.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
75ead184-5e93-4632-9818-731b89d58c4a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,Physiological Context,False,Physiological Context,,,,
e8b1f474-d1d6-4505-94a7-32b6d66c9105,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,"Let us look at the most common physiological scenario: a rise in metabolic rate causes an increase in the production of CO2 by the tissue. This, of course, pushes our equation to the right, and more hydrogen ions are produced. Because of buffering and the way CO2 is transported in the blood (discussed later on), the rise of PCO2 and fall of pH in venous blood is usually minimal, but both of these factors are enough to stimulate an increase in ventilation.",True,Physiological Context,,,,
f472c339-e0ef-4ba8-81c0-bbf486ffa7f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,"This increase in ventilation (more specifically, alveolar ventilation) reduces the alveolar PCO2. This, along with a raised level of CO2 in the venous blood, steepens the diffusion gradient from blood to alveolus. Consequently more CO2 is transferred to the airways and expelled. This lowers blood CO2, driving our equation back toward the left, lowering hydrogen ion concentration and returning pH back to normal.",True,Physiological Context,,,,
a5729fda-c754-4b15-9b80-3293c218447f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,"Because of the importance of maintaining normal CO2 (and thereby pH), alveolar ventilation exponentially increases with decreasing pH. Put simply, the ventilation control mechanisms use negative feedback reflexes to generate the appropriate level of ventilation to keep CO2 and pH constant. Put even more simply, CO2 is a source of acid, and the more you breathe the more CO2 you lose, so pH rises with increased ventilation.",True,Physiological Context,,,,
85990f29-a7c0-4359-809e-91f9f4de0004,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,Summary,False,Summary,,,,
1acbeb2a-c1ab-432b-8db2-7bc5de617280,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,"So now you should be able to predict what will happen to blood pH with a change in PCO2, and what the ventilatory response should be to maintain pH at a constant level.",True,Summary,,,,
0f1a94cd-f1a5-4b03-ab36-ea7ded411cd8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,"These basic principles form the foundation to understanding common and serious clinical situations of metabolic and respiratory acidosis and alkalosis, and how compensation normally prevents deviation from a safe but narrow pH range.",True,Summary,,,,
cccbfb4b-447a-43f3-be03-5d3d6f096fce,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,Text,False,Text,,,,
c7f4c268-560a-4009-8867-a730d1d4a684,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,"Levitsky, Michael G. “Chapter 8: Acid–Base Balance.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
ce0d0dec-b3ee-40ea-abb5-5d1c4182ff9a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-3,"Widdicombe, John G., and Andrew S. Davis. “Chapter 6.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
3fccb680-2058-4fae-abe2-b521d7ca8c4e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,"The reason control of arterial CO2 is so critical is that it influences arterial pH. Too much CO2 in the blood and acidosis arises, while too little raises pH to produce an alkalosis. Any deviation from a set point pH of around 7.4 can be highly dangerous as changes in pH rapidly generate changes in protein shape and function. As enzymes, membrane transporters, channels, and more start to lose function, then cellular and systemic function rapidly deteriorates. With its high metabolic rate and critical need to maintain control over its membrane potential, the nervous system is usually the first to suffer when pH changes.",True,Text,,,,
371b5885-c5ae-4758-b8f4-ddfbc977b67a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,"So we now need to look at the relationships between CO2, arterial pH, and alveolar ventilation. Before starting this chapter you should be completely happy that you have an understanding of pH and what constitutes a weak or a strong acid and reversible reactions.",True,Text,,,,
97b1de2e-3c3c-476b-b171-b87a7bc2022b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,"Active cells produce CO2 through their anerobic and aerobic metabolic pathways. This CO2 rapidly combines with water in the cytoplasm or plasma to produce carbonic acid. Carbonic acid is a weak acid, meaning that some but not all of it dissociates onto a hydrogen ion and bicarbonate ion. Both these molecules are critical players in the maintenance of pH, and this equation explains why CO2 influences arterial pH.",True,Text,,,,
7f4a8c26-d8bd-460e-b6d4-c21bc3c9de89,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,Equation 11.1,True,Text,,,,
5f9ddb1f-5627-421a-ba0d-60d7f45e4acb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],False,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
391f3206-7411-4816-97bf-982ecbcf83ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,"It is well worth committing this equation to memory and ensuring you have a good understanding of it as it is not only crucial in pulmonary pH regulation, but you will also see this equation again in renal physiology, gastrointestinal physiology, and other systems. I would argue that this is the most important equation in physiology. But let us look at it in terms of respiratory gases and the pulmonary system.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
bb62f055-07ce-45b0-8b22-16ebd47fc376,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,"It is critical to understand that this equation is reversible, so it really describes a balance. If CO2 at the tissue rises, the reaction is driven to the right, and consequently the amount of hydrogen ion is increased and pH falls. Conversely, if CO2 falls, then the reaction is driven to the left, so hydrogen ion concentration falls and pH rises. Because the lung has the ability to control the expulsion rate of CO2 from blood, the lung also has the ability to influence pH.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
13aa239d-7965-45a4-a59b-17c1728a97d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,Physiological Context,False,Physiological Context,,,,
2e0889c2-bf6e-43ce-8555-e8a224383296,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,"Let us look at the most common physiological scenario: a rise in metabolic rate causes an increase in the production of CO2 by the tissue. This, of course, pushes our equation to the right, and more hydrogen ions are produced. Because of buffering and the way CO2 is transported in the blood (discussed later on), the rise of PCO2 and fall of pH in venous blood is usually minimal, but both of these factors are enough to stimulate an increase in ventilation.",True,Physiological Context,,,,
457a46f2-d1c5-4678-9248-084488a5d4a3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,"This increase in ventilation (more specifically, alveolar ventilation) reduces the alveolar PCO2. This, along with a raised level of CO2 in the venous blood, steepens the diffusion gradient from blood to alveolus. Consequently more CO2 is transferred to the airways and expelled. This lowers blood CO2, driving our equation back toward the left, lowering hydrogen ion concentration and returning pH back to normal.",True,Physiological Context,,,,
0c82a681-4bc0-4d67-8e25-5f23cfbd7be0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,"Because of the importance of maintaining normal CO2 (and thereby pH), alveolar ventilation exponentially increases with decreasing pH. Put simply, the ventilation control mechanisms use negative feedback reflexes to generate the appropriate level of ventilation to keep CO2 and pH constant. Put even more simply, CO2 is a source of acid, and the more you breathe the more CO2 you lose, so pH rises with increased ventilation.",True,Physiological Context,,,,
24e048d6-4bdf-4c14-9625-b5eaac747017,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,Summary,False,Summary,,,,
428483b3-ee13-481d-8b2e-a837aef1d16d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,"So now you should be able to predict what will happen to blood pH with a change in PCO2, and what the ventilatory response should be to maintain pH at a constant level.",True,Summary,,,,
6ebb7cd6-3e09-4b51-899b-25ab5a7e7c1e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,"These basic principles form the foundation to understanding common and serious clinical situations of metabolic and respiratory acidosis and alkalosis, and how compensation normally prevents deviation from a safe but narrow pH range.",True,Summary,,,,
9a833df2-e9b5-4fc1-bfbf-03fb477d9274,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,Text,False,Text,,,,
22e175b8-040f-4a9a-a31a-da7ce7865823,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,"Levitsky, Michael G. “Chapter 8: Acid–Base Balance.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
81dcaf9d-6c1b-4895-9723-c795186ac5c4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Physiological Context,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-2,"Widdicombe, John G., and Andrew S. Davis. “Chapter 6.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
5248d16a-e7a6-47d8-9006-edd74fe7ffd5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,"The reason control of arterial CO2 is so critical is that it influences arterial pH. Too much CO2 in the blood and acidosis arises, while too little raises pH to produce an alkalosis. Any deviation from a set point pH of around 7.4 can be highly dangerous as changes in pH rapidly generate changes in protein shape and function. As enzymes, membrane transporters, channels, and more start to lose function, then cellular and systemic function rapidly deteriorates. With its high metabolic rate and critical need to maintain control over its membrane potential, the nervous system is usually the first to suffer when pH changes.",True,Text,,,,
3dc4dc18-49d9-4134-a264-4d86adf166cf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,"So we now need to look at the relationships between CO2, arterial pH, and alveolar ventilation. Before starting this chapter you should be completely happy that you have an understanding of pH and what constitutes a weak or a strong acid and reversible reactions.",True,Text,,,,
d677f2f6-999c-4bff-af15-f31179c3d674,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,"Active cells produce CO2 through their anerobic and aerobic metabolic pathways. This CO2 rapidly combines with water in the cytoplasm or plasma to produce carbonic acid. Carbonic acid is a weak acid, meaning that some but not all of it dissociates onto a hydrogen ion and bicarbonate ion. Both these molecules are critical players in the maintenance of pH, and this equation explains why CO2 influences arterial pH.",True,Text,,,,
e62a5151-086e-4ed7-886a-39a264ae3d6e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,Equation 11.1,True,Text,,,,
30cbc5d4-86bb-4884-816a-b3d27f38d764,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,CO2+H2O⇔H2CO3⇔H++HCO−3,False,CO2+H2O⇔H2CO3⇔H++HCO−3,,,,
17bd085f-0e44-4412-ac70-9031161bcfb0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,C,False,C,,,,
c0516004-e911-4053-8dde-b482358bb53f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,O2,False,O2,,,,
304ea8b8-a4e4-4205-b79c-9e9a96b60136,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,O,False,O,,,,
56c2fe93-8793-4902-be78-6045c3ee05d3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,2,False,2,,,,
ec142440-144e-4c94-bf93-41a5ee261176,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,+,False,+,,,,
0a1108b0-8d5b-4ecc-8f57-d391b92ca377,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,H2,False,H2,,,,
da05c9af-9a62-42da-b5fc-68cfd923a18f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,H,False,H,,,,
3e300012-f7c1-4a43-8496-5fa9ffcfd79a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,⇔,False,⇔,,,,
287a48a1-1f6e-45b4-8ed6-7991ced943d0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,O3,False,O3,,,,
6b2a83b6-3735-4035-8472-e7c48b75b946,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,3,False,3,,,,
e5277753-5fdd-488c-8708-78a20f0ce452,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,H+,False,H+,,,,
b894703b-eeaf-4779-85b9-330fff38f5d7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,O−3,False,O−3,,,,
d9b13e88-2198-4e7d-8586-453301b17269,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,−3,False,−3,,,,
8d6cd88e-01d6-485b-9097-402811321dcb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,−,False,−,,,,
f362e2d6-99f8-4165-90ee-1f737f7b5a5c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,"It is well worth committing this equation to memory and ensuring you have a good understanding of it as it is not only crucial in pulmonary pH regulation, but you will also see this equation again in renal physiology, gastrointestinal physiology, and other systems. I would argue that this is the most important equation in physiology. But let us look at it in terms of respiratory gases and the pulmonary system.",True,−,,,,
ae96fe5f-e1c5-44cb-bbe7-5b22504045c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,"It is critical to understand that this equation is reversible, so it really describes a balance. If CO2 at the tissue rises, the reaction is driven to the right, and consequently the amount of hydrogen ion is increased and pH falls. Conversely, if CO2 falls, then the reaction is driven to the left, so hydrogen ion concentration falls and pH rises. Because the lung has the ability to control the expulsion rate of CO2 from blood, the lung also has the ability to influence pH.",True,−,,,,
5d7f1327-abf3-4b52-9b6a-90773d72647d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,Physiological Context,False,Physiological Context,,,,
7fe89fd1-a017-46e4-aeab-e8df42849aef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,"Let us look at the most common physiological scenario: a rise in metabolic rate causes an increase in the production of CO2 by the tissue. This, of course, pushes our equation to the right, and more hydrogen ions are produced. Because of buffering and the way CO2 is transported in the blood (discussed later on), the rise of PCO2 and fall of pH in venous blood is usually minimal, but both of these factors are enough to stimulate an increase in ventilation.",True,Physiological Context,,,,
9cafeffe-3abb-4c9f-90f2-006cc4dbeee5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,"This increase in ventilation (more specifically, alveolar ventilation) reduces the alveolar PCO2. This, along with a raised level of CO2 in the venous blood, steepens the diffusion gradient from blood to alveolus. Consequently more CO2 is transferred to the airways and expelled. This lowers blood CO2, driving our equation back toward the left, lowering hydrogen ion concentration and returning pH back to normal.",True,Physiological Context,,,,
217e1c51-b2d7-44a9-a3a2-46f5ba317c6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,"Because of the importance of maintaining normal CO2 (and thereby pH), alveolar ventilation exponentially increases with decreasing pH. Put simply, the ventilation control mechanisms use negative feedback reflexes to generate the appropriate level of ventilation to keep CO2 and pH constant. Put even more simply, CO2 is a source of acid, and the more you breathe the more CO2 you lose, so pH rises with increased ventilation.",True,Physiological Context,,,,
ca972288-0825-4cbc-89c8-56402d9505d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,Summary,False,Summary,,,,
9f0f7e99-b2a2-4916-b950-53a89a4338a5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,"So now you should be able to predict what will happen to blood pH with a change in PCO2, and what the ventilatory response should be to maintain pH at a constant level.",True,Summary,,,,
fda54fbd-b44e-4227-914f-c8d392e05a4a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,"These basic principles form the foundation to understanding common and serious clinical situations of metabolic and respiratory acidosis and alkalosis, and how compensation normally prevents deviation from a safe but narrow pH range.",True,Summary,,,,
a10909f3-7fff-48f0-baca-9dd017ade432,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,Text,False,Text,,,,
06452b1c-0c33-452a-9f89-3ce8e584a31f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,"Levitsky, Michael G. “Chapter 8: Acid–Base Balance.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
484e2ec6-ceab-49b7-9001-a3dd19fe6cde,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Influence of CO₂ on pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/#chapter-47-section-1,"Widdicombe, John G., and Andrew S. Davis. “Chapter 6.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
c3443bb3-5a58-4959-a1a1-3d000e820fe8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,"The reason control of arterial CO2 is so critical is that it influences arterial pH. Too much CO2 in the blood and acidosis arises, while too little raises pH to produce an alkalosis. Any deviation from a set point pH of around 7.4 can be highly dangerous as changes in pH rapidly generate changes in protein shape and function. As enzymes, membrane transporters, channels, and more start to lose function, then cellular and systemic function rapidly deteriorates. With its high metabolic rate and critical need to maintain control over its membrane potential, the nervous system is usually the first to suffer when pH changes.",True,Text,,,,
51cab289-d397-4b92-981b-a7d3be459e72,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,"So we now need to look at the relationships between CO2, arterial pH, and alveolar ventilation. Before starting this chapter you should be completely happy that you have an understanding of pH and what constitutes a weak or a strong acid and reversible reactions.",True,Text,,,,
22863dd3-e4e4-4942-bc47-19db3277abd8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,"Active cells produce CO2 through their anerobic and aerobic metabolic pathways. This CO2 rapidly combines with water in the cytoplasm or plasma to produce carbonic acid. Carbonic acid is a weak acid, meaning that some but not all of it dissociates onto a hydrogen ion and bicarbonate ion. Both these molecules are critical players in the maintenance of pH, and this equation explains why CO2 influences arterial pH.",True,Text,,,,
f0dc5e25-b636-4cc5-92dd-dd97aa4c2544,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,Equation 11.1,True,Text,,,,
1e8d6b26-1b1f-4ab3-b154-623c12d1b88a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],False,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
44f987b3-ac65-4593-a492-41280d36c1d7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,"It is well worth committing this equation to memory and ensuring you have a good understanding of it as it is not only crucial in pulmonary pH regulation, but you will also see this equation again in renal physiology, gastrointestinal physiology, and other systems. I would argue that this is the most important equation in physiology. But let us look at it in terms of respiratory gases and the pulmonary system.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
6c2b462d-5abb-49e9-8477-e858220973c3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,"It is critical to understand that this equation is reversible, so it really describes a balance. If CO2 at the tissue rises, the reaction is driven to the right, and consequently the amount of hydrogen ion is increased and pH falls. Conversely, if CO2 falls, then the reaction is driven to the left, so hydrogen ion concentration falls and pH rises. Because the lung has the ability to control the expulsion rate of CO2 from blood, the lung also has the ability to influence pH.",True,[latex]CO_2 + H_2O \Leftrightarrow H_2CO_3 \Leftrightarrow H^+ + HCO^-_3[/latex],,,,
f9e9cb7f-efe0-47ba-be52-1239f478932f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,Physiological Context,False,Physiological Context,,,,
e12184eb-13fa-4830-8109-e5c94278b662,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,"Let us look at the most common physiological scenario: a rise in metabolic rate causes an increase in the production of CO2 by the tissue. This, of course, pushes our equation to the right, and more hydrogen ions are produced. Because of buffering and the way CO2 is transported in the blood (discussed later on), the rise of PCO2 and fall of pH in venous blood is usually minimal, but both of these factors are enough to stimulate an increase in ventilation.",True,Physiological Context,,,,
74c07169-9887-4440-a3ff-642cc205b45d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,"This increase in ventilation (more specifically, alveolar ventilation) reduces the alveolar PCO2. This, along with a raised level of CO2 in the venous blood, steepens the diffusion gradient from blood to alveolus. Consequently more CO2 is transferred to the airways and expelled. This lowers blood CO2, driving our equation back toward the left, lowering hydrogen ion concentration and returning pH back to normal.",True,Physiological Context,,,,
414c8a60-49ea-434e-82af-d87b6cd0ffdf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,"Because of the importance of maintaining normal CO2 (and thereby pH), alveolar ventilation exponentially increases with decreasing pH. Put simply, the ventilation control mechanisms use negative feedback reflexes to generate the appropriate level of ventilation to keep CO2 and pH constant. Put even more simply, CO2 is a source of acid, and the more you breathe the more CO2 you lose, so pH rises with increased ventilation.",True,Physiological Context,,,,
9ea40974-6140-462b-a825-ec9db0b0260e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,Summary,False,Summary,,,,
5f44925a-cb00-4760-adb4-7aea319bd844,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,"So now you should be able to predict what will happen to blood pH with a change in PCO2, and what the ventilatory response should be to maintain pH at a constant level.",True,Summary,,,,
9653ebcf-b7f8-4287-b0eb-413c306b7251,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,"These basic principles form the foundation to understanding common and serious clinical situations of metabolic and respiratory acidosis and alkalosis, and how compensation normally prevents deviation from a safe but narrow pH range.",True,Summary,,,,
a7cd6093-d10a-47c4-9b0c-d78cbdf119d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,Text,False,Text,,,,
114e96e3-f6bc-4862-9d98-63751ec10b71,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,"Levitsky, Michael G. “Chapter 8: Acid–Base Balance.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
065e5602-8743-41d4-b8e1-c3789fd59802,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,11. Arterial PCO2 and pH,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/arterial-pco2-and-ph/,"Widdicombe, John G., and Andrew S. Davis. “Chapter 6.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
6845e69b-4f8e-40bb-ade0-06adaf1c6001,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,Introduction,False,Introduction,,,,
09f9eaaf-7b63-41c9-aac8-0eb0bf7d2a75,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,nonventilatory,False,nonventilatory,,,,
57cab8eb-6850-4704-96d8-014e274a3499,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"Before looking at the unique situations that influence movement of fluid into and out of the capillary and alveoli, we will briefly review the usual Starling’s forces that influence fluid movement between a capillary and the surrounding tissue.",True,nonventilatory,,,,
6036b1e3-b9cd-41d6-955c-72034e28f6fe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"First we will look at the balance of hydrostatic forces across the walls of a capillary as it travels through tissue. Being closest to the pumping heart, the hydrostatic pressure at the arterial end is relatively high, and likely much higher than the hydrostatic force in the interstitial space. This forms a hydrostatic pressure gradient that water moves down and out of the capillary into the tissue.",True,nonventilatory,,,,
63a10440-961c-4c4d-a8e0-f49994c4ed6b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"This exit of water from the capillary leaves behind a greater concentration of plasma proteins. This causes the colloid osmotic pressure to progressively rise down the capillary, and thus begins to establish an osmotic gradient with a tendency to drag water back into the capillary from the tissue. This, and the progressive drop in capillary hydrostatic pressure due to the fluid loss to the tissue and increasing distance from the heart, means most of the exuded fluid returns back to the capillary at the venous end down a hydrostatic and osmotic gradient.",True,nonventilatory,,,,
c5a76667-c7ea-4886-8541-d73bf8cfcd3e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"The only other variable to consider here is the permeability of the capillary’s endothelium and other membranes. Pulmonary capillaries are continuous and therefore normally leak relatively little, but exposure to toxins or inflammatory mediators can cause permeabilization of the capillary endothelium and increase outward fluid movement, just like a capillary in the systemic circulation.",True,nonventilatory,,,,
4f9f337e-cfaa-4262-8ad5-8835af1413eb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,permeabilization,False,permeabilization,,,,
cc3ba682-7d67-4567-beb4-5d47ff2bcd24,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"Unlike the systemic capillaries, though, the pulmonary capillaries are exposed to airway and alveolar forces that can influence fluid movement.",True,permeabilization,,,,
46c21060-f9f5-47a0-bd0c-6cb65bf54647,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"Alveolar surface tension caused by the fluid lining of the internal alveolus wall not only drags the alveolar walls inward, but can also cause entry of fluid from the capillary and interstitium into the airspace. Excessive fluid accumulation can produce interstitial or alveolar edema, edema in the alveoli being much more serious as it interferes with gas exchange.",True,permeabilization,,,,
6650a226-d6dd-4d70-b23e-57d8e5348909,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,Nonrespiratory Functions of the Pulmonary Circulation,False,Nonrespiratory Functions of the Pulmonary Circulation,,,,
f0baf849-e326-4ec8-93bb-514e7233bd5f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"Because all cardiac output travels through the pulmonary circulation, it is ideally suited to host the enzymes needed to perform metabolic functions on blood components.",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
c6e65db3-efe0-4c75-aea2-22ddbed0900a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"We will deal with only a few here as it is more effective to address each metabolic pathway in context of its function, rather than merely because of the location in which it occurs.",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
a0a2175b-9e8d-44cd-914c-9d802cc9a705,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"ACE: Perhaps the lung’s most well-known metabolic role is to host the angiotensin-converting enzyme (or ACE). This enzyme is responsible for converting angiotensin I (released during periods of hypotension) to angiotensin II, a powerful vasoconstrictor that helps raise blood pressure. The same enzyme also inactivates 80 percent of circulating bradykinin (a potent vasodilator).",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
37f8cdc0-2060-4076-88d8-9f72c303515e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"Serotonin: Other circulating substances that are controlled by the lung include serotonin, as the lung is the major site for removing serotonin from the circulation. The lung stores the serotonin, rather than breaking it down, and even transfers it to platelets who use serotonin in their hemostatic role.",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
d48f6563-76cf-4d0e-94ea-3da171ab0196,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
d48f6563-76cf-4d0e-94ea-3da171ab0196,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
d48f6563-76cf-4d0e-94ea-3da171ab0196,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
d48f6563-76cf-4d0e-94ea-3da171ab0196,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
7ba7f00e-c645-4d1a-b590-0e14a748db37,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,Summary,False,Summary,,,,
300e0c14-dff2-4bad-bcac-eb32a8f0d68b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"So from this chapter you should be able to determine the direction of fluid movement into and out of the pulmonary capillaries given the Starling and lung forces involved, and appreciate that the lung plays other relatively small but significant metabolic roles.",True,Summary,,,,
95a92541-fd9b-4db2-adff-7039c317401b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,Text,False,Text,,,,
405afb7b-5d31-4d56-b756-36329df0d2fa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"Levitsky, Michael G. “Chapter 10: Nonrespiratory Functions of the Lung.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
9cfd8d5d-3721-4961-8c24-8b2bba6b0e82,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-3,"West, John B. “Chapter 4: Blood Flow and Metabolism—How the Pulmonary Circulation Removes Gas from the Lung and Alters Some Metabolites.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
6e475c9f-ebf4-4fa3-ba43-36e6f42bb785,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,Introduction,False,Introduction,,,,
1a48eb1f-7417-41e8-b522-74b5149cebc9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,nonventilatory,False,nonventilatory,,,,
ab0bdc1f-59c6-42e7-8708-66f67d98cf95,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"Before looking at the unique situations that influence movement of fluid into and out of the capillary and alveoli, we will briefly review the usual Starling’s forces that influence fluid movement between a capillary and the surrounding tissue.",True,nonventilatory,,,,
d3317602-d00f-4f87-9202-0be81676b1ee,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"First we will look at the balance of hydrostatic forces across the walls of a capillary as it travels through tissue. Being closest to the pumping heart, the hydrostatic pressure at the arterial end is relatively high, and likely much higher than the hydrostatic force in the interstitial space. This forms a hydrostatic pressure gradient that water moves down and out of the capillary into the tissue.",True,nonventilatory,,,,
c662afef-d183-455e-a6e9-11de29c10f4f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"This exit of water from the capillary leaves behind a greater concentration of plasma proteins. This causes the colloid osmotic pressure to progressively rise down the capillary, and thus begins to establish an osmotic gradient with a tendency to drag water back into the capillary from the tissue. This, and the progressive drop in capillary hydrostatic pressure due to the fluid loss to the tissue and increasing distance from the heart, means most of the exuded fluid returns back to the capillary at the venous end down a hydrostatic and osmotic gradient.",True,nonventilatory,,,,
05bca51a-adc9-4dc2-b711-aee5440bcc3a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"The only other variable to consider here is the permeability of the capillary’s endothelium and other membranes. Pulmonary capillaries are continuous and therefore normally leak relatively little, but exposure to toxins or inflammatory mediators can cause permeabilization of the capillary endothelium and increase outward fluid movement, just like a capillary in the systemic circulation.",True,nonventilatory,,,,
0514d609-e0bf-4092-a98f-d18ad2a2defa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,permeabilization,False,permeabilization,,,,
7c24d2ac-3865-4bc2-948c-71f59360b1c5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"Unlike the systemic capillaries, though, the pulmonary capillaries are exposed to airway and alveolar forces that can influence fluid movement.",True,permeabilization,,,,
1464c7ce-8c3c-42ca-a964-0f373b44e8f2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"Alveolar surface tension caused by the fluid lining of the internal alveolus wall not only drags the alveolar walls inward, but can also cause entry of fluid from the capillary and interstitium into the airspace. Excessive fluid accumulation can produce interstitial or alveolar edema, edema in the alveoli being much more serious as it interferes with gas exchange.",True,permeabilization,,,,
a89b0707-ba5c-41b3-b91f-bde2056a48b7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,Nonrespiratory Functions of the Pulmonary Circulation,False,Nonrespiratory Functions of the Pulmonary Circulation,,,,
b4fe437f-832f-4551-9448-fbf562992881,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"Because all cardiac output travels through the pulmonary circulation, it is ideally suited to host the enzymes needed to perform metabolic functions on blood components.",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
be64c581-15f1-48f9-81e7-0b4912c37b90,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"We will deal with only a few here as it is more effective to address each metabolic pathway in context of its function, rather than merely because of the location in which it occurs.",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
fcfcafb8-f73c-4eb7-8b2e-aed374aa788f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"ACE: Perhaps the lung’s most well-known metabolic role is to host the angiotensin-converting enzyme (or ACE). This enzyme is responsible for converting angiotensin I (released during periods of hypotension) to angiotensin II, a powerful vasoconstrictor that helps raise blood pressure. The same enzyme also inactivates 80 percent of circulating bradykinin (a potent vasodilator).",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
046e6547-eeca-495f-ac69-87e168ab5ee1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"Serotonin: Other circulating substances that are controlled by the lung include serotonin, as the lung is the major site for removing serotonin from the circulation. The lung stores the serotonin, rather than breaking it down, and even transfers it to platelets who use serotonin in their hemostatic role.",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
64546986-e624-4e05-9dd3-cf881e8f4338,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
64546986-e624-4e05-9dd3-cf881e8f4338,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
64546986-e624-4e05-9dd3-cf881e8f4338,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
64546986-e624-4e05-9dd3-cf881e8f4338,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
4ccabe83-e03c-48b4-8097-dd786b41c544,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,Summary,False,Summary,,,,
d9bce676-69e0-4764-bfaa-bb4e99066943,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"So from this chapter you should be able to determine the direction of fluid movement into and out of the pulmonary capillaries given the Starling and lung forces involved, and appreciate that the lung plays other relatively small but significant metabolic roles.",True,Summary,,,,
1ff035b3-6483-4762-a25f-c4791e087d6e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,Text,False,Text,,,,
01a38f33-fc33-49dc-a0f6-cb9cbca3df91,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"Levitsky, Michael G. “Chapter 10: Nonrespiratory Functions of the Lung.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
fc2cf192-6ab6-40c3-b162-8e37cd328065,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-2,"West, John B. “Chapter 4: Blood Flow and Metabolism—How the Pulmonary Circulation Removes Gas from the Lung and Alters Some Metabolites.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
0f8dfa03-c1e4-49cc-8310-8003f675ba1e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,Introduction,False,Introduction,,,,
7f7c7086-8f30-4c20-b83b-d7354f7e97d0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,nonventilatory,False,nonventilatory,,,,
dff7e5f9-c700-4294-9a6a-7ce313971e77,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"Before looking at the unique situations that influence movement of fluid into and out of the capillary and alveoli, we will briefly review the usual Starling’s forces that influence fluid movement between a capillary and the surrounding tissue.",True,nonventilatory,,,,
9e3b3879-f274-4e38-b837-066bcd5eff63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"First we will look at the balance of hydrostatic forces across the walls of a capillary as it travels through tissue. Being closest to the pumping heart, the hydrostatic pressure at the arterial end is relatively high, and likely much higher than the hydrostatic force in the interstitial space. This forms a hydrostatic pressure gradient that water moves down and out of the capillary into the tissue.",True,nonventilatory,,,,
194f8872-4358-4cfb-a1a4-2250a3a66fbd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"This exit of water from the capillary leaves behind a greater concentration of plasma proteins. This causes the colloid osmotic pressure to progressively rise down the capillary, and thus begins to establish an osmotic gradient with a tendency to drag water back into the capillary from the tissue. This, and the progressive drop in capillary hydrostatic pressure due to the fluid loss to the tissue and increasing distance from the heart, means most of the exuded fluid returns back to the capillary at the venous end down a hydrostatic and osmotic gradient.",True,nonventilatory,,,,
ed59a0fe-770f-495d-83d8-550c2457a6ca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"The only other variable to consider here is the permeability of the capillary’s endothelium and other membranes. Pulmonary capillaries are continuous and therefore normally leak relatively little, but exposure to toxins or inflammatory mediators can cause permeabilization of the capillary endothelium and increase outward fluid movement, just like a capillary in the systemic circulation.",True,nonventilatory,,,,
f943bf5f-94be-4d86-a677-0f38d68269d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,permeabilization,False,permeabilization,,,,
8a300fa7-01a6-49ff-b70f-b3a0fdc4545e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"Unlike the systemic capillaries, though, the pulmonary capillaries are exposed to airway and alveolar forces that can influence fluid movement.",True,permeabilization,,,,
6afa33d6-f635-4cd4-966d-c8c9603cf66f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"Alveolar surface tension caused by the fluid lining of the internal alveolus wall not only drags the alveolar walls inward, but can also cause entry of fluid from the capillary and interstitium into the airspace. Excessive fluid accumulation can produce interstitial or alveolar edema, edema in the alveoli being much more serious as it interferes with gas exchange.",True,permeabilization,,,,
c4d52313-f4b9-43b7-91e6-92b3bf0f04f6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,Nonrespiratory Functions of the Pulmonary Circulation,False,Nonrespiratory Functions of the Pulmonary Circulation,,,,
3d3e4d83-bf9d-4e44-a94c-918484f0ad78,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"Because all cardiac output travels through the pulmonary circulation, it is ideally suited to host the enzymes needed to perform metabolic functions on blood components.",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
564eea79-5d4e-45e6-81a1-e87410246313,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"We will deal with only a few here as it is more effective to address each metabolic pathway in context of its function, rather than merely because of the location in which it occurs.",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
30404a1a-4240-44be-8af7-ef0415e50008,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"ACE: Perhaps the lung’s most well-known metabolic role is to host the angiotensin-converting enzyme (or ACE). This enzyme is responsible for converting angiotensin I (released during periods of hypotension) to angiotensin II, a powerful vasoconstrictor that helps raise blood pressure. The same enzyme also inactivates 80 percent of circulating bradykinin (a potent vasodilator).",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
6e102fa9-b030-46e2-97c9-bb5ba4ad4ba4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"Serotonin: Other circulating substances that are controlled by the lung include serotonin, as the lung is the major site for removing serotonin from the circulation. The lung stores the serotonin, rather than breaking it down, and even transfers it to platelets who use serotonin in their hemostatic role.",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
fe687e47-95e5-49a1-92c1-5e5c8acf2c3d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
fe687e47-95e5-49a1-92c1-5e5c8acf2c3d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
fe687e47-95e5-49a1-92c1-5e5c8acf2c3d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
fe687e47-95e5-49a1-92c1-5e5c8acf2c3d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
6e7c2dcc-a74b-4016-9425-4d36b8b60a7b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,Summary,False,Summary,,,,
aa9b2c23-24ab-4e75-84bb-eb2bcca8cd59,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"So from this chapter you should be able to determine the direction of fluid movement into and out of the pulmonary capillaries given the Starling and lung forces involved, and appreciate that the lung plays other relatively small but significant metabolic roles.",True,Summary,,,,
5240b553-4dd5-4042-80da-0ad8addabea5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,Text,False,Text,,,,
5690a31a-10e0-4d1c-b75f-ab18661e6701,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"Levitsky, Michael G. “Chapter 10: Nonrespiratory Functions of the Lung.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
fce93cc7-2917-4403-9abd-eab4887cf6a0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/#chapter-45-section-1,"West, John B. “Chapter 4: Blood Flow and Metabolism—How the Pulmonary Circulation Removes Gas from the Lung and Alters Some Metabolites.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
a083bb6f-3078-481c-95af-498bafee4a06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,Introduction,False,Introduction,,,,
60468a7a-34be-4185-a8c4-e83981876372,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,nonventilatory,False,nonventilatory,,,,
7f69234b-3760-49b4-8a7f-31123c3e1e7c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"Before looking at the unique situations that influence movement of fluid into and out of the capillary and alveoli, we will briefly review the usual Starling’s forces that influence fluid movement between a capillary and the surrounding tissue.",True,nonventilatory,,,,
e412dec5-f8c2-4b9d-8d16-d8416284c498,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"First we will look at the balance of hydrostatic forces across the walls of a capillary as it travels through tissue. Being closest to the pumping heart, the hydrostatic pressure at the arterial end is relatively high, and likely much higher than the hydrostatic force in the interstitial space. This forms a hydrostatic pressure gradient that water moves down and out of the capillary into the tissue.",True,nonventilatory,,,,
9bd367c3-a05d-4a65-98d0-af8f18235b58,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"This exit of water from the capillary leaves behind a greater concentration of plasma proteins. This causes the colloid osmotic pressure to progressively rise down the capillary, and thus begins to establish an osmotic gradient with a tendency to drag water back into the capillary from the tissue. This, and the progressive drop in capillary hydrostatic pressure due to the fluid loss to the tissue and increasing distance from the heart, means most of the exuded fluid returns back to the capillary at the venous end down a hydrostatic and osmotic gradient.",True,nonventilatory,,,,
d041475f-4feb-4d76-a564-8ef789b32c70,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"The only other variable to consider here is the permeability of the capillary’s endothelium and other membranes. Pulmonary capillaries are continuous and therefore normally leak relatively little, but exposure to toxins or inflammatory mediators can cause permeabilization of the capillary endothelium and increase outward fluid movement, just like a capillary in the systemic circulation.",True,nonventilatory,,,,
bf089848-1b74-46f5-ac05-8d78b0809db0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,permeabilization,False,permeabilization,,,,
f06d4516-829e-4759-a643-6e7c87595738,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"Unlike the systemic capillaries, though, the pulmonary capillaries are exposed to airway and alveolar forces that can influence fluid movement.",True,permeabilization,,,,
09549ebd-0717-42a0-b012-bdf27ca46631,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"Alveolar surface tension caused by the fluid lining of the internal alveolus wall not only drags the alveolar walls inward, but can also cause entry of fluid from the capillary and interstitium into the airspace. Excessive fluid accumulation can produce interstitial or alveolar edema, edema in the alveoli being much more serious as it interferes with gas exchange.",True,permeabilization,,,,
260f11ff-7417-4a5d-a538-13f468734539,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,Nonrespiratory Functions of the Pulmonary Circulation,False,Nonrespiratory Functions of the Pulmonary Circulation,,,,
20cf694f-24c3-4224-ba4c-5a03a84d80c4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"Because all cardiac output travels through the pulmonary circulation, it is ideally suited to host the enzymes needed to perform metabolic functions on blood components.",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
f85dadec-2c09-49dc-888f-562a43a1c839,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"We will deal with only a few here as it is more effective to address each metabolic pathway in context of its function, rather than merely because of the location in which it occurs.",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
930be20c-1998-4acb-a0c4-68db8748944a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"ACE: Perhaps the lung’s most well-known metabolic role is to host the angiotensin-converting enzyme (or ACE). This enzyme is responsible for converting angiotensin I (released during periods of hypotension) to angiotensin II, a powerful vasoconstrictor that helps raise blood pressure. The same enzyme also inactivates 80 percent of circulating bradykinin (a potent vasodilator).",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
9e093b16-0d91-4ae6-841b-6d9e7abe4e2c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"Serotonin: Other circulating substances that are controlled by the lung include serotonin, as the lung is the major site for removing serotonin from the circulation. The lung stores the serotonin, rather than breaking it down, and even transfers it to platelets who use serotonin in their hemostatic role.",True,Nonrespiratory Functions of the Pulmonary Circulation,,,,
2bf666f9-d0d4-4ac0-ba3a-92fc92c8a534,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
2bf666f9-d0d4-4ac0-ba3a-92fc92c8a534,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,Nonrespiratory Functions of the Pulmonary Circulation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
2bf666f9-d0d4-4ac0-ba3a-92fc92c8a534,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,Pulmonary Capillaries and Fluid Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
2bf666f9-d0d4-4ac0-ba3a-92fc92c8a534,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"Arachidonic acid: The lung is also involved in the metabolism of arachidonic acid, which is worth dealing with here as well because not only are the products of this metabolism vasoactive, they can also influence airway smooth muscle and cause bronchoconstriction. In brief, arachidonic acid is produced by the action of a phospholipase on membrane-bound phospholipids. The arachidonic acid can then follow one of two pathways (figure 10.1): to produce leukotrienes, which are involved in the inflammatory response and can cause bronchoconstriction, or to produce prostaglandins and thromboxane through the action of cyclooxygenases. The relevance for us here is that these alternative pathways explain why some asthmatics are sensitive to aspirin and bronchoconstrict when they take aspirin. Aspirin inhibits cyclooxygenase and thus blocks one of these pathways. Consequently there is more substrate, arachidonic acid, available for the alternate pathway and so more leukotrienes are produced, in response to which the hypersensitive airways of the asthmatic bronchoconstrict.",True,Nonrespiratory Functions of the Pulmonary Circulation,Figure 10.1,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/10.1.png,"Figure 10.1: Pulmonary metabolism of arachidonic acid. Blockade of cyclooxygenase by aspirin means more arachidonic acid is available for the production of leukotrienes, which can cause bronchoconstriction."
560dbd2f-963b-4309-8991-a848af2b1569,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,Summary,False,Summary,,,,
f077cc44-a951-414b-b438-e78bce4519cc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"So from this chapter you should be able to determine the direction of fluid movement into and out of the pulmonary capillaries given the Starling and lung forces involved, and appreciate that the lung plays other relatively small but significant metabolic roles.",True,Summary,,,,
985abf03-e96c-4df6-ba39-ad75733084f8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,Text,False,Text,,,,
eac53b3d-c302-4c30-b958-6cae76cd9c85,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"Levitsky, Michael G. “Chapter 10: Nonrespiratory Functions of the Lung.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
a761e19c-783f-4a58-ad50-fbeb1f835232,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,10. Pulmonary Capillaries and Nonventilatory Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-capillaries-and-nonventilatory-function/,"West, John B. “Chapter 4: Blood Flow and Metabolism—How the Pulmonary Circulation Removes Gas from the Lung and Alters Some Metabolites.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
7b0ae5d4-4e95-4b2e-860d-c6077de4c1dc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,Functional anatomy,False,Functional anatomy,,,,
2d656643-3fd1-43fc-96ee-10525d50b3a7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
2d656643-3fd1-43fc-96ee-10525d50b3a7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
2d656643-3fd1-43fc-96ee-10525d50b3a7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
2d656643-3fd1-43fc-96ee-10525d50b3a7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
2d656643-3fd1-43fc-96ee-10525d50b3a7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
203cf211-dc4b-4b38-8067-a5e2bc9c8686,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,Main arteries follow a similar branching pattern to the bronchial tree until the terminal bronchioles are reached. This anatomical arrangement allows perfusion to follow the ventilation. Upon reaching the terminal bronchioles the vessels divide into a vast array of capillaries that wrap around the respiratory ducts and alveoli to form the respiratory zone of the lungs.,True,Functional anatomy,,,,
71adf9d0-36ec-43e0-a596-d39992c60ac8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
71adf9d0-36ec-43e0-a596-d39992c60ac8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
71adf9d0-36ec-43e0-a596-d39992c60ac8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
71adf9d0-36ec-43e0-a596-d39992c60ac8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
71adf9d0-36ec-43e0-a596-d39992c60ac8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
d0577b04-fbad-40d6-a316-b00097d55971,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"The capillary beds converge into small veins after traveling over the alveolar surfaces, and these small veins then collect into four pulmonary veins that lead back to the left heart. This is an unusual example of veins carrying blood with arterial gas pressures.",True,Functional anatomy,,,,
4a245151-c7e3-4f86-a18b-ec19ffdc9e6f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Despite receiving the same blood volume per minute as the systemic circulation the pulmonary circulation is a low-pressure system. Systolic pressure is normally only 25 mmHg, compared to 120 in the systemic circulation, diastolic is 8, compared to 80 and mean pulmonary artery pressure is only 15. These numbers are well worth remembering.",True,Functional anatomy,,,,
e736cb28-7cdf-4455-993e-4b5f2ffa34ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
e736cb28-7cdf-4455-993e-4b5f2ffa34ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
e736cb28-7cdf-4455-993e-4b5f2ffa34ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
e736cb28-7cdf-4455-993e-4b5f2ffa34ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
e736cb28-7cdf-4455-993e-4b5f2ffa34ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
b3758842-3c66-487d-ab1b-6fa24991e892,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"The pulmonary arteries show different characteristic to their systemic counterparts as well. The walls of a pulmonary arterioles are thin compared to systemic arterioles. They also lack the smooth muscle layer seen in the systemic arteriole. In fact pulmonary arterioles look much more like systemic veins and they are often mistaken for such in biopsy or dissection. With little smooth muscle it’s clear that these vessels have little role in controlling the distribution of blood flow – a vital role of their systemic counterparts. As the pulmonary circulation receives all cardiac output, all the time, such precise control isn’t required.",True,Functional anatomy,,,,
36e1ecec-46eb-4a1f-9188-93fae0ef19ae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,The thin walls and lack of smooth muscle also make the pulmonary arterioles highly compliant and so they behave much more like veins in their pressure response – extending when pressure increases. This gives the pulmonary arteriole system a rather unique pressure-resistance relationship that we’ll look at in a moment.,True,Functional anatomy,,,,
d733e2c5-3e4a-4418-a68f-e424ee6e64cc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,This low pressure and compliant system also means that the right heart has much less work to perform to generate its output. In fact the right ventricle has about a tenth of the work of the left heart to move exactly the same blood volume. Hence the structure and work capacity of the right heart is so much smaller than the left – something worth bearing in mind if disease causes changes in the pulmonary vasculature that in turn causes the less substantial right heart to work harder and undergo hypertrophy,True,Functional anatomy,,,,
7940e8cf-06db-46e3-8e5c-f9d7107614a6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",False,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
6325a5d6-c907-458f-84da-8cb60a279adc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
6325a5d6-c907-458f-84da-8cb60a279adc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
6325a5d6-c907-458f-84da-8cb60a279adc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
6325a5d6-c907-458f-84da-8cb60a279adc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
6325a5d6-c907-458f-84da-8cb60a279adc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
2bbb86e4-449d-4278-ad09-1990a2d8b684,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Unlike systemic arterioles there is little autoregulation by the pulmonary arterioles, so the pulmonary arterioles do not actively vasoconstrict when stretched by high pressure. Instead, they passively distend, thereby reducing their resistance with increasing resistance.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
e559d206-42f3-4699-bd6c-3b0df3ae3c3c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"A rise in pulmonary pressure not only distends vessels but initiates flow through otherwise unused, or dormant, vessels, particularly those closer to the apex of the lung (we will see why later on). With more vessels recruited, the total cross-sectional area of used vessels increases and total resistance falls.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
3ec59c37-13fa-479f-8c93-87d98c5f6443,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,But there are other and more complex peculiarities of the pulmonary circulation that determine its resistance…,True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
7adacb8d-da18-41ad-909f-ce30bb37b5f6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,Pulmonary Vascular Resistance and Radial Traction,False,Pulmonary Vascular Resistance and Radial Traction,,,,
18ebdcaa-ba5a-453f-8caa-380515f09552,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,Another unique characteristic of the pulmonary circulation is that it is exposed to the changing pressures in the airways and alveoli. It is also involved in the fiber network that generates radial traction. Consequently pulmonary vessels can be expanded or compressed in a way no other circulation is.,True,Pulmonary Vascular Resistance and Radial Traction,,,,
3f0e9c13-9090-4942-9128-184922b0e4e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
3f0e9c13-9090-4942-9128-184922b0e4e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
3f0e9c13-9090-4942-9128-184922b0e4e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
3f0e9c13-9090-4942-9128-184922b0e4e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
3f0e9c13-9090-4942-9128-184922b0e4e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
30c04fba-638c-4161-875c-e9c874074e28,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Alveolar vessels: These are primarily the capillaries and small vessels in close contact with the alveoli. Consequently they are exposed to the alveolar pressures. First, the surface tension within the alveolus that is tending to pull the alveolus closed also pulls on the vessels between alveoli, tending to pull it open as neighboring alveoli pull inward on themselves, and play tug-of-war with the vessel walls in between, extending them and causing a decrease in vascular resistance.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
a6908a5d-de72-4643-9dbd-7c05bae9db4a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Alternatively, when alveolar pressure increases (e.g., at high lung volumes), the raised alveolar pressure can compress the vessels running over its surface, causing an increase in vascular resistance.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
33efc853-5de8-41ff-8faa-0de4b021fdf1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Extra-alveolar vessels: By definition these vessels are not in contact with the alveoli, so they are not exposed to the same alveolar forces. These are exposed to the intrapleural forces, however, so as we saw airways opening during inspiration when intra-pleural pressure falls, these extra-alveolar vessels are also pulled open during inspiration by radial traction, and their resistance consequently falls as lung volume increases.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
41d6d59f-fe3d-411a-a0c2-66ac80e86083,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"The summation of these forces (alveolar pressure, surface tension, and radial traction) means that pulmonary vasculature resistance has a complex relationship with lung volume.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
63081532-8a20-446b-ad24-9f5594602780,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,Pulmonary Vascular Resistance and Lung Volume,False,Pulmonary Vascular Resistance and Lung Volume,,,,
79ac47de-cbee-4e67-902e-326cf326ff5a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
79ac47de-cbee-4e67-902e-326cf326ff5a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
79ac47de-cbee-4e67-902e-326cf326ff5a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
79ac47de-cbee-4e67-902e-326cf326ff5a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
79ac47de-cbee-4e67-902e-326cf326ff5a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
c8eb161e-6df3-439e-b207-ca61bd6a145b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
c8eb161e-6df3-439e-b207-ca61bd6a145b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
c8eb161e-6df3-439e-b207-ca61bd6a145b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
c8eb161e-6df3-439e-b207-ca61bd6a145b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
c8eb161e-6df3-439e-b207-ca61bd6a145b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
662a01db-ceb5-4631-8916-57168017e69f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
662a01db-ceb5-4631-8916-57168017e69f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
662a01db-ceb5-4631-8916-57168017e69f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
662a01db-ceb5-4631-8916-57168017e69f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
662a01db-ceb5-4631-8916-57168017e69f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
689ce975-ea30-416b-844d-fd839fcb438f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,So vascular resistance and lung volume are related with an inverted bell-shaped relationship. Now let us look at the forces that determine the distribution of blood flow across the lung structure.,True,Pulmonary Vascular Resistance and Lung Volume,,,,
b92b1741-82a5-4389-8cad-d07a5e0d9c99,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,Pulmonary Blood Flow and Gravity,False,Pulmonary Blood Flow and Gravity,,,,
ebf14881-b887-46d5-aa4b-57d239510c35,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"You may recall that gravity affected the distribution of ventilation by generating the gradient of intrapleural pressures down the lung—most negative at the apex, less negative at the base.",True,Pulmonary Blood Flow and Gravity,,,,
3e7ca2e1-e790-4b9f-b380-ae003c217ec6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
3e7ca2e1-e790-4b9f-b380-ae003c217ec6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
3e7ca2e1-e790-4b9f-b380-ae003c217ec6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
3e7ca2e1-e790-4b9f-b380-ae003c217ec6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
3e7ca2e1-e790-4b9f-b380-ae003c217ec6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
79e0cd7b-5ac7-45a0-931b-3a62ca03a970,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,Zones of Perfusion,False,Zones of Perfusion,,,,
af9961ed-cb89-4f06-8d40-6eec104904ca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"We now have to consider the relationship of the pressures in these three systems, arterial, alveolar and venous, at different heights of the lung. Many of the following principles have already been dealt with, but we can put them together to look at how they affect perfusion distribution.",True,Zones of Perfusion,,,,
2147c739-e5c8-44a6-8df7-943fe01fe7a2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Zone 1: At the top of the lung the arterial pressure is relatively low because this is the furthest vertical distance from the heart. In the same zone, as you know, the alveoli here are extended by the low (more negative) intrapleural pressure at the apex. These extended alveoli tend to compress the surrounding capillaries, and the lack of arterial pressure to push past the extended alveolus means blood flow through capillary beds in zone 1 may be relatively low. It is certainly a pronounced effect in patients undergoing positive pressure ventilation where alveolar pressure may exceed arterial pressure and stop blood flow at the apex altogether. This phenomenon of ventilated but underperfused alveoli is referred to as alveolar dead space, as without adequate perfusion, gas exchange is compromised.",True,Zones of Perfusion,,,,
2d0d3094-4f38-436c-bcb2-df7ad18adeb7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Zone 2: In zone 2 we are lower down the lung, and at this point arterial pressure is higher (closer proximity to the heart) and the alveoli are less extended, but venous pressure remains less than alveolar pressure. So flow in zone 2 is determined by the difference between arterial and alveolar pressures.",True,Zones of Perfusion,,,,
12a2f3dd-f3c3-42b2-a3e2-d5e47261a51b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Zone 3: Dropping further down the lung to the base, the arterial and venous pressure have both risen as the column of fluid (blood) above them is greater at this point, and now both are above the now smaller alveolar pressure (near the base the intrapleural pressure is less negative). Consequently the flow through the capillary bed in zone 3 is determined by the arterial–venous pressure difference, just as it is in the systemic circulation.",True,Zones of Perfusion,,,,
2afa1608-c9b0-4550-82bb-63d310167368,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"(There can at times be a fourth zone, which appears only at low lung volumes. At low lung volumes tissue at the base of the lung can be compressed, and this compression can collapse the extra-alveolar vessels.)",True,Zones of Perfusion,,,,
418a3200-e72d-4d95-8a8f-8aa898687a9f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,Summary,False,Summary,,,,
e8c397b8-78a9-4660-b617-1d4f664f890a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"So when considering flow through a systemic capillary bed we only have to think about the arterial and venous pressures, the pulmonary circulation throws us a curve ball by adding alveolar pressures into the mix that produce these perfusion zones.",True,Summary,,,,
16630eca-c3b1-44b0-9492-457d247701a7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,Pulmonary Vasculature’s Response to Hypoxia,False,Pulmonary Vasculature’s Response to Hypoxia,,,,
8df720cc-9a89-4b3e-aae3-53bb6fb0914a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,If systemic tissue becomes hypoxic then local arterioles open to allow more blood flow and increase oxygen delivery. The opposite is true for the pulmonary circulation where the response to local hypoxia is vasoconstriction.,True,Pulmonary Vasculature’s Response to Hypoxia,,,,
464ab310-a3d2-47ba-a61a-4ff9574d7a11,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"First, remember that the bronchial circulation provides oxygen and nutrients to the pulmonary itself, and this behaves as all other systemic circulations. But the pulmonary circulation is for gas exchange. So if an area of the lung has become hypoxic (i.e., has a low oxygen partial pressure), this is indicative of that area having insufficient ventilation.",True,Pulmonary Vasculature’s Response to Hypoxia,,,,
50c601f1-cfb5-4ee9-abb0-0fc7de209eae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"If there is little ventilation going to that area then there is little point sending perfusion to it. So the little smooth muscle there is in the pulmonary vasculature contracts to constrict the vessel when hypoxia is present. The blood follows the path of least resistance and thereby goes to vessels that are open (i.e., to areas where ventilation is maintaining a higher PO2).",True,Pulmonary Vasculature’s Response to Hypoxia,,,,
9b54c899-a7bc-41ae-9f38-770b14694999,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Because of its unique role in gas exchange, rather than supplying local tissue, and the pressures that are present in the lung beyond vasculature pressure, plus the different vasculature structure, the pulmonary circulation has some unusual characteristics. These produce unique blood flow patterns in response to lung volume, gravity, and the need to match ventilated areas with adequate perfusion.",True,Pulmonary Vasculature’s Response to Hypoxia,,,,
b3e5871b-1588-4d90-ace3-29580c32bca9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,Text,False,Text,,,,
5bbf18cb-720e-433f-a97c-7a9a17affa5c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Levitsky, Michael G. “Chapter 4: Blood Flow to the Lung.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
0dccaec5-1a0b-47df-a8e0-bfeef4c33602,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"West, John B. “Chapter 4: Blood Flow and Metabolism—How the Pulmonary Circulation Removes Gas from the Lung and Alters Some Metabolites.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
58f3e187-02d3-4794-a834-033ae16daf9b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-4,"Widdicombe, John G., and Andrew S. Davis. “Chapter 5.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
dc85ebc9-86e5-408c-a03c-5d4b14963686,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,Functional anatomy,False,Functional anatomy,,,,
88f3d09f-18dd-4c33-9a74-dcddea934fd5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
88f3d09f-18dd-4c33-9a74-dcddea934fd5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
88f3d09f-18dd-4c33-9a74-dcddea934fd5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
88f3d09f-18dd-4c33-9a74-dcddea934fd5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
88f3d09f-18dd-4c33-9a74-dcddea934fd5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
84613ce0-0f51-4bed-b2da-cbc58077a412,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,Main arteries follow a similar branching pattern to the bronchial tree until the terminal bronchioles are reached. This anatomical arrangement allows perfusion to follow the ventilation. Upon reaching the terminal bronchioles the vessels divide into a vast array of capillaries that wrap around the respiratory ducts and alveoli to form the respiratory zone of the lungs.,True,Functional anatomy,,,,
f6b7da39-2931-4c5c-b3a9-b9255a0b4e98,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
f6b7da39-2931-4c5c-b3a9-b9255a0b4e98,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
f6b7da39-2931-4c5c-b3a9-b9255a0b4e98,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
f6b7da39-2931-4c5c-b3a9-b9255a0b4e98,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
f6b7da39-2931-4c5c-b3a9-b9255a0b4e98,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
60582796-0402-42de-b70a-ed8133558e52,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"The capillary beds converge into small veins after traveling over the alveolar surfaces, and these small veins then collect into four pulmonary veins that lead back to the left heart. This is an unusual example of veins carrying blood with arterial gas pressures.",True,Functional anatomy,,,,
b108eea7-0437-4584-8d5c-63e25f5706c0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Despite receiving the same blood volume per minute as the systemic circulation the pulmonary circulation is a low-pressure system. Systolic pressure is normally only 25 mmHg, compared to 120 in the systemic circulation, diastolic is 8, compared to 80 and mean pulmonary artery pressure is only 15. These numbers are well worth remembering.",True,Functional anatomy,,,,
5b4f05b9-ab57-4af2-8bbf-e3b8bbd3b885,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
5b4f05b9-ab57-4af2-8bbf-e3b8bbd3b885,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
5b4f05b9-ab57-4af2-8bbf-e3b8bbd3b885,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
5b4f05b9-ab57-4af2-8bbf-e3b8bbd3b885,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
5b4f05b9-ab57-4af2-8bbf-e3b8bbd3b885,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
ef9ca45b-d4ab-4a20-bf5e-e891e836276e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"The pulmonary arteries show different characteristic to their systemic counterparts as well. The walls of a pulmonary arterioles are thin compared to systemic arterioles. They also lack the smooth muscle layer seen in the systemic arteriole. In fact pulmonary arterioles look much more like systemic veins and they are often mistaken for such in biopsy or dissection. With little smooth muscle it’s clear that these vessels have little role in controlling the distribution of blood flow – a vital role of their systemic counterparts. As the pulmonary circulation receives all cardiac output, all the time, such precise control isn’t required.",True,Functional anatomy,,,,
f1328284-e56d-4c7c-baa1-666044a83cdb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,The thin walls and lack of smooth muscle also make the pulmonary arterioles highly compliant and so they behave much more like veins in their pressure response – extending when pressure increases. This gives the pulmonary arteriole system a rather unique pressure-resistance relationship that we’ll look at in a moment.,True,Functional anatomy,,,,
8b066f1a-16b0-486e-84ea-e6306a83401c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,This low pressure and compliant system also means that the right heart has much less work to perform to generate its output. In fact the right ventricle has about a tenth of the work of the left heart to move exactly the same blood volume. Hence the structure and work capacity of the right heart is so much smaller than the left – something worth bearing in mind if disease causes changes in the pulmonary vasculature that in turn causes the less substantial right heart to work harder and undergo hypertrophy,True,Functional anatomy,,,,
7b96771e-1b55-4e22-9026-714647914aaa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",False,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
2c21e552-2350-4636-9879-6b5234643d4e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
2c21e552-2350-4636-9879-6b5234643d4e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
2c21e552-2350-4636-9879-6b5234643d4e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
2c21e552-2350-4636-9879-6b5234643d4e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
2c21e552-2350-4636-9879-6b5234643d4e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
3f07867b-e6b3-46b3-aaa6-91d106935d23,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Unlike systemic arterioles there is little autoregulation by the pulmonary arterioles, so the pulmonary arterioles do not actively vasoconstrict when stretched by high pressure. Instead, they passively distend, thereby reducing their resistance with increasing resistance.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
8571d6d0-ee45-421b-8501-1a19c6ad2449,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"A rise in pulmonary pressure not only distends vessels but initiates flow through otherwise unused, or dormant, vessels, particularly those closer to the apex of the lung (we will see why later on). With more vessels recruited, the total cross-sectional area of used vessels increases and total resistance falls.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
5a1e9861-0520-4dba-81e0-74c34c7482b3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,But there are other and more complex peculiarities of the pulmonary circulation that determine its resistance…,True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
bdc0083f-abad-4ae5-bbd0-545da38a6fe4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,Pulmonary Vascular Resistance and Radial Traction,False,Pulmonary Vascular Resistance and Radial Traction,,,,
79ec1f6e-995f-48a7-929e-4dc855b591d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,Another unique characteristic of the pulmonary circulation is that it is exposed to the changing pressures in the airways and alveoli. It is also involved in the fiber network that generates radial traction. Consequently pulmonary vessels can be expanded or compressed in a way no other circulation is.,True,Pulmonary Vascular Resistance and Radial Traction,,,,
6e517680-f9e1-4e44-a244-2d51daf2e52d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
6e517680-f9e1-4e44-a244-2d51daf2e52d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
6e517680-f9e1-4e44-a244-2d51daf2e52d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
6e517680-f9e1-4e44-a244-2d51daf2e52d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
6e517680-f9e1-4e44-a244-2d51daf2e52d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
f6450351-8026-46c2-9a43-ddeb5316e228,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Alveolar vessels: These are primarily the capillaries and small vessels in close contact with the alveoli. Consequently they are exposed to the alveolar pressures. First, the surface tension within the alveolus that is tending to pull the alveolus closed also pulls on the vessels between alveoli, tending to pull it open as neighboring alveoli pull inward on themselves, and play tug-of-war with the vessel walls in between, extending them and causing a decrease in vascular resistance.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
c346d88a-a7bf-4abc-8f48-66233d635612,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Alternatively, when alveolar pressure increases (e.g., at high lung volumes), the raised alveolar pressure can compress the vessels running over its surface, causing an increase in vascular resistance.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
d4f04672-4674-4ccc-bcf4-174591af8045,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Extra-alveolar vessels: By definition these vessels are not in contact with the alveoli, so they are not exposed to the same alveolar forces. These are exposed to the intrapleural forces, however, so as we saw airways opening during inspiration when intra-pleural pressure falls, these extra-alveolar vessels are also pulled open during inspiration by radial traction, and their resistance consequently falls as lung volume increases.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
90c011da-83bf-4d04-96dc-855321bb1c98,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"The summation of these forces (alveolar pressure, surface tension, and radial traction) means that pulmonary vasculature resistance has a complex relationship with lung volume.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
80b6d85b-007a-40e1-8d68-dd003dc2f301,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,Pulmonary Vascular Resistance and Lung Volume,False,Pulmonary Vascular Resistance and Lung Volume,,,,
bba27019-c292-490c-bc33-d1cc8bd8c0ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
bba27019-c292-490c-bc33-d1cc8bd8c0ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
bba27019-c292-490c-bc33-d1cc8bd8c0ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
bba27019-c292-490c-bc33-d1cc8bd8c0ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
bba27019-c292-490c-bc33-d1cc8bd8c0ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
40139cab-5f52-4f23-89cc-7017097f74f0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
40139cab-5f52-4f23-89cc-7017097f74f0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
40139cab-5f52-4f23-89cc-7017097f74f0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
40139cab-5f52-4f23-89cc-7017097f74f0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
40139cab-5f52-4f23-89cc-7017097f74f0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
f4045eea-f5bc-42b6-ac6e-903b393c4f62,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
f4045eea-f5bc-42b6-ac6e-903b393c4f62,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
f4045eea-f5bc-42b6-ac6e-903b393c4f62,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
f4045eea-f5bc-42b6-ac6e-903b393c4f62,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
f4045eea-f5bc-42b6-ac6e-903b393c4f62,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
ac60d1c4-aaab-49b9-95fc-ecdd0efeb9e3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,So vascular resistance and lung volume are related with an inverted bell-shaped relationship. Now let us look at the forces that determine the distribution of blood flow across the lung structure.,True,Pulmonary Vascular Resistance and Lung Volume,,,,
eeb9a79e-4a65-4fae-8ad5-44549debc74f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,Pulmonary Blood Flow and Gravity,False,Pulmonary Blood Flow and Gravity,,,,
bcb7f0b3-97fe-475f-aa32-c72b8abeda10,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"You may recall that gravity affected the distribution of ventilation by generating the gradient of intrapleural pressures down the lung—most negative at the apex, less negative at the base.",True,Pulmonary Blood Flow and Gravity,,,,
d6af72af-8086-4056-a2a9-c482dbeb07a3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
d6af72af-8086-4056-a2a9-c482dbeb07a3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
d6af72af-8086-4056-a2a9-c482dbeb07a3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
d6af72af-8086-4056-a2a9-c482dbeb07a3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
d6af72af-8086-4056-a2a9-c482dbeb07a3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
b327f54f-fda1-4be1-b8ed-40b8e3ea3313,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,Zones of Perfusion,False,Zones of Perfusion,,,,
bddfb85c-58b5-43cd-9891-b82fbc4ea068,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"We now have to consider the relationship of the pressures in these three systems, arterial, alveolar and venous, at different heights of the lung. Many of the following principles have already been dealt with, but we can put them together to look at how they affect perfusion distribution.",True,Zones of Perfusion,,,,
f039e109-2fee-4324-8e6a-6a4a7eca7921,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Zone 1: At the top of the lung the arterial pressure is relatively low because this is the furthest vertical distance from the heart. In the same zone, as you know, the alveoli here are extended by the low (more negative) intrapleural pressure at the apex. These extended alveoli tend to compress the surrounding capillaries, and the lack of arterial pressure to push past the extended alveolus means blood flow through capillary beds in zone 1 may be relatively low. It is certainly a pronounced effect in patients undergoing positive pressure ventilation where alveolar pressure may exceed arterial pressure and stop blood flow at the apex altogether. This phenomenon of ventilated but underperfused alveoli is referred to as alveolar dead space, as without adequate perfusion, gas exchange is compromised.",True,Zones of Perfusion,,,,
044a44fc-c6de-4f1b-8cf2-9386916fc6c9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Zone 2: In zone 2 we are lower down the lung, and at this point arterial pressure is higher (closer proximity to the heart) and the alveoli are less extended, but venous pressure remains less than alveolar pressure. So flow in zone 2 is determined by the difference between arterial and alveolar pressures.",True,Zones of Perfusion,,,,
9b38c43d-ec1d-4e51-a0c0-dca95db4ed3c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Zone 3: Dropping further down the lung to the base, the arterial and venous pressure have both risen as the column of fluid (blood) above them is greater at this point, and now both are above the now smaller alveolar pressure (near the base the intrapleural pressure is less negative). Consequently the flow through the capillary bed in zone 3 is determined by the arterial–venous pressure difference, just as it is in the systemic circulation.",True,Zones of Perfusion,,,,
1317a4bb-b90f-4f4c-85a3-333d607a03ce,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"(There can at times be a fourth zone, which appears only at low lung volumes. At low lung volumes tissue at the base of the lung can be compressed, and this compression can collapse the extra-alveolar vessels.)",True,Zones of Perfusion,,,,
631611be-affd-411f-bfd8-4aeb0c5643f8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,Summary,False,Summary,,,,
facb154f-2dff-4259-9e1e-ba0121c6975c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"So when considering flow through a systemic capillary bed we only have to think about the arterial and venous pressures, the pulmonary circulation throws us a curve ball by adding alveolar pressures into the mix that produce these perfusion zones.",True,Summary,,,,
75326614-114f-43d1-a834-51f4e1cef5db,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,Pulmonary Vasculature’s Response to Hypoxia,False,Pulmonary Vasculature’s Response to Hypoxia,,,,
28de494e-f661-4106-9b9e-9f7d13458d39,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,If systemic tissue becomes hypoxic then local arterioles open to allow more blood flow and increase oxygen delivery. The opposite is true for the pulmonary circulation where the response to local hypoxia is vasoconstriction.,True,Pulmonary Vasculature’s Response to Hypoxia,,,,
23b780c9-e0b4-4968-ad9b-c75045cedb5d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"First, remember that the bronchial circulation provides oxygen and nutrients to the pulmonary itself, and this behaves as all other systemic circulations. But the pulmonary circulation is for gas exchange. So if an area of the lung has become hypoxic (i.e., has a low oxygen partial pressure), this is indicative of that area having insufficient ventilation.",True,Pulmonary Vasculature’s Response to Hypoxia,,,,
1ac1642b-0c83-4884-b55e-f5cfd33ad4b9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"If there is little ventilation going to that area then there is little point sending perfusion to it. So the little smooth muscle there is in the pulmonary vasculature contracts to constrict the vessel when hypoxia is present. The blood follows the path of least resistance and thereby goes to vessels that are open (i.e., to areas where ventilation is maintaining a higher PO2).",True,Pulmonary Vasculature’s Response to Hypoxia,,,,
1d59f519-2f7a-4a37-af0d-e69b128ab28e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Because of its unique role in gas exchange, rather than supplying local tissue, and the pressures that are present in the lung beyond vasculature pressure, plus the different vasculature structure, the pulmonary circulation has some unusual characteristics. These produce unique blood flow patterns in response to lung volume, gravity, and the need to match ventilated areas with adequate perfusion.",True,Pulmonary Vasculature’s Response to Hypoxia,,,,
c8821233-8397-42d9-9a44-fc2abd26a676,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,Text,False,Text,,,,
2135b784-bf88-48f2-bafa-547464d1c4c0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Levitsky, Michael G. “Chapter 4: Blood Flow to the Lung.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
2fbc36b2-be0c-48b5-a9dc-5e18d6effe3b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"West, John B. “Chapter 4: Blood Flow and Metabolism—How the Pulmonary Circulation Removes Gas from the Lung and Alters Some Metabolites.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
30d21822-2ba9-4f21-951a-a00ff66df38d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Zones of Perfusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-3,"Widdicombe, John G., and Andrew S. Davis. “Chapter 5.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
4f2bbba7-04a4-415c-8d9b-05234ea2f2da,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,Functional anatomy,False,Functional anatomy,,,,
cfeb043b-0e1c-48d3-8980-865488961111,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
cfeb043b-0e1c-48d3-8980-865488961111,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
cfeb043b-0e1c-48d3-8980-865488961111,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
cfeb043b-0e1c-48d3-8980-865488961111,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
cfeb043b-0e1c-48d3-8980-865488961111,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
df80edf5-d59b-4523-a1e3-6b5eeab70921,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,Main arteries follow a similar branching pattern to the bronchial tree until the terminal bronchioles are reached. This anatomical arrangement allows perfusion to follow the ventilation. Upon reaching the terminal bronchioles the vessels divide into a vast array of capillaries that wrap around the respiratory ducts and alveoli to form the respiratory zone of the lungs.,True,Functional anatomy,,,,
dcac3919-768c-42c4-97e2-c82d409c88d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
dcac3919-768c-42c4-97e2-c82d409c88d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
dcac3919-768c-42c4-97e2-c82d409c88d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
dcac3919-768c-42c4-97e2-c82d409c88d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
dcac3919-768c-42c4-97e2-c82d409c88d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
6b26d232-9d2f-45ba-8def-08783a75c887,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"The capillary beds converge into small veins after traveling over the alveolar surfaces, and these small veins then collect into four pulmonary veins that lead back to the left heart. This is an unusual example of veins carrying blood with arterial gas pressures.",True,Functional anatomy,,,,
c2879cae-b712-47d4-ba8b-0791d54d7cb8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Despite receiving the same blood volume per minute as the systemic circulation the pulmonary circulation is a low-pressure system. Systolic pressure is normally only 25 mmHg, compared to 120 in the systemic circulation, diastolic is 8, compared to 80 and mean pulmonary artery pressure is only 15. These numbers are well worth remembering.",True,Functional anatomy,,,,
9a571921-b9d1-438a-914b-b02ee69a8e6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
9a571921-b9d1-438a-914b-b02ee69a8e6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
9a571921-b9d1-438a-914b-b02ee69a8e6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
9a571921-b9d1-438a-914b-b02ee69a8e6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
9a571921-b9d1-438a-914b-b02ee69a8e6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
c38e201b-a406-4700-a78a-76cb0df080a2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"The pulmonary arteries show different characteristic to their systemic counterparts as well. The walls of a pulmonary arterioles are thin compared to systemic arterioles. They also lack the smooth muscle layer seen in the systemic arteriole. In fact pulmonary arterioles look much more like systemic veins and they are often mistaken for such in biopsy or dissection. With little smooth muscle it’s clear that these vessels have little role in controlling the distribution of blood flow – a vital role of their systemic counterparts. As the pulmonary circulation receives all cardiac output, all the time, such precise control isn’t required.",True,Functional anatomy,,,,
2aaf15cb-4101-4063-bafa-ef9dc5494ffa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,The thin walls and lack of smooth muscle also make the pulmonary arterioles highly compliant and so they behave much more like veins in their pressure response – extending when pressure increases. This gives the pulmonary arteriole system a rather unique pressure-resistance relationship that we’ll look at in a moment.,True,Functional anatomy,,,,
0d49aecd-0938-4abb-850e-1e72f52c14cf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,This low pressure and compliant system also means that the right heart has much less work to perform to generate its output. In fact the right ventricle has about a tenth of the work of the left heart to move exactly the same blood volume. Hence the structure and work capacity of the right heart is so much smaller than the left – something worth bearing in mind if disease causes changes in the pulmonary vasculature that in turn causes the less substantial right heart to work harder and undergo hypertrophy,True,Functional anatomy,,,,
b1f36a72-a435-46b3-8dab-cb9abb669819,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",False,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
0c4a1612-8088-4719-8576-4d00237dd27a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
0c4a1612-8088-4719-8576-4d00237dd27a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
0c4a1612-8088-4719-8576-4d00237dd27a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
0c4a1612-8088-4719-8576-4d00237dd27a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
0c4a1612-8088-4719-8576-4d00237dd27a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
7fdb15b5-5e1a-4956-843a-db4d7657085a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Unlike systemic arterioles there is little autoregulation by the pulmonary arterioles, so the pulmonary arterioles do not actively vasoconstrict when stretched by high pressure. Instead, they passively distend, thereby reducing their resistance with increasing resistance.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
4ab10ea0-ca8d-4f8b-8e37-c2cb256eee2d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"A rise in pulmonary pressure not only distends vessels but initiates flow through otherwise unused, or dormant, vessels, particularly those closer to the apex of the lung (we will see why later on). With more vessels recruited, the total cross-sectional area of used vessels increases and total resistance falls.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
df88d8e5-f289-4ec9-b797-7abb814fe035,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,But there are other and more complex peculiarities of the pulmonary circulation that determine its resistance…,True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
cb65b8bb-8104-4718-a8e4-a8febac4e29d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,Pulmonary Vascular Resistance and Radial Traction,False,Pulmonary Vascular Resistance and Radial Traction,,,,
7f16d145-f654-46e5-a468-7e12e5cbd12f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,Another unique characteristic of the pulmonary circulation is that it is exposed to the changing pressures in the airways and alveoli. It is also involved in the fiber network that generates radial traction. Consequently pulmonary vessels can be expanded or compressed in a way no other circulation is.,True,Pulmonary Vascular Resistance and Radial Traction,,,,
867a7b36-d271-4b38-ac2d-fb137cd1733e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
867a7b36-d271-4b38-ac2d-fb137cd1733e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
867a7b36-d271-4b38-ac2d-fb137cd1733e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
867a7b36-d271-4b38-ac2d-fb137cd1733e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
867a7b36-d271-4b38-ac2d-fb137cd1733e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
22e642f4-40a5-4302-a50b-64a9a2569aab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Alveolar vessels: These are primarily the capillaries and small vessels in close contact with the alveoli. Consequently they are exposed to the alveolar pressures. First, the surface tension within the alveolus that is tending to pull the alveolus closed also pulls on the vessels between alveoli, tending to pull it open as neighboring alveoli pull inward on themselves, and play tug-of-war with the vessel walls in between, extending them and causing a decrease in vascular resistance.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
e90d0353-ad88-4087-b583-d97a91a82ad3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Alternatively, when alveolar pressure increases (e.g., at high lung volumes), the raised alveolar pressure can compress the vessels running over its surface, causing an increase in vascular resistance.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
4f0108f5-f640-47b6-a02a-11ced923d3b2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Extra-alveolar vessels: By definition these vessels are not in contact with the alveoli, so they are not exposed to the same alveolar forces. These are exposed to the intrapleural forces, however, so as we saw airways opening during inspiration when intra-pleural pressure falls, these extra-alveolar vessels are also pulled open during inspiration by radial traction, and their resistance consequently falls as lung volume increases.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
d38eacdd-f8eb-4984-b300-71b9bba2a8fd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"The summation of these forces (alveolar pressure, surface tension, and radial traction) means that pulmonary vasculature resistance has a complex relationship with lung volume.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
5bb9ac1c-574a-4772-9b4f-30f0a0babf28,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,Pulmonary Vascular Resistance and Lung Volume,False,Pulmonary Vascular Resistance and Lung Volume,,,,
d3be7061-e7eb-4bd4-b8f2-319175184368,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
d3be7061-e7eb-4bd4-b8f2-319175184368,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
d3be7061-e7eb-4bd4-b8f2-319175184368,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
d3be7061-e7eb-4bd4-b8f2-319175184368,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
d3be7061-e7eb-4bd4-b8f2-319175184368,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
ab40a381-1834-44d5-b9e2-b382ead4ba13,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
ab40a381-1834-44d5-b9e2-b382ead4ba13,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
ab40a381-1834-44d5-b9e2-b382ead4ba13,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
ab40a381-1834-44d5-b9e2-b382ead4ba13,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
ab40a381-1834-44d5-b9e2-b382ead4ba13,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
8a53047f-5074-484e-bb19-44373ceb7892,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
8a53047f-5074-484e-bb19-44373ceb7892,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
8a53047f-5074-484e-bb19-44373ceb7892,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
8a53047f-5074-484e-bb19-44373ceb7892,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
8a53047f-5074-484e-bb19-44373ceb7892,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
9253b39c-337f-4d38-8e55-5b2be90c18cb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,So vascular resistance and lung volume are related with an inverted bell-shaped relationship. Now let us look at the forces that determine the distribution of blood flow across the lung structure.,True,Pulmonary Vascular Resistance and Lung Volume,,,,
a8603716-5918-447b-b006-4cc2faad377b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,Pulmonary Blood Flow and Gravity,False,Pulmonary Blood Flow and Gravity,,,,
6c831ff2-3e5c-4139-856a-c82735a0d396,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"You may recall that gravity affected the distribution of ventilation by generating the gradient of intrapleural pressures down the lung—most negative at the apex, less negative at the base.",True,Pulmonary Blood Flow and Gravity,,,,
d434b1b1-db8c-4ecf-83c9-8b0b3c365f0b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
d434b1b1-db8c-4ecf-83c9-8b0b3c365f0b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
d434b1b1-db8c-4ecf-83c9-8b0b3c365f0b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
d434b1b1-db8c-4ecf-83c9-8b0b3c365f0b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
d434b1b1-db8c-4ecf-83c9-8b0b3c365f0b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
6b86efca-7e4b-4ee3-9cbe-7548b73c0e92,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,Zones of Perfusion,False,Zones of Perfusion,,,,
8b67e6a2-235d-44a1-af9d-c1d66ec1ad73,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"We now have to consider the relationship of the pressures in these three systems, arterial, alveolar and venous, at different heights of the lung. Many of the following principles have already been dealt with, but we can put them together to look at how they affect perfusion distribution.",True,Zones of Perfusion,,,,
2b8dd577-4059-4280-9a2f-ded6401efb87,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Zone 1: At the top of the lung the arterial pressure is relatively low because this is the furthest vertical distance from the heart. In the same zone, as you know, the alveoli here are extended by the low (more negative) intrapleural pressure at the apex. These extended alveoli tend to compress the surrounding capillaries, and the lack of arterial pressure to push past the extended alveolus means blood flow through capillary beds in zone 1 may be relatively low. It is certainly a pronounced effect in patients undergoing positive pressure ventilation where alveolar pressure may exceed arterial pressure and stop blood flow at the apex altogether. This phenomenon of ventilated but underperfused alveoli is referred to as alveolar dead space, as without adequate perfusion, gas exchange is compromised.",True,Zones of Perfusion,,,,
482f5d9a-73cc-4911-9f1a-f02a9815efbc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Zone 2: In zone 2 we are lower down the lung, and at this point arterial pressure is higher (closer proximity to the heart) and the alveoli are less extended, but venous pressure remains less than alveolar pressure. So flow in zone 2 is determined by the difference between arterial and alveolar pressures.",True,Zones of Perfusion,,,,
8ec0742f-5a28-47bb-a25f-7df1f516abe1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Zone 3: Dropping further down the lung to the base, the arterial and venous pressure have both risen as the column of fluid (blood) above them is greater at this point, and now both are above the now smaller alveolar pressure (near the base the intrapleural pressure is less negative). Consequently the flow through the capillary bed in zone 3 is determined by the arterial–venous pressure difference, just as it is in the systemic circulation.",True,Zones of Perfusion,,,,
8ee7fac3-1c78-43c4-941b-0a82bb91f2e9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"(There can at times be a fourth zone, which appears only at low lung volumes. At low lung volumes tissue at the base of the lung can be compressed, and this compression can collapse the extra-alveolar vessels.)",True,Zones of Perfusion,,,,
6aa8c54d-c479-42d7-8389-e77d763cff58,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,Summary,False,Summary,,,,
e35e9ad7-aa00-4585-bd62-cfb879fadf69,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"So when considering flow through a systemic capillary bed we only have to think about the arterial and venous pressures, the pulmonary circulation throws us a curve ball by adding alveolar pressures into the mix that produce these perfusion zones.",True,Summary,,,,
da6eb6c1-c277-4478-9398-e5380683116f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,Pulmonary Vasculature’s Response to Hypoxia,False,Pulmonary Vasculature’s Response to Hypoxia,,,,
7a364f18-bdff-465c-addd-5d06dea029d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,If systemic tissue becomes hypoxic then local arterioles open to allow more blood flow and increase oxygen delivery. The opposite is true for the pulmonary circulation where the response to local hypoxia is vasoconstriction.,True,Pulmonary Vasculature’s Response to Hypoxia,,,,
2e990812-7ab2-40c3-b61b-85fef12ac2fb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"First, remember that the bronchial circulation provides oxygen and nutrients to the pulmonary itself, and this behaves as all other systemic circulations. But the pulmonary circulation is for gas exchange. So if an area of the lung has become hypoxic (i.e., has a low oxygen partial pressure), this is indicative of that area having insufficient ventilation.",True,Pulmonary Vasculature’s Response to Hypoxia,,,,
3c202ac4-a96f-4714-b3f6-a1f1a41e79c2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"If there is little ventilation going to that area then there is little point sending perfusion to it. So the little smooth muscle there is in the pulmonary vasculature contracts to constrict the vessel when hypoxia is present. The blood follows the path of least resistance and thereby goes to vessels that are open (i.e., to areas where ventilation is maintaining a higher PO2).",True,Pulmonary Vasculature’s Response to Hypoxia,,,,
8583b7a5-a5e5-48d9-ab94-9a20ea070aae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Because of its unique role in gas exchange, rather than supplying local tissue, and the pressures that are present in the lung beyond vasculature pressure, plus the different vasculature structure, the pulmonary circulation has some unusual characteristics. These produce unique blood flow patterns in response to lung volume, gravity, and the need to match ventilated areas with adequate perfusion.",True,Pulmonary Vasculature’s Response to Hypoxia,,,,
3b652c37-b264-4c99-b261-44d43021bf1b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,Text,False,Text,,,,
810e1ea3-462e-41ac-b774-7a2dc7f535e6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Levitsky, Michael G. “Chapter 4: Blood Flow to the Lung.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
d41a7c91-55d2-48dd-8ece-8b742cb02e56,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"West, John B. “Chapter 4: Blood Flow and Metabolism—How the Pulmonary Circulation Removes Gas from the Lung and Alters Some Metabolites.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
6539e614-d2ab-435e-bea8-b57f3d808678,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-2,"Widdicombe, John G., and Andrew S. Davis. “Chapter 5.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
46f5cfad-9f57-4cb4-82af-3ec36f11145d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,Functional anatomy,False,Functional anatomy,,,,
6490f7f0-e626-4cfa-ab25-a84da1674032,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
6490f7f0-e626-4cfa-ab25-a84da1674032,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
6490f7f0-e626-4cfa-ab25-a84da1674032,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
6490f7f0-e626-4cfa-ab25-a84da1674032,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
6490f7f0-e626-4cfa-ab25-a84da1674032,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
09e2a701-5ecc-4f7a-abe3-63737caff198,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,Main arteries follow a similar branching pattern to the bronchial tree until the terminal bronchioles are reached. This anatomical arrangement allows perfusion to follow the ventilation. Upon reaching the terminal bronchioles the vessels divide into a vast array of capillaries that wrap around the respiratory ducts and alveoli to form the respiratory zone of the lungs.,True,Functional anatomy,,,,
1bf4a12f-0bff-4a3c-95d6-40c5d2911084,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
1bf4a12f-0bff-4a3c-95d6-40c5d2911084,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
1bf4a12f-0bff-4a3c-95d6-40c5d2911084,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
1bf4a12f-0bff-4a3c-95d6-40c5d2911084,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
1bf4a12f-0bff-4a3c-95d6-40c5d2911084,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
b0349a09-f859-44be-a603-1c2011d83034,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"The capillary beds converge into small veins after traveling over the alveolar surfaces, and these small veins then collect into four pulmonary veins that lead back to the left heart. This is an unusual example of veins carrying blood with arterial gas pressures.",True,Functional anatomy,,,,
cb098d85-063a-4463-af83-eb9d646f178e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Despite receiving the same blood volume per minute as the systemic circulation the pulmonary circulation is a low-pressure system. Systolic pressure is normally only 25 mmHg, compared to 120 in the systemic circulation, diastolic is 8, compared to 80 and mean pulmonary artery pressure is only 15. These numbers are well worth remembering.",True,Functional anatomy,,,,
490fa516-b0bf-4f65-b7ec-a83eaff9b643,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
490fa516-b0bf-4f65-b7ec-a83eaff9b643,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
490fa516-b0bf-4f65-b7ec-a83eaff9b643,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
490fa516-b0bf-4f65-b7ec-a83eaff9b643,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
490fa516-b0bf-4f65-b7ec-a83eaff9b643,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
9fc1b816-a44f-4e1c-96e7-f53493b6fc7a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"The pulmonary arteries show different characteristic to their systemic counterparts as well. The walls of a pulmonary arterioles are thin compared to systemic arterioles. They also lack the smooth muscle layer seen in the systemic arteriole. In fact pulmonary arterioles look much more like systemic veins and they are often mistaken for such in biopsy or dissection. With little smooth muscle it’s clear that these vessels have little role in controlling the distribution of blood flow – a vital role of their systemic counterparts. As the pulmonary circulation receives all cardiac output, all the time, such precise control isn’t required.",True,Functional anatomy,,,,
ccb9001e-30d4-48dc-b7e0-06cc22d0e8bf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,The thin walls and lack of smooth muscle also make the pulmonary arterioles highly compliant and so they behave much more like veins in their pressure response – extending when pressure increases. This gives the pulmonary arteriole system a rather unique pressure-resistance relationship that we’ll look at in a moment.,True,Functional anatomy,,,,
b73cd0c2-5a96-431e-8b86-8a3d075e4756,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,This low pressure and compliant system also means that the right heart has much less work to perform to generate its output. In fact the right ventricle has about a tenth of the work of the left heart to move exactly the same blood volume. Hence the structure and work capacity of the right heart is so much smaller than the left – something worth bearing in mind if disease causes changes in the pulmonary vasculature that in turn causes the less substantial right heart to work harder and undergo hypertrophy,True,Functional anatomy,,,,
04050a95-d022-45a5-b592-831c84bf358d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",False,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
437f784b-1ed5-433c-a796-cc711cc9f2e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
437f784b-1ed5-433c-a796-cc711cc9f2e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
437f784b-1ed5-433c-a796-cc711cc9f2e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
437f784b-1ed5-433c-a796-cc711cc9f2e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
437f784b-1ed5-433c-a796-cc711cc9f2e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
1ab95a94-8639-4c90-87dc-9b0e2e823f03,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Unlike systemic arterioles there is little autoregulation by the pulmonary arterioles, so the pulmonary arterioles do not actively vasoconstrict when stretched by high pressure. Instead, they passively distend, thereby reducing their resistance with increasing resistance.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
639ee591-3bac-4286-b4c1-6d20451f3d71,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"A rise in pulmonary pressure not only distends vessels but initiates flow through otherwise unused, or dormant, vessels, particularly those closer to the apex of the lung (we will see why later on). With more vessels recruited, the total cross-sectional area of used vessels increases and total resistance falls.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
db069324-b538-4b54-a195-84b3066ff918,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,But there are other and more complex peculiarities of the pulmonary circulation that determine its resistance…,True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
ba438620-bd1c-4faa-ade2-0a0dca6f3269,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,Pulmonary Vascular Resistance and Radial Traction,False,Pulmonary Vascular Resistance and Radial Traction,,,,
6a7e73b9-88d9-4c0a-b853-b48e87319f3a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,Another unique characteristic of the pulmonary circulation is that it is exposed to the changing pressures in the airways and alveoli. It is also involved in the fiber network that generates radial traction. Consequently pulmonary vessels can be expanded or compressed in a way no other circulation is.,True,Pulmonary Vascular Resistance and Radial Traction,,,,
efac78f8-7489-4c6d-be4f-f277ce9098de,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
efac78f8-7489-4c6d-be4f-f277ce9098de,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
efac78f8-7489-4c6d-be4f-f277ce9098de,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
efac78f8-7489-4c6d-be4f-f277ce9098de,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
efac78f8-7489-4c6d-be4f-f277ce9098de,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
2b122a8b-f85e-4732-ab41-ad148e2cc664,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Alveolar vessels: These are primarily the capillaries and small vessels in close contact with the alveoli. Consequently they are exposed to the alveolar pressures. First, the surface tension within the alveolus that is tending to pull the alveolus closed also pulls on the vessels between alveoli, tending to pull it open as neighboring alveoli pull inward on themselves, and play tug-of-war with the vessel walls in between, extending them and causing a decrease in vascular resistance.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
dd641154-434e-4fdd-8796-587dcd2d07a4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Alternatively, when alveolar pressure increases (e.g., at high lung volumes), the raised alveolar pressure can compress the vessels running over its surface, causing an increase in vascular resistance.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
c17a6d2d-4750-4b1b-a277-186f7e3d83e6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Extra-alveolar vessels: By definition these vessels are not in contact with the alveoli, so they are not exposed to the same alveolar forces. These are exposed to the intrapleural forces, however, so as we saw airways opening during inspiration when intra-pleural pressure falls, these extra-alveolar vessels are also pulled open during inspiration by radial traction, and their resistance consequently falls as lung volume increases.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
31d54a7e-c7df-4b9e-ace5-5558edbb2ff1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"The summation of these forces (alveolar pressure, surface tension, and radial traction) means that pulmonary vasculature resistance has a complex relationship with lung volume.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
ad7005de-dd39-4dbc-ba1d-56b586b89fd5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,Pulmonary Vascular Resistance and Lung Volume,False,Pulmonary Vascular Resistance and Lung Volume,,,,
12a31713-c646-4ea5-beec-8ee23bef6239,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
12a31713-c646-4ea5-beec-8ee23bef6239,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
12a31713-c646-4ea5-beec-8ee23bef6239,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
12a31713-c646-4ea5-beec-8ee23bef6239,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
12a31713-c646-4ea5-beec-8ee23bef6239,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
a881a6d9-5c77-4b2e-bb90-8f2f937506bd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
a881a6d9-5c77-4b2e-bb90-8f2f937506bd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
a881a6d9-5c77-4b2e-bb90-8f2f937506bd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
a881a6d9-5c77-4b2e-bb90-8f2f937506bd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
a881a6d9-5c77-4b2e-bb90-8f2f937506bd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
272a4fdf-30ae-4f9c-88f9-138c200daf2c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
272a4fdf-30ae-4f9c-88f9-138c200daf2c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
272a4fdf-30ae-4f9c-88f9-138c200daf2c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
272a4fdf-30ae-4f9c-88f9-138c200daf2c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
272a4fdf-30ae-4f9c-88f9-138c200daf2c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
a06fca6f-178d-476e-b0c5-8827de50ee44,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,So vascular resistance and lung volume are related with an inverted bell-shaped relationship. Now let us look at the forces that determine the distribution of blood flow across the lung structure.,True,Pulmonary Vascular Resistance and Lung Volume,,,,
d273ff92-de2d-452e-b8cf-4560454ecb15,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,Pulmonary Blood Flow and Gravity,False,Pulmonary Blood Flow and Gravity,,,,
3c1d598a-4529-436c-afd2-3320a6ac3735,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"You may recall that gravity affected the distribution of ventilation by generating the gradient of intrapleural pressures down the lung—most negative at the apex, less negative at the base.",True,Pulmonary Blood Flow and Gravity,,,,
978f03ad-ae11-4544-b08c-55534ea9273f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
978f03ad-ae11-4544-b08c-55534ea9273f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
978f03ad-ae11-4544-b08c-55534ea9273f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
978f03ad-ae11-4544-b08c-55534ea9273f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
978f03ad-ae11-4544-b08c-55534ea9273f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
514490e8-ade2-4ca5-b0a4-2b9cfcd5fcb4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,Zones of Perfusion,False,Zones of Perfusion,,,,
bf97a953-644a-4c8a-aa26-670d18437959,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"We now have to consider the relationship of the pressures in these three systems, arterial, alveolar and venous, at different heights of the lung. Many of the following principles have already been dealt with, but we can put them together to look at how they affect perfusion distribution.",True,Zones of Perfusion,,,,
8c4127b0-f98f-4478-b275-e97f8bb0f33e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Zone 1: At the top of the lung the arterial pressure is relatively low because this is the furthest vertical distance from the heart. In the same zone, as you know, the alveoli here are extended by the low (more negative) intrapleural pressure at the apex. These extended alveoli tend to compress the surrounding capillaries, and the lack of arterial pressure to push past the extended alveolus means blood flow through capillary beds in zone 1 may be relatively low. It is certainly a pronounced effect in patients undergoing positive pressure ventilation where alveolar pressure may exceed arterial pressure and stop blood flow at the apex altogether. This phenomenon of ventilated but underperfused alveoli is referred to as alveolar dead space, as without adequate perfusion, gas exchange is compromised.",True,Zones of Perfusion,,,,
fdbde047-f888-4149-8b4a-17e3fb8d02a4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Zone 2: In zone 2 we are lower down the lung, and at this point arterial pressure is higher (closer proximity to the heart) and the alveoli are less extended, but venous pressure remains less than alveolar pressure. So flow in zone 2 is determined by the difference between arterial and alveolar pressures.",True,Zones of Perfusion,,,,
cf53d525-8c4a-418a-9dc4-a99daaf02513,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Zone 3: Dropping further down the lung to the base, the arterial and venous pressure have both risen as the column of fluid (blood) above them is greater at this point, and now both are above the now smaller alveolar pressure (near the base the intrapleural pressure is less negative). Consequently the flow through the capillary bed in zone 3 is determined by the arterial–venous pressure difference, just as it is in the systemic circulation.",True,Zones of Perfusion,,,,
775a533f-242d-4a8f-a1d7-76944987e95e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"(There can at times be a fourth zone, which appears only at low lung volumes. At low lung volumes tissue at the base of the lung can be compressed, and this compression can collapse the extra-alveolar vessels.)",True,Zones of Perfusion,,,,
259b4626-6b45-4cd9-b34d-6b6b0d06f613,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,Summary,False,Summary,,,,
9047817b-8a45-44c5-9c04-056d0d1f4c32,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"So when considering flow through a systemic capillary bed we only have to think about the arterial and venous pressures, the pulmonary circulation throws us a curve ball by adding alveolar pressures into the mix that produce these perfusion zones.",True,Summary,,,,
131178a2-e540-4775-be1e-9fea6c1ee6c5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,Pulmonary Vasculature’s Response to Hypoxia,False,Pulmonary Vasculature’s Response to Hypoxia,,,,
4e68d2c7-b091-4c2a-87c2-f7c8930e299d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,If systemic tissue becomes hypoxic then local arterioles open to allow more blood flow and increase oxygen delivery. The opposite is true for the pulmonary circulation where the response to local hypoxia is vasoconstriction.,True,Pulmonary Vasculature’s Response to Hypoxia,,,,
4b57a5b2-9d1d-4ec9-8845-0b0450a47518,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"First, remember that the bronchial circulation provides oxygen and nutrients to the pulmonary itself, and this behaves as all other systemic circulations. But the pulmonary circulation is for gas exchange. So if an area of the lung has become hypoxic (i.e., has a low oxygen partial pressure), this is indicative of that area having insufficient ventilation.",True,Pulmonary Vasculature’s Response to Hypoxia,,,,
3cfb0f69-8e7b-4c20-9e81-30b57523c987,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"If there is little ventilation going to that area then there is little point sending perfusion to it. So the little smooth muscle there is in the pulmonary vasculature contracts to constrict the vessel when hypoxia is present. The blood follows the path of least resistance and thereby goes to vessels that are open (i.e., to areas where ventilation is maintaining a higher PO2).",True,Pulmonary Vasculature’s Response to Hypoxia,,,,
250fd3ab-e017-4171-a4ea-32f12f1ee482,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Because of its unique role in gas exchange, rather than supplying local tissue, and the pressures that are present in the lung beyond vasculature pressure, plus the different vasculature structure, the pulmonary circulation has some unusual characteristics. These produce unique blood flow patterns in response to lung volume, gravity, and the need to match ventilated areas with adequate perfusion.",True,Pulmonary Vasculature’s Response to Hypoxia,,,,
75085d24-7937-4792-a632-802305ae9bd8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,Text,False,Text,,,,
5737e047-1358-4926-a6bd-0a8499aecda4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Levitsky, Michael G. “Chapter 4: Blood Flow to the Lung.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
3108025d-c1fc-48c3-bf2b-2ffe251d03e9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"West, John B. “Chapter 4: Blood Flow and Metabolism—How the Pulmonary Circulation Removes Gas from the Lung and Alters Some Metabolites.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
5ab5b98e-efa9-4a04-a689-dd0e6b9d2646,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/#chapter-43-section-1,"Widdicombe, John G., and Andrew S. Davis. “Chapter 5.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
708c8f25-f7c2-4ccc-aa10-b62447fbae79,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,Functional anatomy,False,Functional anatomy,,,,
4ba67aa0-1182-40cd-8326-e501e38c90b4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
4ba67aa0-1182-40cd-8326-e501e38c90b4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
4ba67aa0-1182-40cd-8326-e501e38c90b4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
4ba67aa0-1182-40cd-8326-e501e38c90b4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
4ba67aa0-1182-40cd-8326-e501e38c90b4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"The pulmonary circulation takes all cardiac output from the right heart via the pulmonary arteries. Thus, even at rest it has a tremendous blood flow – about 5 liters per minute, just the same as the systemic circulation. This volume enters a vast array of vessels that penetrate all the lung structure – so much so that the complete lung structure is visible from the cast of the pulmonary vasculature in figure 9.1.",True,Functional anatomy,Figure 9.1,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.1.jpg,Figure 9.1: The pulmonary circulation. A latex cast of the pulmonary circulation shows the complete and vast penetration of the lung structure by the vasculature.
61f88b15-de04-4a67-93a3-21b13f00bb26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,Main arteries follow a similar branching pattern to the bronchial tree until the terminal bronchioles are reached. This anatomical arrangement allows perfusion to follow the ventilation. Upon reaching the terminal bronchioles the vessels divide into a vast array of capillaries that wrap around the respiratory ducts and alveoli to form the respiratory zone of the lungs.,True,Functional anatomy,,,,
f403a6a5-3fb9-4b3d-bd2f-bf65ecd171ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
f403a6a5-3fb9-4b3d-bd2f-bf65ecd171ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
f403a6a5-3fb9-4b3d-bd2f-bf65ecd171ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
f403a6a5-3fb9-4b3d-bd2f-bf65ecd171ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
f403a6a5-3fb9-4b3d-bd2f-bf65ecd171ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,The density of the capillary beds is so great that individual capillaries can loose their distinct anatomy as can be seen in this electron micrograph where the capillaries are seen to form more sheet-like structures around where the alveoli would be. A common analogy for this is the capillaries look more like a floor of a parking garage with pillars for support but mainly open space – rather (figure 9.3) than the distinct tubes seen in other circulations.,True,Functional anatomy,Figure 9.3,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.3.png,Figure 9.3: Schematic of the pulmonary and systemic circulations – compare capillary densities and pressures.
9b37108e-35ea-4e05-9077-502b2c4d78b2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"The capillary beds converge into small veins after traveling over the alveolar surfaces, and these small veins then collect into four pulmonary veins that lead back to the left heart. This is an unusual example of veins carrying blood with arterial gas pressures.",True,Functional anatomy,,,,
af6923a5-fb81-4de5-a388-78512b5546b8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Despite receiving the same blood volume per minute as the systemic circulation the pulmonary circulation is a low-pressure system. Systolic pressure is normally only 25 mmHg, compared to 120 in the systemic circulation, diastolic is 8, compared to 80 and mean pulmonary artery pressure is only 15. These numbers are well worth remembering.",True,Functional anatomy,,,,
1ddcdbb8-a478-42c6-b54d-5ff6b608e0b7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
1ddcdbb8-a478-42c6-b54d-5ff6b608e0b7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
1ddcdbb8-a478-42c6-b54d-5ff6b608e0b7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
1ddcdbb8-a478-42c6-b54d-5ff6b608e0b7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
1ddcdbb8-a478-42c6-b54d-5ff6b608e0b7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"So how can this one circulation receive so much volume (the complete cardiac output) and yet remain at such low pressure? The first reason is the vast size of the capillary beds. As figure 9.4 suggests, the much higher density of pulmonary capillary beds than that seen in the systemic circulation allows pressure to dissipate much more quickly.",True,Functional anatomy,Figure 9.4,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
ea3c77f1-57b2-4bd4-b4e4-c7541d900a53,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"The pulmonary arteries show different characteristic to their systemic counterparts as well. The walls of a pulmonary arterioles are thin compared to systemic arterioles. They also lack the smooth muscle layer seen in the systemic arteriole. In fact pulmonary arterioles look much more like systemic veins and they are often mistaken for such in biopsy or dissection. With little smooth muscle it’s clear that these vessels have little role in controlling the distribution of blood flow – a vital role of their systemic counterparts. As the pulmonary circulation receives all cardiac output, all the time, such precise control isn’t required.",True,Functional anatomy,,,,
b23ffba1-2b8d-4874-a835-a3b16708c779,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,The thin walls and lack of smooth muscle also make the pulmonary arterioles highly compliant and so they behave much more like veins in their pressure response – extending when pressure increases. This gives the pulmonary arteriole system a rather unique pressure-resistance relationship that we’ll look at in a moment.,True,Functional anatomy,,,,
a58ee7fb-cbd9-4529-a88b-5e26221437ff,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,This low pressure and compliant system also means that the right heart has much less work to perform to generate its output. In fact the right ventricle has about a tenth of the work of the left heart to move exactly the same blood volume. Hence the structure and work capacity of the right heart is so much smaller than the left – something worth bearing in mind if disease causes changes in the pulmonary vasculature that in turn causes the less substantial right heart to work harder and undergo hypertrophy,True,Functional anatomy,,,,
02cab9be-3cf9-4b33-944f-402eff9530bf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",False,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
4f143e84-0c1a-4b99-9a83-4eb77649da64,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
4f143e84-0c1a-4b99-9a83-4eb77649da64,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
4f143e84-0c1a-4b99-9a83-4eb77649da64,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
4f143e84-0c1a-4b99-9a83-4eb77649da64,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
4f143e84-0c1a-4b99-9a83-4eb77649da64,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"As we have just seen, with little smooth muscle and a compliant wall, the arterioles act more like veins. As pulmonary arterial pressure rises, the resistance of the pulmonary circulation falls, as seen in figure 9.4, and this occurs for several reasons.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",Figure 9.4,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.4.png,Figure 9.4: Pulmonary vascular resistance decreases as pressure increases.
49f1c346-e2aa-4689-b99d-a9ba4fe01c03,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Unlike systemic arterioles there is little autoregulation by the pulmonary arterioles, so the pulmonary arterioles do not actively vasoconstrict when stretched by high pressure. Instead, they passively distend, thereby reducing their resistance with increasing resistance.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
bd025b1b-b633-4fb0-aa8c-5fc3701abd7b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"A rise in pulmonary pressure not only distends vessels but initiates flow through otherwise unused, or dormant, vessels, particularly those closer to the apex of the lung (we will see why later on). With more vessels recruited, the total cross-sectional area of used vessels increases and total resistance falls.",True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
f27b92fe-8515-455a-be5e-cc75f9c437b8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,But there are other and more complex peculiarities of the pulmonary circulation that determine its resistance…,True,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",,,,
b0b75470-f09d-4565-8027-08fa4ce9e142,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,Pulmonary Vascular Resistance and Radial Traction,False,Pulmonary Vascular Resistance and Radial Traction,,,,
25b60750-c9ec-41c6-9041-5dba14a4de6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,Another unique characteristic of the pulmonary circulation is that it is exposed to the changing pressures in the airways and alveoli. It is also involved in the fiber network that generates radial traction. Consequently pulmonary vessels can be expanded or compressed in a way no other circulation is.,True,Pulmonary Vascular Resistance and Radial Traction,,,,
e288548c-fe58-4645-9c42-b6b7c622417e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
e288548c-fe58-4645-9c42-b6b7c622417e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
e288548c-fe58-4645-9c42-b6b7c622417e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
e288548c-fe58-4645-9c42-b6b7c622417e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
e288548c-fe58-4645-9c42-b6b7c622417e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"To explain these phenomena we have to divide the pulmonary circulation into two subdivisions, the alveolar vessels and the extra-alveolar vessels (figure 9.5). These two vessel types behave differently, so we will deal with them separately.",True,Pulmonary Vascular Resistance and Radial Traction,Figure 9.5,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.5-new.png,Figure 9.5: Pulmonary vessels can be categorized as alveolar or extra-alveolar.
f4e02fb4-e5a1-4dcf-8ddf-9e9495619460,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Alveolar vessels: These are primarily the capillaries and small vessels in close contact with the alveoli. Consequently they are exposed to the alveolar pressures. First, the surface tension within the alveolus that is tending to pull the alveolus closed also pulls on the vessels between alveoli, tending to pull it open as neighboring alveoli pull inward on themselves, and play tug-of-war with the vessel walls in between, extending them and causing a decrease in vascular resistance.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
cb6e2a4d-9139-43b1-871c-b35ed4da2f2c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Alternatively, when alveolar pressure increases (e.g., at high lung volumes), the raised alveolar pressure can compress the vessels running over its surface, causing an increase in vascular resistance.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
114b86bf-4248-4f41-b8a8-a82b491b9662,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Extra-alveolar vessels: By definition these vessels are not in contact with the alveoli, so they are not exposed to the same alveolar forces. These are exposed to the intrapleural forces, however, so as we saw airways opening during inspiration when intra-pleural pressure falls, these extra-alveolar vessels are also pulled open during inspiration by radial traction, and their resistance consequently falls as lung volume increases.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
cd8ad73a-7727-4a5e-87ce-4ae807e9a307,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"The summation of these forces (alveolar pressure, surface tension, and radial traction) means that pulmonary vasculature resistance has a complex relationship with lung volume.",True,Pulmonary Vascular Resistance and Radial Traction,,,,
7373763c-550c-49b7-ad91-aa32077ce65b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,Pulmonary Vascular Resistance and Lung Volume,False,Pulmonary Vascular Resistance and Lung Volume,,,,
c44f466c-a8d1-41e1-9ee8-073bf33e2008,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
c44f466c-a8d1-41e1-9ee8-073bf33e2008,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
c44f466c-a8d1-41e1-9ee8-073bf33e2008,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
c44f466c-a8d1-41e1-9ee8-073bf33e2008,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
c44f466c-a8d1-41e1-9ee8-073bf33e2008,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Vascular resistance at low lung volumes: At low lung volumes (figure 9.6, gray zone on the left), you should know that intra-pleural pressure is less negative because the lung recoil is less. With less negative pressure to hold open the extra-alveolar vessels via radial traction, these tend to narrow and vasculature resistance becomes relatively high.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
d3b56e32-3f71-4217-b2c8-3d9f4836df55,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
d3b56e32-3f71-4217-b2c8-3d9f4836df55,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
d3b56e32-3f71-4217-b2c8-3d9f4836df55,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
d3b56e32-3f71-4217-b2c8-3d9f4836df55,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
d3b56e32-3f71-4217-b2c8-3d9f4836df55,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Vascular resistance at medium lung volumes: As lung volume increases (figure 9.6, tan zone in the middle), the intrapleural pressure becomes more negative. Radial or parenchymal traction now begins to pull the extra-alveolar vessels open, and as they become wider, vascular resistance falls. Common sense would tell you that this effect would increase with continually larger lung volumes, and one might expect that vascular resistance would continue to decrease as lung volume increased. But this is evidently not the case.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
6e8a9010-4304-4fbe-b930-081756d2fe3a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
6e8a9010-4304-4fbe-b930-081756d2fe3a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
6e8a9010-4304-4fbe-b930-081756d2fe3a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
6e8a9010-4304-4fbe-b930-081756d2fe3a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
6e8a9010-4304-4fbe-b930-081756d2fe3a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Vascular resistance at high lung volumes: With further increases in lung volume (figure 9.6, pink zone on the right), vascular resistance rises. At high lung volumes the alveoli are enlarging, and this causes the capillaries running around them to stretch. As the capillaries stretch, they narrow—a little like how a piece of latex tubing narrows when it is stretched. This narrowing of a large number of capillaries overcomes the radial traction effect on the extra-alveolar vessels, and there is a net increase in vascular resistance.",True,Pulmonary Vascular Resistance and Lung Volume,Figure 9.6,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.6.png,Figure 9.6: The relationship between lung volume and pulmonary vascular resistance.
605dc09a-fbc6-4f9c-af1f-acc37a0caf5f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,So vascular resistance and lung volume are related with an inverted bell-shaped relationship. Now let us look at the forces that determine the distribution of blood flow across the lung structure.,True,Pulmonary Vascular Resistance and Lung Volume,,,,
a26d9532-f715-42cd-aae7-9a6a6792e016,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,Pulmonary Blood Flow and Gravity,False,Pulmonary Blood Flow and Gravity,,,,
27c9402e-5a2d-4701-9fdb-a819724ba5c8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"You may recall that gravity affected the distribution of ventilation by generating the gradient of intrapleural pressures down the lung—most negative at the apex, less negative at the base.",True,Pulmonary Blood Flow and Gravity,,,,
9e7e8140-e4a9-461e-b000-8bd583d879e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,Pulmonary Vasculature’s Response to Hypoxia,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
9e7e8140-e4a9-461e-b000-8bd583d879e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,Zones of Perfusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
9e7e8140-e4a9-461e-b000-8bd583d879e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,"Pulmonary Vascular Resistance, Lung Volume, and Gravity",https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
9e7e8140-e4a9-461e-b000-8bd583d879e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,The Pulmonary Vasculature,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
9e7e8140-e4a9-461e-b000-8bd583d879e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"We see a similar distribution of blood flow in the lung as well, as figure 9.7 shows with blood flow being greater at the base of the lung than it is at the apex. Again this is simply due to gravity. Gravity pushes against the blood rising from heart level, hence the base is better perfused than the apex. Because of this, gravity is responsible for matching the level of perfusion and ventilation up the lung; both are high at the bottom, and both are low at the apex. This is advantageous, as well ventilated areas need more perfusion for efficient gas exchange, and likewise there is little point in sending large amounts of pulmonary blood to poorly ventilated areas. The relationship between ventilation and perfusion (known as the V/Q ratio) that gravity establishes is not quite ideal, however, and we will see the ramifications of this less-than-perfect relationship later on. There are also other forces affecting the distribution of perfusion as well, and we can look at them now.",True,Pulmonary Blood Flow and Gravity,Figure 9.7,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/9.7.png,Figure 9.7: Perfusion distribution up the lung.
22ed0ded-c9f4-4052-af15-7c714b0ff94e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,Zones of Perfusion,False,Zones of Perfusion,,,,
0fb5af51-c26a-4a07-b20f-e50f8f402b8f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"We now have to consider the relationship of the pressures in these three systems, arterial, alveolar and venous, at different heights of the lung. Many of the following principles have already been dealt with, but we can put them together to look at how they affect perfusion distribution.",True,Zones of Perfusion,,,,
382cb0b1-8f02-4d01-acf7-1fd7092f1e8b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Zone 1: At the top of the lung the arterial pressure is relatively low because this is the furthest vertical distance from the heart. In the same zone, as you know, the alveoli here are extended by the low (more negative) intrapleural pressure at the apex. These extended alveoli tend to compress the surrounding capillaries, and the lack of arterial pressure to push past the extended alveolus means blood flow through capillary beds in zone 1 may be relatively low. It is certainly a pronounced effect in patients undergoing positive pressure ventilation where alveolar pressure may exceed arterial pressure and stop blood flow at the apex altogether. This phenomenon of ventilated but underperfused alveoli is referred to as alveolar dead space, as without adequate perfusion, gas exchange is compromised.",True,Zones of Perfusion,,,,
1c6b85d1-d178-47cf-99d9-07eb941b69c4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Zone 2: In zone 2 we are lower down the lung, and at this point arterial pressure is higher (closer proximity to the heart) and the alveoli are less extended, but venous pressure remains less than alveolar pressure. So flow in zone 2 is determined by the difference between arterial and alveolar pressures.",True,Zones of Perfusion,,,,
813e43cb-d3e2-4aef-9ccd-d54e913edf2b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Zone 3: Dropping further down the lung to the base, the arterial and venous pressure have both risen as the column of fluid (blood) above them is greater at this point, and now both are above the now smaller alveolar pressure (near the base the intrapleural pressure is less negative). Consequently the flow through the capillary bed in zone 3 is determined by the arterial–venous pressure difference, just as it is in the systemic circulation.",True,Zones of Perfusion,,,,
d787a7ec-0051-401c-bf69-8bfc479ff7c6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"(There can at times be a fourth zone, which appears only at low lung volumes. At low lung volumes tissue at the base of the lung can be compressed, and this compression can collapse the extra-alveolar vessels.)",True,Zones of Perfusion,,,,
65dc920e-c3e9-4517-86c6-035cfff24280,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,Summary,False,Summary,,,,
3b8ef7b8-c84e-480b-99eb-b06ba2ab7588,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"So when considering flow through a systemic capillary bed we only have to think about the arterial and venous pressures, the pulmonary circulation throws us a curve ball by adding alveolar pressures into the mix that produce these perfusion zones.",True,Summary,,,,
a92d8b24-2cae-4a8a-95f7-531944f488f2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,Pulmonary Vasculature’s Response to Hypoxia,False,Pulmonary Vasculature’s Response to Hypoxia,,,,
6e75f80b-2fc3-4e7c-b76d-495203f9ed12,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,If systemic tissue becomes hypoxic then local arterioles open to allow more blood flow and increase oxygen delivery. The opposite is true for the pulmonary circulation where the response to local hypoxia is vasoconstriction.,True,Pulmonary Vasculature’s Response to Hypoxia,,,,
28007c04-db33-48ab-a525-a4fea71f9cc1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"First, remember that the bronchial circulation provides oxygen and nutrients to the pulmonary itself, and this behaves as all other systemic circulations. But the pulmonary circulation is for gas exchange. So if an area of the lung has become hypoxic (i.e., has a low oxygen partial pressure), this is indicative of that area having insufficient ventilation.",True,Pulmonary Vasculature’s Response to Hypoxia,,,,
f0016605-a84f-4965-bc33-6b44e7636ef5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"If there is little ventilation going to that area then there is little point sending perfusion to it. So the little smooth muscle there is in the pulmonary vasculature contracts to constrict the vessel when hypoxia is present. The blood follows the path of least resistance and thereby goes to vessels that are open (i.e., to areas where ventilation is maintaining a higher PO2).",True,Pulmonary Vasculature’s Response to Hypoxia,,,,
93951372-244c-463e-abae-482f56b6d090,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Because of its unique role in gas exchange, rather than supplying local tissue, and the pressures that are present in the lung beyond vasculature pressure, plus the different vasculature structure, the pulmonary circulation has some unusual characteristics. These produce unique blood flow patterns in response to lung volume, gravity, and the need to match ventilated areas with adequate perfusion.",True,Pulmonary Vasculature’s Response to Hypoxia,,,,
900fdab7-4541-4d05-9d08-f880bda5e452,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,Text,False,Text,,,,
b7eeaeab-3665-4c33-9661-c4e6d748ba09,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Levitsky, Michael G. “Chapter 4: Blood Flow to the Lung.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
b64efc96-0b2f-4860-afb3-869a3be7fee1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"West, John B. “Chapter 4: Blood Flow and Metabolism—How the Pulmonary Circulation Removes Gas from the Lung and Alters Some Metabolites.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
63cb5ca3-f834-45b6-b8e7-571028100e8c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,9. Pulmonary Blood Flow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/pulmonary-blood-flow/,"Widdicombe, John G., and Andrew S. Davis. “Chapter 5.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
3248525b-afb8-434f-b240-a0dd6a050569,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,OR,False,OR,,,,
ea085c56-bcc8-4188-83d6-9514a3d788c6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"Identifying whether deranged blood gases are due to diffusion or perfusion limitations can help in the diagnosis of an underlying pathological issue, so we will look at them here.",True,OR,,,,
463fa892-1416-4654-be18-50ff142f7f54,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
463fa892-1416-4654-be18-50ff142f7f54,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
463fa892-1416-4654-be18-50ff142f7f54,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
463fa892-1416-4654-be18-50ff142f7f54,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
3c95b469-429c-4487-826d-731547875baa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
3c95b469-429c-4487-826d-731547875baa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
3c95b469-429c-4487-826d-731547875baa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
3c95b469-429c-4487-826d-731547875baa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
6c66fe37-5877-45a5-8184-401b37c5900c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,We can illustrate these diffusion and perfusion limitations with the behavior of two nonphysiological gases transferring from the alveolus to the bloodstream.,True,OR,,,,
2e41ac57-5da4-462e-a1ea-a28cb636db14,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,Carbon monoxide is well known for its affinity for hemoglobin. When CO passes across the membrane it rapidly binds to hemoglobin and is thus removed from solution. This removal from solution maintains the pressure gradient across the membrane. So with a maintained pressure gradient the major impediment to CO transfer is diffusion across the membrane. Therefore CO transfer is referred to as diffusion limited and dependent on the properties of the membrane. (Consequently CO is used in diffusion limitation testing (DLCO) in pulmonary function labs.),True,OR,,,,
79366767-25f0-4533-89cb-10bcd3076920,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"Nitrous oxide, alternatively, does not bind with hemoglobin at all, so its arterial partial pressure rises rapidly as it stays in solution. So maintaining the pressure gradient is dependent on how quickly the transferred nitrous oxide is washed away by blood flow. Because of this, nitrous oxide is referred to as perfusion limited.",True,OR,,,,
984378f8-8885-440a-93fe-2ed0658d9617,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"So while our two nonphysiological gases provide good examples of diffusion and perfusion limitations, let us see how oxygen behaves.",True,OR,,,,
5112588e-a1a8-4d11-ab6b-ec9e9a12b260,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
5112588e-a1a8-4d11-ab6b-ec9e9a12b260,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
5112588e-a1a8-4d11-ab6b-ec9e9a12b260,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
5112588e-a1a8-4d11-ab6b-ec9e9a12b260,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
fcb04a87-d9cf-452a-bfc9-9e25aede1a08,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
fcb04a87-d9cf-452a-bfc9-9e25aede1a08,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
fcb04a87-d9cf-452a-bfc9-9e25aede1a08,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
fcb04a87-d9cf-452a-bfc9-9e25aede1a08,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
07c87127-f693-453f-bb01-92a16e7f2c7d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
07c87127-f693-453f-bb01-92a16e7f2c7d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
07c87127-f693-453f-bb01-92a16e7f2c7d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
07c87127-f693-453f-bb01-92a16e7f2c7d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
7c077748-f7da-4e48-82c8-e8c12aa90d58,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"The transfer of O2 is also hampered by having to start off at venous partial pressures (40 mmHg), compared to our test gases that start off at zero. Consequently the initial pressure gradient is less. Despite this, the arterial partial pressure of oxygen equilibrates with alveolar pressures within 0.25 seconds (i.e., a third of the distance around the capillary). With the blood still having another 0.5 seconds in the capillary, this provides a large reserve time.",True,OR,,,,
a832895e-d2aa-49dd-8fc7-669911a24b06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
a832895e-d2aa-49dd-8fc7-669911a24b06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
a832895e-d2aa-49dd-8fc7-669911a24b06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
a832895e-d2aa-49dd-8fc7-669911a24b06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
00d5d42c-2cac-4631-a847-74fc82e3cfce,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"While in the normal state the transfer of oxygen is perfusion limited, in lung diseases that affect the surface area or membrane thickness of the gas exchange surface, the transfer of oxygen may become diffusion limited. Being able to measure the transfer of gas into the blood provides a valuable diagnostic tool. This is what we will look at here, not only because of its clinical pertinence, but also because it summarizes some physiological principles.",True,OR,,,,
dfacba25-5a02-4be8-b44d-ff105ff4ea5f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,Testing the Diffusion Capacity of the Lung,False,Testing the Diffusion Capacity of the Lung,,,,
5a6530c6-b883-4dc9-9634-21639f6c6958,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"The gas used to test the diffusion capacity of the lung is carbon monoxide. Why? Because as you have seen, carbon monoxide is diffusion limited, so any change in membrane characteristics will affect its movement into the bloodstream. So fundamentally, we will have the patient inhale a little carbon monoxide and hold their breath for a few seconds. During the breath-hold some CO will move into the bloodstream—the greater the disease (diffusion limitation), the more will stay in the lung. As the patient breathes out, the exhaled carbon monoxide (i.e., that not transferred) is measured. The difference between the amount inhaled and the amount returned in the exhalation is the amount that crossed into the blood. The more CO that comes back in the exhalation, the less that crossed into the blood and the worse diffusion limitation is.",True,Testing the Diffusion Capacity of the Lung,,,,
8250fc10-37e5-48e2-97ab-bbb16f3bab5c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,Let us look at this more formally.,False,Let us look at this more formally.,,,,
c56b5d78-a406-4e4f-aaee-34714643e722,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"The transfer factor is primarily dictated by the factors within Fick’s law of diffusion. Because we cannot independently measure membrane area and thickness, we lump these terms and the diffusion coefficient of the gas we are interested in into one term, the diffusing capacity of the lung, or DL (equations below).",True,Let us look at this more formally.,,,,
224fdfcb-baee-4d17-9dde-868ee8e881a6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,Equation 8.1,True,Let us look at this more formally.,,,,
fda9ad4e-18e4-48ac-805c-d7da69cc5586,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,[latex]\dot{V}_{gas} = \frac{A}{T} \times D \times (P_1 - P_2)[/latex],False,[latex]\dot{V}_{gas} = \frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
b469c136-10fa-4cb0-a6cc-f947b8b666ee,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,↓,False,↓,,,,
a8d30229-e745-4fb9-a152-e2675774464c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,Equation 8.2,True,↓,,,,
3b4bb7ec-0e5f-484f-ae86-2f8134faf6b2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,[latex]\dot{V}_{gas} = D_L \times (P_1 - P_2)[/latex],False,[latex]\dot{V}_{gas} = D_L \times (P_1 - P_2)[/latex],,,,
25642507-f496-4380-8e93-2566b49d6a8b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,Equation 8.3,True,[latex]\dot{V}_{gas} = D_L \times (P_1 - P_2)[/latex],,,,
271f428a-6883-4afc-9b29-76592888cda9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_1 - P_2}[/latex],False,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_1 - P_2}[/latex],,,,
68e63b92-cda8-4a3e-b2b2-6d3eff583dc2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,Equation 8.4,True,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_1 - P_2}[/latex],,,,
e64e9780-a038-4969-ac48-8dd2ac04ce02,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_{A_{CO}}}[/latex],False,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_{A_{CO}}}[/latex],,,,
0b0b7401-8a9a-49d6-b8f2-da909601e4ba,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"In the lab test, we are specifically looking at the transfer, or flow, of CO across the membrane, and if we rearrange this equation for transfer factor we see the transfer factor is the flow of CO divided by the pressure gradient of CO (equation 8.4). We can assume that the arterial partial pressure of CO is zero, so our equation for transfer factor ends up as the flow, or transfer, of CO across the membrane, divided by the alveolar partial pressure of CO.",True,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_{A_{CO}}}[/latex],,,,
6a153cc7-d489-47f4-b8b1-eb69a95e082f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"But the movement of gases such as CO, and more physiologically important, oxygen, is also determined by the rate of binding with hemoglobin when it gets into the bloodstream. So our transfer factor has to contain an additional term to account for this. The rate of binding to hemoglobin is determined by two factors; first, the affinity of the gas for hemoglobin, denoted here by theta, and second, by the amount of hemoglobin present in the capillary, denoted as Vc, or capillary volume.",True,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_{A_{CO}}}[/latex],,,,
ca9a9fb1-8932-4866-a277-090804daf777,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,Equation 8.5,True,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_{A_{CO}}}[/latex],,,,
2fdf4da0-03fb-46a1-930f-33e935055526,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,[latex]\displaystyle\frac{1}{D_L} = \displaystyle\frac{1}{D_M} + \displaystyle\frac{1}{\theta \times V_c}[/latex],False,[latex]\displaystyle\frac{1}{D_L} = \displaystyle\frac{1}{D_M} + \displaystyle\frac{1}{\theta \times V_c}[/latex],,,,
9d4fa9a6-e062-4ba6-8391-4a4909541b16,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"So now if we rename our initial value of DL that described the factors associated with the membrane as DM and add our term to account for binding with hemoglobin (equation 8.5), the sum of these two gives a more complete description of transfer, or DL. This more complete term now reflects that the transfer of gas is not solely dependent on membrane properties.",True,[latex]\displaystyle\frac{1}{D_L} = \displaystyle\frac{1}{D_M} + \displaystyle\frac{1}{\theta \times V_c}[/latex],,,,
125930a1-e498-4bcd-b7b9-a1906ed993e2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,This provides a relatively simple and powerful diagnostic technique to assess disease stage and reduced function of the lung as a gas exchange organ.,True,[latex]\displaystyle\frac{1}{D_L} = \displaystyle\frac{1}{D_M} + \displaystyle\frac{1}{\theta \times V_c}[/latex],,,,
e9be68ec-6be9-40f5-8b18-efe37764ce0c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,Summary,False,Summary,,,,
111ccdb1-28e8-416f-9d22-c1ec31f466ce,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"So we have seen the two major factors that affect the rate of gas transfer across the lung: the rate of diffusion that is determined by the characteristics of the membrane (as described in Fick’s law of diffusion), and also the rate of perfusion, which involves the rate of blood flow, volume, and binding affinity with hemoglobin. Diffusion limitation is really a description of the impediment caused by the membrane with a constant partial pressure gradient; and perfusion limitation describes whether the partial pressure gradient is being maintained.",True,Summary,,,,
ba90c805-bb72-4a46-9128-3982f25f3f57,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,Text,False,Text,,,,
7ee7bd78-ee76-462c-8326-3223973d9968,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"Levitsky, Michael G. “Chapter 6: Diffusion of Gases and Interpretation of Pulmonary Function Tests.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
7098f0e3-8f6c-4a7f-8bb9-019917fbc96e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"West, John B. “Chapter 3: Diffusion—How Gas Gets Across the Blood–Gas Barrier.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
83eef49d-f1b3-4248-908d-fe1c99a681e8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Summary,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-3,"Widdicombe, John G., and Andrew S. Davis. “Chapter 4.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
7bf23f79-6b28-43da-b732-30936e532baf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,OR,False,OR,,,,
04af8620-cac8-4642-ac14-2ebc8d7e3049,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"Identifying whether deranged blood gases are due to diffusion or perfusion limitations can help in the diagnosis of an underlying pathological issue, so we will look at them here.",True,OR,,,,
35f1d1da-1db1-4ca3-adea-6934378837c5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
35f1d1da-1db1-4ca3-adea-6934378837c5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
35f1d1da-1db1-4ca3-adea-6934378837c5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
35f1d1da-1db1-4ca3-adea-6934378837c5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
2e0578d5-e29f-4c3a-8b9e-a0aa57164880,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
2e0578d5-e29f-4c3a-8b9e-a0aa57164880,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
2e0578d5-e29f-4c3a-8b9e-a0aa57164880,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
2e0578d5-e29f-4c3a-8b9e-a0aa57164880,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
bb5e6010-7042-4472-b1f7-3a6ffde85221,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,We can illustrate these diffusion and perfusion limitations with the behavior of two nonphysiological gases transferring from the alveolus to the bloodstream.,True,OR,,,,
57b6648a-4951-48c3-aad6-24562320d572,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,Carbon monoxide is well known for its affinity for hemoglobin. When CO passes across the membrane it rapidly binds to hemoglobin and is thus removed from solution. This removal from solution maintains the pressure gradient across the membrane. So with a maintained pressure gradient the major impediment to CO transfer is diffusion across the membrane. Therefore CO transfer is referred to as diffusion limited and dependent on the properties of the membrane. (Consequently CO is used in diffusion limitation testing (DLCO) in pulmonary function labs.),True,OR,,,,
85aaacec-633b-487e-a316-eee648e6e45b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"Nitrous oxide, alternatively, does not bind with hemoglobin at all, so its arterial partial pressure rises rapidly as it stays in solution. So maintaining the pressure gradient is dependent on how quickly the transferred nitrous oxide is washed away by blood flow. Because of this, nitrous oxide is referred to as perfusion limited.",True,OR,,,,
54c39a15-b7fe-4f95-88aa-d1b2b8d6e5bf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"So while our two nonphysiological gases provide good examples of diffusion and perfusion limitations, let us see how oxygen behaves.",True,OR,,,,
f47a827c-0879-4135-8eaf-0ee32f6f376a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
f47a827c-0879-4135-8eaf-0ee32f6f376a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
f47a827c-0879-4135-8eaf-0ee32f6f376a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
f47a827c-0879-4135-8eaf-0ee32f6f376a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
70884e55-9956-42d5-ae99-e67a259371cb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
70884e55-9956-42d5-ae99-e67a259371cb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
70884e55-9956-42d5-ae99-e67a259371cb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
70884e55-9956-42d5-ae99-e67a259371cb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
6b68b69c-6bf4-459e-8c28-0db0bc588913,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
6b68b69c-6bf4-459e-8c28-0db0bc588913,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
6b68b69c-6bf4-459e-8c28-0db0bc588913,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
6b68b69c-6bf4-459e-8c28-0db0bc588913,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
bf1d0064-3c1d-487b-bd7d-7a6bfe210e88,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"The transfer of O2 is also hampered by having to start off at venous partial pressures (40 mmHg), compared to our test gases that start off at zero. Consequently the initial pressure gradient is less. Despite this, the arterial partial pressure of oxygen equilibrates with alveolar pressures within 0.25 seconds (i.e., a third of the distance around the capillary). With the blood still having another 0.5 seconds in the capillary, this provides a large reserve time.",True,OR,,,,
23a7bba5-ae71-48dc-a952-1507771c1583,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
23a7bba5-ae71-48dc-a952-1507771c1583,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
23a7bba5-ae71-48dc-a952-1507771c1583,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
23a7bba5-ae71-48dc-a952-1507771c1583,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
a8605fe1-d73e-46ed-8f12-8bcbf3e70a33,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"While in the normal state the transfer of oxygen is perfusion limited, in lung diseases that affect the surface area or membrane thickness of the gas exchange surface, the transfer of oxygen may become diffusion limited. Being able to measure the transfer of gas into the blood provides a valuable diagnostic tool. This is what we will look at here, not only because of its clinical pertinence, but also because it summarizes some physiological principles.",True,OR,,,,
760a13cc-21ee-4e53-b128-f186724dbf92,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,Testing the Diffusion Capacity of the Lung,False,Testing the Diffusion Capacity of the Lung,,,,
4db1743f-4166-410e-b371-bc35239becba,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"The gas used to test the diffusion capacity of the lung is carbon monoxide. Why? Because as you have seen, carbon monoxide is diffusion limited, so any change in membrane characteristics will affect its movement into the bloodstream. So fundamentally, we will have the patient inhale a little carbon monoxide and hold their breath for a few seconds. During the breath-hold some CO will move into the bloodstream—the greater the disease (diffusion limitation), the more will stay in the lung. As the patient breathes out, the exhaled carbon monoxide (i.e., that not transferred) is measured. The difference between the amount inhaled and the amount returned in the exhalation is the amount that crossed into the blood. The more CO that comes back in the exhalation, the less that crossed into the blood and the worse diffusion limitation is.",True,Testing the Diffusion Capacity of the Lung,,,,
94580dad-60c6-40a2-87bf-6b1204a00239,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,Let us look at this more formally.,False,Let us look at this more formally.,,,,
eaab6b91-40f7-439a-8fd8-92ec5b5123e3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"The transfer factor is primarily dictated by the factors within Fick’s law of diffusion. Because we cannot independently measure membrane area and thickness, we lump these terms and the diffusion coefficient of the gas we are interested in into one term, the diffusing capacity of the lung, or DL (equations below).",True,Let us look at this more formally.,,,,
509804ec-d736-4176-8606-9f6f800d24cb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,Equation 8.1,True,Let us look at this more formally.,,,,
181cf066-c78b-4714-868f-edc276f8d653,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,[latex]\dot{V}_{gas} = \frac{A}{T} \times D \times (P_1 - P_2)[/latex],False,[latex]\dot{V}_{gas} = \frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
29655c73-efa7-4dd3-96da-66d75a259f83,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,↓,False,↓,,,,
e324286c-bf5a-4fa7-a019-fc3073b0bdcf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,Equation 8.2,True,↓,,,,
f1937d98-dd9b-4eee-8d12-76db2fc90631,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,[latex]\dot{V}_{gas} = D_L \times (P_1 - P_2)[/latex],False,[latex]\dot{V}_{gas} = D_L \times (P_1 - P_2)[/latex],,,,
a526bbf4-9014-46f2-89f6-ff2d1db677de,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,Equation 8.3,True,[latex]\dot{V}_{gas} = D_L \times (P_1 - P_2)[/latex],,,,
42b4e1d6-8901-4a23-ac29-bb66f3e5c474,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_1 - P_2}[/latex],False,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_1 - P_2}[/latex],,,,
4a6723be-fbc8-438b-aa8b-db494063f2df,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,Equation 8.4,True,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_1 - P_2}[/latex],,,,
5c9dd4d5-446d-4d30-882e-876220cd2b59,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_{A_{CO}}}[/latex],False,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_{A_{CO}}}[/latex],,,,
88265549-ef69-4587-b787-3c85422cbfdf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"In the lab test, we are specifically looking at the transfer, or flow, of CO across the membrane, and if we rearrange this equation for transfer factor we see the transfer factor is the flow of CO divided by the pressure gradient of CO (equation 8.4). We can assume that the arterial partial pressure of CO is zero, so our equation for transfer factor ends up as the flow, or transfer, of CO across the membrane, divided by the alveolar partial pressure of CO.",True,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_{A_{CO}}}[/latex],,,,
81872785-09e1-42ac-bf2c-d7dbb9298448,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"But the movement of gases such as CO, and more physiologically important, oxygen, is also determined by the rate of binding with hemoglobin when it gets into the bloodstream. So our transfer factor has to contain an additional term to account for this. The rate of binding to hemoglobin is determined by two factors; first, the affinity of the gas for hemoglobin, denoted here by theta, and second, by the amount of hemoglobin present in the capillary, denoted as Vc, or capillary volume.",True,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_{A_{CO}}}[/latex],,,,
377f6e88-a11d-47d0-826c-213ec73cac34,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,Equation 8.5,True,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_{A_{CO}}}[/latex],,,,
5d9b9fdd-11b4-4362-861a-2a9cd9daa1b3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,[latex]\displaystyle\frac{1}{D_L} = \displaystyle\frac{1}{D_M} + \displaystyle\frac{1}{\theta \times V_c}[/latex],False,[latex]\displaystyle\frac{1}{D_L} = \displaystyle\frac{1}{D_M} + \displaystyle\frac{1}{\theta \times V_c}[/latex],,,,
5833bbb1-725d-49cf-9983-849553dbc8a2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"So now if we rename our initial value of DL that described the factors associated with the membrane as DM and add our term to account for binding with hemoglobin (equation 8.5), the sum of these two gives a more complete description of transfer, or DL. This more complete term now reflects that the transfer of gas is not solely dependent on membrane properties.",True,[latex]\displaystyle\frac{1}{D_L} = \displaystyle\frac{1}{D_M} + \displaystyle\frac{1}{\theta \times V_c}[/latex],,,,
81173963-c915-443f-96e8-9af319e54f7b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,This provides a relatively simple and powerful diagnostic technique to assess disease stage and reduced function of the lung as a gas exchange organ.,True,[latex]\displaystyle\frac{1}{D_L} = \displaystyle\frac{1}{D_M} + \displaystyle\frac{1}{\theta \times V_c}[/latex],,,,
c70e4b70-639e-45cb-b9e3-17a4bb7e973f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,Summary,False,Summary,,,,
6b88bc19-d416-4546-9317-d741a2735c5e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"So we have seen the two major factors that affect the rate of gas transfer across the lung: the rate of diffusion that is determined by the characteristics of the membrane (as described in Fick’s law of diffusion), and also the rate of perfusion, which involves the rate of blood flow, volume, and binding affinity with hemoglobin. Diffusion limitation is really a description of the impediment caused by the membrane with a constant partial pressure gradient; and perfusion limitation describes whether the partial pressure gradient is being maintained.",True,Summary,,,,
922f6cbc-d3e4-4ba2-aea6-e80febbfbc16,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,Text,False,Text,,,,
2c66bf0e-220c-4ada-b84d-bb11a31e5c71,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"Levitsky, Michael G. “Chapter 6: Diffusion of Gases and Interpretation of Pulmonary Function Tests.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
bfbd8a09-0c37-4aec-9b01-492b6052ed93,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"West, John B. “Chapter 3: Diffusion—How Gas Gets Across the Blood–Gas Barrier.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
816786a3-0a59-4519-ba55-818024922177,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-2,"Widdicombe, John G., and Andrew S. Davis. “Chapter 4.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
f94142fb-47d4-4e72-b0bb-1034c96d1185,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,OR,False,OR,,,,
ce51e967-43ae-42c4-8894-be56d2a4d53e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"Identifying whether deranged blood gases are due to diffusion or perfusion limitations can help in the diagnosis of an underlying pathological issue, so we will look at them here.",True,OR,,,,
b229b15e-b31e-4a61-832a-aa5faa0a125e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
b229b15e-b31e-4a61-832a-aa5faa0a125e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
b229b15e-b31e-4a61-832a-aa5faa0a125e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
b229b15e-b31e-4a61-832a-aa5faa0a125e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
ec98e221-2b51-4a5f-8921-b7c0b10026f8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
ec98e221-2b51-4a5f-8921-b7c0b10026f8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
ec98e221-2b51-4a5f-8921-b7c0b10026f8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
ec98e221-2b51-4a5f-8921-b7c0b10026f8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
4663ac59-c4a3-42d0-b862-93dcf18d525a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,We can illustrate these diffusion and perfusion limitations with the behavior of two nonphysiological gases transferring from the alveolus to the bloodstream.,True,OR,,,,
099ad18f-9768-4a9d-af29-8c375a6890aa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,Carbon monoxide is well known for its affinity for hemoglobin. When CO passes across the membrane it rapidly binds to hemoglobin and is thus removed from solution. This removal from solution maintains the pressure gradient across the membrane. So with a maintained pressure gradient the major impediment to CO transfer is diffusion across the membrane. Therefore CO transfer is referred to as diffusion limited and dependent on the properties of the membrane. (Consequently CO is used in diffusion limitation testing (DLCO) in pulmonary function labs.),True,OR,,,,
926a2437-376d-4cbf-b9a7-f8336acf5f2e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"Nitrous oxide, alternatively, does not bind with hemoglobin at all, so its arterial partial pressure rises rapidly as it stays in solution. So maintaining the pressure gradient is dependent on how quickly the transferred nitrous oxide is washed away by blood flow. Because of this, nitrous oxide is referred to as perfusion limited.",True,OR,,,,
6d78e44c-369e-4db3-b79e-5d4e758ccb54,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"So while our two nonphysiological gases provide good examples of diffusion and perfusion limitations, let us see how oxygen behaves.",True,OR,,,,
2796816e-e885-4fdb-b248-9c7d3fa23493,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
2796816e-e885-4fdb-b248-9c7d3fa23493,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
2796816e-e885-4fdb-b248-9c7d3fa23493,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
2796816e-e885-4fdb-b248-9c7d3fa23493,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
afd38899-8168-41a0-9eb0-ae63f379d9c5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
afd38899-8168-41a0-9eb0-ae63f379d9c5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
afd38899-8168-41a0-9eb0-ae63f379d9c5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
afd38899-8168-41a0-9eb0-ae63f379d9c5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
f23e4914-14ab-4a9b-a45a-909124508c69,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
f23e4914-14ab-4a9b-a45a-909124508c69,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
f23e4914-14ab-4a9b-a45a-909124508c69,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
f23e4914-14ab-4a9b-a45a-909124508c69,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
a1d7425f-841a-4947-8799-a9b5bd2331f0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"The transfer of O2 is also hampered by having to start off at venous partial pressures (40 mmHg), compared to our test gases that start off at zero. Consequently the initial pressure gradient is less. Despite this, the arterial partial pressure of oxygen equilibrates with alveolar pressures within 0.25 seconds (i.e., a third of the distance around the capillary). With the blood still having another 0.5 seconds in the capillary, this provides a large reserve time.",True,OR,,,,
74c8f3d3-03dd-475e-816e-530580283b29,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
74c8f3d3-03dd-475e-816e-530580283b29,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
74c8f3d3-03dd-475e-816e-530580283b29,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
74c8f3d3-03dd-475e-816e-530580283b29,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
4bcab715-2bb5-4321-ac80-b471d237b0c3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"While in the normal state the transfer of oxygen is perfusion limited, in lung diseases that affect the surface area or membrane thickness of the gas exchange surface, the transfer of oxygen may become diffusion limited. Being able to measure the transfer of gas into the blood provides a valuable diagnostic tool. This is what we will look at here, not only because of its clinical pertinence, but also because it summarizes some physiological principles.",True,OR,,,,
489f59b8-5e07-47ce-aa72-70de1dfb7f3c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,Testing the Diffusion Capacity of the Lung,False,Testing the Diffusion Capacity of the Lung,,,,
3ea000d7-832f-4de6-bc56-92eeb82d64b5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"The gas used to test the diffusion capacity of the lung is carbon monoxide. Why? Because as you have seen, carbon monoxide is diffusion limited, so any change in membrane characteristics will affect its movement into the bloodstream. So fundamentally, we will have the patient inhale a little carbon monoxide and hold their breath for a few seconds. During the breath-hold some CO will move into the bloodstream—the greater the disease (diffusion limitation), the more will stay in the lung. As the patient breathes out, the exhaled carbon monoxide (i.e., that not transferred) is measured. The difference between the amount inhaled and the amount returned in the exhalation is the amount that crossed into the blood. The more CO that comes back in the exhalation, the less that crossed into the blood and the worse diffusion limitation is.",True,Testing the Diffusion Capacity of the Lung,,,,
71aca562-b11f-49ab-b6af-0ceb5b427123,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,Let us look at this more formally.,False,Let us look at this more formally.,,,,
abb04b46-c0e6-4cab-a2a9-7e1518229c05,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"The transfer factor is primarily dictated by the factors within Fick’s law of diffusion. Because we cannot independently measure membrane area and thickness, we lump these terms and the diffusion coefficient of the gas we are interested in into one term, the diffusing capacity of the lung, or DL (equations below).",True,Let us look at this more formally.,,,,
8b84a156-fb5e-41a7-8157-6b7e4489b0da,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,Equation 8.1,True,Let us look at this more formally.,,,,
82133f60-5348-48da-9f7d-0fb3fe761d26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,˙Vgas=AT×D×(P1−P2),False,˙Vgas=AT×D×(P1−P2),,,,
341efe33-1557-4c09-b4bb-ca3a1003d09b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,˙Vgas,False,˙Vgas,,,,
8f053089-7e90-4dca-a009-18f813d6750a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,˙V,False,˙V,,,,
4d1d1824-7a6e-4e70-ac85-a551abad8ec6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,˙,False,˙,,,,
56ede589-2b28-45f8-8b00-c02395409171,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,V,False,V,,,,
f8c14182-4e62-432f-ba71-ebf166212a40,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,gas,False,gas,,,,
bb9df214-323a-4742-8ec2-43ee6f1f02c0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,g,False,g,,,,
6169fb8a-7d7a-49ee-862b-10b11306d207,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,a,False,a,,,,
dd20d5e0-6453-4af2-82e6-a0e361e9bf78,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,s,False,s,,,,
0644d3de-c19b-4f75-ae06-71e81ca74389,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,=,False,=,,,,
ea833810-83d3-4ea6-8f1b-99b39ea4a4dc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,AT,False,AT,,,,
21bbfed1-b5ae-47ac-8f75-fe4cce347af2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,A,False,A,,,,
3f9d14e7-aaf1-4023-b164-82cbe37a7ff7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,T,False,T,,,,
a6e0f6d1-3c14-4e88-b966-2ee046985276,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,×,False,×,,,,
b58369aa-f5b4-4ab9-888d-04a3d42aeccd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,D,False,D,,,,
41dcbec6-c3dc-4575-81dd-9df8e51a23b2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,(,False,(,,,,
e262db95-d861-45c9-a26b-8a853112405e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,P1,False,P1,,,,
a5b4db4c-62fe-4c50-94d2-532d67f6de00,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,P,False,P,,,,
1f34d981-49c1-43e6-b62e-5054f24bacd3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,1,False,1,,,,
a0d62a0c-d65c-4ab8-9717-fee318f9b4ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,−,False,−,,,,
599c1762-a081-4581-8e03-1abeae494ede,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,P2,False,P2,,,,
a101055d-9725-4a01-8fb3-2bb9fbe08c5e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,2,False,2,,,,
04615fc7-d49b-4650-b9d8-91245dfaa84b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,),False,),,,,
3779386f-d3c2-4b22-9a78-b4baf59f3e21,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,↓,False,↓,,,,
dbf4f24c-257e-4b08-9612-c41484512363,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,Equation 8.2,True,↓,,,,
6aec0700-f118-4c6e-aa61-8eec94e5a407,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,˙Vgas=DL×(P1−P2),False,˙Vgas=DL×(P1−P2),,,,
d5e8ebac-6d7d-47c0-bafc-fcebfe8838ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,DL,False,DL,,,,
6ab0d7f1-06a8-405c-b64f-a163ca67f84a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,L,False,L,,,,
817c1c64-f619-452b-840e-55fddaab4b14,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,Equation 8.3,True,L,,,,
4577f6c0-ca6e-48c7-9758-c66771058b55,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,DL=˙VCOP1−P2,False,DL=˙VCOP1−P2,,,,
f81a3006-05cc-424a-8375-b86c67f45ce9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,˙VCOP1−P2,False,˙VCOP1−P2,,,,
6b73e53b-8881-4fff-98e6-14536e4ec4af,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,˙VCO,False,˙VCO,,,,
7a3bb527-d3a7-44db-9f1b-1316423a2099,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,CO,False,CO,,,,
ce788d93-1ddc-4f08-8f7a-ea27da5afe83,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,C,False,C,,,,
8f84a6b6-8940-4452-9d4f-5f342495b143,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,O,False,O,,,,
a7f5b4ff-60f2-4a7c-8d08-7a3637626fd7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,P1−P2,False,P1−P2,,,,
c861797f-134c-4909-82cb-fcadceff8e19,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,Equation 8.4,True,P1−P2,,,,
b38c342d-ee91-4ee3-a29a-10995cbcb215,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,DL=˙VCOPACO,False,DL=˙VCOPACO,,,,
7cf089d1-740e-42ba-af93-840d59869e49,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,˙VCOPACO,False,˙VCOPACO,,,,
a4ac4e18-f486-44e8-a07e-6b18be1d2297,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,PACO,False,PACO,,,,
4c31e4d8-8894-4919-af54-9904c2040423,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,ACO,False,ACO,,,,
eaab5e5e-9fa6-4a24-88b6-ef8188c52d59,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"In the lab test, we are specifically looking at the transfer, or flow, of CO across the membrane, and if we rearrange this equation for transfer factor we see the transfer factor is the flow of CO divided by the pressure gradient of CO (equation 8.4). We can assume that the arterial partial pressure of CO is zero, so our equation for transfer factor ends up as the flow, or transfer, of CO across the membrane, divided by the alveolar partial pressure of CO.",True,ACO,,,,
e4dabd8b-bcd3-4f20-a6e2-38a6cfd92cf0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"But the movement of gases such as CO, and more physiologically important, oxygen, is also determined by the rate of binding with hemoglobin when it gets into the bloodstream. So our transfer factor has to contain an additional term to account for this. The rate of binding to hemoglobin is determined by two factors; first, the affinity of the gas for hemoglobin, denoted here by theta, and second, by the amount of hemoglobin present in the capillary, denoted as Vc, or capillary volume.",True,ACO,,,,
a6a89fdb-aa34-490f-9721-3b0a7aebe7f6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,Equation 8.5,True,ACO,,,,
d195a51b-6dd9-45c2-b0fb-8470a7482043,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,1DL=1DM+1θ×Vc,False,1DL=1DM+1θ×Vc,,,,
6b459ecc-36df-45f4-83f7-b7e061c2b550,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,1DL,False,1DL,,,,
d551cde6-3946-4c3f-9932-5735ec031a43,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,1DM+1θ×Vc,False,1DM+1θ×Vc,,,,
bf1df4fc-5aae-42ce-89a4-f37c328ce278,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,1DM,False,1DM,,,,
433c233a-9607-417b-8304-aece895b749f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,DM,False,DM,,,,
d4f5ddec-307e-4ef3-9df2-12fde45cb302,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,M,False,M,,,,
20f471ab-0534-4acb-9c2b-d8e0198032bc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,+,False,+,,,,
3bb58a4b-3c8c-48a2-8aa6-d5aae66ad46e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,1θ×Vc,False,1θ×Vc,,,,
ad9da688-3774-436a-9ff6-df92c7dbafa9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,θ×Vc,False,θ×Vc,,,,
816f926a-5700-4db6-a13e-822b6419e389,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,θ,False,θ,,,,
6be1a185-5b33-45e1-a21f-ce4574ba1e69,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,Vc,False,Vc,,,,
4a990b5e-5194-46ba-911b-4ff1acaa7311,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,c,False,c,,,,
35d104dc-ecd2-4706-8a23-821d2924305d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"So now if we rename our initial value of DL that described the factors associated with the membrane as DM and add our term to account for binding with hemoglobin (equation 8.5), the sum of these two gives a more complete description of transfer, or DL. This more complete term now reflects that the transfer of gas is not solely dependent on membrane properties.",True,c,,,,
d4c79d0c-845f-40ab-aa96-6ac2e1368e25,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,This provides a relatively simple and powerful diagnostic technique to assess disease stage and reduced function of the lung as a gas exchange organ.,True,c,,,,
d6dd363c-0e36-4b5f-a1f2-c18b42e1b74b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,Summary,False,Summary,,,,
9bc514b6-5f14-41b9-949f-36455d2d8959,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"So we have seen the two major factors that affect the rate of gas transfer across the lung: the rate of diffusion that is determined by the characteristics of the membrane (as described in Fick’s law of diffusion), and also the rate of perfusion, which involves the rate of blood flow, volume, and binding affinity with hemoglobin. Diffusion limitation is really a description of the impediment caused by the membrane with a constant partial pressure gradient; and perfusion limitation describes whether the partial pressure gradient is being maintained.",True,Summary,,,,
e0d9a872-e62f-4aff-9cc7-2640509845d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,Text,False,Text,,,,
a71247d9-40a7-4667-bac9-1b3001429d91,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"Levitsky, Michael G. “Chapter 6: Diffusion of Gases and Interpretation of Pulmonary Function Tests.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
919ed0dc-690d-4632-920c-09b9b26b57d7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"West, John B. “Chapter 3: Diffusion—How Gas Gets Across the Blood–Gas Barrier.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
cd47d7ea-7fdc-436c-937d-7110bd477b6a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/#chapter-41-section-1,"Widdicombe, John G., and Andrew S. Davis. “Chapter 4.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
8f997830-a7a5-4844-97e4-b11ae83de6ba,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,OR,False,OR,,,,
425d2966-1bee-49d6-8bc6-63b87093c6ca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"Identifying whether deranged blood gases are due to diffusion or perfusion limitations can help in the diagnosis of an underlying pathological issue, so we will look at them here.",True,OR,,,,
13b5f799-d317-4b36-928f-68f5a303b405,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
13b5f799-d317-4b36-928f-68f5a303b405,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
13b5f799-d317-4b36-928f-68f5a303b405,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
13b5f799-d317-4b36-928f-68f5a303b405,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"If a sufficient diffusion gradient exists across a membrane, then the rate of transfer of gas is primarily dependent on the properties of the membrane (see the left side of the figure 8.1). The transfer of gas in this case is referred to as a diffusion limitation.",True,OR,Figure 8.1,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
a45805eb-e660-46cd-9f82-b21a45c296ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
a45805eb-e660-46cd-9f82-b21a45c296ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
a45805eb-e660-46cd-9f82-b21a45c296ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
a45805eb-e660-46cd-9f82-b21a45c296ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"If gas starts to accumulate on the other side of the membrane, however, the pressure gradient will dissipate and transfer rates become limited (right side of figure 8.1). This is referred to as a perfusion limitation, as it is indicative of low blood flow that is insufficient to “wash away” transferred gas, keep blood gas partial pressure low, and maintain the diffusion gradient.",True,OR,Figure 8.1,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.1.png,Figure 8.1: Diffusion and perfusion limitations.
54656453-fd20-4bd3-a3a1-a4c63686b516,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,We can illustrate these diffusion and perfusion limitations with the behavior of two nonphysiological gases transferring from the alveolus to the bloodstream.,True,OR,,,,
3499f9c9-0cf9-4b5b-9c47-da39f84fcf5e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,Carbon monoxide is well known for its affinity for hemoglobin. When CO passes across the membrane it rapidly binds to hemoglobin and is thus removed from solution. This removal from solution maintains the pressure gradient across the membrane. So with a maintained pressure gradient the major impediment to CO transfer is diffusion across the membrane. Therefore CO transfer is referred to as diffusion limited and dependent on the properties of the membrane. (Consequently CO is used in diffusion limitation testing (DLCO) in pulmonary function labs.),True,OR,,,,
2422f269-4250-447a-aaf9-8da6aec9e831,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"Nitrous oxide, alternatively, does not bind with hemoglobin at all, so its arterial partial pressure rises rapidly as it stays in solution. So maintaining the pressure gradient is dependent on how quickly the transferred nitrous oxide is washed away by blood flow. Because of this, nitrous oxide is referred to as perfusion limited.",True,OR,,,,
6cf7e073-dc5f-4a46-9c50-9dbb06cb070f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"So while our two nonphysiological gases provide good examples of diffusion and perfusion limitations, let us see how oxygen behaves.",True,OR,,,,
71bb19ff-f4de-4d54-86b9-572aaef68949,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
71bb19ff-f4de-4d54-86b9-572aaef68949,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
71bb19ff-f4de-4d54-86b9-572aaef68949,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
71bb19ff-f4de-4d54-86b9-572aaef68949,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"The blood partial pressure of CO rises very little along the capillary as it is rapidly binding to hemoglobin (Hb) (figure 8.2), the pressure gradient is maintained, and the CO is only limited by the membrane; it exhibits diffusion limitation.",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
a4afcbd7-69e3-4704-a9e1-e43c14073578,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
a4afcbd7-69e3-4704-a9e1-e43c14073578,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
a4afcbd7-69e3-4704-a9e1-e43c14073578,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
a4afcbd7-69e3-4704-a9e1-e43c14073578,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"The blood partial pressure of nitrous oxide, alternatively, rapidly rises (figure 8.2), and the transfer of NO becomes reliant on the rate of perfusion to maintain the gradient and gas transfer (i.e., it is perfusion limited).",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
8ee32286-80ba-4690-8d2e-e53f63b8144a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
8ee32286-80ba-4690-8d2e-e53f63b8144a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
8ee32286-80ba-4690-8d2e-e53f63b8144a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
8ee32286-80ba-4690-8d2e-e53f63b8144a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"The results for O2 fall much closer to the perfusion limitation (NO) line than the diffusion limitation line (figure 8.2, O2 normal). Oxygen binds to hemoglobin so the arterial PO2 does not rise as quickly as nitrous oxide, but the binding of O2 is so much less than carbon monoxide it actually demonstrates more perfusion, rather than diffusion limitation.",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
9994067f-33cd-4aca-8f26-7dd54c1e1d14,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"The transfer of O2 is also hampered by having to start off at venous partial pressures (40 mmHg), compared to our test gases that start off at zero. Consequently the initial pressure gradient is less. Despite this, the arterial partial pressure of oxygen equilibrates with alveolar pressures within 0.25 seconds (i.e., a third of the distance around the capillary). With the blood still having another 0.5 seconds in the capillary, this provides a large reserve time.",True,OR,,,,
01e6f2e8-cd43-4473-bc97-6051ee9b610b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,Summary,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
01e6f2e8-cd43-4473-bc97-6051ee9b610b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,Testing the Diffusion Capacity of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
01e6f2e8-cd43-4473-bc97-6051ee9b610b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,Diffusion Versus Perfusion Limitations,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
01e6f2e8-cd43-4473-bc97-6051ee9b610b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"This reserve time is often eaten into in some disease states (figure 8.2, abnormal); if for example a diffusion problem arises, such as thickening of the membrane, then that extra 0.5 seconds, or last 2/3 seconds of the transit time around the alveolus, can still allow alveolar and arterial PO2s to equilibrate. The patient may still show normal oxygen pressures until they exercise, during which the velocity of pulmonary blood flow increases and transit time is reduced; you can see from figure 8.2 if transit time is reduced to 0.5 seconds then arterial PO2 will not equilibrate with alveolar values in the abnormal lung.",True,OR,Figure 8.2,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/8.2.png,Figure 8.2: Transfer of gases from alveolus to capillary.
4ebcbe6d-37ef-4c72-84d2-2b0451d3172d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"While in the normal state the transfer of oxygen is perfusion limited, in lung diseases that affect the surface area or membrane thickness of the gas exchange surface, the transfer of oxygen may become diffusion limited. Being able to measure the transfer of gas into the blood provides a valuable diagnostic tool. This is what we will look at here, not only because of its clinical pertinence, but also because it summarizes some physiological principles.",True,OR,,,,
73e0cdb9-6d35-4e88-8127-b275ef94d3db,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,Testing the Diffusion Capacity of the Lung,False,Testing the Diffusion Capacity of the Lung,,,,
ad5e06e8-b04d-4687-be6f-0ed6a8b527bb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"The gas used to test the diffusion capacity of the lung is carbon monoxide. Why? Because as you have seen, carbon monoxide is diffusion limited, so any change in membrane characteristics will affect its movement into the bloodstream. So fundamentally, we will have the patient inhale a little carbon monoxide and hold their breath for a few seconds. During the breath-hold some CO will move into the bloodstream—the greater the disease (diffusion limitation), the more will stay in the lung. As the patient breathes out, the exhaled carbon monoxide (i.e., that not transferred) is measured. The difference between the amount inhaled and the amount returned in the exhalation is the amount that crossed into the blood. The more CO that comes back in the exhalation, the less that crossed into the blood and the worse diffusion limitation is.",True,Testing the Diffusion Capacity of the Lung,,,,
70c7beb5-9715-427c-ab0f-b544e57e908f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,Let us look at this more formally.,False,Let us look at this more formally.,,,,
c05c5395-dda4-4fe4-9f65-38fdcfeb21e6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"The transfer factor is primarily dictated by the factors within Fick’s law of diffusion. Because we cannot independently measure membrane area and thickness, we lump these terms and the diffusion coefficient of the gas we are interested in into one term, the diffusing capacity of the lung, or DL (equations below).",True,Let us look at this more formally.,,,,
40c2346b-497b-4ca3-8a2a-4d41cf18224d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,Equation 8.1,True,Let us look at this more formally.,,,,
22992bb6-36a0-457c-bca8-26d3dab2f32b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,[latex]\dot{V}_{gas} = \frac{A}{T} \times D \times (P_1 - P_2)[/latex],False,[latex]\dot{V}_{gas} = \frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
92f995a8-741b-4cc6-ba6c-663482a0b66f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,↓,False,↓,,,,
8ced152b-8326-4a31-861d-4db6abaeb526,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,Equation 8.2,True,↓,,,,
85adce47-4f60-438b-a217-9addc9411301,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,[latex]\dot{V}_{gas} = D_L \times (P_1 - P_2)[/latex],False,[latex]\dot{V}_{gas} = D_L \times (P_1 - P_2)[/latex],,,,
878a3c23-52b4-41de-a4c4-6b8f48ab6807,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,Equation 8.3,True,[latex]\dot{V}_{gas} = D_L \times (P_1 - P_2)[/latex],,,,
8622b777-f7d8-49e2-812c-e6883a54ebb9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_1 - P_2}[/latex],False,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_1 - P_2}[/latex],,,,
bcd4565c-50fc-4d2e-9ae9-4ea74b11d9be,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,Equation 8.4,True,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_1 - P_2}[/latex],,,,
14fc8caa-8abd-4545-bb37-f61df4135b31,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_{A_{CO}}}[/latex],False,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_{A_{CO}}}[/latex],,,,
ca37bebb-ee50-4211-b4fc-2ca97b9389c1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"In the lab test, we are specifically looking at the transfer, or flow, of CO across the membrane, and if we rearrange this equation for transfer factor we see the transfer factor is the flow of CO divided by the pressure gradient of CO (equation 8.4). We can assume that the arterial partial pressure of CO is zero, so our equation for transfer factor ends up as the flow, or transfer, of CO across the membrane, divided by the alveolar partial pressure of CO.",True,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_{A_{CO}}}[/latex],,,,
19710d7e-ff8a-41f7-ae9d-ad82807fd030,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"But the movement of gases such as CO, and more physiologically important, oxygen, is also determined by the rate of binding with hemoglobin when it gets into the bloodstream. So our transfer factor has to contain an additional term to account for this. The rate of binding to hemoglobin is determined by two factors; first, the affinity of the gas for hemoglobin, denoted here by theta, and second, by the amount of hemoglobin present in the capillary, denoted as Vc, or capillary volume.",True,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_{A_{CO}}}[/latex],,,,
b128efab-de58-41cb-a08a-d63ce742cb2f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,Equation 8.5,True,[latex]D_L = \displaystyle\frac{\dot{V}_{CO}}{P_{A_{CO}}}[/latex],,,,
758e279c-f6a7-4099-9d99-e6ba4897d28f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,[latex]\displaystyle\frac{1}{D_L} = \displaystyle\frac{1}{D_M} + \displaystyle\frac{1}{\theta \times V_c}[/latex],False,[latex]\displaystyle\frac{1}{D_L} = \displaystyle\frac{1}{D_M} + \displaystyle\frac{1}{\theta \times V_c}[/latex],,,,
70475400-d66a-4868-8f0b-3a5d02f9afd4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"So now if we rename our initial value of DL that described the factors associated with the membrane as DM and add our term to account for binding with hemoglobin (equation 8.5), the sum of these two gives a more complete description of transfer, or DL. This more complete term now reflects that the transfer of gas is not solely dependent on membrane properties.",True,[latex]\displaystyle\frac{1}{D_L} = \displaystyle\frac{1}{D_M} + \displaystyle\frac{1}{\theta \times V_c}[/latex],,,,
a4a1d3a6-b638-4d4e-90f0-3e85618d909d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,This provides a relatively simple and powerful diagnostic technique to assess disease stage and reduced function of the lung as a gas exchange organ.,True,[latex]\displaystyle\frac{1}{D_L} = \displaystyle\frac{1}{D_M} + \displaystyle\frac{1}{\theta \times V_c}[/latex],,,,
516c0f54-be8d-435f-a7b8-6a1c6869c5a8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,Summary,False,Summary,,,,
627e5b5c-c5dd-49a6-8217-6c5255c9c765,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"So we have seen the two major factors that affect the rate of gas transfer across the lung: the rate of diffusion that is determined by the characteristics of the membrane (as described in Fick’s law of diffusion), and also the rate of perfusion, which involves the rate of blood flow, volume, and binding affinity with hemoglobin. Diffusion limitation is really a description of the impediment caused by the membrane with a constant partial pressure gradient; and perfusion limitation describes whether the partial pressure gradient is being maintained.",True,Summary,,,,
1f90d09d-4ed8-4fa9-aa1d-bfd042fcfff1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,Text,False,Text,,,,
a33d1307-940a-4754-a3c6-77acb9705695,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"Levitsky, Michael G. “Chapter 6: Diffusion of Gases and Interpretation of Pulmonary Function Tests.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
e90402c5-b03d-4cc2-b40c-7309c0366598,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"West, John B. “Chapter 3: Diffusion—How Gas Gets Across the Blood–Gas Barrier.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
31964248-f3af-401f-aade-6a4b025e4b5c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,8. Perfusion and Diffusion Limitations in Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/perfusion-and-diffusion-limitations-in-gas-exchange/,"Widdicombe, John G., and Andrew S. Davis. “Chapter 4.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
94a2e555-32f9-4cc7-8f5b-ef7daead5687,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"Before we do that though, we need to be able to calculate the units of measurement we use when describing gas exchange. When referring to gas exchange we are really referring to diffusion of gases down their concentration gradient, but rather than use concentrations, we use partial pressures.",True,Text,,,,
83d5f78d-9abb-48e8-b071-bef116366b8f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,Partial pressures describe what proportion of the total pressure is exerted by a particular component of a mixed gas. Let us look at the specific situation we are interested in to illustrate this description.,True,Text,,,,
d82456a7-eec8-4a00-acb8-976db3f8f866,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"Atmospheric pressure at sea level is 760 mmHg. This pressure is generated by the collisions of all the molecules with each other and other objects. At high altitude there are fewer molecules, so fewer collisions, and hence atmospheric pressure is lower.",True,Text,,,,
a630d4b8-fca5-42f2-b5b5-7435455e5bc6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"Now looking at the composition of our atmosphere we know that 79 percent is nitrogen, 20.9 percent is oxygen, and some trace gases collectively get us to 100 percent. Now let us calculate a partial pressure. If 79 percent of the atmosphere is nitrogen, then 79 percent of our atmospheric pressure is generated by the collisions by nitrogen molecules. Likewise 20.9 percent of the atmospheric pressure is due to oxygen, so to calculate the partial pressure of oxygen (PO2) we simply multiply atmospheric pressure (PB) by the percentage of oxygen, which means our atmosphere has a partial pressure of oxygen of 159 mmHg.",True,Text,,,,
5f37b31b-d4da-42f2-aba8-69b9e32bd795,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,[latex]PO_2 = \%O_2 \times P_B[/latex],False,[latex]PO_2 = \%O_2 \times P_B[/latex],,,,
271b75fb-b62c-4dfb-8a5e-c125c2c035f6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,[latex]PO_2 = 20.9\% \times 760\:mmHg = 159\:mmHg[/latex],True,[latex]PO_2 = \%O_2 \times P_B[/latex],,,,
82f758e9-c640-4065-9865-ec24be6dba5b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,Alveolar PO2,False,Alveolar PO2,,,,
6bcbe39a-d68e-4fea-8188-d9c23f4383ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"Although related, we are more interested in the PO2 at the gas exchange surface—that is the alveolar PO2 denoted as PAO2 (note the uppercase A; lowercase refers to arterial PO2 (i.e., PaO2)). This value differs significantly from atmospheric PO2 at about 100 mmHg. So why the drop of nearly 60 mmHg from atmospheric PO2?",True,Alveolar PO2,,,,
7d6b0339-1db0-4d46-84b6-30081c05179c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,PAO2,False,PAO2,,,,
0981cc2f-d928-47fc-b068-ed8ae34e6357,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,PaO2,False,PaO2,,,,
e05798d0-51c0-4eaf-9124-90ebfc0b3dbf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"To calculate alveolar PO2 we need to account for the water vapor that is added to the inspired air as it enters the airways. This is equivalent to adding another gas and must be accounted for. Water vapor exerts a pressure of 47 mmHg. Subtracting this from our atmospheric pressure, our total gaseous pressure is 713 mmHg; multiplying this by our fraction of inspired O2 (FiO2 is merely the percentage (fraction) of oxygen inspired), we see our alveolar PO2 is theoretically 149.7 mmHg (i.e., ~150 mmHg).",True,PaO2,,,,
eceba820-ad93-418a-9168-77c8e851b8e4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],False,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],,,,
58d7a984-0b05-480d-a977-641d70b4ff44,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,[latex]P_AO_2 = 20.9\% \times (760 - 47) = 149.7\:mmHg\:or \sim 150\:mmHg[/latex],True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],,,,
d78ff3df-9ffa-46b9-b14f-8135c3c1a230,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"If we understand that there will be mixing with air remaining from the previous breath, the real PAO2 is 100 mmHg (however, we will see this varies across the regions of the lung).",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],,,,
08e5a60b-4262-4849-8300-e592f290d3d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"So how does this value relate to gas exchange in the lung? The venous blood PO2 (PVO2), returning from the systemic tissue where oxygen has been consumed, is 40 mmHg (see figure 7.1). This blood passes the gas exchange surface, and a pressure gradient of 60 mmHg allows oxygen to move into the pulmonary blood. By the time the blood has passed the alveolus, arterial PO2 will have equilibrated with the alveolar PO2 and will also be 100 mmHg. These numbers are well worth committing to memory.",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],Figure 7.1,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.1.png,Figure 7.1: Oxygen tensions around the alveolus.
08e5a60b-4262-4849-8300-e592f290d3d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"So how does this value relate to gas exchange in the lung? The venous blood PO2 (PVO2), returning from the systemic tissue where oxygen has been consumed, is 40 mmHg (see figure 7.1). This blood passes the gas exchange surface, and a pressure gradient of 60 mmHg allows oxygen to move into the pulmonary blood. By the time the blood has passed the alveolus, arterial PO2 will have equilibrated with the alveolar PO2 and will also be 100 mmHg. These numbers are well worth committing to memory.",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],Figure 7.1,Partial Pressures,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.1.png,Figure 7.1: Oxygen tensions around the alveolus.
08e5a60b-4262-4849-8300-e592f290d3d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"So how does this value relate to gas exchange in the lung? The venous blood PO2 (PVO2), returning from the systemic tissue where oxygen has been consumed, is 40 mmHg (see figure 7.1). This blood passes the gas exchange surface, and a pressure gradient of 60 mmHg allows oxygen to move into the pulmonary blood. By the time the blood has passed the alveolus, arterial PO2 will have equilibrated with the alveolar PO2 and will also be 100 mmHg. These numbers are well worth committing to memory.",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],Figure 7.1,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.1.png,Figure 7.1: Oxygen tensions around the alveolus.
ed53b093-27bf-4647-99ec-a32df33bc45a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"The other critical values we need to address here are the partial pressures of CO2 (see figure 7.2). Venous blood returning from the tissue has a PCO2 of 45 mmHg, compared to alveolar PCO2 that is 40 mmHg. This pressure gradient of 5 mmHg is enough to allow blood to equilibrate with the alveolus, and so arterial PCO2 is 40 mmHg. Again, these numbers are worth remembering.",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],Figure 7.2,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.2.png,Figure 7.2: Carbon dioxide tensions around the alveolus.
ed53b093-27bf-4647-99ec-a32df33bc45a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"The other critical values we need to address here are the partial pressures of CO2 (see figure 7.2). Venous blood returning from the tissue has a PCO2 of 45 mmHg, compared to alveolar PCO2 that is 40 mmHg. This pressure gradient of 5 mmHg is enough to allow blood to equilibrate with the alveolus, and so arterial PCO2 is 40 mmHg. Again, these numbers are worth remembering.",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],Figure 7.2,Partial Pressures,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.2.png,Figure 7.2: Carbon dioxide tensions around the alveolus.
ed53b093-27bf-4647-99ec-a32df33bc45a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"The other critical values we need to address here are the partial pressures of CO2 (see figure 7.2). Venous blood returning from the tissue has a PCO2 of 45 mmHg, compared to alveolar PCO2 that is 40 mmHg. This pressure gradient of 5 mmHg is enough to allow blood to equilibrate with the alveolus, and so arterial PCO2 is 40 mmHg. Again, these numbers are worth remembering.",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],Figure 7.2,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.2.png,Figure 7.2: Carbon dioxide tensions around the alveolus.
80f14e98-6d0d-46d5-a094-2dd9f1a23aa6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"A much smaller diffusion gradient is needed for CO2 because CO2 is much more soluble than oxygen, a factor among others that is included in Fick’s law of diffusion.",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],,,,
7b078ad0-d88b-4e76-9cd0-c043c881a35f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,Fick’s Law of Diffusion,False,Fick’s Law of Diffusion,,,,
785844a4-2f7f-40fb-bc0c-231169e46107,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"Fick’s law of diffusion (equation 7.1) describes all the factors that influence the transfer of gas (or flow, V) across a membrane.",True,Fick’s Law of Diffusion,,,,
4245e993-555f-4e26-97d2-7104b69edf40,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,Equation 7.1,True,Fick’s Law of Diffusion,,,,
f465ccac-eed0-4508-8dce-8c4a4242a923,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],False,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
8dca1687-82b4-49ca-8ea5-b76ac65f54e1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,We will look at each factor in the equation and see how it relates to the physiology of the lung.,True,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
c111fe31-7355-4c6d-b8a8-3f2d0a641894,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"Pressure gradient (P1−P2): The higher the pressure gradient, the greater the transfer of gas, and the pressure gradient must be maintained for gas exchange to continue. The maintenance of the gradient is achieved by adequate ventilation to the alveolus to refresh the alveolar gases, and adequate perfusion to flush oxygen away from the gas exchange surface and supply more CO2. We will look at the importance of matching ventilation and perfusion in chapter 13.",True,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
30613f0f-6fb1-4313-ab7e-de7303b85abb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,Other factors in Fick’s law are fairly obvious and are reflected in the lung’s structure.,True,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
3ca943e1-d69f-4558-ab75-d578a5cbb04c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"Surface area (A): The greater the surface area available for exchange, the greater the exchange. The lung has a surface area of 100 m2, which is more than adequate to maintain sufficient gas transfer, even during maximal exercise.",True,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
c3b32db8-11df-4ba0-9a25-673c9629e987,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"Membrane thickness (T): The thickness of the membrane that gas has to cross also determines the rate of transfer; the thinner the membrane, the more rapid the transfer. The gas exchange membrane in the lung is approximately a 0.3 um thick—and poses little opposition to gas movement.",True,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
002b493a-4e40-49b3-b65a-ac4294846cb9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"Diffusion constant (D): The last variable is the diffusion constant of the gases in question, which for us are O2 and CO2. The important issue here is that CO2 is much more soluble (x 20) than O2 and so has a much greater diffusion constant; hence it transfers across the membrane much more readily and does not need the large pressure gradient like the relatively insoluble oxygen (5 mmHg compared with 60 mmHg).",True,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
5599cd0a-f222-443d-8220-ec940bec4498,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"Some of these factors can change in lung disease and can result in decreased gas exchange and so result in deranged blood gases. Loss of surface area occurs in diseases, such as emphysema, that destroy the lung architecture, and cause a loss of gas transfer. Likewise, any disease that causes thickening of the alveolar membrane, such as pulmonary fibrosis, increases the distance for, and resistance to, gas transfer. If ventilation or perfusion of the gas exchange surface fails—for example, a mucus plug blocking an airway or a pulmonary embolus blocking a vessel—then the pressure gradient across the membrane is lost and gas exchange is reduced compared to the ideal situation of ventilation and perfusion being matched.",True,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
912aa1ae-df3c-473a-a95b-f881be9ee3f0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,Summary,False,Summary,,,,
da7da9ee-69af-494c-bef6-64c3e1342329,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,After this chapter you should be able to calculate the alveolar partial pressure of a gas at any atmospheric pressure and relate it to the rate of gas exchange.,True,Summary,,,,
ba6d348e-7679-420a-8bdb-a3ca3d680d28,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,You should also now understand the different factors that contribute to the rate of gas exchange described in Fick’s law of diffusion and be able to appreciate how they might change in disease.,True,Summary,,,,
3bc4ed08-9887-4d09-ae4b-8db5c502df0b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,Text,False,Text,,,,
d7ce3b1c-6375-4f8e-9dbf-13b77ddebff7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"Levitsky, Michael G. “Chapter 6: Diffusion of Gases and Interpretation of Pulmonary Function Tests.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
8bc7a0c2-f138-4f6e-a0ee-bff605d6bed1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"West, John B. “Chapter 3: Diffusion—How Gas Gets Across the Blood–Gas Barrier.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
d62691f8-5c5e-49f0-890a-f5bc6fafaad4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-2,"Widdicombe, John G., and Andrew S. Davis. “Chapter 4.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
7699058a-c379-4838-ad17-20de8e522d6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"Before we do that though, we need to be able to calculate the units of measurement we use when describing gas exchange. When referring to gas exchange we are really referring to diffusion of gases down their concentration gradient, but rather than use concentrations, we use partial pressures.",True,Text,,,,
35f68c8d-c93d-4b95-9bf5-5af272129128,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,Partial pressures describe what proportion of the total pressure is exerted by a particular component of a mixed gas. Let us look at the specific situation we are interested in to illustrate this description.,True,Text,,,,
12caeefc-2317-49e3-8e88-9c5a1774ce07,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"Atmospheric pressure at sea level is 760 mmHg. This pressure is generated by the collisions of all the molecules with each other and other objects. At high altitude there are fewer molecules, so fewer collisions, and hence atmospheric pressure is lower.",True,Text,,,,
a3b38537-16b8-458a-8ce5-edc3b14da838,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"Now looking at the composition of our atmosphere we know that 79 percent is nitrogen, 20.9 percent is oxygen, and some trace gases collectively get us to 100 percent. Now let us calculate a partial pressure. If 79 percent of the atmosphere is nitrogen, then 79 percent of our atmospheric pressure is generated by the collisions by nitrogen molecules. Likewise 20.9 percent of the atmospheric pressure is due to oxygen, so to calculate the partial pressure of oxygen (PO2) we simply multiply atmospheric pressure (PB) by the percentage of oxygen, which means our atmosphere has a partial pressure of oxygen of 159 mmHg.",True,Text,,,,
48fe785c-b955-433b-a70c-b84d915e5492,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,PO2=%O2×PB,False,PO2=%O2×PB,,,,
59162568-9b32-4a87-8548-5aac890e4c1b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,P,False,P,,,,
359ac4ac-ee1c-474a-8180-c810545a434c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,O2,False,O2,,,,
a5771006-7697-4e04-8f1b-5b1412ad6b4c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,O,False,O,,,,
3f0236bf-7046-4bd5-a6c2-2d1d0edaae83,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,2,False,2,,,,
d41ec597-5b7f-4dab-8481-1b71392f3ccd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,=,False,=,,,,
c95de27a-8725-41a6-9db3-d9633da87918,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,%,False,%,,,,
70bfbbea-8b2a-4712-b05c-53fed0d55f20,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,×,False,×,,,,
866db574-8f18-45ed-ad13-07a8b4b11a1b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,PB,False,PB,,,,
b9423d58-979f-46a7-a52f-67669153a79b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,B,False,B,,,,
5d2625dd-c00f-406e-89b7-bf17e3d042c0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,PO2=20.9%×760mmHg=159mmHg,True,B,,,,
7e8e8e0e-3038-405c-8d7a-fd9238de44aa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,20.9,True,B,,,,
b7b6f978-d495-447b-89ef-b1584dc24372,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,760,False,760,,,,
26cfe24b-d655-4563-b5d2-92e471330984,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,m,False,m,,,,
99fb25e6-ea80-411d-a4b5-a00241aa6219,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,H,False,H,,,,
025a69ee-d4ce-431b-a9f1-928751875baf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,g,False,g,,,,
b3513d85-bf88-44a8-805f-e8f5149332ef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,159,False,159,,,,
f352d387-3b02-48a5-9f51-c42bfcb87fac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,Alveolar PO2,False,Alveolar PO2,,,,
41496e40-b5ca-42f0-8e66-29888f54d53a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"Although related, we are more interested in the PO2 at the gas exchange surface—that is the alveolar PO2 denoted as PAO2 (note the uppercase A; lowercase refers to arterial PO2 (i.e., PaO2)). This value differs significantly from atmospheric PO2 at about 100 mmHg. So why the drop of nearly 60 mmHg from atmospheric PO2?",True,Alveolar PO2,,,,
234ce049-bc40-4f90-b4dd-e2f1c099d03a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,PAO2,False,PAO2,,,,
23913847-059e-4010-a9b7-3277de4c5eeb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,PaO2,False,PaO2,,,,
afb41197-e37c-4ba4-b9ee-c104cf2fbb9c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"To calculate alveolar PO2 we need to account for the water vapor that is added to the inspired air as it enters the airways. This is equivalent to adding another gas and must be accounted for. Water vapor exerts a pressure of 47 mmHg. Subtracting this from our atmospheric pressure, our total gaseous pressure is 713 mmHg; multiplying this by our fraction of inspired O2 (FiO2 is merely the percentage (fraction) of oxygen inspired), we see our alveolar PO2 is theoretically 149.7 mmHg (i.e., ~150 mmHg).",True,PaO2,,,,
6d230db9-4930-441f-9960-207a1a09b267,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,PAO2=FiO2×(PB−PH2O),False,PAO2=FiO2×(PB−PH2O),,,,
81faf230-43de-4731-b918-98aaaeeecb16,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,PA,False,PA,,,,
aa5aa1c4-c729-4a7c-b40d-d92cc835e873,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,A,False,A,,,,
6637137b-1999-48b4-967f-4d1f7a57033f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,F,False,F,,,,
a66c50ec-0627-457d-b983-85fd14208bac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,i,False,i,,,,
ccf387fa-3d07-4e9e-b758-02cc07247892,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,(,False,(,,,,
c738fe50-7c67-4917-b4b0-3d71508ecd01,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,−,False,−,,,,
6b6fd9e2-1f36-41ae-80ef-98afc84ad617,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,PH2O,False,PH2O,,,,
23609fa4-06e2-40ed-8e0e-0637e53ae44f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,H2O,False,H2O,,,,
6f52bec1-f321-4db6-a3c4-322aeb4443dc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,H2,False,H2,,,,
b4e6da73-d152-4391-979f-4d8503501a26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,),False,),,,,
5ebd5f2f-5746-4bbc-a036-3921e85c3205,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,PAO2=20.9%×(760−47)=149.7mmHgor∼150mmHg,True,),,,,
05035079-75dc-4eb0-bab5-6949ec4ca963,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,47,False,47,,,,
2417ccf9-6f8c-41eb-8afa-8fd9f8f8b13b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,149.7,True,47,,,,
f4d270bc-c20b-4757-8b99-48d257702768,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,o,False,o,,,,
e149b8e9-51b4-4a26-b258-eecdfaa5b603,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,r,False,r,,,,
0b7274fc-3cb8-4a6e-b117-8b9e3ad5f694,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,∼,False,∼,,,,
767a34a3-77f3-4408-94e4-41e06e76eca8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,150,False,150,,,,
13a434a2-a210-4515-b491-79328c81f946,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"If we understand that there will be mixing with air remaining from the previous breath, the real PAO2 is 100 mmHg (however, we will see this varies across the regions of the lung).",True,150,,,,
6b3e61de-17f8-43e8-b4b5-29cd036e4437,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"So how does this value relate to gas exchange in the lung? The venous blood PO2 (PVO2), returning from the systemic tissue where oxygen has been consumed, is 40 mmHg (see figure 7.1). This blood passes the gas exchange surface, and a pressure gradient of 60 mmHg allows oxygen to move into the pulmonary blood. By the time the blood has passed the alveolus, arterial PO2 will have equilibrated with the alveolar PO2 and will also be 100 mmHg. These numbers are well worth committing to memory.",True,150,Figure 7.1,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.1.png,Figure 7.1: Oxygen tensions around the alveolus.
6b3e61de-17f8-43e8-b4b5-29cd036e4437,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"So how does this value relate to gas exchange in the lung? The venous blood PO2 (PVO2), returning from the systemic tissue where oxygen has been consumed, is 40 mmHg (see figure 7.1). This blood passes the gas exchange surface, and a pressure gradient of 60 mmHg allows oxygen to move into the pulmonary blood. By the time the blood has passed the alveolus, arterial PO2 will have equilibrated with the alveolar PO2 and will also be 100 mmHg. These numbers are well worth committing to memory.",True,150,Figure 7.1,Partial Pressures,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.1.png,Figure 7.1: Oxygen tensions around the alveolus.
6b3e61de-17f8-43e8-b4b5-29cd036e4437,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"So how does this value relate to gas exchange in the lung? The venous blood PO2 (PVO2), returning from the systemic tissue where oxygen has been consumed, is 40 mmHg (see figure 7.1). This blood passes the gas exchange surface, and a pressure gradient of 60 mmHg allows oxygen to move into the pulmonary blood. By the time the blood has passed the alveolus, arterial PO2 will have equilibrated with the alveolar PO2 and will also be 100 mmHg. These numbers are well worth committing to memory.",True,150,Figure 7.1,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.1.png,Figure 7.1: Oxygen tensions around the alveolus.
9b5a9e33-e9cf-4f6c-815c-91e89cccdb1f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"The other critical values we need to address here are the partial pressures of CO2 (see figure 7.2). Venous blood returning from the tissue has a PCO2 of 45 mmHg, compared to alveolar PCO2 that is 40 mmHg. This pressure gradient of 5 mmHg is enough to allow blood to equilibrate with the alveolus, and so arterial PCO2 is 40 mmHg. Again, these numbers are worth remembering.",True,150,Figure 7.2,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.2.png,Figure 7.2: Carbon dioxide tensions around the alveolus.
9b5a9e33-e9cf-4f6c-815c-91e89cccdb1f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"The other critical values we need to address here are the partial pressures of CO2 (see figure 7.2). Venous blood returning from the tissue has a PCO2 of 45 mmHg, compared to alveolar PCO2 that is 40 mmHg. This pressure gradient of 5 mmHg is enough to allow blood to equilibrate with the alveolus, and so arterial PCO2 is 40 mmHg. Again, these numbers are worth remembering.",True,150,Figure 7.2,Partial Pressures,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.2.png,Figure 7.2: Carbon dioxide tensions around the alveolus.
9b5a9e33-e9cf-4f6c-815c-91e89cccdb1f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"The other critical values we need to address here are the partial pressures of CO2 (see figure 7.2). Venous blood returning from the tissue has a PCO2 of 45 mmHg, compared to alveolar PCO2 that is 40 mmHg. This pressure gradient of 5 mmHg is enough to allow blood to equilibrate with the alveolus, and so arterial PCO2 is 40 mmHg. Again, these numbers are worth remembering.",True,150,Figure 7.2,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.2.png,Figure 7.2: Carbon dioxide tensions around the alveolus.
192ef0bd-449f-425b-b717-b96acdce47b9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"A much smaller diffusion gradient is needed for CO2 because CO2 is much more soluble than oxygen, a factor among others that is included in Fick’s law of diffusion.",True,150,,,,
6f561b6e-efc4-4a11-a160-59c363b26aac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,Fick’s Law of Diffusion,False,Fick’s Law of Diffusion,,,,
a74b9d3e-820d-43c3-be3e-368f9e259b38,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"Fick’s law of diffusion (equation 7.1) describes all the factors that influence the transfer of gas (or flow, V) across a membrane.",True,Fick’s Law of Diffusion,,,,
869865df-24ed-4e92-9c31-6f6c850f3f32,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,Equation 7.1,True,Fick’s Law of Diffusion,,,,
cb429ac2-db0e-461d-b93f-213e8e95927a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,˙V∝AT×D×(P1−P2),False,˙V∝AT×D×(P1−P2),,,,
9f007119-c1a4-4001-87ff-0d7a96c0876a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,˙V,False,˙V,,,,
78c02930-37c0-4828-aa08-fe036c834421,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,˙,False,˙,,,,
7aa035a6-46ce-4152-81d4-86b5a473b897,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,V,False,V,,,,
75a275df-9c83-4afb-b129-0fa9ad120ae9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,∝,False,∝,,,,
798f6751-7259-4b2b-a858-35f9a7424d51,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,AT×D×(P1−P2),False,AT×D×(P1−P2),,,,
33d28c0e-fd91-479d-bbe3-6052b9bbadd3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,AT,False,AT,,,,
0473650f-d822-402e-9b0a-af9ea3f7105a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,T,False,T,,,,
26be4c31-5857-43af-9c72-c5aa7f99044a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,D,False,D,,,,
9acd842f-e629-4b27-9a51-de3b747e66d4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,P1,False,P1,,,,
70aeda87-1936-4cee-8861-b08178e751a0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,1,False,1,,,,
bed5346d-0722-411d-8ef0-5168840dc12e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,P2,False,P2,,,,
a61fe5fe-bb98-4ab3-aa54-54bff822fc15,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,We will look at each factor in the equation and see how it relates to the physiology of the lung.,True,P2,,,,
57280347-ce41-454f-bb64-8237cd031f49,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"Pressure gradient (P1−P2): The higher the pressure gradient, the greater the transfer of gas, and the pressure gradient must be maintained for gas exchange to continue. The maintenance of the gradient is achieved by adequate ventilation to the alveolus to refresh the alveolar gases, and adequate perfusion to flush oxygen away from the gas exchange surface and supply more CO2. We will look at the importance of matching ventilation and perfusion in chapter 13.",True,P2,,,,
7c532ab5-cea7-4dcc-8251-12efd6f43198,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,Other factors in Fick’s law are fairly obvious and are reflected in the lung’s structure.,True,P2,,,,
b3ccaaf8-02ac-432a-8005-c6b7a420dcee,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"Surface area (A): The greater the surface area available for exchange, the greater the exchange. The lung has a surface area of 100 m2, which is more than adequate to maintain sufficient gas transfer, even during maximal exercise.",True,P2,,,,
a73efc4b-40f0-4540-b897-155f2d5be49d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"Membrane thickness (T): The thickness of the membrane that gas has to cross also determines the rate of transfer; the thinner the membrane, the more rapid the transfer. The gas exchange membrane in the lung is approximately a 0.3 um thick—and poses little opposition to gas movement.",True,P2,,,,
5d9d558f-8c21-480e-93fc-f2c0dcdbe245,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"Diffusion constant (D): The last variable is the diffusion constant of the gases in question, which for us are O2 and CO2. The important issue here is that CO2 is much more soluble (x 20) than O2 and so has a much greater diffusion constant; hence it transfers across the membrane much more readily and does not need the large pressure gradient like the relatively insoluble oxygen (5 mmHg compared with 60 mmHg).",True,P2,,,,
abfc8357-bba4-4048-a0d7-4110c0118227,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"Some of these factors can change in lung disease and can result in decreased gas exchange and so result in deranged blood gases. Loss of surface area occurs in diseases, such as emphysema, that destroy the lung architecture, and cause a loss of gas transfer. Likewise, any disease that causes thickening of the alveolar membrane, such as pulmonary fibrosis, increases the distance for, and resistance to, gas transfer. If ventilation or perfusion of the gas exchange surface fails—for example, a mucus plug blocking an airway or a pulmonary embolus blocking a vessel—then the pressure gradient across the membrane is lost and gas exchange is reduced compared to the ideal situation of ventilation and perfusion being matched.",True,P2,,,,
26c1d409-cd49-4592-844f-b68bd277d82d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,Summary,False,Summary,,,,
1b838367-6562-4751-a97a-4319c9cf33e1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,After this chapter you should be able to calculate the alveolar partial pressure of a gas at any atmospheric pressure and relate it to the rate of gas exchange.,True,Summary,,,,
5245e1bb-6440-4c20-aa14-6719158d210d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,You should also now understand the different factors that contribute to the rate of gas exchange described in Fick’s law of diffusion and be able to appreciate how they might change in disease.,True,Summary,,,,
88753da5-f7d6-453b-9c40-26e24993f1d4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,Text,False,Text,,,,
3709dabe-d860-4439-a1e3-f1bd0086fbe6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"Levitsky, Michael G. “Chapter 6: Diffusion of Gases and Interpretation of Pulmonary Function Tests.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
82a2ca2b-33e5-4359-9b38-8b7a5d6c195b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"West, John B. “Chapter 3: Diffusion—How Gas Gets Across the Blood–Gas Barrier.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
26061fca-b7a0-4d0f-bd97-1e051f8fb1d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Partial Pressures,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/#chapter-39-section-1,"Widdicombe, John G., and Andrew S. Davis. “Chapter 4.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
c4a43396-0776-49e3-9b9b-2c9680b19de5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"Before we do that though, we need to be able to calculate the units of measurement we use when describing gas exchange. When referring to gas exchange we are really referring to diffusion of gases down their concentration gradient, but rather than use concentrations, we use partial pressures.",True,Text,,,,
d4e16bce-c3f2-497d-88ca-cc3f9c789f37,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,Partial pressures describe what proportion of the total pressure is exerted by a particular component of a mixed gas. Let us look at the specific situation we are interested in to illustrate this description.,True,Text,,,,
f7a2ca21-06f2-45ed-b084-a0bd65c038c2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"Atmospheric pressure at sea level is 760 mmHg. This pressure is generated by the collisions of all the molecules with each other and other objects. At high altitude there are fewer molecules, so fewer collisions, and hence atmospheric pressure is lower.",True,Text,,,,
fe518da5-0b50-4a8c-a70a-48f5bce6c3e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"Now looking at the composition of our atmosphere we know that 79 percent is nitrogen, 20.9 percent is oxygen, and some trace gases collectively get us to 100 percent. Now let us calculate a partial pressure. If 79 percent of the atmosphere is nitrogen, then 79 percent of our atmospheric pressure is generated by the collisions by nitrogen molecules. Likewise 20.9 percent of the atmospheric pressure is due to oxygen, so to calculate the partial pressure of oxygen (PO2) we simply multiply atmospheric pressure (PB) by the percentage of oxygen, which means our atmosphere has a partial pressure of oxygen of 159 mmHg.",True,Text,,,,
e1e020ac-1665-4abc-b0d2-52d347b2f60a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,[latex]PO_2 = \%O_2 \times P_B[/latex],False,[latex]PO_2 = \%O_2 \times P_B[/latex],,,,
7e9ad266-8e9d-476c-86bb-96deb8836183,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,[latex]PO_2 = 20.9\% \times 760\:mmHg = 159\:mmHg[/latex],True,[latex]PO_2 = \%O_2 \times P_B[/latex],,,,
b57ca97e-2506-4517-ac41-88d9d268429b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,Alveolar PO2,False,Alveolar PO2,,,,
a7013972-f56f-40c5-a06e-e44c80c27afa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"Although related, we are more interested in the PO2 at the gas exchange surface—that is the alveolar PO2 denoted as PAO2 (note the uppercase A; lowercase refers to arterial PO2 (i.e., PaO2)). This value differs significantly from atmospheric PO2 at about 100 mmHg. So why the drop of nearly 60 mmHg from atmospheric PO2?",True,Alveolar PO2,,,,
5a371f14-5dee-4eba-bda7-1781f002f264,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,PAO2,False,PAO2,,,,
d1a9b6e1-83fa-49dc-bde3-56ccb0cb73a5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,PaO2,False,PaO2,,,,
58a00f32-0bad-4fb5-ba85-1fbb02c11875,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"To calculate alveolar PO2 we need to account for the water vapor that is added to the inspired air as it enters the airways. This is equivalent to adding another gas and must be accounted for. Water vapor exerts a pressure of 47 mmHg. Subtracting this from our atmospheric pressure, our total gaseous pressure is 713 mmHg; multiplying this by our fraction of inspired O2 (FiO2 is merely the percentage (fraction) of oxygen inspired), we see our alveolar PO2 is theoretically 149.7 mmHg (i.e., ~150 mmHg).",True,PaO2,,,,
5135ede8-3b2c-4cd3-acca-be11ab36f5d1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],False,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],,,,
e3a6caae-b346-450f-9ff7-31f41e2339a8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,[latex]P_AO_2 = 20.9\% \times (760 - 47) = 149.7\:mmHg\:or \sim 150\:mmHg[/latex],True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],,,,
4d9ea52b-b0db-4573-a571-e9edeaa1c276,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"If we understand that there will be mixing with air remaining from the previous breath, the real PAO2 is 100 mmHg (however, we will see this varies across the regions of the lung).",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],,,,
c453bc6f-4b9f-4f49-8dbf-609194d047e3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"So how does this value relate to gas exchange in the lung? The venous blood PO2 (PVO2), returning from the systemic tissue where oxygen has been consumed, is 40 mmHg (see figure 7.1). This blood passes the gas exchange surface, and a pressure gradient of 60 mmHg allows oxygen to move into the pulmonary blood. By the time the blood has passed the alveolus, arterial PO2 will have equilibrated with the alveolar PO2 and will also be 100 mmHg. These numbers are well worth committing to memory.",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],Figure 7.1,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.1.png,Figure 7.1: Oxygen tensions around the alveolus.
c453bc6f-4b9f-4f49-8dbf-609194d047e3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"So how does this value relate to gas exchange in the lung? The venous blood PO2 (PVO2), returning from the systemic tissue where oxygen has been consumed, is 40 mmHg (see figure 7.1). This blood passes the gas exchange surface, and a pressure gradient of 60 mmHg allows oxygen to move into the pulmonary blood. By the time the blood has passed the alveolus, arterial PO2 will have equilibrated with the alveolar PO2 and will also be 100 mmHg. These numbers are well worth committing to memory.",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],Figure 7.1,Partial Pressures,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.1.png,Figure 7.1: Oxygen tensions around the alveolus.
c453bc6f-4b9f-4f49-8dbf-609194d047e3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"So how does this value relate to gas exchange in the lung? The venous blood PO2 (PVO2), returning from the systemic tissue where oxygen has been consumed, is 40 mmHg (see figure 7.1). This blood passes the gas exchange surface, and a pressure gradient of 60 mmHg allows oxygen to move into the pulmonary blood. By the time the blood has passed the alveolus, arterial PO2 will have equilibrated with the alveolar PO2 and will also be 100 mmHg. These numbers are well worth committing to memory.",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],Figure 7.1,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.1.png,Figure 7.1: Oxygen tensions around the alveolus.
ecc6bf78-8012-439a-a4a6-6fbf62a6d0d4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"The other critical values we need to address here are the partial pressures of CO2 (see figure 7.2). Venous blood returning from the tissue has a PCO2 of 45 mmHg, compared to alveolar PCO2 that is 40 mmHg. This pressure gradient of 5 mmHg is enough to allow blood to equilibrate with the alveolus, and so arterial PCO2 is 40 mmHg. Again, these numbers are worth remembering.",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],Figure 7.2,Fick’s Law of Diffusion,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.2.png,Figure 7.2: Carbon dioxide tensions around the alveolus.
ecc6bf78-8012-439a-a4a6-6fbf62a6d0d4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"The other critical values we need to address here are the partial pressures of CO2 (see figure 7.2). Venous blood returning from the tissue has a PCO2 of 45 mmHg, compared to alveolar PCO2 that is 40 mmHg. This pressure gradient of 5 mmHg is enough to allow blood to equilibrate with the alveolus, and so arterial PCO2 is 40 mmHg. Again, these numbers are worth remembering.",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],Figure 7.2,Partial Pressures,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.2.png,Figure 7.2: Carbon dioxide tensions around the alveolus.
ecc6bf78-8012-439a-a4a6-6fbf62a6d0d4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"The other critical values we need to address here are the partial pressures of CO2 (see figure 7.2). Venous blood returning from the tissue has a PCO2 of 45 mmHg, compared to alveolar PCO2 that is 40 mmHg. This pressure gradient of 5 mmHg is enough to allow blood to equilibrate with the alveolus, and so arterial PCO2 is 40 mmHg. Again, these numbers are worth remembering.",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],Figure 7.2,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/7.2.png,Figure 7.2: Carbon dioxide tensions around the alveolus.
2e8bef32-5d9d-4ac7-94d8-50d0cdf9e44b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"A much smaller diffusion gradient is needed for CO2 because CO2 is much more soluble than oxygen, a factor among others that is included in Fick’s law of diffusion.",True,[latex]P_AO_2 = FiO_2 \times (P_B - P_{H_2O})[/latex],,,,
bcbe3471-ecb5-41ee-b710-0b53cc5b1b27,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,Fick’s Law of Diffusion,False,Fick’s Law of Diffusion,,,,
6ca2db56-0d97-4f73-8ba5-274be853735b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"Fick’s law of diffusion (equation 7.1) describes all the factors that influence the transfer of gas (or flow, V) across a membrane.",True,Fick’s Law of Diffusion,,,,
37c337ea-46f5-4667-a26e-d73c1035cb65,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,Equation 7.1,True,Fick’s Law of Diffusion,,,,
70632314-1d33-4b05-a52f-532946b7792f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],False,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
abd7b26c-69d5-4292-8995-5953dd5266b9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,We will look at each factor in the equation and see how it relates to the physiology of the lung.,True,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
772b7fa0-4937-4566-9407-2c0356b09b79,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"Pressure gradient (P1−P2): The higher the pressure gradient, the greater the transfer of gas, and the pressure gradient must be maintained for gas exchange to continue. The maintenance of the gradient is achieved by adequate ventilation to the alveolus to refresh the alveolar gases, and adequate perfusion to flush oxygen away from the gas exchange surface and supply more CO2. We will look at the importance of matching ventilation and perfusion in chapter 13.",True,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
eed3d4a8-ba85-4410-b22e-972c08d719d8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,Other factors in Fick’s law are fairly obvious and are reflected in the lung’s structure.,True,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
1e6fcda9-3ec1-468e-973f-47778424f277,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"Surface area (A): The greater the surface area available for exchange, the greater the exchange. The lung has a surface area of 100 m2, which is more than adequate to maintain sufficient gas transfer, even during maximal exercise.",True,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
80984480-7e2e-49a7-a8ee-d5d33a352fea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"Membrane thickness (T): The thickness of the membrane that gas has to cross also determines the rate of transfer; the thinner the membrane, the more rapid the transfer. The gas exchange membrane in the lung is approximately a 0.3 um thick—and poses little opposition to gas movement.",True,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
70405c3d-ea88-4b1c-b9fc-fec0131b34e8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"Diffusion constant (D): The last variable is the diffusion constant of the gases in question, which for us are O2 and CO2. The important issue here is that CO2 is much more soluble (x 20) than O2 and so has a much greater diffusion constant; hence it transfers across the membrane much more readily and does not need the large pressure gradient like the relatively insoluble oxygen (5 mmHg compared with 60 mmHg).",True,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
96e58331-4e22-4b75-b94d-0b81daa9128f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"Some of these factors can change in lung disease and can result in decreased gas exchange and so result in deranged blood gases. Loss of surface area occurs in diseases, such as emphysema, that destroy the lung architecture, and cause a loss of gas transfer. Likewise, any disease that causes thickening of the alveolar membrane, such as pulmonary fibrosis, increases the distance for, and resistance to, gas transfer. If ventilation or perfusion of the gas exchange surface fails—for example, a mucus plug blocking an airway or a pulmonary embolus blocking a vessel—then the pressure gradient across the membrane is lost and gas exchange is reduced compared to the ideal situation of ventilation and perfusion being matched.",True,[latex]\dot{V} \propto \displaystyle\frac{A}{T} \times D \times (P_1 - P_2)[/latex],,,,
d7def588-03ce-4ccf-a4b9-cfd26696768a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,Summary,False,Summary,,,,
7c42f8f6-bfec-40e0-b776-7968c4408d3e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,After this chapter you should be able to calculate the alveolar partial pressure of a gas at any atmospheric pressure and relate it to the rate of gas exchange.,True,Summary,,,,
e66bec65-2da0-418e-bdf3-a08add97d45c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,You should also now understand the different factors that contribute to the rate of gas exchange described in Fick’s law of diffusion and be able to appreciate how they might change in disease.,True,Summary,,,,
ff627f60-5131-404a-b4a3-fb84c5e18927,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,Text,False,Text,,,,
8c78ee6f-c7f6-4d37-8caf-706c922522d7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"Levitsky, Michael G. “Chapter 6: Diffusion of Gases and Interpretation of Pulmonary Function Tests.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
3bdec1e9-7f6c-4599-8893-c7a274ae06bd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"West, John B. “Chapter 3: Diffusion—How Gas Gets Across the Blood–Gas Barrier.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
fc2a5ba2-b912-457c-a9af-741e1590d3ae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,7. Fundamentals of Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/fundamentals-of-gas-exchange/,"Widdicombe, John G., and Andrew S. Davis. “Chapter 4.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
e125ba2f-6da8-4e10-bea6-e132c5f31f62,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"Although this phenomenon is present in the healthy lung, we will see how it is exacerbated in certain disease states and how this exacerbation can be detected by common pulmonary function tests.",True,Text,,,,
6443f20b-c2ba-4f2a-912d-b820480b48dc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"First, let us look at the forces involved during a normal, passive expiration.",True,Text,,,,
b41f13e9-f936-4f36-a5cf-fb0da07ecd91,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"For simplicity, the schematic in figure 6.1 shows one airway and an alveolus within the thoracic cavity. At the onset of passive expiration (driven by the recoil of the expanded lung), the intrapleural pressure is negative (about −8 cm H2O). As it remains negative, intrapleural pressure helps keep the airways open.",True,Text,Figure 6.1,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.1.png,Figure 6.1: Intrapleural and airway pressures during normal/passive expiration.
b41f13e9-f936-4f36-a5cf-fb0da07ecd91,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"For simplicity, the schematic in figure 6.1 shows one airway and an alveolus within the thoracic cavity. At the onset of passive expiration (driven by the recoil of the expanded lung), the intrapleural pressure is negative (about −8 cm H2O). As it remains negative, intrapleural pressure helps keep the airways open.",True,Text,Figure 6.1,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.1.png,Figure 6.1: Intrapleural and airway pressures during normal/passive expiration.
b41f13e9-f936-4f36-a5cf-fb0da07ecd91,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"For simplicity, the schematic in figure 6.1 shows one airway and an alveolus within the thoracic cavity. At the onset of passive expiration (driven by the recoil of the expanded lung), the intrapleural pressure is negative (about −8 cm H2O). As it remains negative, intrapleural pressure helps keep the airways open.",True,Text,Figure 6.1,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.1.png,Figure 6.1: Intrapleural and airway pressures during normal/passive expiration.
97a2ec68-1d99-48b6-92c7-4173a01db3d1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,H2O,False,H2O,,,,
b2595d16-3472-4347-8652-8a5041e897ec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"The elastic forces of the alveolus wall exert an inward force of about +10 cm H2O. This results in a net force of +2 cm H2O in the alveolus, and a gradient between this positive pressure is established between the alveolus and the atmosphere outside the lung. That means that along the airway toward the mouth there is a gradient of progressively decreasing pressure to zero (shown in maroon).",True,H2O,,,,
4d8eebf9-c2a1-4fc0-af77-1f63bd8d903f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"Importantly in this example of passive expiration the airway pressure is greater than the pleural pressure along the whole length of the airway toward the mouth. Along with the radial traction provided by the surrounding parenchymal tissue, this favorable transmural pressure gradient helps keep the airway open during expiration.",True,H2O,,,,
85336abb-ae09-42b1-8f3d-90c22ce05bb5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"Now let us look at what happens if expiration is forceful, or active, rather than passively relying on lung recoil.",True,H2O,,,,
6141bd45-9a97-4ead-8439-2dddc888dac7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"In a forced expiration (see figure 6.2) the intrapleural pressure can become positive (as much as 120 cm H2O), but in this example we will say it is 25 cm H2O. This positive pressure in the pleural cavity comes from the chest wall and diaphragm now “pushing” the pleural membranes together and compressing the lung.",True,H2O,Figure 6.2,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
6141bd45-9a97-4ead-8439-2dddc888dac7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"In a forced expiration (see figure 6.2) the intrapleural pressure can become positive (as much as 120 cm H2O), but in this example we will say it is 25 cm H2O. This positive pressure in the pleural cavity comes from the chest wall and diaphragm now “pushing” the pleural membranes together and compressing the lung.",True,H2O,Figure 6.2,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
6141bd45-9a97-4ead-8439-2dddc888dac7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"In a forced expiration (see figure 6.2) the intrapleural pressure can become positive (as much as 120 cm H2O), but in this example we will say it is 25 cm H2O. This positive pressure in the pleural cavity comes from the chest wall and diaphragm now “pushing” the pleural membranes together and compressing the lung.",True,H2O,Figure 6.2,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
8b63e01d-2e8d-46d0-90ae-dad23f3025c1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"Again, we have the elastic forces of the alveolus generating an inward force (still +10 cm H2O), and when summed with the now positive intrapleural forces, we end up with an alveolar pressure of +35 cm H2O.",True,H2O,,,,
2aefa857-cbcc-430c-96cb-ba4ef825fd3d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"Again, a pressure gradient between the alveolus and the atmosphere is established (again shown in maroon), but this time there is a fundamental difference caused by the larger intrapleural pressure.",True,H2O,,,,
8da683bb-c7ee-4f58-b005-bf64671bdced,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"At some point along the airway, as airway pressure is decreasing, the intrapleural pressure exceeds airway pressure (in this example it is 25 cm H2O). At this “choke” point (arrows pointing toward airway in figure 6.2), the airway can become compressed or even collapse.",True,H2O,Figure 6.2,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
8da683bb-c7ee-4f58-b005-bf64671bdced,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"At some point along the airway, as airway pressure is decreasing, the intrapleural pressure exceeds airway pressure (in this example it is 25 cm H2O). At this “choke” point (arrows pointing toward airway in figure 6.2), the airway can become compressed or even collapse.",True,H2O,Figure 6.2,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
8da683bb-c7ee-4f58-b005-bf64671bdced,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"At some point along the airway, as airway pressure is decreasing, the intrapleural pressure exceeds airway pressure (in this example it is 25 cm H2O). At this “choke” point (arrows pointing toward airway in figure 6.2), the airway can become compressed or even collapse.",True,H2O,Figure 6.2,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
480559ff-b1ff-40db-8773-ae708a2320e6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"This effect is somewhat reduced by the radial traction of the parenchyma, but airway compression occurs even in the healthy normal lung, and the greater the effort of expiration (i.e., the more positive the intrapleural pressure), the greater degree airways compress and compression occurs closer to the alveoli (i.e., further up the pressure gradient in the airway).",True,H2O,,,,
e843288a-9a88-4e3a-b197-33a90f9c8ed9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"If airways are already narrowed, as in obstructive lung diseases such as asthma, or parenchymal traction is lost, such as in emphysema, dynamic airway compression occurs to a greater extent. In these obstructive diseases the increased airway resistance results in the patient having to forcefully expire to overcome the increased resistance of the narrowed airways. This promotes airway compression and leads to air being trapped behind the choke point, causing hyperinflation (breathing at an elevated lung volume).",True,H2O,,,,
f1570577-d8ed-42e9-afb5-85e530a4feb6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"This airway compression or any other increase in airway resistance can be demonstrated by a common pulmonary function test, the flow-volume loop.",True,H2O,,,,
58431e18-7209-4c70-8ad9-6929e9430aae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,Flow-Volume Loops,False,Flow-Volume Loops,,,,
2d0afc3b-7842-421e-810c-7315aa2dca00,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"Flow-volume loops are briefly discussed in context of the relevant physiology. Figure 6.3 shows a normal flow-volume loop. Note that the volume axis seems to be the wrong way around; this is because expired volume and flow are generally more useful, so the plot has expiratory flow as positive and lung volume orientated for expiration. While breathing on a spirometer, the patient begins to breathe in from residual volume (bottom half of maroon line). As inspiration continues, lung volume increases (moves toward the y-axis) and airflow increases (moves downward). The patient continues inhaling until they are at total lung capacity (or TLC).",True,Flow-Volume Loops,Figure 6.3,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.3.png,Figure 6.3: Typical and normal flow-volume loop. FVC: forved vital capacity.
2d0afc3b-7842-421e-810c-7315aa2dca00,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"Flow-volume loops are briefly discussed in context of the relevant physiology. Figure 6.3 shows a normal flow-volume loop. Note that the volume axis seems to be the wrong way around; this is because expired volume and flow are generally more useful, so the plot has expiratory flow as positive and lung volume orientated for expiration. While breathing on a spirometer, the patient begins to breathe in from residual volume (bottom half of maroon line). As inspiration continues, lung volume increases (moves toward the y-axis) and airflow increases (moves downward). The patient continues inhaling until they are at total lung capacity (or TLC).",True,Flow-Volume Loops,Figure 6.3,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.3.png,Figure 6.3: Typical and normal flow-volume loop. FVC: forved vital capacity.
2d0afc3b-7842-421e-810c-7315aa2dca00,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"Flow-volume loops are briefly discussed in context of the relevant physiology. Figure 6.3 shows a normal flow-volume loop. Note that the volume axis seems to be the wrong way around; this is because expired volume and flow are generally more useful, so the plot has expiratory flow as positive and lung volume orientated for expiration. While breathing on a spirometer, the patient begins to breathe in from residual volume (bottom half of maroon line). As inspiration continues, lung volume increases (moves toward the y-axis) and airflow increases (moves downward). The patient continues inhaling until they are at total lung capacity (or TLC).",True,Flow-Volume Loops,Figure 6.3,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.3.png,Figure 6.3: Typical and normal flow-volume loop. FVC: forved vital capacity.
3c648ba2-73e4-47f5-b712-da0d0aea9f7f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"They then exhale as hard and as fast as they can, forcefully emptying the lung as quickly as possible. During forced exhalation of the first liter or so, expiratory flow rapidly increases until it reaches peak expiratory flow; this is the first clinically pertinent measure. After this point expiratory flow begins an exponential decline; as lung volume continues to decrease, so does the flow rate until flow reaches zero when the lung is emptied (at residual volume).",True,Flow-Volume Loops,,,,
ef8ca426-319c-46e9-8681-ab7bb5b4aa47,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,The rate of this decline in flow rate is also an important clinical measure and brings together a couple of important physiological points:,True,Flow-Volume Loops,,,,
76b0deb9-f98e-4fd6-afdf-0e3793be0296,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"Although there are a number of measurements that are calculated from this forced exhalation, two are most commonly reported. First, the total volume that is expelled from the lung is referred to as the forced vital capacity (FVC). The forced expiratory volume that is expelled from the lung in the first second of expiration is referred to as FEV1. The ratio of these two values, known as FEV1/FVC, describes the percentage of lung volume that can be emptied in one second and is a useful indicator of airway resistance. A normal FEV1/FVC is 90 percent or higher, meaning over 90 percent of vital capacity can be emptied from the lung within a second. This value is dependent on age, gender, and body size, but commonly used predicted values take these variables into account when assessing for disease.",True,Flow-Volume Loops,,,,
af0623a0-f625-4fb4-a96a-cfe9d008d918,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,FEV1,False,FEV1,,,,
6eae07de-134e-4157-b1f9-2c21589e94f1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"The loop produced by a patient with chronic obstructive lung disease, or COPD, looks very different (gray line in figure 6.4). With disease causing airway narrowing, the peak expiratory flow is significantly reduced, and the decay in expiratory flow as lung volume declines is much more pronounced as the narrowed airways can be easier to collapse due to a lower starting radius and/or loss of radial traction.",True,FEV1,Figure 6.4,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.4.png,Figure 6.4: Normal (maroon) and obstructive disease (gray) flow-volume loops.
6eae07de-134e-4157-b1f9-2c21589e94f1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"The loop produced by a patient with chronic obstructive lung disease, or COPD, looks very different (gray line in figure 6.4). With disease causing airway narrowing, the peak expiratory flow is significantly reduced, and the decay in expiratory flow as lung volume declines is much more pronounced as the narrowed airways can be easier to collapse due to a lower starting radius and/or loss of radial traction.",True,FEV1,Figure 6.4,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.4.png,Figure 6.4: Normal (maroon) and obstructive disease (gray) flow-volume loops.
6eae07de-134e-4157-b1f9-2c21589e94f1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"The loop produced by a patient with chronic obstructive lung disease, or COPD, looks very different (gray line in figure 6.4). With disease causing airway narrowing, the peak expiratory flow is significantly reduced, and the decay in expiratory flow as lung volume declines is much more pronounced as the narrowed airways can be easier to collapse due to a lower starting radius and/or loss of radial traction.",True,FEV1,Figure 6.4,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.4.png,Figure 6.4: Normal (maroon) and obstructive disease (gray) flow-volume loops.
a9447d8a-043e-40ac-9a3d-eaf68ecb640f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"This means that FEV1 is significantly reduced, but FVC may remain unchanged (i.e., the lung volume is the same, but it takes longer to empty). An FEV1/FVC significantly less than 90 percent is indicative of obstructive disease. Notice that the inspiratory loop of the COPD patient appears normal, illustrating the effect of increasingly negative intrapleural pressure, increasing lung volume and radial traction on airway resistance.",True,FEV1,,,,
b1f7270f-a1a0-42ea-840c-1b10afdbc09d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"Alternatively, diseases that restrict lung expansion (figure 6.5), such as pulmonary fibrosis, demonstrate a reduced lung volume, where FVC is substantially reduced, but FEV1 may not be significantly affected; in fact it is not uncommon for FEV1/FVC to increase to about normal in restricted diseases, but this is of course due to a decline in FVC rather than a rise in FEV1. Notice also that the inspiratory loop is affected, with volumes being reduced here as well.",True,FEV1,Figure 6.5,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.5.png,Figure 6.5: Normal (maroon) and restrictive (gray) flow-volume loops.
b1f7270f-a1a0-42ea-840c-1b10afdbc09d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"Alternatively, diseases that restrict lung expansion (figure 6.5), such as pulmonary fibrosis, demonstrate a reduced lung volume, where FVC is substantially reduced, but FEV1 may not be significantly affected; in fact it is not uncommon for FEV1/FVC to increase to about normal in restricted diseases, but this is of course due to a decline in FVC rather than a rise in FEV1. Notice also that the inspiratory loop is affected, with volumes being reduced here as well.",True,FEV1,Figure 6.5,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.5.png,Figure 6.5: Normal (maroon) and restrictive (gray) flow-volume loops.
b1f7270f-a1a0-42ea-840c-1b10afdbc09d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"Alternatively, diseases that restrict lung expansion (figure 6.5), such as pulmonary fibrosis, demonstrate a reduced lung volume, where FVC is substantially reduced, but FEV1 may not be significantly affected; in fact it is not uncommon for FEV1/FVC to increase to about normal in restricted diseases, but this is of course due to a decline in FVC rather than a rise in FEV1. Notice also that the inspiratory loop is affected, with volumes being reduced here as well.",True,FEV1,Figure 6.5,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.5.png,Figure 6.5: Normal (maroon) and restrictive (gray) flow-volume loops.
bfae96d4-8f73-47a3-bc15-1e4a8b89fe16,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"A flow-volume loop is a quick, cheap, and powerful diagnostic measure, but it is highly dependent on the patient performing a forced expiration to encourage dynamic compression and peak flows be obtained so that any airway abnormalities can be seen. This is why you may hear a pulmonary function technologist (PFT) shouting encouragement to a patient as you walk past the lab.",True,FEV1,,,,
a52d6803-01b7-43ed-87a6-81083de9bad7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,Summary,False,Summary,,,,
c2a28e29-e429-433c-aa9c-20fdfa1e6ad4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"So we have dealt with a couple of relatively complex issues in this chapter, particularly the interaction between intrapleural pressure and airway pressure during forced or active expirations and how airways can become compressed.",True,Summary,,,,
b1f3896b-28a3-48a5-a578-79d067745772,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,We have also looked at the use of flow-volume loops to determine the degree of airway obstruction and to distinguish between obstructive and restrictive disorders.,True,Summary,,,,
3d579548-1fbb-4119-a8bd-6a18a2ce12f9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,Text,False,Text,,,,
65586ba3-7ec6-4943-b392-b8410642bee9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"Levitsky, Michael G. “Chapter 3: Alveolar Ventilation.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
e3fd9346-74ee-4550-ac3d-c10b889a9616,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
f3d82c09-4fa4-4232-b7c2-ca82c3f0e4d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow-Volume Loops,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-2,"Widdicombe, John G., and Andrew S. Davis. “Chapter 3.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
867b1bdf-336f-41aa-a69a-3c7e6e0fcd96,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"Although this phenomenon is present in the healthy lung, we will see how it is exacerbated in certain disease states and how this exacerbation can be detected by common pulmonary function tests.",True,Text,,,,
c6991c68-1914-4f95-a439-0e29351df771,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"First, let us look at the forces involved during a normal, passive expiration.",True,Text,,,,
c2594d74-fb26-48ba-9ea5-49396c44c6af,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"For simplicity, the schematic in figure 6.1 shows one airway and an alveolus within the thoracic cavity. At the onset of passive expiration (driven by the recoil of the expanded lung), the intrapleural pressure is negative (about −8 cm H2O). As it remains negative, intrapleural pressure helps keep the airways open.",True,Text,Figure 6.1,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.1.png,Figure 6.1: Intrapleural and airway pressures during normal/passive expiration.
c2594d74-fb26-48ba-9ea5-49396c44c6af,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"For simplicity, the schematic in figure 6.1 shows one airway and an alveolus within the thoracic cavity. At the onset of passive expiration (driven by the recoil of the expanded lung), the intrapleural pressure is negative (about −8 cm H2O). As it remains negative, intrapleural pressure helps keep the airways open.",True,Text,Figure 6.1,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.1.png,Figure 6.1: Intrapleural and airway pressures during normal/passive expiration.
c2594d74-fb26-48ba-9ea5-49396c44c6af,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"For simplicity, the schematic in figure 6.1 shows one airway and an alveolus within the thoracic cavity. At the onset of passive expiration (driven by the recoil of the expanded lung), the intrapleural pressure is negative (about −8 cm H2O). As it remains negative, intrapleural pressure helps keep the airways open.",True,Text,Figure 6.1,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.1.png,Figure 6.1: Intrapleural and airway pressures during normal/passive expiration.
eb937abb-7093-45ba-a227-37acd3e37a72,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,H2O,False,H2O,,,,
13749366-078e-4538-8589-a426ebd410e4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"The elastic forces of the alveolus wall exert an inward force of about +10 cm H2O. This results in a net force of +2 cm H2O in the alveolus, and a gradient between this positive pressure is established between the alveolus and the atmosphere outside the lung. That means that along the airway toward the mouth there is a gradient of progressively decreasing pressure to zero (shown in maroon).",True,H2O,,,,
f573d71d-a7b8-4a54-9335-a5369308871d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"Importantly in this example of passive expiration the airway pressure is greater than the pleural pressure along the whole length of the airway toward the mouth. Along with the radial traction provided by the surrounding parenchymal tissue, this favorable transmural pressure gradient helps keep the airway open during expiration.",True,H2O,,,,
500928e4-5c74-4645-9ac1-5d3b5892b3db,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"Now let us look at what happens if expiration is forceful, or active, rather than passively relying on lung recoil.",True,H2O,,,,
ea13da32-1c95-4ab1-abac-428a24e45bf5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"In a forced expiration (see figure 6.2) the intrapleural pressure can become positive (as much as 120 cm H2O), but in this example we will say it is 25 cm H2O. This positive pressure in the pleural cavity comes from the chest wall and diaphragm now “pushing” the pleural membranes together and compressing the lung.",True,H2O,Figure 6.2,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
ea13da32-1c95-4ab1-abac-428a24e45bf5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"In a forced expiration (see figure 6.2) the intrapleural pressure can become positive (as much as 120 cm H2O), but in this example we will say it is 25 cm H2O. This positive pressure in the pleural cavity comes from the chest wall and diaphragm now “pushing” the pleural membranes together and compressing the lung.",True,H2O,Figure 6.2,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
ea13da32-1c95-4ab1-abac-428a24e45bf5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"In a forced expiration (see figure 6.2) the intrapleural pressure can become positive (as much as 120 cm H2O), but in this example we will say it is 25 cm H2O. This positive pressure in the pleural cavity comes from the chest wall and diaphragm now “pushing” the pleural membranes together and compressing the lung.",True,H2O,Figure 6.2,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
abfe9635-f549-4101-85e4-abac628e210b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"Again, we have the elastic forces of the alveolus generating an inward force (still +10 cm H2O), and when summed with the now positive intrapleural forces, we end up with an alveolar pressure of +35 cm H2O.",True,H2O,,,,
21f2341e-300a-4f10-8068-ff2d33993f85,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"Again, a pressure gradient between the alveolus and the atmosphere is established (again shown in maroon), but this time there is a fundamental difference caused by the larger intrapleural pressure.",True,H2O,,,,
8a3412a2-b09e-436a-9247-a91132fa6af8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"At some point along the airway, as airway pressure is decreasing, the intrapleural pressure exceeds airway pressure (in this example it is 25 cm H2O). At this “choke” point (arrows pointing toward airway in figure 6.2), the airway can become compressed or even collapse.",True,H2O,Figure 6.2,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
8a3412a2-b09e-436a-9247-a91132fa6af8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"At some point along the airway, as airway pressure is decreasing, the intrapleural pressure exceeds airway pressure (in this example it is 25 cm H2O). At this “choke” point (arrows pointing toward airway in figure 6.2), the airway can become compressed or even collapse.",True,H2O,Figure 6.2,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
8a3412a2-b09e-436a-9247-a91132fa6af8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"At some point along the airway, as airway pressure is decreasing, the intrapleural pressure exceeds airway pressure (in this example it is 25 cm H2O). At this “choke” point (arrows pointing toward airway in figure 6.2), the airway can become compressed or even collapse.",True,H2O,Figure 6.2,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
9ebe7174-d4fd-46e7-8e26-a825ad78cffb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"This effect is somewhat reduced by the radial traction of the parenchyma, but airway compression occurs even in the healthy normal lung, and the greater the effort of expiration (i.e., the more positive the intrapleural pressure), the greater degree airways compress and compression occurs closer to the alveoli (i.e., further up the pressure gradient in the airway).",True,H2O,,,,
802c0d49-f5fa-483a-9271-5c97b635adc5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"If airways are already narrowed, as in obstructive lung diseases such as asthma, or parenchymal traction is lost, such as in emphysema, dynamic airway compression occurs to a greater extent. In these obstructive diseases the increased airway resistance results in the patient having to forcefully expire to overcome the increased resistance of the narrowed airways. This promotes airway compression and leads to air being trapped behind the choke point, causing hyperinflation (breathing at an elevated lung volume).",True,H2O,,,,
e5dfb7e6-0a6d-49fc-9334-55e84a558b0b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"This airway compression or any other increase in airway resistance can be demonstrated by a common pulmonary function test, the flow-volume loop.",True,H2O,,,,
9b527069-c9ee-4224-9e88-507941f59dcd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,Flow-Volume Loops,False,Flow-Volume Loops,,,,
739382bf-7aa6-4777-b972-ea8e528ff645,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"Flow-volume loops are briefly discussed in context of the relevant physiology. Figure 6.3 shows a normal flow-volume loop. Note that the volume axis seems to be the wrong way around; this is because expired volume and flow are generally more useful, so the plot has expiratory flow as positive and lung volume orientated for expiration. While breathing on a spirometer, the patient begins to breathe in from residual volume (bottom half of maroon line). As inspiration continues, lung volume increases (moves toward the y-axis) and airflow increases (moves downward). The patient continues inhaling until they are at total lung capacity (or TLC).",True,Flow-Volume Loops,Figure 6.3,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.3.png,Figure 6.3: Typical and normal flow-volume loop. FVC: forved vital capacity.
739382bf-7aa6-4777-b972-ea8e528ff645,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"Flow-volume loops are briefly discussed in context of the relevant physiology. Figure 6.3 shows a normal flow-volume loop. Note that the volume axis seems to be the wrong way around; this is because expired volume and flow are generally more useful, so the plot has expiratory flow as positive and lung volume orientated for expiration. While breathing on a spirometer, the patient begins to breathe in from residual volume (bottom half of maroon line). As inspiration continues, lung volume increases (moves toward the y-axis) and airflow increases (moves downward). The patient continues inhaling until they are at total lung capacity (or TLC).",True,Flow-Volume Loops,Figure 6.3,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.3.png,Figure 6.3: Typical and normal flow-volume loop. FVC: forved vital capacity.
739382bf-7aa6-4777-b972-ea8e528ff645,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"Flow-volume loops are briefly discussed in context of the relevant physiology. Figure 6.3 shows a normal flow-volume loop. Note that the volume axis seems to be the wrong way around; this is because expired volume and flow are generally more useful, so the plot has expiratory flow as positive and lung volume orientated for expiration. While breathing on a spirometer, the patient begins to breathe in from residual volume (bottom half of maroon line). As inspiration continues, lung volume increases (moves toward the y-axis) and airflow increases (moves downward). The patient continues inhaling until they are at total lung capacity (or TLC).",True,Flow-Volume Loops,Figure 6.3,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.3.png,Figure 6.3: Typical and normal flow-volume loop. FVC: forved vital capacity.
bf70edcc-1f38-49c5-83a8-494ceba8eee4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"They then exhale as hard and as fast as they can, forcefully emptying the lung as quickly as possible. During forced exhalation of the first liter or so, expiratory flow rapidly increases until it reaches peak expiratory flow; this is the first clinically pertinent measure. After this point expiratory flow begins an exponential decline; as lung volume continues to decrease, so does the flow rate until flow reaches zero when the lung is emptied (at residual volume).",True,Flow-Volume Loops,,,,
3c277b2b-b98b-45d9-8f94-93c6ccf41cdf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,The rate of this decline in flow rate is also an important clinical measure and brings together a couple of important physiological points:,True,Flow-Volume Loops,,,,
cc35a0d6-04fd-41ba-959d-c2ae707ea3eb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"Although there are a number of measurements that are calculated from this forced exhalation, two are most commonly reported. First, the total volume that is expelled from the lung is referred to as the forced vital capacity (FVC). The forced expiratory volume that is expelled from the lung in the first second of expiration is referred to as FEV1. The ratio of these two values, known as FEV1/FVC, describes the percentage of lung volume that can be emptied in one second and is a useful indicator of airway resistance. A normal FEV1/FVC is 90 percent or higher, meaning over 90 percent of vital capacity can be emptied from the lung within a second. This value is dependent on age, gender, and body size, but commonly used predicted values take these variables into account when assessing for disease.",True,Flow-Volume Loops,,,,
fc29de00-c61c-458b-b66e-53a9b9a7067d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,FEV1,False,FEV1,,,,
54839cdc-fbfe-440d-b513-ebfdc37e9850,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"The loop produced by a patient with chronic obstructive lung disease, or COPD, looks very different (gray line in figure 6.4). With disease causing airway narrowing, the peak expiratory flow is significantly reduced, and the decay in expiratory flow as lung volume declines is much more pronounced as the narrowed airways can be easier to collapse due to a lower starting radius and/or loss of radial traction.",True,FEV1,Figure 6.4,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.4.png,Figure 6.4: Normal (maroon) and obstructive disease (gray) flow-volume loops.
54839cdc-fbfe-440d-b513-ebfdc37e9850,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"The loop produced by a patient with chronic obstructive lung disease, or COPD, looks very different (gray line in figure 6.4). With disease causing airway narrowing, the peak expiratory flow is significantly reduced, and the decay in expiratory flow as lung volume declines is much more pronounced as the narrowed airways can be easier to collapse due to a lower starting radius and/or loss of radial traction.",True,FEV1,Figure 6.4,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.4.png,Figure 6.4: Normal (maroon) and obstructive disease (gray) flow-volume loops.
54839cdc-fbfe-440d-b513-ebfdc37e9850,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"The loop produced by a patient with chronic obstructive lung disease, or COPD, looks very different (gray line in figure 6.4). With disease causing airway narrowing, the peak expiratory flow is significantly reduced, and the decay in expiratory flow as lung volume declines is much more pronounced as the narrowed airways can be easier to collapse due to a lower starting radius and/or loss of radial traction.",True,FEV1,Figure 6.4,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.4.png,Figure 6.4: Normal (maroon) and obstructive disease (gray) flow-volume loops.
b3fc9aad-2f86-4713-bda4-954f3a22a40d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"This means that FEV1 is significantly reduced, but FVC may remain unchanged (i.e., the lung volume is the same, but it takes longer to empty). An FEV1/FVC significantly less than 90 percent is indicative of obstructive disease. Notice that the inspiratory loop of the COPD patient appears normal, illustrating the effect of increasingly negative intrapleural pressure, increasing lung volume and radial traction on airway resistance.",True,FEV1,,,,
c9c5217a-74ea-4873-b118-2a9a1c9e007c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"Alternatively, diseases that restrict lung expansion (figure 6.5), such as pulmonary fibrosis, demonstrate a reduced lung volume, where FVC is substantially reduced, but FEV1 may not be significantly affected; in fact it is not uncommon for FEV1/FVC to increase to about normal in restricted diseases, but this is of course due to a decline in FVC rather than a rise in FEV1. Notice also that the inspiratory loop is affected, with volumes being reduced here as well.",True,FEV1,Figure 6.5,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.5.png,Figure 6.5: Normal (maroon) and restrictive (gray) flow-volume loops.
c9c5217a-74ea-4873-b118-2a9a1c9e007c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"Alternatively, diseases that restrict lung expansion (figure 6.5), such as pulmonary fibrosis, demonstrate a reduced lung volume, where FVC is substantially reduced, but FEV1 may not be significantly affected; in fact it is not uncommon for FEV1/FVC to increase to about normal in restricted diseases, but this is of course due to a decline in FVC rather than a rise in FEV1. Notice also that the inspiratory loop is affected, with volumes being reduced here as well.",True,FEV1,Figure 6.5,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.5.png,Figure 6.5: Normal (maroon) and restrictive (gray) flow-volume loops.
c9c5217a-74ea-4873-b118-2a9a1c9e007c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"Alternatively, diseases that restrict lung expansion (figure 6.5), such as pulmonary fibrosis, demonstrate a reduced lung volume, where FVC is substantially reduced, but FEV1 may not be significantly affected; in fact it is not uncommon for FEV1/FVC to increase to about normal in restricted diseases, but this is of course due to a decline in FVC rather than a rise in FEV1. Notice also that the inspiratory loop is affected, with volumes being reduced here as well.",True,FEV1,Figure 6.5,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.5.png,Figure 6.5: Normal (maroon) and restrictive (gray) flow-volume loops.
41fe3439-542e-48fc-bd3e-cbf61870fb3c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"A flow-volume loop is a quick, cheap, and powerful diagnostic measure, but it is highly dependent on the patient performing a forced expiration to encourage dynamic compression and peak flows be obtained so that any airway abnormalities can be seen. This is why you may hear a pulmonary function technologist (PFT) shouting encouragement to a patient as you walk past the lab.",True,FEV1,,,,
59643e57-793a-4021-9bfc-6bd531fc1053,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,Summary,False,Summary,,,,
8180407c-213e-49d8-90a8-764c99989d35,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"So we have dealt with a couple of relatively complex issues in this chapter, particularly the interaction between intrapleural pressure and airway pressure during forced or active expirations and how airways can become compressed.",True,Summary,,,,
93dbb554-0e6a-492b-8e10-3296ae08eb36,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,We have also looked at the use of flow-volume loops to determine the degree of airway obstruction and to distinguish between obstructive and restrictive disorders.,True,Summary,,,,
64d2ac93-40da-4b18-ab0e-f04d69b67b91,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,Text,False,Text,,,,
a4e1e4cb-5060-4da3-8519-77b7fa4b7d39,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"Levitsky, Michael G. “Chapter 3: Alveolar Ventilation.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
893f0410-cace-4e90-83cd-bd692844105e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
34621726-1869-4e44-b82d-00865fb7a5c6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/#chapter-35-section-1,"Widdicombe, John G., and Andrew S. Davis. “Chapter 3.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
398d99ef-fd99-4a62-8736-43750d9777ec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"Although this phenomenon is present in the healthy lung, we will see how it is exacerbated in certain disease states and how this exacerbation can be detected by common pulmonary function tests.",True,Text,,,,
ff461ad7-df47-4a0e-ab9a-00dffaf1c16c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"First, let us look at the forces involved during a normal, passive expiration.",True,Text,,,,
67a10159-1757-4a3a-8e6d-662b92021d02,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"For simplicity, the schematic in figure 6.1 shows one airway and an alveolus within the thoracic cavity. At the onset of passive expiration (driven by the recoil of the expanded lung), the intrapleural pressure is negative (about −8 cm H2O). As it remains negative, intrapleural pressure helps keep the airways open.",True,Text,Figure 6.1,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.1.png,Figure 6.1: Intrapleural and airway pressures during normal/passive expiration.
67a10159-1757-4a3a-8e6d-662b92021d02,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"For simplicity, the schematic in figure 6.1 shows one airway and an alveolus within the thoracic cavity. At the onset of passive expiration (driven by the recoil of the expanded lung), the intrapleural pressure is negative (about −8 cm H2O). As it remains negative, intrapleural pressure helps keep the airways open.",True,Text,Figure 6.1,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.1.png,Figure 6.1: Intrapleural and airway pressures during normal/passive expiration.
67a10159-1757-4a3a-8e6d-662b92021d02,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"For simplicity, the schematic in figure 6.1 shows one airway and an alveolus within the thoracic cavity. At the onset of passive expiration (driven by the recoil of the expanded lung), the intrapleural pressure is negative (about −8 cm H2O). As it remains negative, intrapleural pressure helps keep the airways open.",True,Text,Figure 6.1,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.1.png,Figure 6.1: Intrapleural and airway pressures during normal/passive expiration.
8156ecaa-c0f9-4a16-acd7-ac7c157c0b9c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,H2O,False,H2O,,,,
b559cbfc-c597-4550-af98-f044c22c2fb2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"The elastic forces of the alveolus wall exert an inward force of about +10 cm H2O. This results in a net force of +2 cm H2O in the alveolus, and a gradient between this positive pressure is established between the alveolus and the atmosphere outside the lung. That means that along the airway toward the mouth there is a gradient of progressively decreasing pressure to zero (shown in maroon).",True,H2O,,,,
5e2f4ba7-7563-4fef-8d89-84452c28501c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"Importantly in this example of passive expiration the airway pressure is greater than the pleural pressure along the whole length of the airway toward the mouth. Along with the radial traction provided by the surrounding parenchymal tissue, this favorable transmural pressure gradient helps keep the airway open during expiration.",True,H2O,,,,
4bd1cfb2-a3df-447d-836a-49a16a7d6fa6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"Now let us look at what happens if expiration is forceful, or active, rather than passively relying on lung recoil.",True,H2O,,,,
80fbca1f-71f3-4de2-9ff1-3e85f4963092,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"In a forced expiration (see figure 6.2) the intrapleural pressure can become positive (as much as 120 cm H2O), but in this example we will say it is 25 cm H2O. This positive pressure in the pleural cavity comes from the chest wall and diaphragm now “pushing” the pleural membranes together and compressing the lung.",True,H2O,Figure 6.2,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
80fbca1f-71f3-4de2-9ff1-3e85f4963092,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"In a forced expiration (see figure 6.2) the intrapleural pressure can become positive (as much as 120 cm H2O), but in this example we will say it is 25 cm H2O. This positive pressure in the pleural cavity comes from the chest wall and diaphragm now “pushing” the pleural membranes together and compressing the lung.",True,H2O,Figure 6.2,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
80fbca1f-71f3-4de2-9ff1-3e85f4963092,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"In a forced expiration (see figure 6.2) the intrapleural pressure can become positive (as much as 120 cm H2O), but in this example we will say it is 25 cm H2O. This positive pressure in the pleural cavity comes from the chest wall and diaphragm now “pushing” the pleural membranes together and compressing the lung.",True,H2O,Figure 6.2,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
d3099b8e-4dc9-42bb-b82a-74018225d338,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"Again, we have the elastic forces of the alveolus generating an inward force (still +10 cm H2O), and when summed with the now positive intrapleural forces, we end up with an alveolar pressure of +35 cm H2O.",True,H2O,,,,
d4519595-3c7a-4175-802f-f73a3fe925a6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"Again, a pressure gradient between the alveolus and the atmosphere is established (again shown in maroon), but this time there is a fundamental difference caused by the larger intrapleural pressure.",True,H2O,,,,
79b23dc0-b150-44a1-bc62-b64f23a4f717,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"At some point along the airway, as airway pressure is decreasing, the intrapleural pressure exceeds airway pressure (in this example it is 25 cm H2O). At this “choke” point (arrows pointing toward airway in figure 6.2), the airway can become compressed or even collapse.",True,H2O,Figure 6.2,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
79b23dc0-b150-44a1-bc62-b64f23a4f717,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"At some point along the airway, as airway pressure is decreasing, the intrapleural pressure exceeds airway pressure (in this example it is 25 cm H2O). At this “choke” point (arrows pointing toward airway in figure 6.2), the airway can become compressed or even collapse.",True,H2O,Figure 6.2,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
79b23dc0-b150-44a1-bc62-b64f23a4f717,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"At some point along the airway, as airway pressure is decreasing, the intrapleural pressure exceeds airway pressure (in this example it is 25 cm H2O). At this “choke” point (arrows pointing toward airway in figure 6.2), the airway can become compressed or even collapse.",True,H2O,Figure 6.2,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.2-newer.png,Figure 6.2: Intrapleural and airway pressures during forced expiration.
867abff8-df17-4c09-9df0-870fabfc19ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"This effect is somewhat reduced by the radial traction of the parenchyma, but airway compression occurs even in the healthy normal lung, and the greater the effort of expiration (i.e., the more positive the intrapleural pressure), the greater degree airways compress and compression occurs closer to the alveoli (i.e., further up the pressure gradient in the airway).",True,H2O,,,,
5ff0e059-0256-4cfa-90c3-dea6334bf649,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"If airways are already narrowed, as in obstructive lung diseases such as asthma, or parenchymal traction is lost, such as in emphysema, dynamic airway compression occurs to a greater extent. In these obstructive diseases the increased airway resistance results in the patient having to forcefully expire to overcome the increased resistance of the narrowed airways. This promotes airway compression and leads to air being trapped behind the choke point, causing hyperinflation (breathing at an elevated lung volume).",True,H2O,,,,
fc4d675b-cedc-4243-afe1-a634ecc578b4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"This airway compression or any other increase in airway resistance can be demonstrated by a common pulmonary function test, the flow-volume loop.",True,H2O,,,,
7b41c0b2-44d4-4ebf-b91b-4028e8620457,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,Flow-Volume Loops,False,Flow-Volume Loops,,,,
bfeb4d2e-27f2-431f-b1ec-1ea887bbfb96,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"Flow-volume loops are briefly discussed in context of the relevant physiology. Figure 6.3 shows a normal flow-volume loop. Note that the volume axis seems to be the wrong way around; this is because expired volume and flow are generally more useful, so the plot has expiratory flow as positive and lung volume orientated for expiration. While breathing on a spirometer, the patient begins to breathe in from residual volume (bottom half of maroon line). As inspiration continues, lung volume increases (moves toward the y-axis) and airflow increases (moves downward). The patient continues inhaling until they are at total lung capacity (or TLC).",True,Flow-Volume Loops,Figure 6.3,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.3.png,Figure 6.3: Typical and normal flow-volume loop. FVC: forved vital capacity.
bfeb4d2e-27f2-431f-b1ec-1ea887bbfb96,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"Flow-volume loops are briefly discussed in context of the relevant physiology. Figure 6.3 shows a normal flow-volume loop. Note that the volume axis seems to be the wrong way around; this is because expired volume and flow are generally more useful, so the plot has expiratory flow as positive and lung volume orientated for expiration. While breathing on a spirometer, the patient begins to breathe in from residual volume (bottom half of maroon line). As inspiration continues, lung volume increases (moves toward the y-axis) and airflow increases (moves downward). The patient continues inhaling until they are at total lung capacity (or TLC).",True,Flow-Volume Loops,Figure 6.3,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.3.png,Figure 6.3: Typical and normal flow-volume loop. FVC: forved vital capacity.
bfeb4d2e-27f2-431f-b1ec-1ea887bbfb96,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"Flow-volume loops are briefly discussed in context of the relevant physiology. Figure 6.3 shows a normal flow-volume loop. Note that the volume axis seems to be the wrong way around; this is because expired volume and flow are generally more useful, so the plot has expiratory flow as positive and lung volume orientated for expiration. While breathing on a spirometer, the patient begins to breathe in from residual volume (bottom half of maroon line). As inspiration continues, lung volume increases (moves toward the y-axis) and airflow increases (moves downward). The patient continues inhaling until they are at total lung capacity (or TLC).",True,Flow-Volume Loops,Figure 6.3,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.3.png,Figure 6.3: Typical and normal flow-volume loop. FVC: forved vital capacity.
e46b6c79-56d2-4fa9-9d22-e031f86b96f9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"They then exhale as hard and as fast as they can, forcefully emptying the lung as quickly as possible. During forced exhalation of the first liter or so, expiratory flow rapidly increases until it reaches peak expiratory flow; this is the first clinically pertinent measure. After this point expiratory flow begins an exponential decline; as lung volume continues to decrease, so does the flow rate until flow reaches zero when the lung is emptied (at residual volume).",True,Flow-Volume Loops,,,,
24ac9605-b187-4fb6-a459-cb5678abbab5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,The rate of this decline in flow rate is also an important clinical measure and brings together a couple of important physiological points:,True,Flow-Volume Loops,,,,
c81f6141-8368-4659-bda0-0123becce1d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"Although there are a number of measurements that are calculated from this forced exhalation, two are most commonly reported. First, the total volume that is expelled from the lung is referred to as the forced vital capacity (FVC). The forced expiratory volume that is expelled from the lung in the first second of expiration is referred to as FEV1. The ratio of these two values, known as FEV1/FVC, describes the percentage of lung volume that can be emptied in one second and is a useful indicator of airway resistance. A normal FEV1/FVC is 90 percent or higher, meaning over 90 percent of vital capacity can be emptied from the lung within a second. This value is dependent on age, gender, and body size, but commonly used predicted values take these variables into account when assessing for disease.",True,Flow-Volume Loops,,,,
93cf3f94-44aa-4305-a056-9676b11441cc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,FEV1,False,FEV1,,,,
ca1d1909-b9e1-4cee-b294-b182b47b2cbb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"The loop produced by a patient with chronic obstructive lung disease, or COPD, looks very different (gray line in figure 6.4). With disease causing airway narrowing, the peak expiratory flow is significantly reduced, and the decay in expiratory flow as lung volume declines is much more pronounced as the narrowed airways can be easier to collapse due to a lower starting radius and/or loss of radial traction.",True,FEV1,Figure 6.4,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.4.png,Figure 6.4: Normal (maroon) and obstructive disease (gray) flow-volume loops.
ca1d1909-b9e1-4cee-b294-b182b47b2cbb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"The loop produced by a patient with chronic obstructive lung disease, or COPD, looks very different (gray line in figure 6.4). With disease causing airway narrowing, the peak expiratory flow is significantly reduced, and the decay in expiratory flow as lung volume declines is much more pronounced as the narrowed airways can be easier to collapse due to a lower starting radius and/or loss of radial traction.",True,FEV1,Figure 6.4,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.4.png,Figure 6.4: Normal (maroon) and obstructive disease (gray) flow-volume loops.
ca1d1909-b9e1-4cee-b294-b182b47b2cbb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"The loop produced by a patient with chronic obstructive lung disease, or COPD, looks very different (gray line in figure 6.4). With disease causing airway narrowing, the peak expiratory flow is significantly reduced, and the decay in expiratory flow as lung volume declines is much more pronounced as the narrowed airways can be easier to collapse due to a lower starting radius and/or loss of radial traction.",True,FEV1,Figure 6.4,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.4.png,Figure 6.4: Normal (maroon) and obstructive disease (gray) flow-volume loops.
ae3ab054-9e57-4844-868a-b7f85d8b59b2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"This means that FEV1 is significantly reduced, but FVC may remain unchanged (i.e., the lung volume is the same, but it takes longer to empty). An FEV1/FVC significantly less than 90 percent is indicative of obstructive disease. Notice that the inspiratory loop of the COPD patient appears normal, illustrating the effect of increasingly negative intrapleural pressure, increasing lung volume and radial traction on airway resistance.",True,FEV1,,,,
12dbd24f-65e5-4ae3-b3b3-524ed142d0e7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"Alternatively, diseases that restrict lung expansion (figure 6.5), such as pulmonary fibrosis, demonstrate a reduced lung volume, where FVC is substantially reduced, but FEV1 may not be significantly affected; in fact it is not uncommon for FEV1/FVC to increase to about normal in restricted diseases, but this is of course due to a decline in FVC rather than a rise in FEV1. Notice also that the inspiratory loop is affected, with volumes being reduced here as well.",True,FEV1,Figure 6.5,Flow-Volume Loops,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.5.png,Figure 6.5: Normal (maroon) and restrictive (gray) flow-volume loops.
12dbd24f-65e5-4ae3-b3b3-524ed142d0e7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"Alternatively, diseases that restrict lung expansion (figure 6.5), such as pulmonary fibrosis, demonstrate a reduced lung volume, where FVC is substantially reduced, but FEV1 may not be significantly affected; in fact it is not uncommon for FEV1/FVC to increase to about normal in restricted diseases, but this is of course due to a decline in FVC rather than a rise in FEV1. Notice also that the inspiratory loop is affected, with volumes being reduced here as well.",True,FEV1,Figure 6.5,Compression of Airways During Expiration,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.5.png,Figure 6.5: Normal (maroon) and restrictive (gray) flow-volume loops.
12dbd24f-65e5-4ae3-b3b3-524ed142d0e7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"Alternatively, diseases that restrict lung expansion (figure 6.5), such as pulmonary fibrosis, demonstrate a reduced lung volume, where FVC is substantially reduced, but FEV1 may not be significantly affected; in fact it is not uncommon for FEV1/FVC to increase to about normal in restricted diseases, but this is of course due to a decline in FVC rather than a rise in FEV1. Notice also that the inspiratory loop is affected, with volumes being reduced here as well.",True,FEV1,Figure 6.5,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/6.5.png,Figure 6.5: Normal (maroon) and restrictive (gray) flow-volume loops.
652fd886-03be-4b05-a62b-25fc649ba951,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"A flow-volume loop is a quick, cheap, and powerful diagnostic measure, but it is highly dependent on the patient performing a forced expiration to encourage dynamic compression and peak flows be obtained so that any airway abnormalities can be seen. This is why you may hear a pulmonary function technologist (PFT) shouting encouragement to a patient as you walk past the lab.",True,FEV1,,,,
bd0ddd3e-7ae9-445b-bc9f-0b17de8cd509,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,Summary,False,Summary,,,,
17767fc4-be0f-40a2-8cde-6252a2608628,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"So we have dealt with a couple of relatively complex issues in this chapter, particularly the interaction between intrapleural pressure and airway pressure during forced or active expirations and how airways can become compressed.",True,Summary,,,,
a2918899-2271-4e0e-89c7-a35718b474b9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,We have also looked at the use of flow-volume loops to determine the degree of airway obstruction and to distinguish between obstructive and restrictive disorders.,True,Summary,,,,
ddc8a617-9c16-44db-b88a-a89e5d05684f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,Text,False,Text,,,,
397ceeee-390a-41e5-944b-933989de99be,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"Levitsky, Michael G. “Chapter 3: Alveolar Ventilation.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
adf0064c-8bf3-494d-aada-dec58c33bc72,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
6248e4ad-1b98-4999-95aa-4dafad6b316d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,6. Dynamic Airway Compression,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/dynamic-airway-compression/,"Widdicombe, John G., and Andrew S. Davis. “Chapter 3.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
2abbd8fc-bc45-4021-95f3-7cc764fb7854,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,The first factor we must consider when thinking about airflow is the type of flow that is occurring.,True,Text,,,,
90b7c113-9453-48ab-af12-da3e977c0466,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"The most efficient form of flow is laminar (i.e., laminar flow takes the lowest pressure differential for flow to occur). In laminar flow the molecules are moving in an orderly manner, those at the side of the tube moving a little slower due to contact with tube walls and those in the middle moving fastest (figure 5.1).",True,Text,Figure 5.1,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.1.png,Figure 5.1: Laminar flow.
90b7c113-9453-48ab-af12-da3e977c0466,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"The most efficient form of flow is laminar (i.e., laminar flow takes the lowest pressure differential for flow to occur). In laminar flow the molecules are moving in an orderly manner, those at the side of the tube moving a little slower due to contact with tube walls and those in the middle moving fastest (figure 5.1).",True,Text,Figure 5.1,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.1.png,Figure 5.1: Laminar flow.
90b7c113-9453-48ab-af12-da3e977c0466,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"The most efficient form of flow is laminar (i.e., laminar flow takes the lowest pressure differential for flow to occur). In laminar flow the molecules are moving in an orderly manner, those at the side of the tube moving a little slower due to contact with tube walls and those in the middle moving fastest (figure 5.1).",True,Text,Figure 5.1,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.1.png,Figure 5.1: Laminar flow.
185f8384-ae77-4ecc-8216-cf9651f31397,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"When velocity increases or tube radius decreases then this organization is lost. Collisions between molecules and with the tube wall are now more frequent and movement is more chaotic, and the flow becomes turbulent (figure 5.2). At this point some molecules are at times moving against the pressure gradient due to these collisions. Consequently, to generate the same amount of molecule movement (i.e., flow) from one end of the tube to another, a greater pressure differential is needed when flow becomes turbulent. Turbulent flow is more common in the large airways where velocity and airway radius are high.",True,Text,Figure 5.2,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.2.png,Figure 5.2: Turbulent flow.
185f8384-ae77-4ecc-8216-cf9651f31397,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"When velocity increases or tube radius decreases then this organization is lost. Collisions between molecules and with the tube wall are now more frequent and movement is more chaotic, and the flow becomes turbulent (figure 5.2). At this point some molecules are at times moving against the pressure gradient due to these collisions. Consequently, to generate the same amount of molecule movement (i.e., flow) from one end of the tube to another, a greater pressure differential is needed when flow becomes turbulent. Turbulent flow is more common in the large airways where velocity and airway radius are high.",True,Text,Figure 5.2,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.2.png,Figure 5.2: Turbulent flow.
185f8384-ae77-4ecc-8216-cf9651f31397,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"When velocity increases or tube radius decreases then this organization is lost. Collisions between molecules and with the tube wall are now more frequent and movement is more chaotic, and the flow becomes turbulent (figure 5.2). At this point some molecules are at times moving against the pressure gradient due to these collisions. Consequently, to generate the same amount of molecule movement (i.e., flow) from one end of the tube to another, a greater pressure differential is needed when flow becomes turbulent. Turbulent flow is more common in the large airways where velocity and airway radius are high.",True,Text,Figure 5.2,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.2.png,Figure 5.2: Turbulent flow.
78016837-1b1e-4b72-9459-159a81636088,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"In reality, the vast majority of the airways are branching small tubes, so we see a mixture of the two above—mostly laminar flow but some turbulence generated at the branch (or transitional) points (figure 5.3).",True,Text,Figure 5.3,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.3.png,Figure 5.3: Transitional flow.
78016837-1b1e-4b72-9459-159a81636088,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"In reality, the vast majority of the airways are branching small tubes, so we see a mixture of the two above—mostly laminar flow but some turbulence generated at the branch (or transitional) points (figure 5.3).",True,Text,Figure 5.3,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.3.png,Figure 5.3: Transitional flow.
78016837-1b1e-4b72-9459-159a81636088,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"In reality, the vast majority of the airways are branching small tubes, so we see a mixture of the two above—mostly laminar flow but some turbulence generated at the branch (or transitional) points (figure 5.3).",True,Text,Figure 5.3,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.3.png,Figure 5.3: Transitional flow.
d8c9a412-74b3-47d6-9885-10a68f3195dc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"For our purposes though we are going to look at the factors that affect flow when it is laminar—the dominant form of flow in the majority of airways. These factors are described by Poiselle’s equation. We will now break down Poiselle’s equation in relation to flow of air down airways. Although initially an intimidating equation, there are some things we can generally ignore.",True,Text,,,,
329ee30f-0280-4186-a272-76cda4611f6d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,Equation 5.1,True,Text,,,,
5d98b316-14ae-4aeb-9345-37822013e6db,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],False,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
5e3fb3a7-a053-4acc-86e9-d182ddf86042,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"First, Poiselle says that flow decreases when length of the tube increases; because the airways have constant length, we do not have to worry about it.",True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
61591784-2605-49b6-90c8-7235cba59477,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"Then there is the viscosity of the gas. This is not usually a concern either when breathing humidified air at a constant biological temperature. It does become important when breathing other gas mixtures, however, such as a helium/oxygen blend that has a lower viscosity and is given to respiratory patients or deep water divers to increase flow. But we will assume it is another constant. Pi (π) is also a constant.",True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
a5a1a5d4-c643-4a7a-b174-3e51a5e3e4e9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"So the two remaining variables are the important ones to understand. The pressure differential created by expansion and relaxation of the lung generates a proportional flow, and we have dealt with this in previous chapters.",True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
5213b635-ab48-405e-8029-e5110cb26cfc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"What we will look at more closely now is airway radius as this has a profound effect on flow. Radius is critical for two main reasons. First it is variable, as the caliber of an airway changes with lung volume and by the action of airway smooth muscle. Second, it has a very powerful effect on flow; as you can see in Poiselle’s equation, radius is to the fourth power. This means a small increase in radius has a large effect on flow. For example, if the radius of an airway is doubled from 1 mm to 2 mm, the flow rate through the tube increases sixteenfold, which of course is two to the fourth power (i.e., 2x2x2x2). The inverse is of course true—halve the radius and flow reduces sixteenfold.",True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
ebe62cb3-d7dd-46a2-9281-1ebc290a834a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"So far we have couched everything in terms of flow, but really we need to look at airway resistance. Because resistance is simply the reciprocal (or opposite) of flow, we can flip Poiselle’s equation upside down to describe resistance, and we now see that a reduction in radius (r) causes a large increase in resistance (R).",True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
d563dc7e-7fa3-4742-9a9d-0fe9c19a3eac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,Equation 5.2,True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
d238c523-a3c0-4cf0-92c3-2b202b5c85a0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,[latex]R = \displaystyle\frac{8n \times L}{\Delta P \times \pi \times r^4}[/latex],False,[latex]R = \displaystyle\frac{8n \times L}{\Delta P \times \pi \times r^4}[/latex],,,,
cb70ce03-4c48-49b0-8b0f-44c590d8ca66,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,Airway Resistance,False,Airway Resistance,,,,
c7af50f6-2c05-47d3-9087-5b1f80d3fccb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"So with radius having such a powerful effect on airway resistance we would expect that the early and larger generations of airways would offer the least resistance to flow, and resistance would increase as we descended deeper into the lung to the smaller and later airway generations. Figure 5.4 shows the opposite is true—that airway resistance decreases as the airway generations are descended. This is because the total cross-sectional area increases with each generation—while the early and large airways are wide, they are few. The lower and smaller airways are much more numerous, and so collectively they have a greater cross-sectional area and therefore offer less resistance.",True,Airway Resistance,Figure 5.4,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.4.png,Figure 5.4: Airway resistance down the bronchial tree.
c7af50f6-2c05-47d3-9087-5b1f80d3fccb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"So with radius having such a powerful effect on airway resistance we would expect that the early and larger generations of airways would offer the least resistance to flow, and resistance would increase as we descended deeper into the lung to the smaller and later airway generations. Figure 5.4 shows the opposite is true—that airway resistance decreases as the airway generations are descended. This is because the total cross-sectional area increases with each generation—while the early and large airways are wide, they are few. The lower and smaller airways are much more numerous, and so collectively they have a greater cross-sectional area and therefore offer less resistance.",True,Airway Resistance,Figure 5.4,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.4.png,Figure 5.4: Airway resistance down the bronchial tree.
c7af50f6-2c05-47d3-9087-5b1f80d3fccb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"So with radius having such a powerful effect on airway resistance we would expect that the early and larger generations of airways would offer the least resistance to flow, and resistance would increase as we descended deeper into the lung to the smaller and later airway generations. Figure 5.4 shows the opposite is true—that airway resistance decreases as the airway generations are descended. This is because the total cross-sectional area increases with each generation—while the early and large airways are wide, they are few. The lower and smaller airways are much more numerous, and so collectively they have a greater cross-sectional area and therefore offer less resistance.",True,Airway Resistance,Figure 5.4,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.4.png,Figure 5.4: Airway resistance down the bronchial tree.
b1b161a6-1bb8-45d6-88e1-70fe35847671,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,The highest point of resistance is actually the midsize bronchioles. There are a couple of clinically important points to make here:,True,Airway Resistance,,,,
bbbc3d82-8140-4629-886b-eb5f54f76b70,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,Airway Resistance and Lung Volume,False,Airway Resistance and Lung Volume,,,,
cbb7a36b-87fc-4845-9394-57c7374d4733,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"The airways without cartilaginous support significantly change their radius when the lung expands due to the radial traction. In brief, parenchymal fibers tethered to the alveoli and exterior of the airways allow the airways to be pulled open by the expanding alveoli when lung volume increases (illustrated in figure 5.5).",True,Airway Resistance and Lung Volume,Figure 5.5,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.5.png,Figure 5.5: Radial traction decreases airway resistance as lung volume increases.
cbb7a36b-87fc-4845-9394-57c7374d4733,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"The airways without cartilaginous support significantly change their radius when the lung expands due to the radial traction. In brief, parenchymal fibers tethered to the alveoli and exterior of the airways allow the airways to be pulled open by the expanding alveoli when lung volume increases (illustrated in figure 5.5).",True,Airway Resistance and Lung Volume,Figure 5.5,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.5.png,Figure 5.5: Radial traction decreases airway resistance as lung volume increases.
cbb7a36b-87fc-4845-9394-57c7374d4733,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"The airways without cartilaginous support significantly change their radius when the lung expands due to the radial traction. In brief, parenchymal fibers tethered to the alveoli and exterior of the airways allow the airways to be pulled open by the expanding alveoli when lung volume increases (illustrated in figure 5.5).",True,Airway Resistance and Lung Volume,Figure 5.5,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.5.png,Figure 5.5: Radial traction decreases airway resistance as lung volume increases.
16bcda72-2e9a-413f-ae1d-b5d369159840,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"This increase in airway diameter means that airway resistance falls as lung volume increases. This is demonstrated by figure 5.6; as lung volume increases, then airway resistance falls exponentially.",True,Airway Resistance and Lung Volume,Figure 5.6,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.6.png,Figure 5.6: Airway resistance and lung volume.
16bcda72-2e9a-413f-ae1d-b5d369159840,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"This increase in airway diameter means that airway resistance falls as lung volume increases. This is demonstrated by figure 5.6; as lung volume increases, then airway resistance falls exponentially.",True,Airway Resistance and Lung Volume,Figure 5.6,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.6.png,Figure 5.6: Airway resistance and lung volume.
16bcda72-2e9a-413f-ae1d-b5d369159840,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"This increase in airway diameter means that airway resistance falls as lung volume increases. This is demonstrated by figure 5.6; as lung volume increases, then airway resistance falls exponentially.",True,Airway Resistance and Lung Volume,Figure 5.6,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.6.png,Figure 5.6: Airway resistance and lung volume.
ce71d882-d522-4f75-9d9c-d0057c48fede,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"The inverse is also true, that as lung volume decreases, airway radius declines. This may happen to a sufficient extent to allow small airways to collapse. It is worth noting here that respiratory patients frequently breathe at higher lung volumes. While there are mechanical reasons for this that we will discover in the next chapter, the higher lung volume may at least improve airway conductance (although it carries many other disadvantages).",True,Airway Resistance and Lung Volume,,,,
83b89a7a-3dee-4eaf-8d84-a0c89d41ae8f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,Airway Resistance and Neural Control,False,Airway Resistance and Neural Control,,,,
7fbedb37-b1a1-4e8e-9b75-3174278e913b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"As well as the lung volume effect, the tone of airway smooth muscle is also a powerful determinant of airway radius and therefore resistance. The muscle is arranged in a ring pattern around the airway circumference. Contraction of the smooth muscle causes bronchoconstriction, decreasing the airway radius. Relaxation of the smooth muscle allows bronchodilation.",True,Airway Resistance and Neural Control,,,,
b6fab127-b070-4907-b6f1-c7e002e1f264,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"Airway smooth muscle is under the control of the autonomic nervous system. Parasympathetic release of acetylcholine causes activation of muscarinic receptors. This causes a rise in intracellular calcium that activates the smooth muscle. Muscle is relaxed by sympathetic stimulation of β2 adrenergic receptors. These β2 receptors are the target of bronchodilator drugs, such as albuterol, that resolve the inappropriate contraction of smooth muscle seen in the hypersensitive airways of asthmatics.",True,Airway Resistance and Neural Control,,,,
21f8a7bc-59af-4aeb-a2e7-6f804effab65,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"The bronchoconstrictive pathway is utilized by the irritant reflex that is initiated by airway wall receptors detecting the arrival of inspired particulates. This defensive reflex results in bronchoconstriction, presumably to limit the entry of more particulates.",True,Airway Resistance and Neural Control,,,,
711d35bf-e5b0-4935-a96e-0fc4dc439037,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,A number of inflammatory mediators also cause bronchoconstriction and probably play a significant role in the bronchoconstriction of asthma (which frequently also involves airway inflammation).,True,Airway Resistance and Neural Control,,,,
58667a67-1b20-472a-ad8b-cb483a27c09a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,Low airway PCO2 also has a direct stimulatory effect on airway smooth muscle and a bronchoconstrictive effect. This is presumably to shunt air to other regions of the lung and away from regions where overventilation caused the low PCO2.,True,Airway Resistance and Neural Control,,,,
17055ef3-6433-44c6-ab37-dbc676290ba1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,Summary,False,Summary,,,,
e9f4b749-54a9-484b-8c35-4c8a005ea450,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"So now you should be able to understand how the type of flow, airway radius, lung volume, and autonomic nervous system all influence airway resistance and so can either oppose or promote the flow of air in the lung.",True,Summary,,,,
5ccdd5f4-f3e6-4b7a-84ea-cecfcd5c7516,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,Text,False,Text,,,,
ccf522d3-ed2e-4e8f-951d-b5f59bf4614f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"Levitsky, Michael G. “Chapter 2: Mechanics of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
89ed6639-fe0b-41c3-b083-556aff144b01,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
928f839a-4071-4966-86b1-3ddbcc332b43,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-2,"Widdicombe, John G., and Andrew S. Davis. “Chapter 3.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
8a513b03-6b51-4ef3-b35b-41f1eeb83bf6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,The first factor we must consider when thinking about airflow is the type of flow that is occurring.,True,Text,,,,
0b270403-445b-4f54-96dc-f9dbee0d5ba2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"The most efficient form of flow is laminar (i.e., laminar flow takes the lowest pressure differential for flow to occur). In laminar flow the molecules are moving in an orderly manner, those at the side of the tube moving a little slower due to contact with tube walls and those in the middle moving fastest (figure 5.1).",True,Text,Figure 5.1,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.1.png,Figure 5.1: Laminar flow.
0b270403-445b-4f54-96dc-f9dbee0d5ba2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"The most efficient form of flow is laminar (i.e., laminar flow takes the lowest pressure differential for flow to occur). In laminar flow the molecules are moving in an orderly manner, those at the side of the tube moving a little slower due to contact with tube walls and those in the middle moving fastest (figure 5.1).",True,Text,Figure 5.1,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.1.png,Figure 5.1: Laminar flow.
0b270403-445b-4f54-96dc-f9dbee0d5ba2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"The most efficient form of flow is laminar (i.e., laminar flow takes the lowest pressure differential for flow to occur). In laminar flow the molecules are moving in an orderly manner, those at the side of the tube moving a little slower due to contact with tube walls and those in the middle moving fastest (figure 5.1).",True,Text,Figure 5.1,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.1.png,Figure 5.1: Laminar flow.
e989c98d-b134-4295-8dca-3683fb6a085b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"When velocity increases or tube radius decreases then this organization is lost. Collisions between molecules and with the tube wall are now more frequent and movement is more chaotic, and the flow becomes turbulent (figure 5.2). At this point some molecules are at times moving against the pressure gradient due to these collisions. Consequently, to generate the same amount of molecule movement (i.e., flow) from one end of the tube to another, a greater pressure differential is needed when flow becomes turbulent. Turbulent flow is more common in the large airways where velocity and airway radius are high.",True,Text,Figure 5.2,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.2.png,Figure 5.2: Turbulent flow.
e989c98d-b134-4295-8dca-3683fb6a085b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"When velocity increases or tube radius decreases then this organization is lost. Collisions between molecules and with the tube wall are now more frequent and movement is more chaotic, and the flow becomes turbulent (figure 5.2). At this point some molecules are at times moving against the pressure gradient due to these collisions. Consequently, to generate the same amount of molecule movement (i.e., flow) from one end of the tube to another, a greater pressure differential is needed when flow becomes turbulent. Turbulent flow is more common in the large airways where velocity and airway radius are high.",True,Text,Figure 5.2,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.2.png,Figure 5.2: Turbulent flow.
e989c98d-b134-4295-8dca-3683fb6a085b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"When velocity increases or tube radius decreases then this organization is lost. Collisions between molecules and with the tube wall are now more frequent and movement is more chaotic, and the flow becomes turbulent (figure 5.2). At this point some molecules are at times moving against the pressure gradient due to these collisions. Consequently, to generate the same amount of molecule movement (i.e., flow) from one end of the tube to another, a greater pressure differential is needed when flow becomes turbulent. Turbulent flow is more common in the large airways where velocity and airway radius are high.",True,Text,Figure 5.2,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.2.png,Figure 5.2: Turbulent flow.
f0eb6bb3-fa8c-42b5-b7b9-c5d1ab1b153b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"In reality, the vast majority of the airways are branching small tubes, so we see a mixture of the two above—mostly laminar flow but some turbulence generated at the branch (or transitional) points (figure 5.3).",True,Text,Figure 5.3,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.3.png,Figure 5.3: Transitional flow.
f0eb6bb3-fa8c-42b5-b7b9-c5d1ab1b153b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"In reality, the vast majority of the airways are branching small tubes, so we see a mixture of the two above—mostly laminar flow but some turbulence generated at the branch (or transitional) points (figure 5.3).",True,Text,Figure 5.3,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.3.png,Figure 5.3: Transitional flow.
f0eb6bb3-fa8c-42b5-b7b9-c5d1ab1b153b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"In reality, the vast majority of the airways are branching small tubes, so we see a mixture of the two above—mostly laminar flow but some turbulence generated at the branch (or transitional) points (figure 5.3).",True,Text,Figure 5.3,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.3.png,Figure 5.3: Transitional flow.
f32e28db-95f8-49b0-a671-898ae633eae1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"For our purposes though we are going to look at the factors that affect flow when it is laminar—the dominant form of flow in the majority of airways. These factors are described by Poiselle’s equation. We will now break down Poiselle’s equation in relation to flow of air down airways. Although initially an intimidating equation, there are some things we can generally ignore.",True,Text,,,,
fb335173-85b5-48c4-80af-16614009be72,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,Equation 5.1,True,Text,,,,
2875f408-1783-421c-b2c5-9dc8bb5663dd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],False,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
5b81920f-9c40-4e03-aea7-8ffb81690b1d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"First, Poiselle says that flow decreases when length of the tube increases; because the airways have constant length, we do not have to worry about it.",True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
b5087ae1-6d2a-4f5d-937e-38e0d42d691e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"Then there is the viscosity of the gas. This is not usually a concern either when breathing humidified air at a constant biological temperature. It does become important when breathing other gas mixtures, however, such as a helium/oxygen blend that has a lower viscosity and is given to respiratory patients or deep water divers to increase flow. But we will assume it is another constant. Pi (π) is also a constant.",True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
a82780ae-955d-4e00-ac5a-64cb5cbf9b4f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"So the two remaining variables are the important ones to understand. The pressure differential created by expansion and relaxation of the lung generates a proportional flow, and we have dealt with this in previous chapters.",True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
72bb22e7-277f-4719-985c-a7abee094e0f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"What we will look at more closely now is airway radius as this has a profound effect on flow. Radius is critical for two main reasons. First it is variable, as the caliber of an airway changes with lung volume and by the action of airway smooth muscle. Second, it has a very powerful effect on flow; as you can see in Poiselle’s equation, radius is to the fourth power. This means a small increase in radius has a large effect on flow. For example, if the radius of an airway is doubled from 1 mm to 2 mm, the flow rate through the tube increases sixteenfold, which of course is two to the fourth power (i.e., 2x2x2x2). The inverse is of course true—halve the radius and flow reduces sixteenfold.",True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
294bb9ca-2855-4651-96c3-da838c680f63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"So far we have couched everything in terms of flow, but really we need to look at airway resistance. Because resistance is simply the reciprocal (or opposite) of flow, we can flip Poiselle’s equation upside down to describe resistance, and we now see that a reduction in radius (r) causes a large increase in resistance (R).",True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
00d2fac7-d58d-48e1-8429-2196e7fb6c8c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,Equation 5.2,True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
352ad151-b064-448f-bf8c-27e2b789ddcb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,[latex]R = \displaystyle\frac{8n \times L}{\Delta P \times \pi \times r^4}[/latex],False,[latex]R = \displaystyle\frac{8n \times L}{\Delta P \times \pi \times r^4}[/latex],,,,
b3c1f9c8-b441-4498-ac23-29638df5f8e6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,Airway Resistance,False,Airway Resistance,,,,
bb983e6f-6de2-4719-bfc0-506c6edbb49d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"So with radius having such a powerful effect on airway resistance we would expect that the early and larger generations of airways would offer the least resistance to flow, and resistance would increase as we descended deeper into the lung to the smaller and later airway generations. Figure 5.4 shows the opposite is true—that airway resistance decreases as the airway generations are descended. This is because the total cross-sectional area increases with each generation—while the early and large airways are wide, they are few. The lower and smaller airways are much more numerous, and so collectively they have a greater cross-sectional area and therefore offer less resistance.",True,Airway Resistance,Figure 5.4,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.4.png,Figure 5.4: Airway resistance down the bronchial tree.
bb983e6f-6de2-4719-bfc0-506c6edbb49d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"So with radius having such a powerful effect on airway resistance we would expect that the early and larger generations of airways would offer the least resistance to flow, and resistance would increase as we descended deeper into the lung to the smaller and later airway generations. Figure 5.4 shows the opposite is true—that airway resistance decreases as the airway generations are descended. This is because the total cross-sectional area increases with each generation—while the early and large airways are wide, they are few. The lower and smaller airways are much more numerous, and so collectively they have a greater cross-sectional area and therefore offer less resistance.",True,Airway Resistance,Figure 5.4,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.4.png,Figure 5.4: Airway resistance down the bronchial tree.
bb983e6f-6de2-4719-bfc0-506c6edbb49d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"So with radius having such a powerful effect on airway resistance we would expect that the early and larger generations of airways would offer the least resistance to flow, and resistance would increase as we descended deeper into the lung to the smaller and later airway generations. Figure 5.4 shows the opposite is true—that airway resistance decreases as the airway generations are descended. This is because the total cross-sectional area increases with each generation—while the early and large airways are wide, they are few. The lower and smaller airways are much more numerous, and so collectively they have a greater cross-sectional area and therefore offer less resistance.",True,Airway Resistance,Figure 5.4,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.4.png,Figure 5.4: Airway resistance down the bronchial tree.
c8b5721e-16cb-44de-8cf6-5ee785f79e72,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,The highest point of resistance is actually the midsize bronchioles. There are a couple of clinically important points to make here:,True,Airway Resistance,,,,
df010242-f6a7-44be-b8e8-dae3780e03f0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,Airway Resistance and Lung Volume,False,Airway Resistance and Lung Volume,,,,
e5cefd80-00c9-49d1-958c-112adce01e61,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"The airways without cartilaginous support significantly change their radius when the lung expands due to the radial traction. In brief, parenchymal fibers tethered to the alveoli and exterior of the airways allow the airways to be pulled open by the expanding alveoli when lung volume increases (illustrated in figure 5.5).",True,Airway Resistance and Lung Volume,Figure 5.5,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.5.png,Figure 5.5: Radial traction decreases airway resistance as lung volume increases.
e5cefd80-00c9-49d1-958c-112adce01e61,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"The airways without cartilaginous support significantly change their radius when the lung expands due to the radial traction. In brief, parenchymal fibers tethered to the alveoli and exterior of the airways allow the airways to be pulled open by the expanding alveoli when lung volume increases (illustrated in figure 5.5).",True,Airway Resistance and Lung Volume,Figure 5.5,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.5.png,Figure 5.5: Radial traction decreases airway resistance as lung volume increases.
e5cefd80-00c9-49d1-958c-112adce01e61,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"The airways without cartilaginous support significantly change their radius when the lung expands due to the radial traction. In brief, parenchymal fibers tethered to the alveoli and exterior of the airways allow the airways to be pulled open by the expanding alveoli when lung volume increases (illustrated in figure 5.5).",True,Airway Resistance and Lung Volume,Figure 5.5,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.5.png,Figure 5.5: Radial traction decreases airway resistance as lung volume increases.
75875429-196e-4de4-9e41-5353873ab289,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"This increase in airway diameter means that airway resistance falls as lung volume increases. This is demonstrated by figure 5.6; as lung volume increases, then airway resistance falls exponentially.",True,Airway Resistance and Lung Volume,Figure 5.6,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.6.png,Figure 5.6: Airway resistance and lung volume.
75875429-196e-4de4-9e41-5353873ab289,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"This increase in airway diameter means that airway resistance falls as lung volume increases. This is demonstrated by figure 5.6; as lung volume increases, then airway resistance falls exponentially.",True,Airway Resistance and Lung Volume,Figure 5.6,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.6.png,Figure 5.6: Airway resistance and lung volume.
75875429-196e-4de4-9e41-5353873ab289,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"This increase in airway diameter means that airway resistance falls as lung volume increases. This is demonstrated by figure 5.6; as lung volume increases, then airway resistance falls exponentially.",True,Airway Resistance and Lung Volume,Figure 5.6,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.6.png,Figure 5.6: Airway resistance and lung volume.
10ca9f5b-0c56-4b6c-a82b-62fa215bd145,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"The inverse is also true, that as lung volume decreases, airway radius declines. This may happen to a sufficient extent to allow small airways to collapse. It is worth noting here that respiratory patients frequently breathe at higher lung volumes. While there are mechanical reasons for this that we will discover in the next chapter, the higher lung volume may at least improve airway conductance (although it carries many other disadvantages).",True,Airway Resistance and Lung Volume,,,,
af5cb18d-1565-4da4-8ec6-5f20a59035b1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,Airway Resistance and Neural Control,False,Airway Resistance and Neural Control,,,,
af8dfba6-f8c3-40b9-a4d6-d591d62803e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"As well as the lung volume effect, the tone of airway smooth muscle is also a powerful determinant of airway radius and therefore resistance. The muscle is arranged in a ring pattern around the airway circumference. Contraction of the smooth muscle causes bronchoconstriction, decreasing the airway radius. Relaxation of the smooth muscle allows bronchodilation.",True,Airway Resistance and Neural Control,,,,
72f2886d-dee0-47d8-b0d9-986b3ecd07b4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"Airway smooth muscle is under the control of the autonomic nervous system. Parasympathetic release of acetylcholine causes activation of muscarinic receptors. This causes a rise in intracellular calcium that activates the smooth muscle. Muscle is relaxed by sympathetic stimulation of β2 adrenergic receptors. These β2 receptors are the target of bronchodilator drugs, such as albuterol, that resolve the inappropriate contraction of smooth muscle seen in the hypersensitive airways of asthmatics.",True,Airway Resistance and Neural Control,,,,
82949015-59c2-46b2-b2e9-7a10c5128b71,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"The bronchoconstrictive pathway is utilized by the irritant reflex that is initiated by airway wall receptors detecting the arrival of inspired particulates. This defensive reflex results in bronchoconstriction, presumably to limit the entry of more particulates.",True,Airway Resistance and Neural Control,,,,
801c4825-c76f-4968-8db3-670541a3069c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,A number of inflammatory mediators also cause bronchoconstriction and probably play a significant role in the bronchoconstriction of asthma (which frequently also involves airway inflammation).,True,Airway Resistance and Neural Control,,,,
e6f3b7ba-fb29-4e0a-b7f7-e37808b9a709,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,Low airway PCO2 also has a direct stimulatory effect on airway smooth muscle and a bronchoconstrictive effect. This is presumably to shunt air to other regions of the lung and away from regions where overventilation caused the low PCO2.,True,Airway Resistance and Neural Control,,,,
eb04e683-3741-474c-b3d0-791c250b6020,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,Summary,False,Summary,,,,
0234d8ab-a62b-4a90-8257-cc6a90fbeef4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"So now you should be able to understand how the type of flow, airway radius, lung volume, and autonomic nervous system all influence airway resistance and so can either oppose or promote the flow of air in the lung.",True,Summary,,,,
5e1cedfd-45f4-439f-825d-5dae16aa31c7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,Text,False,Text,,,,
24ff717a-2286-41a4-9fd9-45ecdf73fc37,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"Levitsky, Michael G. “Chapter 2: Mechanics of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
1c082841-a7b2-4113-b73d-e0937b7e48e2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
989b3860-a723-4df3-8c8c-7a1fcde59125,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/#chapter-33-section-1,"Widdicombe, John G., and Andrew S. Davis. “Chapter 3.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
c7b393f1-39d9-4a75-b4d1-076f4698915f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,The first factor we must consider when thinking about airflow is the type of flow that is occurring.,True,Text,,,,
e4bce8d7-b5fa-42a1-9c98-462d7ffea033,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"The most efficient form of flow is laminar (i.e., laminar flow takes the lowest pressure differential for flow to occur). In laminar flow the molecules are moving in an orderly manner, those at the side of the tube moving a little slower due to contact with tube walls and those in the middle moving fastest (figure 5.1).",True,Text,Figure 5.1,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.1.png,Figure 5.1: Laminar flow.
e4bce8d7-b5fa-42a1-9c98-462d7ffea033,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"The most efficient form of flow is laminar (i.e., laminar flow takes the lowest pressure differential for flow to occur). In laminar flow the molecules are moving in an orderly manner, those at the side of the tube moving a little slower due to contact with tube walls and those in the middle moving fastest (figure 5.1).",True,Text,Figure 5.1,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.1.png,Figure 5.1: Laminar flow.
e4bce8d7-b5fa-42a1-9c98-462d7ffea033,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"The most efficient form of flow is laminar (i.e., laminar flow takes the lowest pressure differential for flow to occur). In laminar flow the molecules are moving in an orderly manner, those at the side of the tube moving a little slower due to contact with tube walls and those in the middle moving fastest (figure 5.1).",True,Text,Figure 5.1,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.1.png,Figure 5.1: Laminar flow.
f6d7ffa9-54fe-4091-a695-315be802e901,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"When velocity increases or tube radius decreases then this organization is lost. Collisions between molecules and with the tube wall are now more frequent and movement is more chaotic, and the flow becomes turbulent (figure 5.2). At this point some molecules are at times moving against the pressure gradient due to these collisions. Consequently, to generate the same amount of molecule movement (i.e., flow) from one end of the tube to another, a greater pressure differential is needed when flow becomes turbulent. Turbulent flow is more common in the large airways where velocity and airway radius are high.",True,Text,Figure 5.2,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.2.png,Figure 5.2: Turbulent flow.
f6d7ffa9-54fe-4091-a695-315be802e901,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"When velocity increases or tube radius decreases then this organization is lost. Collisions between molecules and with the tube wall are now more frequent and movement is more chaotic, and the flow becomes turbulent (figure 5.2). At this point some molecules are at times moving against the pressure gradient due to these collisions. Consequently, to generate the same amount of molecule movement (i.e., flow) from one end of the tube to another, a greater pressure differential is needed when flow becomes turbulent. Turbulent flow is more common in the large airways where velocity and airway radius are high.",True,Text,Figure 5.2,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.2.png,Figure 5.2: Turbulent flow.
f6d7ffa9-54fe-4091-a695-315be802e901,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"When velocity increases or tube radius decreases then this organization is lost. Collisions between molecules and with the tube wall are now more frequent and movement is more chaotic, and the flow becomes turbulent (figure 5.2). At this point some molecules are at times moving against the pressure gradient due to these collisions. Consequently, to generate the same amount of molecule movement (i.e., flow) from one end of the tube to another, a greater pressure differential is needed when flow becomes turbulent. Turbulent flow is more common in the large airways where velocity and airway radius are high.",True,Text,Figure 5.2,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.2.png,Figure 5.2: Turbulent flow.
90fdaa3c-ab68-4f55-a687-abe07bb2e53f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"In reality, the vast majority of the airways are branching small tubes, so we see a mixture of the two above—mostly laminar flow but some turbulence generated at the branch (or transitional) points (figure 5.3).",True,Text,Figure 5.3,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.3.png,Figure 5.3: Transitional flow.
90fdaa3c-ab68-4f55-a687-abe07bb2e53f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"In reality, the vast majority of the airways are branching small tubes, so we see a mixture of the two above—mostly laminar flow but some turbulence generated at the branch (or transitional) points (figure 5.3).",True,Text,Figure 5.3,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.3.png,Figure 5.3: Transitional flow.
90fdaa3c-ab68-4f55-a687-abe07bb2e53f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"In reality, the vast majority of the airways are branching small tubes, so we see a mixture of the two above—mostly laminar flow but some turbulence generated at the branch (or transitional) points (figure 5.3).",True,Text,Figure 5.3,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.3.png,Figure 5.3: Transitional flow.
62315e3c-8689-4c27-80f5-a3db8cd82609,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"For our purposes though we are going to look at the factors that affect flow when it is laminar—the dominant form of flow in the majority of airways. These factors are described by Poiselle’s equation. We will now break down Poiselle’s equation in relation to flow of air down airways. Although initially an intimidating equation, there are some things we can generally ignore.",True,Text,,,,
84f8f467-0f64-4fec-8d68-adf050f44a88,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,Equation 5.1,True,Text,,,,
f5e7f0ea-06e8-4491-b06f-41a69dcd3621,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],False,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
7b7a1c4a-b34e-43e9-a126-8d3c35eeb88c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"First, Poiselle says that flow decreases when length of the tube increases; because the airways have constant length, we do not have to worry about it.",True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
c7e325c6-a729-4bf8-9162-b48aad87088a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"Then there is the viscosity of the gas. This is not usually a concern either when breathing humidified air at a constant biological temperature. It does become important when breathing other gas mixtures, however, such as a helium/oxygen blend that has a lower viscosity and is given to respiratory patients or deep water divers to increase flow. But we will assume it is another constant. Pi (π) is also a constant.",True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
77e7a033-5321-485b-8685-2009889647de,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"So the two remaining variables are the important ones to understand. The pressure differential created by expansion and relaxation of the lung generates a proportional flow, and we have dealt with this in previous chapters.",True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
a0ce46ac-05dd-48fb-8b1d-42a5d6c2b298,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"What we will look at more closely now is airway radius as this has a profound effect on flow. Radius is critical for two main reasons. First it is variable, as the caliber of an airway changes with lung volume and by the action of airway smooth muscle. Second, it has a very powerful effect on flow; as you can see in Poiselle’s equation, radius is to the fourth power. This means a small increase in radius has a large effect on flow. For example, if the radius of an airway is doubled from 1 mm to 2 mm, the flow rate through the tube increases sixteenfold, which of course is two to the fourth power (i.e., 2x2x2x2). The inverse is of course true—halve the radius and flow reduces sixteenfold.",True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
1e9bca06-b7c0-47c7-ab12-f86e1cf2dbf9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"So far we have couched everything in terms of flow, but really we need to look at airway resistance. Because resistance is simply the reciprocal (or opposite) of flow, we can flip Poiselle’s equation upside down to describe resistance, and we now see that a reduction in radius (r) causes a large increase in resistance (R).",True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
f8f3919d-bf3b-42a1-86c9-d03e1bfd64ec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,Equation 5.2,True,[latex]\dot{V} = \displaystyle\frac{\Delta P \times \pi \times r^4}{8n \times L}[/latex],,,,
ba54a1d6-0d3a-4a6a-badb-a3813a325d5d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,[latex]R = \displaystyle\frac{8n \times L}{\Delta P \times \pi \times r^4}[/latex],False,[latex]R = \displaystyle\frac{8n \times L}{\Delta P \times \pi \times r^4}[/latex],,,,
1a86985b-f3e0-4ae3-8835-c5c2098d53bd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,Airway Resistance,False,Airway Resistance,,,,
4cadbb19-3ffa-40ed-b257-d7251c63caa4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"So with radius having such a powerful effect on airway resistance we would expect that the early and larger generations of airways would offer the least resistance to flow, and resistance would increase as we descended deeper into the lung to the smaller and later airway generations. Figure 5.4 shows the opposite is true—that airway resistance decreases as the airway generations are descended. This is because the total cross-sectional area increases with each generation—while the early and large airways are wide, they are few. The lower and smaller airways are much more numerous, and so collectively they have a greater cross-sectional area and therefore offer less resistance.",True,Airway Resistance,Figure 5.4,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.4.png,Figure 5.4: Airway resistance down the bronchial tree.
4cadbb19-3ffa-40ed-b257-d7251c63caa4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"So with radius having such a powerful effect on airway resistance we would expect that the early and larger generations of airways would offer the least resistance to flow, and resistance would increase as we descended deeper into the lung to the smaller and later airway generations. Figure 5.4 shows the opposite is true—that airway resistance decreases as the airway generations are descended. This is because the total cross-sectional area increases with each generation—while the early and large airways are wide, they are few. The lower and smaller airways are much more numerous, and so collectively they have a greater cross-sectional area and therefore offer less resistance.",True,Airway Resistance,Figure 5.4,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.4.png,Figure 5.4: Airway resistance down the bronchial tree.
4cadbb19-3ffa-40ed-b257-d7251c63caa4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"So with radius having such a powerful effect on airway resistance we would expect that the early and larger generations of airways would offer the least resistance to flow, and resistance would increase as we descended deeper into the lung to the smaller and later airway generations. Figure 5.4 shows the opposite is true—that airway resistance decreases as the airway generations are descended. This is because the total cross-sectional area increases with each generation—while the early and large airways are wide, they are few. The lower and smaller airways are much more numerous, and so collectively they have a greater cross-sectional area and therefore offer less resistance.",True,Airway Resistance,Figure 5.4,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.4.png,Figure 5.4: Airway resistance down the bronchial tree.
5c29eeeb-6493-477a-802a-1e31e7bdcaa5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,The highest point of resistance is actually the midsize bronchioles. There are a couple of clinically important points to make here:,True,Airway Resistance,,,,
6931932a-abce-4349-987d-40d28af57838,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,Airway Resistance and Lung Volume,False,Airway Resistance and Lung Volume,,,,
6faa3af1-08d4-4525-ba05-c828d21380e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"The airways without cartilaginous support significantly change their radius when the lung expands due to the radial traction. In brief, parenchymal fibers tethered to the alveoli and exterior of the airways allow the airways to be pulled open by the expanding alveoli when lung volume increases (illustrated in figure 5.5).",True,Airway Resistance and Lung Volume,Figure 5.5,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.5.png,Figure 5.5: Radial traction decreases airway resistance as lung volume increases.
6faa3af1-08d4-4525-ba05-c828d21380e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"The airways without cartilaginous support significantly change their radius when the lung expands due to the radial traction. In brief, parenchymal fibers tethered to the alveoli and exterior of the airways allow the airways to be pulled open by the expanding alveoli when lung volume increases (illustrated in figure 5.5).",True,Airway Resistance and Lung Volume,Figure 5.5,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.5.png,Figure 5.5: Radial traction decreases airway resistance as lung volume increases.
6faa3af1-08d4-4525-ba05-c828d21380e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"The airways without cartilaginous support significantly change their radius when the lung expands due to the radial traction. In brief, parenchymal fibers tethered to the alveoli and exterior of the airways allow the airways to be pulled open by the expanding alveoli when lung volume increases (illustrated in figure 5.5).",True,Airway Resistance and Lung Volume,Figure 5.5,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.5.png,Figure 5.5: Radial traction decreases airway resistance as lung volume increases.
186b2a7f-ba02-4213-b6c1-b163b56a2556,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"This increase in airway diameter means that airway resistance falls as lung volume increases. This is demonstrated by figure 5.6; as lung volume increases, then airway resistance falls exponentially.",True,Airway Resistance and Lung Volume,Figure 5.6,Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.6.png,Figure 5.6: Airway resistance and lung volume.
186b2a7f-ba02-4213-b6c1-b163b56a2556,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"This increase in airway diameter means that airway resistance falls as lung volume increases. This is demonstrated by figure 5.6; as lung volume increases, then airway resistance falls exponentially.",True,Airway Resistance and Lung Volume,Figure 5.6,Fundamentals of Airflow,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.6.png,Figure 5.6: Airway resistance and lung volume.
186b2a7f-ba02-4213-b6c1-b163b56a2556,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"This increase in airway diameter means that airway resistance falls as lung volume increases. This is demonstrated by figure 5.6; as lung volume increases, then airway resistance falls exponentially.",True,Airway Resistance and Lung Volume,Figure 5.6,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/5.6.png,Figure 5.6: Airway resistance and lung volume.
6b513029-81f4-4761-aa67-c4170db8c28b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"The inverse is also true, that as lung volume decreases, airway radius declines. This may happen to a sufficient extent to allow small airways to collapse. It is worth noting here that respiratory patients frequently breathe at higher lung volumes. While there are mechanical reasons for this that we will discover in the next chapter, the higher lung volume may at least improve airway conductance (although it carries many other disadvantages).",True,Airway Resistance and Lung Volume,,,,
3f6219af-5228-40ed-884a-143e03acbebc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,Airway Resistance and Neural Control,False,Airway Resistance and Neural Control,,,,
204c22f9-9772-472c-b321-25182bf56286,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"As well as the lung volume effect, the tone of airway smooth muscle is also a powerful determinant of airway radius and therefore resistance. The muscle is arranged in a ring pattern around the airway circumference. Contraction of the smooth muscle causes bronchoconstriction, decreasing the airway radius. Relaxation of the smooth muscle allows bronchodilation.",True,Airway Resistance and Neural Control,,,,
e01ced53-89d9-4805-b830-6dd8184a38da,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"Airway smooth muscle is under the control of the autonomic nervous system. Parasympathetic release of acetylcholine causes activation of muscarinic receptors. This causes a rise in intracellular calcium that activates the smooth muscle. Muscle is relaxed by sympathetic stimulation of β2 adrenergic receptors. These β2 receptors are the target of bronchodilator drugs, such as albuterol, that resolve the inappropriate contraction of smooth muscle seen in the hypersensitive airways of asthmatics.",True,Airway Resistance and Neural Control,,,,
afb9e071-67f6-4506-89f6-93a0ca9f5c09,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"The bronchoconstrictive pathway is utilized by the irritant reflex that is initiated by airway wall receptors detecting the arrival of inspired particulates. This defensive reflex results in bronchoconstriction, presumably to limit the entry of more particulates.",True,Airway Resistance and Neural Control,,,,
1d210a00-3591-42eb-ad76-b2d1184f7fe6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,A number of inflammatory mediators also cause bronchoconstriction and probably play a significant role in the bronchoconstriction of asthma (which frequently also involves airway inflammation).,True,Airway Resistance and Neural Control,,,,
bf1bbf32-6521-4e99-902c-9db9b2005da3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,Low airway PCO2 also has a direct stimulatory effect on airway smooth muscle and a bronchoconstrictive effect. This is presumably to shunt air to other regions of the lung and away from regions where overventilation caused the low PCO2.,True,Airway Resistance and Neural Control,,,,
dc9c58bc-4d0c-4959-9445-f8c4baf5cb4c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,Summary,False,Summary,,,,
72d04a35-5ed8-47ab-892e-177dd866c796,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"So now you should be able to understand how the type of flow, airway radius, lung volume, and autonomic nervous system all influence airway resistance and so can either oppose or promote the flow of air in the lung.",True,Summary,,,,
cb4f0c75-e3df-4eaf-a875-0da2a237d72d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,Text,False,Text,,,,
4b2acdd2-66c1-491e-87f2-27861d53a135,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"Levitsky, Michael G. “Chapter 2: Mechanics of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
36455ae2-04f4-4fd6-94e0-ed4b0403ae5b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
c31dca92-0e8e-4d85-a96c-f50537046e0c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,5. Airflow and Airway Resistance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/airflow-and-airway-resistance/,"Widdicombe, John G., and Andrew S. Davis. “Chapter 3.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
61bb9cca-0afd-492f-8ebd-599e2b474f4d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,Introduction,False,Introduction,,,,
8111fca7-baa1-496b-90d3-ef1c8d02b32e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,Lung Parenchyma and Radial Traction,False,Lung Parenchyma and Radial Traction,,,,
a51c7485-ccc2-408b-b8e4-81a967726da8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"Before we look at ventilation distribution we need to understand a little more about lung structure. Although the lung is composed of individual components, such as the alveoli within distinct ascini, the airways, and the blood vessels, the parenchymal tissue between these components helps form the mechanical structure of the lung.",True,Lung Parenchyma and Radial Traction,,,,
09fc2fc3-6f3e-400f-9d1a-8f68ce4cd87c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,ascini,False,ascini,,,,
be8b78cd-0195-4b08-b835-d711e5910ebf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"In brief, collagenous and elastic fibers run the length of the large airways and into the lobes forming the axial network. Fibers beneath the pleura and within the septal spaces between the lobes form a peripheral network, and finally thin fibers surrounding the alveoli within the lobes form the septal network. Together these networks form a fibrous “web” of the lung (figure 4.1).",True,ascini,Figure 4.1,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.1.png,Figure 4.1: The fiber networks of the lung.
be8b78cd-0195-4b08-b835-d711e5910ebf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"In brief, collagenous and elastic fibers run the length of the large airways and into the lobes forming the axial network. Fibers beneath the pleura and within the septal spaces between the lobes form a peripheral network, and finally thin fibers surrounding the alveoli within the lobes form the septal network. Together these networks form a fibrous “web” of the lung (figure 4.1).",True,ascini,Figure 4.1,Radial Traction,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.1.png,Figure 4.1: The fiber networks of the lung.
be8b78cd-0195-4b08-b835-d711e5910ebf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"In brief, collagenous and elastic fibers run the length of the large airways and into the lobes forming the axial network. Fibers beneath the pleura and within the septal spaces between the lobes form a peripheral network, and finally thin fibers surrounding the alveoli within the lobes form the septal network. Together these networks form a fibrous “web” of the lung (figure 4.1).",True,ascini,Figure 4.1,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.1.png,Figure 4.1: The fiber networks of the lung.
05b86415-fa0a-4fd9-bcd2-ac5248007ef1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"Functionally what this means is that movement of one lung structure is transferred to others. As the lung inflates these fibrous connections have a significant impact on lung function and the pulmonary vasculature. Expanding alveoli pull on fibers that are attached to neighboring airways and blood vessels and, indeed, other alveoli.",True,ascini,,,,
e6b3312f-2269-4d95-a367-9aa35274f3d4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"The expanding lung volume tends to pull open airways and blood vessels, lowering the resistance of both as inspiration continues, as is illustrated in figure 4.2.",True,ascini,Figure 4.2,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.2.png,Figure 4.2: The action of radial traction.
e6b3312f-2269-4d95-a367-9aa35274f3d4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"The expanding lung volume tends to pull open airways and blood vessels, lowering the resistance of both as inspiration continues, as is illustrated in figure 4.2.",True,ascini,Figure 4.2,Radial Traction,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.2.png,Figure 4.2: The action of radial traction.
e6b3312f-2269-4d95-a367-9aa35274f3d4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"The expanding lung volume tends to pull open airways and blood vessels, lowering the resistance of both as inspiration continues, as is illustrated in figure 4.2.",True,ascini,Figure 4.2,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.2.png,Figure 4.2: The action of radial traction.
e09c9161-fc78-4197-acb5-13e6b2517377,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"Radial traction (sometimes called parenchymal traction) is an important component of the lung’s mechanical behavior, and it means that lung volume has an effect on airway and vascular resistance.",True,ascini,,,,
7fac62a3-dcfc-4f2a-9ed3-f2ad58606fce,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"More important for us now though is the understanding that the lung is highly connected within itself. And it is a good thing that it is these fiber networks transfer changes in pleural pressure from the lung periphery to its center; without the networks, only the alveoli at the periphery of the lung would expand when pleural pressure became negative during inspiration.",True,ascini,,,,
b86a276d-3ccd-419d-80d8-19a1ed9b8520,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"It also means that the effects of gravity are transferred to the lung as a single unit, and we will look at that now.",True,ascini,,,,
b41e11b3-41b4-44c1-9c3d-bfa3898b6b9b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,Distribution of Ventilation Across the Lung,False,Distribution of Ventilation Across the Lung,,,,
37d203a4-7994-4997-9a6d-f7c0e178c7b7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"The lung hangs in the thorax supported by the trachea and the surface tension adhering its outer surface to the inside of the thoracic cavity. Gravity obviously tends to pull the lung downward, and this pull has an unequal effect on alveoli at different heights of the lung.",True,Distribution of Ventilation Across the Lung,,,,
f387b6f8-aa1f-4f5d-a949-9400ba45da0a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,Distribution of Ventilation and Gravity,False,Distribution of Ventilation and Gravity,,,,
0d6fedce-9752-4d68-81b5-7494c5f5e736,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"Alveoli at the apex (top) of the lung have a substantial amount of lung tissue below them for gravity to act on, so there is a large force pulling the lung away from the pleural space here and hence at the top of the lung intrapleural pressure is more negative. As we descend down the lung the mass below each point becomes less and less, so the pull on the pleural space declines, and we see intrapleural pressure become less and less negative.",True,Distribution of Ventilation and Gravity,,,,
d88f06b7-a07c-477f-a356-9b5556a97395,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"Simply because of gravity, therefore, we have a distribution of intrapleural pressures. As you know from the previous chapter, intrapleural pressure determines alveolus size (figure 4.3). So at the apex of the lung alveoli tend to be large because of the more negative intrapleural pressure, while at the base, alveoli are less extended because of the less negative intrapleural pressure. If an analogy would help, look at this slinky being held up (figure 4.4). The coils near the top of it are pulled far apart because of the weight of the slinky below the top. As you travel down the slinky the coils are less and less extended as less and less weight below pulls on them. The lung acts just the same; alveoli at the top are extended at rest, while those at the base have a smaller volume.",True,Distribution of Ventilation and Gravity,Figure 4.3,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
d88f06b7-a07c-477f-a356-9b5556a97395,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"Simply because of gravity, therefore, we have a distribution of intrapleural pressures. As you know from the previous chapter, intrapleural pressure determines alveolus size (figure 4.3). So at the apex of the lung alveoli tend to be large because of the more negative intrapleural pressure, while at the base, alveoli are less extended because of the less negative intrapleural pressure. If an analogy would help, look at this slinky being held up (figure 4.4). The coils near the top of it are pulled far apart because of the weight of the slinky below the top. As you travel down the slinky the coils are less and less extended as less and less weight below pulls on them. The lung acts just the same; alveoli at the top are extended at rest, while those at the base have a smaller volume.",True,Distribution of Ventilation and Gravity,Figure 4.3,Radial Traction,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
d88f06b7-a07c-477f-a356-9b5556a97395,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"Simply because of gravity, therefore, we have a distribution of intrapleural pressures. As you know from the previous chapter, intrapleural pressure determines alveolus size (figure 4.3). So at the apex of the lung alveoli tend to be large because of the more negative intrapleural pressure, while at the base, alveoli are less extended because of the less negative intrapleural pressure. If an analogy would help, look at this slinky being held up (figure 4.4). The coils near the top of it are pulled far apart because of the weight of the slinky below the top. As you travel down the slinky the coils are less and less extended as less and less weight below pulls on them. The lung acts just the same; alveoli at the top are extended at rest, while those at the base have a smaller volume.",True,Distribution of Ventilation and Gravity,Figure 4.3,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
9e36424f-a1ab-4191-8732-63f704c81294,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"This has ramifications on where air entering the lung goes and how ventilation is distributed across the lung (more on the implications of this in chapter 13). Alveoli at the apex of the lung are already extended and therefore have limited capacity to take in more air; their resting volume is also close to the flat part of the compliance curve (figure 4.3), so they are more difficult to inflate. The smaller alveoli at the base of the lung, however, still have a greater capacity for expansion, and the smaller resting volume places them on the steeper section of the compliance curve; consequently they are easier to inflate, and air takes the path of least resistance.",True,Distribution of Ventilation and Gravity,Figure 4.3,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
9e36424f-a1ab-4191-8732-63f704c81294,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"This has ramifications on where air entering the lung goes and how ventilation is distributed across the lung (more on the implications of this in chapter 13). Alveoli at the apex of the lung are already extended and therefore have limited capacity to take in more air; their resting volume is also close to the flat part of the compliance curve (figure 4.3), so they are more difficult to inflate. The smaller alveoli at the base of the lung, however, still have a greater capacity for expansion, and the smaller resting volume places them on the steeper section of the compliance curve; consequently they are easier to inflate, and air takes the path of least resistance.",True,Distribution of Ventilation and Gravity,Figure 4.3,Radial Traction,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
9e36424f-a1ab-4191-8732-63f704c81294,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"This has ramifications on where air entering the lung goes and how ventilation is distributed across the lung (more on the implications of this in chapter 13). Alveoli at the apex of the lung are already extended and therefore have limited capacity to take in more air; their resting volume is also close to the flat part of the compliance curve (figure 4.3), so they are more difficult to inflate. The smaller alveoli at the base of the lung, however, still have a greater capacity for expansion, and the smaller resting volume places them on the steeper section of the compliance curve; consequently they are easier to inflate, and air takes the path of least resistance.",True,Distribution of Ventilation and Gravity,Figure 4.3,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
18e21582-f8de-47df-b66f-013595cc7781,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"Because of this, the alveoli at the apex of the lung rapidly fill to capacity on inspiration, and the vast majority of inspired air descends toward the base toward the more compliant and less extended alveoli. This uneven distribution of ventilation is something we will return to when we address other learning objectives, so it is worth understanding.",True,Distribution of Ventilation and Gravity,,,,
e562fc82-ae59-4e9c-a721-9b1f56348365,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,Distribution of Ventilation and Lung Volume,False,Distribution of Ventilation and Lung Volume,,,,
c97d9bb0-e9af-41df-a403-3810771f74cb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"The distribution of ventilation is also effected by lung volume, and at low lung volumes the apex of the lung is actually better ventilated than the base—again, this is due to changes in alveolar compliance.",True,Distribution of Ventilation and Lung Volume,,,,
61698af8-8f5e-423c-b912-4307c8078a9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"As the lung is emptied below functional residual capacity, that is below the normal point that expiration ends, the recoil of the lung is reduced and therefore intrapleural pressure becomes progressively less negative (or more positive if that is the way you would like to think of it). Compared to the normal resting volume we just dealt with, at low lung volumes the intrapleural pressure may be up to −4 cm H2O (compared to −10). This pushes the apical alveoli down on to the steep part of the compliance curve, and therefore they are easier to inflate.",True,Distribution of Ventilation and Lung Volume,,,,
3610db22-ab8c-4579-a5cb-6301265a033f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,H2O,False,H2O,,,,
f471b51b-53e8-4a5c-8be6-104466a4f6cc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"The intrapleural pressure at the base of the lung may actually become positive at low lung volumes. Now that force that tended to open up alveoli is actually a force that tends to compress alveoli. In our example here the intrapleural reaches 3.5 cm H2O, a force that may lead to airway compression and thereby reduce ventilation to the basal alveoli. This intrapleural pressure will certainly place these alveoli on the very flat and therefore noncompliant section of the compliance curve and make them difficult to inflate because of the surface tension and small radius effect we have discussed previously.",True,H2O,,,,
18e1b47a-5c63-4308-bf13-87bdd7bd0d3b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,Summary,False,Summary,,,,
51c22bee-8d26-45c5-b56d-5e272b4882ca,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,Ventilation is unevenly distributed across the lung because of the range of intrapleural pressures that are established down the lung by gravity. At normal lung volumes the base of the lung is better ventilated than the apex.,True,Summary,,,,
34c1cc59-112f-438a-969f-fc135a5ae24c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"At low lung volumes this relationship is reversed as intrapleural pressures at the base of the lung become compressive, reducing the compliance of basal alveoli, while the compliance of apical alveoli is increased.",True,Summary,,,,
ff19f223-63d9-4e1e-9eed-47a243dee067,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,Text,False,Text,,,,
a727ff1b-c7d9-44d4-b217-4264f3ca8110,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"Levitsky, Michael G. “Chapter 2: Mechanics of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
da1b93a3-47e5-48af-8b9b-ac0e598767d4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
6122ed24-6881-4243-b127-64fd05cdb94a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-2,"Widdicombe, John G., and Andrew S. Davis. “Chapter 1.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
7816385b-be3f-4cc1-bde5-8d7587a3e876,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,Introduction,False,Introduction,,,,
b2676751-088f-4ba1-b7b9-27bf1c6d5f80,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,Lung Parenchyma and Radial Traction,False,Lung Parenchyma and Radial Traction,,,,
49f7ad03-bee0-4c5c-b6f5-3c63d1c02c42,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"Before we look at ventilation distribution we need to understand a little more about lung structure. Although the lung is composed of individual components, such as the alveoli within distinct ascini, the airways, and the blood vessels, the parenchymal tissue between these components helps form the mechanical structure of the lung.",True,Lung Parenchyma and Radial Traction,,,,
42a34cd5-3382-4745-a8c2-890caa1ccf00,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,ascini,False,ascini,,,,
a7f60d34-dda7-493e-9665-fbae05feae31,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"In brief, collagenous and elastic fibers run the length of the large airways and into the lobes forming the axial network. Fibers beneath the pleura and within the septal spaces between the lobes form a peripheral network, and finally thin fibers surrounding the alveoli within the lobes form the septal network. Together these networks form a fibrous “web” of the lung (figure 4.1).",True,ascini,Figure 4.1,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.1.png,Figure 4.1: The fiber networks of the lung.
a7f60d34-dda7-493e-9665-fbae05feae31,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"In brief, collagenous and elastic fibers run the length of the large airways and into the lobes forming the axial network. Fibers beneath the pleura and within the septal spaces between the lobes form a peripheral network, and finally thin fibers surrounding the alveoli within the lobes form the septal network. Together these networks form a fibrous “web” of the lung (figure 4.1).",True,ascini,Figure 4.1,Radial Traction,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.1.png,Figure 4.1: The fiber networks of the lung.
a7f60d34-dda7-493e-9665-fbae05feae31,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"In brief, collagenous and elastic fibers run the length of the large airways and into the lobes forming the axial network. Fibers beneath the pleura and within the septal spaces between the lobes form a peripheral network, and finally thin fibers surrounding the alveoli within the lobes form the septal network. Together these networks form a fibrous “web” of the lung (figure 4.1).",True,ascini,Figure 4.1,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.1.png,Figure 4.1: The fiber networks of the lung.
0690534e-3020-4f8b-8942-90c64c799ff3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"Functionally what this means is that movement of one lung structure is transferred to others. As the lung inflates these fibrous connections have a significant impact on lung function and the pulmonary vasculature. Expanding alveoli pull on fibers that are attached to neighboring airways and blood vessels and, indeed, other alveoli.",True,ascini,,,,
ee8c2c86-23d2-42c1-aaa4-b16160f3b75f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"The expanding lung volume tends to pull open airways and blood vessels, lowering the resistance of both as inspiration continues, as is illustrated in figure 4.2.",True,ascini,Figure 4.2,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.2.png,Figure 4.2: The action of radial traction.
ee8c2c86-23d2-42c1-aaa4-b16160f3b75f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"The expanding lung volume tends to pull open airways and blood vessels, lowering the resistance of both as inspiration continues, as is illustrated in figure 4.2.",True,ascini,Figure 4.2,Radial Traction,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.2.png,Figure 4.2: The action of radial traction.
ee8c2c86-23d2-42c1-aaa4-b16160f3b75f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"The expanding lung volume tends to pull open airways and blood vessels, lowering the resistance of both as inspiration continues, as is illustrated in figure 4.2.",True,ascini,Figure 4.2,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.2.png,Figure 4.2: The action of radial traction.
1bef8bda-2633-4f1e-b327-db002257d02f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"Radial traction (sometimes called parenchymal traction) is an important component of the lung’s mechanical behavior, and it means that lung volume has an effect on airway and vascular resistance.",True,ascini,,,,
17e514d3-c5ab-4687-82e7-f53ea116f0db,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"More important for us now though is the understanding that the lung is highly connected within itself. And it is a good thing that it is these fiber networks transfer changes in pleural pressure from the lung periphery to its center; without the networks, only the alveoli at the periphery of the lung would expand when pleural pressure became negative during inspiration.",True,ascini,,,,
579ef00d-7589-4ecd-91d7-7d61e0fa4ba6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"It also means that the effects of gravity are transferred to the lung as a single unit, and we will look at that now.",True,ascini,,,,
145bf6ff-1d5e-4006-b3ee-18bd80bf8d02,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,Distribution of Ventilation Across the Lung,False,Distribution of Ventilation Across the Lung,,,,
f8fccc77-8e54-4588-aac3-77b64a2f8323,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"The lung hangs in the thorax supported by the trachea and the surface tension adhering its outer surface to the inside of the thoracic cavity. Gravity obviously tends to pull the lung downward, and this pull has an unequal effect on alveoli at different heights of the lung.",True,Distribution of Ventilation Across the Lung,,,,
60af04a6-440e-460a-a75c-b8d3c9c4c0b2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,Distribution of Ventilation and Gravity,False,Distribution of Ventilation and Gravity,,,,
ccb7b667-7b29-418c-96c0-5cd76f290ad4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"Alveoli at the apex (top) of the lung have a substantial amount of lung tissue below them for gravity to act on, so there is a large force pulling the lung away from the pleural space here and hence at the top of the lung intrapleural pressure is more negative. As we descend down the lung the mass below each point becomes less and less, so the pull on the pleural space declines, and we see intrapleural pressure become less and less negative.",True,Distribution of Ventilation and Gravity,,,,
1bcb99c6-e00a-4e56-84c6-21ed4aae49f1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"Simply because of gravity, therefore, we have a distribution of intrapleural pressures. As you know from the previous chapter, intrapleural pressure determines alveolus size (figure 4.3). So at the apex of the lung alveoli tend to be large because of the more negative intrapleural pressure, while at the base, alveoli are less extended because of the less negative intrapleural pressure. If an analogy would help, look at this slinky being held up (figure 4.4). The coils near the top of it are pulled far apart because of the weight of the slinky below the top. As you travel down the slinky the coils are less and less extended as less and less weight below pulls on them. The lung acts just the same; alveoli at the top are extended at rest, while those at the base have a smaller volume.",True,Distribution of Ventilation and Gravity,Figure 4.3,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
1bcb99c6-e00a-4e56-84c6-21ed4aae49f1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"Simply because of gravity, therefore, we have a distribution of intrapleural pressures. As you know from the previous chapter, intrapleural pressure determines alveolus size (figure 4.3). So at the apex of the lung alveoli tend to be large because of the more negative intrapleural pressure, while at the base, alveoli are less extended because of the less negative intrapleural pressure. If an analogy would help, look at this slinky being held up (figure 4.4). The coils near the top of it are pulled far apart because of the weight of the slinky below the top. As you travel down the slinky the coils are less and less extended as less and less weight below pulls on them. The lung acts just the same; alveoli at the top are extended at rest, while those at the base have a smaller volume.",True,Distribution of Ventilation and Gravity,Figure 4.3,Radial Traction,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
1bcb99c6-e00a-4e56-84c6-21ed4aae49f1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"Simply because of gravity, therefore, we have a distribution of intrapleural pressures. As you know from the previous chapter, intrapleural pressure determines alveolus size (figure 4.3). So at the apex of the lung alveoli tend to be large because of the more negative intrapleural pressure, while at the base, alveoli are less extended because of the less negative intrapleural pressure. If an analogy would help, look at this slinky being held up (figure 4.4). The coils near the top of it are pulled far apart because of the weight of the slinky below the top. As you travel down the slinky the coils are less and less extended as less and less weight below pulls on them. The lung acts just the same; alveoli at the top are extended at rest, while those at the base have a smaller volume.",True,Distribution of Ventilation and Gravity,Figure 4.3,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
17e19667-7b89-4d90-9714-770329779c2f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"This has ramifications on where air entering the lung goes and how ventilation is distributed across the lung (more on the implications of this in chapter 13). Alveoli at the apex of the lung are already extended and therefore have limited capacity to take in more air; their resting volume is also close to the flat part of the compliance curve (figure 4.3), so they are more difficult to inflate. The smaller alveoli at the base of the lung, however, still have a greater capacity for expansion, and the smaller resting volume places them on the steeper section of the compliance curve; consequently they are easier to inflate, and air takes the path of least resistance.",True,Distribution of Ventilation and Gravity,Figure 4.3,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
17e19667-7b89-4d90-9714-770329779c2f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"This has ramifications on where air entering the lung goes and how ventilation is distributed across the lung (more on the implications of this in chapter 13). Alveoli at the apex of the lung are already extended and therefore have limited capacity to take in more air; their resting volume is also close to the flat part of the compliance curve (figure 4.3), so they are more difficult to inflate. The smaller alveoli at the base of the lung, however, still have a greater capacity for expansion, and the smaller resting volume places them on the steeper section of the compliance curve; consequently they are easier to inflate, and air takes the path of least resistance.",True,Distribution of Ventilation and Gravity,Figure 4.3,Radial Traction,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
17e19667-7b89-4d90-9714-770329779c2f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"This has ramifications on where air entering the lung goes and how ventilation is distributed across the lung (more on the implications of this in chapter 13). Alveoli at the apex of the lung are already extended and therefore have limited capacity to take in more air; their resting volume is also close to the flat part of the compliance curve (figure 4.3), so they are more difficult to inflate. The smaller alveoli at the base of the lung, however, still have a greater capacity for expansion, and the smaller resting volume places them on the steeper section of the compliance curve; consequently they are easier to inflate, and air takes the path of least resistance.",True,Distribution of Ventilation and Gravity,Figure 4.3,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
0ac2395c-f60d-4afa-b754-52c97031649b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"Because of this, the alveoli at the apex of the lung rapidly fill to capacity on inspiration, and the vast majority of inspired air descends toward the base toward the more compliant and less extended alveoli. This uneven distribution of ventilation is something we will return to when we address other learning objectives, so it is worth understanding.",True,Distribution of Ventilation and Gravity,,,,
bafc33ac-f983-47ac-930f-584e32874d42,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,Distribution of Ventilation and Lung Volume,False,Distribution of Ventilation and Lung Volume,,,,
831dac5d-8490-495e-9bb0-5fbbf4d88727,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"The distribution of ventilation is also effected by lung volume, and at low lung volumes the apex of the lung is actually better ventilated than the base—again, this is due to changes in alveolar compliance.",True,Distribution of Ventilation and Lung Volume,,,,
f9bffe05-58b0-4fde-a49d-d093fd36e3c2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"As the lung is emptied below functional residual capacity, that is below the normal point that expiration ends, the recoil of the lung is reduced and therefore intrapleural pressure becomes progressively less negative (or more positive if that is the way you would like to think of it). Compared to the normal resting volume we just dealt with, at low lung volumes the intrapleural pressure may be up to −4 cm H2O (compared to −10). This pushes the apical alveoli down on to the steep part of the compliance curve, and therefore they are easier to inflate.",True,Distribution of Ventilation and Lung Volume,,,,
1ea5a3a7-c89f-49e6-99a5-6887b825166f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,H2O,False,H2O,,,,
8c5cd4cc-25fe-4e75-b469-6bc2700cf426,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"The intrapleural pressure at the base of the lung may actually become positive at low lung volumes. Now that force that tended to open up alveoli is actually a force that tends to compress alveoli. In our example here the intrapleural reaches 3.5 cm H2O, a force that may lead to airway compression and thereby reduce ventilation to the basal alveoli. This intrapleural pressure will certainly place these alveoli on the very flat and therefore noncompliant section of the compliance curve and make them difficult to inflate because of the surface tension and small radius effect we have discussed previously.",True,H2O,,,,
33f7c668-b5fe-4dfe-9e1c-5e8cd064aac5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,Summary,False,Summary,,,,
abee7ccd-3545-4aa5-9094-1ec33f0fbe2c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,Ventilation is unevenly distributed across the lung because of the range of intrapleural pressures that are established down the lung by gravity. At normal lung volumes the base of the lung is better ventilated than the apex.,True,Summary,,,,
1286ac7b-6410-49a1-82ec-cac300f60fb8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"At low lung volumes this relationship is reversed as intrapleural pressures at the base of the lung become compressive, reducing the compliance of basal alveoli, while the compliance of apical alveoli is increased.",True,Summary,,,,
751477c4-6273-4969-8ad9-15fa3cb08497,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,Text,False,Text,,,,
d738e7eb-17a9-49fa-bb84-b4245d684678,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"Levitsky, Michael G. “Chapter 2: Mechanics of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
91f0b465-f8e2-4d3e-b068-0d4e87fd4441,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
5833310b-0f0c-4fad-9f95-1fb7ca1974c0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Radial Traction,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/#chapter-31-section-1,"Widdicombe, John G., and Andrew S. Davis. “Chapter 1.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
673428f3-7c76-4a7a-8d50-55e9831c001c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,Introduction,False,Introduction,,,,
b70d5bbe-01b5-4f15-a9f2-fe1b14c9e26b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,Lung Parenchyma and Radial Traction,False,Lung Parenchyma and Radial Traction,,,,
df22dea0-b2ea-4ac9-9a2a-e95e692c53d3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"Before we look at ventilation distribution we need to understand a little more about lung structure. Although the lung is composed of individual components, such as the alveoli within distinct ascini, the airways, and the blood vessels, the parenchymal tissue between these components helps form the mechanical structure of the lung.",True,Lung Parenchyma and Radial Traction,,,,
e3e6b6d0-9744-4281-9966-17efb8da080d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,ascini,False,ascini,,,,
353c5f09-7c3a-453b-8f8c-3ab390cb4c59,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"In brief, collagenous and elastic fibers run the length of the large airways and into the lobes forming the axial network. Fibers beneath the pleura and within the septal spaces between the lobes form a peripheral network, and finally thin fibers surrounding the alveoli within the lobes form the septal network. Together these networks form a fibrous “web” of the lung (figure 4.1).",True,ascini,Figure 4.1,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.1.png,Figure 4.1: The fiber networks of the lung.
353c5f09-7c3a-453b-8f8c-3ab390cb4c59,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"In brief, collagenous and elastic fibers run the length of the large airways and into the lobes forming the axial network. Fibers beneath the pleura and within the septal spaces between the lobes form a peripheral network, and finally thin fibers surrounding the alveoli within the lobes form the septal network. Together these networks form a fibrous “web” of the lung (figure 4.1).",True,ascini,Figure 4.1,Radial Traction,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.1.png,Figure 4.1: The fiber networks of the lung.
353c5f09-7c3a-453b-8f8c-3ab390cb4c59,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"In brief, collagenous and elastic fibers run the length of the large airways and into the lobes forming the axial network. Fibers beneath the pleura and within the septal spaces between the lobes form a peripheral network, and finally thin fibers surrounding the alveoli within the lobes form the septal network. Together these networks form a fibrous “web” of the lung (figure 4.1).",True,ascini,Figure 4.1,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.1.png,Figure 4.1: The fiber networks of the lung.
b9809270-11ef-4407-856f-70bc5aa62de5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"Functionally what this means is that movement of one lung structure is transferred to others. As the lung inflates these fibrous connections have a significant impact on lung function and the pulmonary vasculature. Expanding alveoli pull on fibers that are attached to neighboring airways and blood vessels and, indeed, other alveoli.",True,ascini,,,,
88675d74-d3b0-467a-9229-58117ef74884,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"The expanding lung volume tends to pull open airways and blood vessels, lowering the resistance of both as inspiration continues, as is illustrated in figure 4.2.",True,ascini,Figure 4.2,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.2.png,Figure 4.2: The action of radial traction.
88675d74-d3b0-467a-9229-58117ef74884,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"The expanding lung volume tends to pull open airways and blood vessels, lowering the resistance of both as inspiration continues, as is illustrated in figure 4.2.",True,ascini,Figure 4.2,Radial Traction,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.2.png,Figure 4.2: The action of radial traction.
88675d74-d3b0-467a-9229-58117ef74884,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"The expanding lung volume tends to pull open airways and blood vessels, lowering the resistance of both as inspiration continues, as is illustrated in figure 4.2.",True,ascini,Figure 4.2,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.2.png,Figure 4.2: The action of radial traction.
618e3db2-9704-4d96-8502-842523c44ea2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"Radial traction (sometimes called parenchymal traction) is an important component of the lung’s mechanical behavior, and it means that lung volume has an effect on airway and vascular resistance.",True,ascini,,,,
f1644882-0248-467f-9c64-6f17f4c77803,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"More important for us now though is the understanding that the lung is highly connected within itself. And it is a good thing that it is these fiber networks transfer changes in pleural pressure from the lung periphery to its center; without the networks, only the alveoli at the periphery of the lung would expand when pleural pressure became negative during inspiration.",True,ascini,,,,
1b2dea99-0d62-4d83-b15c-f5cf1f6fff52,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"It also means that the effects of gravity are transferred to the lung as a single unit, and we will look at that now.",True,ascini,,,,
f835afc5-b3ae-4fcc-8697-1dbba5744654,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,Distribution of Ventilation Across the Lung,False,Distribution of Ventilation Across the Lung,,,,
4137a43d-31d5-4e00-876c-77e1980f923d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"The lung hangs in the thorax supported by the trachea and the surface tension adhering its outer surface to the inside of the thoracic cavity. Gravity obviously tends to pull the lung downward, and this pull has an unequal effect on alveoli at different heights of the lung.",True,Distribution of Ventilation Across the Lung,,,,
900c3b42-9e78-41fc-a6ff-6d3f4d261815,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,Distribution of Ventilation and Gravity,False,Distribution of Ventilation and Gravity,,,,
a56ea1ad-1d8b-4bb3-9997-f5cd96e63b94,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"Alveoli at the apex (top) of the lung have a substantial amount of lung tissue below them for gravity to act on, so there is a large force pulling the lung away from the pleural space here and hence at the top of the lung intrapleural pressure is more negative. As we descend down the lung the mass below each point becomes less and less, so the pull on the pleural space declines, and we see intrapleural pressure become less and less negative.",True,Distribution of Ventilation and Gravity,,,,
d24897fd-5a16-4fb2-8061-1e3bfee2ff6e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"Simply because of gravity, therefore, we have a distribution of intrapleural pressures. As you know from the previous chapter, intrapleural pressure determines alveolus size (figure 4.3). So at the apex of the lung alveoli tend to be large because of the more negative intrapleural pressure, while at the base, alveoli are less extended because of the less negative intrapleural pressure. If an analogy would help, look at this slinky being held up (figure 4.4). The coils near the top of it are pulled far apart because of the weight of the slinky below the top. As you travel down the slinky the coils are less and less extended as less and less weight below pulls on them. The lung acts just the same; alveoli at the top are extended at rest, while those at the base have a smaller volume.",True,Distribution of Ventilation and Gravity,Figure 4.3,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
d24897fd-5a16-4fb2-8061-1e3bfee2ff6e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"Simply because of gravity, therefore, we have a distribution of intrapleural pressures. As you know from the previous chapter, intrapleural pressure determines alveolus size (figure 4.3). So at the apex of the lung alveoli tend to be large because of the more negative intrapleural pressure, while at the base, alveoli are less extended because of the less negative intrapleural pressure. If an analogy would help, look at this slinky being held up (figure 4.4). The coils near the top of it are pulled far apart because of the weight of the slinky below the top. As you travel down the slinky the coils are less and less extended as less and less weight below pulls on them. The lung acts just the same; alveoli at the top are extended at rest, while those at the base have a smaller volume.",True,Distribution of Ventilation and Gravity,Figure 4.3,Radial Traction,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
d24897fd-5a16-4fb2-8061-1e3bfee2ff6e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"Simply because of gravity, therefore, we have a distribution of intrapleural pressures. As you know from the previous chapter, intrapleural pressure determines alveolus size (figure 4.3). So at the apex of the lung alveoli tend to be large because of the more negative intrapleural pressure, while at the base, alveoli are less extended because of the less negative intrapleural pressure. If an analogy would help, look at this slinky being held up (figure 4.4). The coils near the top of it are pulled far apart because of the weight of the slinky below the top. As you travel down the slinky the coils are less and less extended as less and less weight below pulls on them. The lung acts just the same; alveoli at the top are extended at rest, while those at the base have a smaller volume.",True,Distribution of Ventilation and Gravity,Figure 4.3,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
036c928d-6a85-43cf-ad1f-0c33e63d8bd1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"This has ramifications on where air entering the lung goes and how ventilation is distributed across the lung (more on the implications of this in chapter 13). Alveoli at the apex of the lung are already extended and therefore have limited capacity to take in more air; their resting volume is also close to the flat part of the compliance curve (figure 4.3), so they are more difficult to inflate. The smaller alveoli at the base of the lung, however, still have a greater capacity for expansion, and the smaller resting volume places them on the steeper section of the compliance curve; consequently they are easier to inflate, and air takes the path of least resistance.",True,Distribution of Ventilation and Gravity,Figure 4.3,Distribution of Ventilation Across the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
036c928d-6a85-43cf-ad1f-0c33e63d8bd1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"This has ramifications on where air entering the lung goes and how ventilation is distributed across the lung (more on the implications of this in chapter 13). Alveoli at the apex of the lung are already extended and therefore have limited capacity to take in more air; their resting volume is also close to the flat part of the compliance curve (figure 4.3), so they are more difficult to inflate. The smaller alveoli at the base of the lung, however, still have a greater capacity for expansion, and the smaller resting volume places them on the steeper section of the compliance curve; consequently they are easier to inflate, and air takes the path of least resistance.",True,Distribution of Ventilation and Gravity,Figure 4.3,Radial Traction,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
036c928d-6a85-43cf-ad1f-0c33e63d8bd1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"This has ramifications on where air entering the lung goes and how ventilation is distributed across the lung (more on the implications of this in chapter 13). Alveoli at the apex of the lung are already extended and therefore have limited capacity to take in more air; their resting volume is also close to the flat part of the compliance curve (figure 4.3), so they are more difficult to inflate. The smaller alveoli at the base of the lung, however, still have a greater capacity for expansion, and the smaller resting volume places them on the steeper section of the compliance curve; consequently they are easier to inflate, and air takes the path of least resistance.",True,Distribution of Ventilation and Gravity,Figure 4.3,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/4.3.png,"Figure 4.3: Interaction of lung volume, compliance, and distribution of ventilation."
c17643d9-6bc8-4969-969d-474fafdf7932,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"Because of this, the alveoli at the apex of the lung rapidly fill to capacity on inspiration, and the vast majority of inspired air descends toward the base toward the more compliant and less extended alveoli. This uneven distribution of ventilation is something we will return to when we address other learning objectives, so it is worth understanding.",True,Distribution of Ventilation and Gravity,,,,
77834b55-9d74-47c0-8a08-904ad021a1a1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,Distribution of Ventilation and Lung Volume,False,Distribution of Ventilation and Lung Volume,,,,
04c3b8f0-f4b4-4255-9592-4c13959716aa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"The distribution of ventilation is also effected by lung volume, and at low lung volumes the apex of the lung is actually better ventilated than the base—again, this is due to changes in alveolar compliance.",True,Distribution of Ventilation and Lung Volume,,,,
89f79d23-f6ee-47cc-b4ef-307acad2836c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"As the lung is emptied below functional residual capacity, that is below the normal point that expiration ends, the recoil of the lung is reduced and therefore intrapleural pressure becomes progressively less negative (or more positive if that is the way you would like to think of it). Compared to the normal resting volume we just dealt with, at low lung volumes the intrapleural pressure may be up to −4 cm H2O (compared to −10). This pushes the apical alveoli down on to the steep part of the compliance curve, and therefore they are easier to inflate.",True,Distribution of Ventilation and Lung Volume,,,,
d73b66ac-a811-4312-9b56-dcb05bed81ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,H2O,False,H2O,,,,
1c667632-6429-47ed-a842-357fd1efdbd2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"The intrapleural pressure at the base of the lung may actually become positive at low lung volumes. Now that force that tended to open up alveoli is actually a force that tends to compress alveoli. In our example here the intrapleural reaches 3.5 cm H2O, a force that may lead to airway compression and thereby reduce ventilation to the basal alveoli. This intrapleural pressure will certainly place these alveoli on the very flat and therefore noncompliant section of the compliance curve and make them difficult to inflate because of the surface tension and small radius effect we have discussed previously.",True,H2O,,,,
367da034-57b4-4af5-a1db-9f7a95bc583f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,Summary,False,Summary,,,,
c3525d6d-834f-4920-9c89-f107bbd2fabe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,Ventilation is unevenly distributed across the lung because of the range of intrapleural pressures that are established down the lung by gravity. At normal lung volumes the base of the lung is better ventilated than the apex.,True,Summary,,,,
60f7bc81-9aa0-4544-97e5-82fe7820f2fb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"At low lung volumes this relationship is reversed as intrapleural pressures at the base of the lung become compressive, reducing the compliance of basal alveoli, while the compliance of apical alveoli is increased.",True,Summary,,,,
9081d21b-1e28-47d1-ac31-b48d146c8f4f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,Text,False,Text,,,,
7aeeabf0-bab9-4e6a-b30c-00340ba7e7f3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"Levitsky, Michael G. “Chapter 2: Mechanics of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
c9f1112b-7ab5-49b1-88c1-949eeae2bca0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
eb2b13dd-f27a-4c96-a214-fed8d4c3a16a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,4. Distribution of Ventilation,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/distribution-of-ventilation/,"Widdicombe, John G., and Andrew S. Davis. “Chapter 1.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
3a3e4666-e3eb-47e5-b5d5-48bf12f7d875,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,Introduction,False,Introduction,,,,
c7d85909-2009-453b-8eb7-c62cb1645522,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,Lung Volumes,False,Lung Volumes,,,,
6ba80913-757c-4bf2-9fae-0abce683e342,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,First let us look at lung volumes. This trace from a spirometer (figure 3.1) shows the change in lung volume as a patient breathes normally and then performs some specific maneuvers.,True,Lung Volumes,Figure 3.1,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
6ba80913-757c-4bf2-9fae-0abce683e342,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,First let us look at lung volumes. This trace from a spirometer (figure 3.1) shows the change in lung volume as a patient breathes normally and then performs some specific maneuvers.,True,Lung Volumes,Figure 3.1,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
6ba80913-757c-4bf2-9fae-0abce683e342,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,First let us look at lung volumes. This trace from a spirometer (figure 3.1) shows the change in lung volume as a patient breathes normally and then performs some specific maneuvers.,True,Lung Volumes,Figure 3.1,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
ac8ec9e3-516a-425c-b7ce-a82558e6e9e2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,Let us work through the trace from left to right. The initial part of the trace shows resting or “tidal” breathing. The amount of volume inspired during each breath is referred to as tidal volume.,True,Lung Volumes,,,,
f67812e4-2a8d-4331-bec3-b0fae9916f7f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Once a normal expiration is complete, however, the lung is far from empty, and when instructed, this patient (figure 3.1) breathes out as far as they can; this excess that comes out the lung is referred to as the expiratory reserve volume.",True,Lung Volumes,Figure 3.1,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
f67812e4-2a8d-4331-bec3-b0fae9916f7f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Once a normal expiration is complete, however, the lung is far from empty, and when instructed, this patient (figure 3.1) breathes out as far as they can; this excess that comes out the lung is referred to as the expiratory reserve volume.",True,Lung Volumes,Figure 3.1,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
f67812e4-2a8d-4331-bec3-b0fae9916f7f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Once a normal expiration is complete, however, the lung is far from empty, and when instructed, this patient (figure 3.1) breathes out as far as they can; this excess that comes out the lung is referred to as the expiratory reserve volume.",True,Lung Volumes,Figure 3.1,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
dc56756d-41ee-4ec8-b969-4573065f4b6b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Even at this point, however, some air remains in the lung, and this is referred to as residual volume. Even with maximal efforts, this volume cannot be exhaled, so at no point can the lung be fully emptied. This also means that residual volume can never be measured with a spirometer.",True,Lung Volumes,,,,
f288c178-32e1-4731-8af8-c03a67151b63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Our patient (figure 3.1) returns to normal tidal breathing for two breaths before taking a full breath in, filling the lungs as much as they can. This extra volume into the lung after a normal tidal inspiration is referred to as inspiratory reserve volume. Related to this volume is the inspiratory capacity, which is the volume that can be taken into the lung after a normal expiration; inspiratory capacity is a useful clinical measurement that we will return to when we deal with some disease states.",True,Lung Volumes,Figure 3.1,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
f288c178-32e1-4731-8af8-c03a67151b63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Our patient (figure 3.1) returns to normal tidal breathing for two breaths before taking a full breath in, filling the lungs as much as they can. This extra volume into the lung after a normal tidal inspiration is referred to as inspiratory reserve volume. Related to this volume is the inspiratory capacity, which is the volume that can be taken into the lung after a normal expiration; inspiratory capacity is a useful clinical measurement that we will return to when we deal with some disease states.",True,Lung Volumes,Figure 3.1,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
f288c178-32e1-4731-8af8-c03a67151b63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Our patient (figure 3.1) returns to normal tidal breathing for two breaths before taking a full breath in, filling the lungs as much as they can. This extra volume into the lung after a normal tidal inspiration is referred to as inspiratory reserve volume. Related to this volume is the inspiratory capacity, which is the volume that can be taken into the lung after a normal expiration; inspiratory capacity is a useful clinical measurement that we will return to when we deal with some disease states.",True,Lung Volumes,Figure 3.1,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
8763a675-1a95-47e8-9ccf-01a538f10261,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Another clinically valuable measurement is vital capacity, which is the volume of air that our patient can move out of the lung after a full inspiration, that is, the total lung capacity, minus the residual volume (remember: residual volume cannot be expelled). Forced vital capacity is a common measure taken in pulmonary function testing, and this is simply the volume that can be expelled from total lung capacity during a forceful expiration. The importance of this maneuver being forced will be dealt with when we look at airway compression (chapter 6).",True,Lung Volumes,,,,
f9e309dc-7742-4d89-91f5-00041b8b6a6d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"While the volumes we have just seen measured by spirometry in the pulmonary function lab provide valuable clinical information, we need to now look at some physiological variables that are also critical for our understanding of lung function and disease.",True,Lung Volumes,,,,
d819021e-a68e-4187-a995-01e2e9d3c4d6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,Components of Tidal Breathing,False,Components of Tidal Breathing,,,,
68b1385e-fd77-4886-a987-7a43f6cc9f83,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"As you have seen, the volume of air inspired during a normal breath is tidal volume, and the size of this is dependent on body size, but in the example here is listed as 500 mL (a good approximation). Not all this 500 mL reaches the gas exchange surfaces in the respiratory zone, however, as some never gets further than the conducting zone (i.e., it stays in the anatomical dead space). From chapter 1 we know that this dead space has a volume of 150 mL, so the amount of air reaching the alveoli in the respiratory zone is our tidal volume (500 mL), minus the dead space volume, so alveolar volume is 350 mL.",True,Components of Tidal Breathing,,,,
8193e390-06e1-4d2e-b7ef-d1f349a3c8bb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"This brings us to an important point of clarification. Minute ventilation (denoted as Ve) is the volume of air exchanged in the lung within a minute. This is analogous to cardiac output, the volume of blood pumped by the heart in a minute. As such, minute ventilation is the average tidal volume (VT) multiplied by the number of breaths taken in a minute (RR).",True,Components of Tidal Breathing,,,,
e3c8077b-c703-4e84-9cd8-ca4328c7e75e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,Equation 3.1,True,Components of Tidal Breathing,,,,
8110ec6c-2e61-45c7-9e6d-d63e35013e6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,[latex]Ve = RR \times V_T[/latex],False,[latex]Ve = RR \times V_T[/latex],,,,
d7b20370-3cc9-4e56-8211-5b1064e3ce09,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"So if respiratory rate is 10 bpm and tidal volume is 500 mL, minute ventilation is 5,000 mL.",True,[latex]Ve = RR \times V_T[/latex],,,,
0fe8cf12-ee11-477b-91fc-153382912cd4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,Equation 3.2,True,[latex]Ve = RR \times V_T[/latex],,,,
3f06a589-0e7c-484f-9030-6bbf7f46dd72,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"[latex]Ve = 10\:bpm \times 500\:mL = 5,000\:mL\:per\:min[/latex]",False,"[latex]Ve = 10\:bpm \times 500\:mL = 5,000\:mL\:per\:min[/latex]",,,,
ec2e7604-bc85-4c48-b6e8-1d2ee48175b1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Physiologically more important, however, is the alveolar minute ventilation (VA) that accounts for the “wasted” ventilation that never reached a gas exchange surface but remained in the anatomical dead space. So the calculation for VA is",True,"[latex]Ve = 10\:bpm \times 500\:mL = 5,000\:mL\:per\:min[/latex]",,,,
cc6f9246-3b61-4f24-96fb-cfa80f6019a4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,Equation 3.3,True,"[latex]Ve = 10\:bpm \times 500\:mL = 5,000\:mL\:per\:min[/latex]",,,,
b1ade39c-7ce6-43b0-8796-de835d768281,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,[latex]V_A = RR \times (V_T - V_D)[/latex],False,[latex]V_A = RR \times (V_T - V_D)[/latex],,,,
6b97a405-83a4-4da1-b864-00f13ec9449a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"where VD is the anatomical dead space (approximately 150 mL). So for our previous example, alveolar minute ventilation is",True,[latex]V_A = RR \times (V_T - V_D)[/latex],,,,
7e881735-623c-4d4e-adbf-7a3a8be20017,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,Equation 3.4,True,[latex]V_A = RR \times (V_T - V_D)[/latex],,,,
b1736f51-0207-414c-bc79-25cf858ab3d3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"[latex]V_A = 10 \times (500 - 150\:mL) = 3,500\:mL\:per\:min[/latex]",False,"[latex]V_A = 10 \times (500 - 150\:mL) = 3,500\:mL\:per\:min[/latex]",,,,
4f0e51a2-b584-48a8-b20e-1f41f292d9c4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,describing only the volume of air that reached the respiratory zone.,True,"[latex]V_A = 10 \times (500 - 150\:mL) = 3,500\:mL\:per\:min[/latex]",,,,
86aade39-a50e-4e6e-8c61-efa554b7c295,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"So far the involvement of anatomical dead space might seem academic, as it remains constant. But let us consider a different breathing pattern (as often occurs in disease states).",True,"[latex]V_A = 10 \times (500 - 150\:mL) = 3,500\:mL\:per\:min[/latex]",,,,
c028ddf4-66e2-475f-a128-70862da12d38,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"In our example above minute ventilation is 5,000 mL, but accounting for dead space we see that alveolar minute ventilation is 3,500 mL. Now let us consider another breathing pattern—one typical of a patient with restrictive lung disease where tidal volume is reduced and respiratory rate is increased. With a tidal volume of 250 mL and rate of 20, the minute ventilation remains the same, 5,000 mL.",True,"[latex]V_A = 10 \times (500 - 150\:mL) = 3,500\:mL\:per\:min[/latex]",,,,
7d3f3158-f721-4cc8-bb5a-037202006657,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,Equation 3.5,True,"[latex]V_A = 10 \times (500 - 150\:mL) = 3,500\:mL\:per\:min[/latex]",,,,
7d1d7828-f689-4710-813c-3388d069d4a6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"[latex]Ve = 20\:bpm \times 250\:mL = 5,000\:mL\:per\:min[/latex]",False,"[latex]Ve = 20\:bpm \times 250\:mL = 5,000\:mL\:per\:min[/latex]",,,,
59d9cbc6-11cd-4fbe-bb3c-94b27f90374b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,But calculating alveolar minute ventilation we see that a greater proportion of the reduced tidal volume is consumed by dead space.,True,"[latex]Ve = 20\:bpm \times 250\:mL = 5,000\:mL\:per\:min[/latex]",,,,
63e82b96-e727-4cc3-bcf3-1c951420b92c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,Equation 3.6,True,"[latex]Ve = 20\:bpm \times 250\:mL = 5,000\:mL\:per\:min[/latex]",,,,
6d457d43-83ba-479e-9cad-9e0ac31238c2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"[latex]V_A = 20 \times (250 - 150\:mL) = 2,000\:mL\:per\:min[/latex]",False,"[latex]V_A = 20 \times (250 - 150\:mL) = 2,000\:mL\:per\:min[/latex]",,,,
1c16b300-39ec-49c1-bfc7-5a2dc76d4d07,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"So despite maintaining the same minute ventilation, the second patient’s alveolar minute ventilation is reduced by 1,500 mL, which is significant given that this is the volume of air going to the gas exchange surfaces.",True,"[latex]V_A = 20 \times (250 - 150\:mL) = 2,000\:mL\:per\:min[/latex]",,,,
37c67bfc-e104-4064-89dc-96788fcfaf6a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"This partially explains why increases in ventilation are initially achieved by increases in tidal volume; as shown in figure 3.2, as tidal volume increases during exercise intensity (represented by oxygen uptake) until it reaches a plateau. Only when this plateau is reached are further increases in minute ventilation achieved by increasing respiratory rate.",True,"[latex]V_A = 20 \times (250 - 150\:mL) = 2,000\:mL\:per\:min[/latex]",Figure 3.2,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.2.png,Figure 3.2: Changes in breathing tidal volume and respiratory rate with increasing levels of exercise.
37c67bfc-e104-4064-89dc-96788fcfaf6a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"This partially explains why increases in ventilation are initially achieved by increases in tidal volume; as shown in figure 3.2, as tidal volume increases during exercise intensity (represented by oxygen uptake) until it reaches a plateau. Only when this plateau is reached are further increases in minute ventilation achieved by increasing respiratory rate.",True,"[latex]V_A = 20 \times (250 - 150\:mL) = 2,000\:mL\:per\:min[/latex]",Figure 3.2,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.2.png,Figure 3.2: Changes in breathing tidal volume and respiratory rate with increasing levels of exercise.
37c67bfc-e104-4064-89dc-96788fcfaf6a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"This partially explains why increases in ventilation are initially achieved by increases in tidal volume; as shown in figure 3.2, as tidal volume increases during exercise intensity (represented by oxygen uptake) until it reaches a plateau. Only when this plateau is reached are further increases in minute ventilation achieved by increasing respiratory rate.",True,"[latex]V_A = 20 \times (250 - 150\:mL) = 2,000\:mL\:per\:min[/latex]",Figure 3.2,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.2.png,Figure 3.2: Changes in breathing tidal volume and respiratory rate with increasing levels of exercise.
f9badee4-82c4-4073-9f76-7490c77f53b7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"So why not keep increasing tidal volume? At higher lung volumes the elastic limit of the lung is approached, and it takes more energy (muscular force) to expand, so it is more efficient and the work of breathing is less if the rate of breathing is increased to achieve higher levels of minute ventilation. This brings us to our next topic, lung compliance.",True,"[latex]V_A = 20 \times (250 - 150\:mL) = 2,000\:mL\:per\:min[/latex]",,,,
fe71d954-aa61-48bc-b23f-e8d775b2224a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,Lung Compliance,False,Lung Compliance,,,,
eb090bbf-c764-42ea-a0e8-7f58725e4d00,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Lung compliance is a description of how easy the lung is to inflate, more specifically, how much volume will change for a given pressure differential. Figure 3.3 shows a typical and normal lung compliance curve. The lower line shows how volume changes as intrapleural pressure becomes more negative (as the chest wall and diaphragm expand the thorax). The upper curve is the compliance of the lung during expiration, and it is clearly different; this is an example of hysteresis, meaning that the relationship depends on direction, and we will see why this exists later.",True,Lung Compliance,Figure 3.3,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
eb090bbf-c764-42ea-a0e8-7f58725e4d00,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Lung compliance is a description of how easy the lung is to inflate, more specifically, how much volume will change for a given pressure differential. Figure 3.3 shows a typical and normal lung compliance curve. The lower line shows how volume changes as intrapleural pressure becomes more negative (as the chest wall and diaphragm expand the thorax). The upper curve is the compliance of the lung during expiration, and it is clearly different; this is an example of hysteresis, meaning that the relationship depends on direction, and we will see why this exists later.",True,Lung Compliance,Figure 3.3,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
eb090bbf-c764-42ea-a0e8-7f58725e4d00,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Lung compliance is a description of how easy the lung is to inflate, more specifically, how much volume will change for a given pressure differential. Figure 3.3 shows a typical and normal lung compliance curve. The lower line shows how volume changes as intrapleural pressure becomes more negative (as the chest wall and diaphragm expand the thorax). The upper curve is the compliance of the lung during expiration, and it is clearly different; this is an example of hysteresis, meaning that the relationship depends on direction, and we will see why this exists later.",True,Lung Compliance,Figure 3.3,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
11bf4d41-a016-46dd-8fc1-fa130d760fd9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,Lung Compliance During Inspiration,False,Lung Compliance During Inspiration,,,,
bf688c7a-ae87-4784-bff0-a4fc4b6648af,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"You will notice at low lung volumes the slope of the compliance curve (figure 3.3) is shallower, meaning that it takes a relatively large pressure change to cause an increase in volume. This tells us at low lung volumes the lung is less distensible, or has low compliance.",True,Lung Compliance During Inspiration,Figure 3.3,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
bf688c7a-ae87-4784-bff0-a4fc4b6648af,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"You will notice at low lung volumes the slope of the compliance curve (figure 3.3) is shallower, meaning that it takes a relatively large pressure change to cause an increase in volume. This tells us at low lung volumes the lung is less distensible, or has low compliance.",True,Lung Compliance During Inspiration,Figure 3.3,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
bf688c7a-ae87-4784-bff0-a4fc4b6648af,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"You will notice at low lung volumes the slope of the compliance curve (figure 3.3) is shallower, meaning that it takes a relatively large pressure change to cause an increase in volume. This tells us at low lung volumes the lung is less distensible, or has low compliance.",True,Lung Compliance During Inspiration,Figure 3.3,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
4568b50b-5850-4ce8-87d7-3a44de82dbfb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"If we start to breathe at a higher lung volume, the slope of the curve is steeper, meaning that for a similar change in pressure there is a greater change in volume (i.e., the lung is more compliant).",True,Lung Compliance During Inspiration,,,,
938ef1ff-989b-4d01-8605-5f387607d321,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"If we start breathing at a higher lung volume still, closer to total lung capacity, we see the slope of the compliance curve flatten out again, showing that at the lung volumes the compliance of the lung is low.",True,Lung Compliance During Inspiration,,,,
8a48fba0-bb2d-407f-98e1-170502f90531,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"As you might imagine, the normal range for breathing is in the middle range where the slope is steep and the lung compliant. This corresponds to an intrapleural pressure range of −5 to −10 cm H2O, which you should know is the normal range of intrapleural pressures during tidal breathing. This means we normally breathe at a lung volume at which the lung is most compliant and therefore takes less work to inflate.",True,Lung Compliance During Inspiration,,,,
7169eb7f-c35b-4f02-aead-79505ca90aab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,H2O,False,H2O,,,,
d16ea004-19ec-4b3b-9a78-420bddc6679f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Too low a lung volume and compliance falls and work of breathing increases, likewise during breathing at high lung volumes, another contributing reason for why tidal volume plateaus during exercise.",True,H2O,,,,
451b76e9-589e-4a74-bfc0-49991bb084ef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"So now let us look at why compliance is low at high and low lung volumes, starting with the cause of low lung compliance at low volumes.",True,H2O,,,,
b3fcd35a-6d91-4bc7-b257-ff73349fa7b3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Low compliance at low volumes—Surface tension: The reason why the lung takes more pressure to inflate at low volumes is surface tension. As mentioned in chapter 1 the alveoli have a thin layer of fluid lining their inner surface. As we saw in the pleural space, this causes surface tension. Unlike the surface tension in the pleural space, in the alveoli surface tension is a disadvantage.",True,H2O,,,,
ca8faa42-d2ec-4bae-952e-07edccef8f5d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Surface tension is generated as water molecules cluster together to reduce their exposure to the gas in the alveolar space. As they gather together they drag the alveolar wall with them, producing a force that tends to pull the alveolar walls inward. The alveolar pressure opposes this force and should prevent the alveolus from collapsing (figure 3.4).",True,H2O,Figure 3.4,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.4.png,Figure 3.4: Opposing forces of alveolar pressure and surface tension.
ca8faa42-d2ec-4bae-952e-07edccef8f5d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Surface tension is generated as water molecules cluster together to reduce their exposure to the gas in the alveolar space. As they gather together they drag the alveolar wall with them, producing a force that tends to pull the alveolar walls inward. The alveolar pressure opposes this force and should prevent the alveolus from collapsing (figure 3.4).",True,H2O,Figure 3.4,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.4.png,Figure 3.4: Opposing forces of alveolar pressure and surface tension.
ca8faa42-d2ec-4bae-952e-07edccef8f5d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Surface tension is generated as water molecules cluster together to reduce their exposure to the gas in the alveolar space. As they gather together they drag the alveolar wall with them, producing a force that tends to pull the alveolar walls inward. The alveolar pressure opposes this force and should prevent the alveolus from collapsing (figure 3.4).",True,H2O,Figure 3.4,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.4.png,Figure 3.4: Opposing forces of alveolar pressure and surface tension.
da746387-5ed7-484c-bf0b-c88bcb2f1276,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"The relationship between these two opposing forces is described by Laplace’s law that states the outward (alveolar) pressure needed to oppose the inwardly directed tension is proportionate to the tension (obviously), but also inversely related to the radius of the alveolus (i.e., the smaller the radius, the greater the inwardly acting force).",True,H2O,,,,
3509f1ca-8ecc-4ad2-b9cf-3eff570619b3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"This explains why compliance is low at low lung volumes. At low lung volumes the alveoli are smaller and thus have a smaller radius. Laplace’s law states that with a low radius the pressure needed to overcome the inward force will be greater, explaining why a larger alveolar (outward) pressure is needed to inflate the alveolus from a low starting volume.",True,H2O,,,,
036a0fe8-5632-4d81-bf4b-f27259dbb8ed,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"As lung volume increases, and thus alveolar radius increases, the pressure needed to overcome the inward acting force becomes less and the compliance of the lung increases. This explains why compliance is improved at the normal operating range of lung volumes.",True,H2O,,,,
000e0120-8738-495c-8cd9-a9f3b7a795c5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"This also explains the hysteresis of the compliance curve. During expiration as alveoli are becoming progressively smaller, the inwardly acting force generated by surface tension becomes progressively greater. This phenomenon consequently assists expiration and contributes to expiration being a passive process.",True,H2O,,,,
da35cdea-8870-4095-b7fa-9c77d9540a3e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Low compliance at high lung volumes—Elastic limit: At high lung volumes the alveolar radius has increased further, suggesting that compliance should be further improved as the effect of surface tension will be much less. But surface tension is not the only factor involved, and the compliance curve flattens here, meaning a greater pressure is needed to achieve a volume change at high lung volumes. The low compliance at high lung volumes is caused by another phenomenon altogether. At high lung volumes expansion of the lung becomes limited by the elastic limit of the lung, a little like trying to further stretched an already stretch elastic band—it is harder to do.",True,H2O,,,,
8484b092-d7eb-44a1-b241-2fecb31ef15e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"So with surface tension causing problems at low lung volumes and tissue elastic limit causing problems at high lung volumes, the compliance curve is steepest (i.e., most favorable) in the middle, as mentioned before, which is the operating volume of the lung. These principles are summarized in figure 3.5.",True,H2O,Figure 3.5,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.5.png,"Figure 3.5: Summary of lung volumes and compliance. At low volumes alveoli are small and subject to greater surface tension forces that generate an inwardly acting force that requires greater alveolar pressure to achieve inflation. At higher lung volumes surface tension is less effective at generating an inward force, so less pressure is required to cause inflation (the lung is more compliant). At very high lung volumes surface tension poses even less of a problem, but the elastic limits of the lung are being reached, and increases in volume require alveolar pressures to overcome elastic recoil."
8484b092-d7eb-44a1-b241-2fecb31ef15e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"So with surface tension causing problems at low lung volumes and tissue elastic limit causing problems at high lung volumes, the compliance curve is steepest (i.e., most favorable) in the middle, as mentioned before, which is the operating volume of the lung. These principles are summarized in figure 3.5.",True,H2O,Figure 3.5,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.5.png,"Figure 3.5: Summary of lung volumes and compliance. At low volumes alveoli are small and subject to greater surface tension forces that generate an inwardly acting force that requires greater alveolar pressure to achieve inflation. At higher lung volumes surface tension is less effective at generating an inward force, so less pressure is required to cause inflation (the lung is more compliant). At very high lung volumes surface tension poses even less of a problem, but the elastic limits of the lung are being reached, and increases in volume require alveolar pressures to overcome elastic recoil."
8484b092-d7eb-44a1-b241-2fecb31ef15e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"So with surface tension causing problems at low lung volumes and tissue elastic limit causing problems at high lung volumes, the compliance curve is steepest (i.e., most favorable) in the middle, as mentioned before, which is the operating volume of the lung. These principles are summarized in figure 3.5.",True,H2O,Figure 3.5,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.5.png,"Figure 3.5: Summary of lung volumes and compliance. At low volumes alveoli are small and subject to greater surface tension forces that generate an inwardly acting force that requires greater alveolar pressure to achieve inflation. At higher lung volumes surface tension is less effective at generating an inward force, so less pressure is required to cause inflation (the lung is more compliant). At very high lung volumes surface tension poses even less of a problem, but the elastic limits of the lung are being reached, and increases in volume require alveolar pressures to overcome elastic recoil."
29a73de0-3529-4d42-9213-a65ad7fce041,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Improving lung compliance with surfactant: So after that information on how surface tension is a problem for the lung, we now have to look at how it could be so much worse if the lung did not protect itself.",True,H2O,,,,
4e9740cc-c080-4ddb-8640-dac07d5ffc9a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Despite it having an effect, particularly at low lung volumes, the lung actually reduces the effect of alveolar surface tension by releasing “surfactant,” a molecule that disrupts surface tension. In brief, the surfactant molecule (dipalmitoyl phosphatidylcholine) has a similar structure to the phospholipids that make up cell membranes with a hydrophobic end and a hydrophilic end, allowing it to surround water and repel it at the same time, thus breaking up the interaction between water molecules. So as surfactant significantly reduces surface tension, it thereby increases lung compliance and the risk of alveolar collapse. It also helps keep the air space dry, as excessive surface tension tends to draw water into the space from the capillaries and interstitial spaces.",True,H2O,,,,
fdc63085-2513-4355-8ded-f5d0c9698671,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,Surfactant is released onto the alveolar inner surface by Type II alveolar cells (recall Type I cells are those making up the alveolar wall). Type II cells produce surfactant at a high rate and thus demand a constant and generous blood flow; therefore any condition that disrupts this blood supply will cause surfactant concentrations to decline and therefore put the alveolus at risk of collapse as surface tension is allowed to increase.,True,H2O,,,,
08ca76c6-e7cf-44d2-ac4f-713cf0644d61,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"A good illustration of the effect of surfactant is respiratory distress syndrome of the newborn. The underdeveloped lungs of infants born prematurely (at about twenty-eight weeks), cannot produce sufficient surfactant. Alveoli rapidly collapse (known as atelectasis), and pulmonary edema develops because of the excessive surface tension in the alveolar walls.",True,H2O,,,,
99233183-1243-418a-922d-9382a50104a0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,Text,False,Text,,,,
3a126fc2-c595-468b-a2bf-31322d4888e4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Levitsky, Michael G. “Chapter 2: Mechanics of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
54d89019-6776-4a9e-90b6-2f592381b74d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
3265bb73-23ce-4e55-b347-c6a6e3d0f4a2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-2,"Widdicombe, John G., and Andrew S. Davis. “Chapter 2.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
d32b3565-b4bc-4c17-b8ba-b1c825fb4efb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,Introduction,False,Introduction,,,,
7263370a-07ae-4fd1-8925-bf533eb949a8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,Lung Volumes,False,Lung Volumes,,,,
7192e321-d98f-4e35-a65f-49658bc3f073,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,First let us look at lung volumes. This trace from a spirometer (figure 3.1) shows the change in lung volume as a patient breathes normally and then performs some specific maneuvers.,True,Lung Volumes,Figure 3.1,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
7192e321-d98f-4e35-a65f-49658bc3f073,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,First let us look at lung volumes. This trace from a spirometer (figure 3.1) shows the change in lung volume as a patient breathes normally and then performs some specific maneuvers.,True,Lung Volumes,Figure 3.1,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
7192e321-d98f-4e35-a65f-49658bc3f073,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,First let us look at lung volumes. This trace from a spirometer (figure 3.1) shows the change in lung volume as a patient breathes normally and then performs some specific maneuvers.,True,Lung Volumes,Figure 3.1,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
09548a5f-abb7-4c3e-89d4-0c57bbb78d39,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,Let us work through the trace from left to right. The initial part of the trace shows resting or “tidal” breathing. The amount of volume inspired during each breath is referred to as tidal volume.,True,Lung Volumes,,,,
5ac77b73-8b4e-4fd4-a594-352f6de2cea6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Once a normal expiration is complete, however, the lung is far from empty, and when instructed, this patient (figure 3.1) breathes out as far as they can; this excess that comes out the lung is referred to as the expiratory reserve volume.",True,Lung Volumes,Figure 3.1,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
5ac77b73-8b4e-4fd4-a594-352f6de2cea6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Once a normal expiration is complete, however, the lung is far from empty, and when instructed, this patient (figure 3.1) breathes out as far as they can; this excess that comes out the lung is referred to as the expiratory reserve volume.",True,Lung Volumes,Figure 3.1,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
5ac77b73-8b4e-4fd4-a594-352f6de2cea6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Once a normal expiration is complete, however, the lung is far from empty, and when instructed, this patient (figure 3.1) breathes out as far as they can; this excess that comes out the lung is referred to as the expiratory reserve volume.",True,Lung Volumes,Figure 3.1,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
6e0a06f9-25d9-442d-820b-ce39927ce81b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Even at this point, however, some air remains in the lung, and this is referred to as residual volume. Even with maximal efforts, this volume cannot be exhaled, so at no point can the lung be fully emptied. This also means that residual volume can never be measured with a spirometer.",True,Lung Volumes,,,,
404706b3-6142-4b15-a403-89782729ff87,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Our patient (figure 3.1) returns to normal tidal breathing for two breaths before taking a full breath in, filling the lungs as much as they can. This extra volume into the lung after a normal tidal inspiration is referred to as inspiratory reserve volume. Related to this volume is the inspiratory capacity, which is the volume that can be taken into the lung after a normal expiration; inspiratory capacity is a useful clinical measurement that we will return to when we deal with some disease states.",True,Lung Volumes,Figure 3.1,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
404706b3-6142-4b15-a403-89782729ff87,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Our patient (figure 3.1) returns to normal tidal breathing for two breaths before taking a full breath in, filling the lungs as much as they can. This extra volume into the lung after a normal tidal inspiration is referred to as inspiratory reserve volume. Related to this volume is the inspiratory capacity, which is the volume that can be taken into the lung after a normal expiration; inspiratory capacity is a useful clinical measurement that we will return to when we deal with some disease states.",True,Lung Volumes,Figure 3.1,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
404706b3-6142-4b15-a403-89782729ff87,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Our patient (figure 3.1) returns to normal tidal breathing for two breaths before taking a full breath in, filling the lungs as much as they can. This extra volume into the lung after a normal tidal inspiration is referred to as inspiratory reserve volume. Related to this volume is the inspiratory capacity, which is the volume that can be taken into the lung after a normal expiration; inspiratory capacity is a useful clinical measurement that we will return to when we deal with some disease states.",True,Lung Volumes,Figure 3.1,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
e268aad9-56e5-4913-90aa-c956607469bb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Another clinically valuable measurement is vital capacity, which is the volume of air that our patient can move out of the lung after a full inspiration, that is, the total lung capacity, minus the residual volume (remember: residual volume cannot be expelled). Forced vital capacity is a common measure taken in pulmonary function testing, and this is simply the volume that can be expelled from total lung capacity during a forceful expiration. The importance of this maneuver being forced will be dealt with when we look at airway compression (chapter 6).",True,Lung Volumes,,,,
03aa6274-2810-495d-a46f-6ed0fea49488,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"While the volumes we have just seen measured by spirometry in the pulmonary function lab provide valuable clinical information, we need to now look at some physiological variables that are also critical for our understanding of lung function and disease.",True,Lung Volumes,,,,
bf1de516-5818-40a5-8881-ea4d46790d1e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,Components of Tidal Breathing,False,Components of Tidal Breathing,,,,
1d99493c-0773-414b-bb22-7c8f3b24c939,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"As you have seen, the volume of air inspired during a normal breath is tidal volume, and the size of this is dependent on body size, but in the example here is listed as 500 mL (a good approximation). Not all this 500 mL reaches the gas exchange surfaces in the respiratory zone, however, as some never gets further than the conducting zone (i.e., it stays in the anatomical dead space). From chapter 1 we know that this dead space has a volume of 150 mL, so the amount of air reaching the alveoli in the respiratory zone is our tidal volume (500 mL), minus the dead space volume, so alveolar volume is 350 mL.",True,Components of Tidal Breathing,,,,
f2133dad-10f6-40ec-88ef-9c844e2c5032,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"This brings us to an important point of clarification. Minute ventilation (denoted as Ve) is the volume of air exchanged in the lung within a minute. This is analogous to cardiac output, the volume of blood pumped by the heart in a minute. As such, minute ventilation is the average tidal volume (VT) multiplied by the number of breaths taken in a minute (RR).",True,Components of Tidal Breathing,,,,
26c562fb-dc46-4f0f-9862-67341d214b64,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,Equation 3.1,True,Components of Tidal Breathing,,,,
5229e2d7-a0d7-41c5-8983-35e804b9425f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,Ve=RR×VT,False,Ve=RR×VT,,,,
a811bd46-e7d9-4514-a286-747a92f5548f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,V,False,V,,,,
2c6a0dba-ffb0-4cbd-8c52-4c561ab66eae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,e,False,e,,,,
bf58effc-0a6c-44cd-8d7c-2c1035616c6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,=,False,=,,,,
525a6086-43a3-4487-8376-52250c456789,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,R,False,R,,,,
b39ab2cf-463c-4135-bec6-6f69b6edaeb5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,×,False,×,,,,
4ea00c92-7b43-4aa7-83ae-30fd5836fedf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,VT,False,VT,,,,
a26a231d-9943-4550-954f-45ecad72bb54,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,T,False,T,,,,
118f22f1-00a6-424a-acb6-617c97ecce8f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"So if respiratory rate is 10 bpm and tidal volume is 500 mL, minute ventilation is 5,000 mL.",True,T,,,,
775bf9e5-9c11-424e-b4a9-291a425790df,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,Equation 3.2,True,T,,,,
2e071edb-b195-43ba-b86c-2656a3b86d1d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Ve=10bpm×500mL=5,000mLpermin",False,"Ve=10bpm×500mL=5,000mLpermin",,,,
a3c989b6-d8e2-44bd-a4b8-a629cc5151c2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,10,False,10,,,,
f9655574-3974-4f1e-b365-5d372d92809a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,b,False,b,,,,
0f4809de-8625-49ca-a79d-caff5c4036c7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,p,False,p,,,,
29c12feb-0dec-4348-a4db-bb90123ccd1e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,m,False,m,,,,
c348b13a-b70c-48db-95fa-fc67c63f5dcc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,500,False,500,,,,
77998674-48f2-49d9-afa6-67584e5074d1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,L,False,L,,,,
91ef90c2-df02-4df8-9c70-8ad4cf298ef4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,5,False,5,,,,
15c7a734-89d3-46cf-837c-60c3c7af18db,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,",",False,",",,,,
3d82aeac-b8c5-4e73-b643-4af4f9837737,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,000,False,000,,,,
cdf16196-5ff3-4f2c-8ac7-7744c999d683,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,r,False,r,,,,
5dfcd120-6002-40f6-b36d-01560c675510,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,i,False,i,,,,
ad17cc75-0b0e-4da6-ab58-18a9df1b480a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,n,False,n,,,,
9cb6e198-1b6e-44f5-bbf5-1f983e257c23,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Physiologically more important, however, is the alveolar minute ventilation (VA) that accounts for the “wasted” ventilation that never reached a gas exchange surface but remained in the anatomical dead space. So the calculation for VA is",True,n,,,,
2858321a-7e06-4ed8-abd9-f84ed968c009,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,Equation 3.3,True,n,,,,
852f53df-468a-4596-bc5b-f54ad50ac414,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,VA=RR×(VT−VD),False,VA=RR×(VT−VD),,,,
e8939b00-d073-4f31-82bd-4f4cd08a247d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,VA,False,VA,,,,
9d00ccea-0814-4d36-adf9-253aff84ce30,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,A,False,A,,,,
3524f7d6-bf1b-4694-b903-d1006cb1b642,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,(,False,(,,,,
29c7f463-2a15-42e2-8567-bd0a6eab6ef5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,−,False,−,,,,
f2b87aeb-8573-4315-afbd-3d79fb5ef202,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,VD,False,VD,,,,
86f1cb3b-8f46-4ad7-b504-00e64f9c60ce,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,D,False,D,,,,
fc775221-235c-4e88-a257-79f191a86b00,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,),False,),,,,
e7df798c-2427-4814-b0f8-100de5c76852,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"where VD is the anatomical dead space (approximately 150 mL). So for our previous example, alveolar minute ventilation is",True,),,,,
372f70ae-d12f-4d96-9f88-c1a9935e8936,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,Equation 3.4,True,),,,,
693f7d6b-da04-4472-8616-207fb9d60710,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"VA=10×(500−150mL)=3,500mLpermin",False,"VA=10×(500−150mL)=3,500mLpermin",,,,
24236ad3-bae2-4c2b-8354-66ae261ca822,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,150,False,150,,,,
1dbc9dee-b585-459b-8281-d3b54051b653,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,3,False,3,,,,
dd9ce240-23ea-4905-ba20-37b81159d7ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,describing only the volume of air that reached the respiratory zone.,True,3,,,,
9763f70e-3dec-459a-a2bf-612d6a7eb39d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"So far the involvement of anatomical dead space might seem academic, as it remains constant. But let us consider a different breathing pattern (as often occurs in disease states).",True,3,,,,
7224648c-e6fc-42e2-8278-76d3542face5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"In our example above minute ventilation is 5,000 mL, but accounting for dead space we see that alveolar minute ventilation is 3,500 mL. Now let us consider another breathing pattern—one typical of a patient with restrictive lung disease where tidal volume is reduced and respiratory rate is increased. With a tidal volume of 250 mL and rate of 20, the minute ventilation remains the same, 5,000 mL.",True,3,,,,
706edbeb-927b-4fe5-84fb-5cef8f8b39e7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,Equation 3.5,True,3,,,,
1240184e-022c-4eb9-b2af-1544a952b153,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Ve=20bpm×250mL=5,000mLpermin",False,"Ve=20bpm×250mL=5,000mLpermin",,,,
4c1b3e25-7e8b-41dd-9a8d-439f8c098173,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,20,False,20,,,,
789c111b-a9f2-4a65-870c-f4081741fb98,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,250,False,250,,,,
d8972e84-0baf-487e-bbee-1be3c40438ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,But calculating alveolar minute ventilation we see that a greater proportion of the reduced tidal volume is consumed by dead space.,True,250,,,,
191be6a5-ebcc-4e05-882c-db07154b611a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,Equation 3.6,True,250,,,,
f5164884-09ff-42d5-94eb-eeee35325120,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"VA=20×(250−150mL)=2,000mLpermin",False,"VA=20×(250−150mL)=2,000mLpermin",,,,
3fa237bf-8dfb-43a9-a931-92e93b948399,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,2,False,2,,,,
64a2c6b0-ff55-4cf2-bfe8-1046624ef6ce,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"So despite maintaining the same minute ventilation, the second patient’s alveolar minute ventilation is reduced by 1,500 mL, which is significant given that this is the volume of air going to the gas exchange surfaces.",True,2,,,,
043f2c18-2825-455c-8cc2-34962a301b5c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"This partially explains why increases in ventilation are initially achieved by increases in tidal volume; as shown in figure 3.2, as tidal volume increases during exercise intensity (represented by oxygen uptake) until it reaches a plateau. Only when this plateau is reached are further increases in minute ventilation achieved by increasing respiratory rate.",True,2,Figure 3.2,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.2.png,Figure 3.2: Changes in breathing tidal volume and respiratory rate with increasing levels of exercise.
043f2c18-2825-455c-8cc2-34962a301b5c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"This partially explains why increases in ventilation are initially achieved by increases in tidal volume; as shown in figure 3.2, as tidal volume increases during exercise intensity (represented by oxygen uptake) until it reaches a plateau. Only when this plateau is reached are further increases in minute ventilation achieved by increasing respiratory rate.",True,2,Figure 3.2,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.2.png,Figure 3.2: Changes in breathing tidal volume and respiratory rate with increasing levels of exercise.
043f2c18-2825-455c-8cc2-34962a301b5c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"This partially explains why increases in ventilation are initially achieved by increases in tidal volume; as shown in figure 3.2, as tidal volume increases during exercise intensity (represented by oxygen uptake) until it reaches a plateau. Only when this plateau is reached are further increases in minute ventilation achieved by increasing respiratory rate.",True,2,Figure 3.2,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.2.png,Figure 3.2: Changes in breathing tidal volume and respiratory rate with increasing levels of exercise.
7342333f-4885-4934-9602-5cbbb4348c84,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"So why not keep increasing tidal volume? At higher lung volumes the elastic limit of the lung is approached, and it takes more energy (muscular force) to expand, so it is more efficient and the work of breathing is less if the rate of breathing is increased to achieve higher levels of minute ventilation. This brings us to our next topic, lung compliance.",True,2,,,,
c49b6d96-2e95-4d48-8997-4ab7ffa42677,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,Lung Compliance,False,Lung Compliance,,,,
092f65d9-a9d0-4f67-9599-e45d817fe1fb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Lung compliance is a description of how easy the lung is to inflate, more specifically, how much volume will change for a given pressure differential. Figure 3.3 shows a typical and normal lung compliance curve. The lower line shows how volume changes as intrapleural pressure becomes more negative (as the chest wall and diaphragm expand the thorax). The upper curve is the compliance of the lung during expiration, and it is clearly different; this is an example of hysteresis, meaning that the relationship depends on direction, and we will see why this exists later.",True,Lung Compliance,Figure 3.3,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
092f65d9-a9d0-4f67-9599-e45d817fe1fb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Lung compliance is a description of how easy the lung is to inflate, more specifically, how much volume will change for a given pressure differential. Figure 3.3 shows a typical and normal lung compliance curve. The lower line shows how volume changes as intrapleural pressure becomes more negative (as the chest wall and diaphragm expand the thorax). The upper curve is the compliance of the lung during expiration, and it is clearly different; this is an example of hysteresis, meaning that the relationship depends on direction, and we will see why this exists later.",True,Lung Compliance,Figure 3.3,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
092f65d9-a9d0-4f67-9599-e45d817fe1fb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Lung compliance is a description of how easy the lung is to inflate, more specifically, how much volume will change for a given pressure differential. Figure 3.3 shows a typical and normal lung compliance curve. The lower line shows how volume changes as intrapleural pressure becomes more negative (as the chest wall and diaphragm expand the thorax). The upper curve is the compliance of the lung during expiration, and it is clearly different; this is an example of hysteresis, meaning that the relationship depends on direction, and we will see why this exists later.",True,Lung Compliance,Figure 3.3,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
9c8d2988-264f-4635-8961-b0139e6bd7bc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,Lung Compliance During Inspiration,False,Lung Compliance During Inspiration,,,,
12d03457-27d2-49f7-979e-35fa8e39307d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"You will notice at low lung volumes the slope of the compliance curve (figure 3.3) is shallower, meaning that it takes a relatively large pressure change to cause an increase in volume. This tells us at low lung volumes the lung is less distensible, or has low compliance.",True,Lung Compliance During Inspiration,Figure 3.3,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
12d03457-27d2-49f7-979e-35fa8e39307d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"You will notice at low lung volumes the slope of the compliance curve (figure 3.3) is shallower, meaning that it takes a relatively large pressure change to cause an increase in volume. This tells us at low lung volumes the lung is less distensible, or has low compliance.",True,Lung Compliance During Inspiration,Figure 3.3,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
12d03457-27d2-49f7-979e-35fa8e39307d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"You will notice at low lung volumes the slope of the compliance curve (figure 3.3) is shallower, meaning that it takes a relatively large pressure change to cause an increase in volume. This tells us at low lung volumes the lung is less distensible, or has low compliance.",True,Lung Compliance During Inspiration,Figure 3.3,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
7df787d5-b66c-4db5-a36d-9e0d7b57b967,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"If we start to breathe at a higher lung volume, the slope of the curve is steeper, meaning that for a similar change in pressure there is a greater change in volume (i.e., the lung is more compliant).",True,Lung Compliance During Inspiration,,,,
d950a7de-c149-42fc-99e9-6de70c8fb7ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"If we start breathing at a higher lung volume still, closer to total lung capacity, we see the slope of the compliance curve flatten out again, showing that at the lung volumes the compliance of the lung is low.",True,Lung Compliance During Inspiration,,,,
af797a35-2e0e-4264-8413-74969dc1af3d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"As you might imagine, the normal range for breathing is in the middle range where the slope is steep and the lung compliant. This corresponds to an intrapleural pressure range of −5 to −10 cm H2O, which you should know is the normal range of intrapleural pressures during tidal breathing. This means we normally breathe at a lung volume at which the lung is most compliant and therefore takes less work to inflate.",True,Lung Compliance During Inspiration,,,,
cfefa029-9e21-4862-a601-62e8923bb44f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,H2O,False,H2O,,,,
eaf21078-54fc-4bde-9f54-396582b63e8f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Too low a lung volume and compliance falls and work of breathing increases, likewise during breathing at high lung volumes, another contributing reason for why tidal volume plateaus during exercise.",True,H2O,,,,
134e0abb-a7b1-4f09-a389-b5a37b2b7c9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"So now let us look at why compliance is low at high and low lung volumes, starting with the cause of low lung compliance at low volumes.",True,H2O,,,,
ac15ad28-0d4f-4d25-a2ee-705d95d3df4d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Low compliance at low volumes—Surface tension: The reason why the lung takes more pressure to inflate at low volumes is surface tension. As mentioned in chapter 1 the alveoli have a thin layer of fluid lining their inner surface. As we saw in the pleural space, this causes surface tension. Unlike the surface tension in the pleural space, in the alveoli surface tension is a disadvantage.",True,H2O,,,,
6a277e16-2c48-44de-bb28-8ba5ea674a70,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Surface tension is generated as water molecules cluster together to reduce their exposure to the gas in the alveolar space. As they gather together they drag the alveolar wall with them, producing a force that tends to pull the alveolar walls inward. The alveolar pressure opposes this force and should prevent the alveolus from collapsing (figure 3.4).",True,H2O,Figure 3.4,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.4.png,Figure 3.4: Opposing forces of alveolar pressure and surface tension.
6a277e16-2c48-44de-bb28-8ba5ea674a70,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Surface tension is generated as water molecules cluster together to reduce their exposure to the gas in the alveolar space. As they gather together they drag the alveolar wall with them, producing a force that tends to pull the alveolar walls inward. The alveolar pressure opposes this force and should prevent the alveolus from collapsing (figure 3.4).",True,H2O,Figure 3.4,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.4.png,Figure 3.4: Opposing forces of alveolar pressure and surface tension.
6a277e16-2c48-44de-bb28-8ba5ea674a70,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Surface tension is generated as water molecules cluster together to reduce their exposure to the gas in the alveolar space. As they gather together they drag the alveolar wall with them, producing a force that tends to pull the alveolar walls inward. The alveolar pressure opposes this force and should prevent the alveolus from collapsing (figure 3.4).",True,H2O,Figure 3.4,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.4.png,Figure 3.4: Opposing forces of alveolar pressure and surface tension.
cbf89dc1-f2a8-4a43-85d4-c3ef2614ca26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"The relationship between these two opposing forces is described by Laplace’s law that states the outward (alveolar) pressure needed to oppose the inwardly directed tension is proportionate to the tension (obviously), but also inversely related to the radius of the alveolus (i.e., the smaller the radius, the greater the inwardly acting force).",True,H2O,,,,
6d03ad31-9b7c-4ab8-97f5-a261dcc5afce,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"This explains why compliance is low at low lung volumes. At low lung volumes the alveoli are smaller and thus have a smaller radius. Laplace’s law states that with a low radius the pressure needed to overcome the inward force will be greater, explaining why a larger alveolar (outward) pressure is needed to inflate the alveolus from a low starting volume.",True,H2O,,,,
8968075c-ff46-47ba-a3d5-bff563d63293,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"As lung volume increases, and thus alveolar radius increases, the pressure needed to overcome the inward acting force becomes less and the compliance of the lung increases. This explains why compliance is improved at the normal operating range of lung volumes.",True,H2O,,,,
cc8e11f9-82b7-49eb-9f45-b32abcbf50ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"This also explains the hysteresis of the compliance curve. During expiration as alveoli are becoming progressively smaller, the inwardly acting force generated by surface tension becomes progressively greater. This phenomenon consequently assists expiration and contributes to expiration being a passive process.",True,H2O,,,,
1bdce420-abf2-4441-bf4f-a402342ece3d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Low compliance at high lung volumes—Elastic limit: At high lung volumes the alveolar radius has increased further, suggesting that compliance should be further improved as the effect of surface tension will be much less. But surface tension is not the only factor involved, and the compliance curve flattens here, meaning a greater pressure is needed to achieve a volume change at high lung volumes. The low compliance at high lung volumes is caused by another phenomenon altogether. At high lung volumes expansion of the lung becomes limited by the elastic limit of the lung, a little like trying to further stretched an already stretch elastic band—it is harder to do.",True,H2O,,,,
a67b9dcc-3169-406b-9925-471c1ce398f6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"So with surface tension causing problems at low lung volumes and tissue elastic limit causing problems at high lung volumes, the compliance curve is steepest (i.e., most favorable) in the middle, as mentioned before, which is the operating volume of the lung. These principles are summarized in figure 3.5.",True,H2O,Figure 3.5,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.5.png,"Figure 3.5: Summary of lung volumes and compliance. At low volumes alveoli are small and subject to greater surface tension forces that generate an inwardly acting force that requires greater alveolar pressure to achieve inflation. At higher lung volumes surface tension is less effective at generating an inward force, so less pressure is required to cause inflation (the lung is more compliant). At very high lung volumes surface tension poses even less of a problem, but the elastic limits of the lung are being reached, and increases in volume require alveolar pressures to overcome elastic recoil."
a67b9dcc-3169-406b-9925-471c1ce398f6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"So with surface tension causing problems at low lung volumes and tissue elastic limit causing problems at high lung volumes, the compliance curve is steepest (i.e., most favorable) in the middle, as mentioned before, which is the operating volume of the lung. These principles are summarized in figure 3.5.",True,H2O,Figure 3.5,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.5.png,"Figure 3.5: Summary of lung volumes and compliance. At low volumes alveoli are small and subject to greater surface tension forces that generate an inwardly acting force that requires greater alveolar pressure to achieve inflation. At higher lung volumes surface tension is less effective at generating an inward force, so less pressure is required to cause inflation (the lung is more compliant). At very high lung volumes surface tension poses even less of a problem, but the elastic limits of the lung are being reached, and increases in volume require alveolar pressures to overcome elastic recoil."
a67b9dcc-3169-406b-9925-471c1ce398f6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"So with surface tension causing problems at low lung volumes and tissue elastic limit causing problems at high lung volumes, the compliance curve is steepest (i.e., most favorable) in the middle, as mentioned before, which is the operating volume of the lung. These principles are summarized in figure 3.5.",True,H2O,Figure 3.5,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.5.png,"Figure 3.5: Summary of lung volumes and compliance. At low volumes alveoli are small and subject to greater surface tension forces that generate an inwardly acting force that requires greater alveolar pressure to achieve inflation. At higher lung volumes surface tension is less effective at generating an inward force, so less pressure is required to cause inflation (the lung is more compliant). At very high lung volumes surface tension poses even less of a problem, but the elastic limits of the lung are being reached, and increases in volume require alveolar pressures to overcome elastic recoil."
4b31e26b-0d42-4123-99fd-031f944e97be,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Improving lung compliance with surfactant: So after that information on how surface tension is a problem for the lung, we now have to look at how it could be so much worse if the lung did not protect itself.",True,H2O,,,,
6afa470a-7bde-49f0-83c2-49f8d0174edc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Despite it having an effect, particularly at low lung volumes, the lung actually reduces the effect of alveolar surface tension by releasing “surfactant,” a molecule that disrupts surface tension. In brief, the surfactant molecule (dipalmitoyl phosphatidylcholine) has a similar structure to the phospholipids that make up cell membranes with a hydrophobic end and a hydrophilic end, allowing it to surround water and repel it at the same time, thus breaking up the interaction between water molecules. So as surfactant significantly reduces surface tension, it thereby increases lung compliance and the risk of alveolar collapse. It also helps keep the air space dry, as excessive surface tension tends to draw water into the space from the capillaries and interstitial spaces.",True,H2O,,,,
0a0cdffb-57a0-46c5-8211-2578bbbab3de,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,Surfactant is released onto the alveolar inner surface by Type II alveolar cells (recall Type I cells are those making up the alveolar wall). Type II cells produce surfactant at a high rate and thus demand a constant and generous blood flow; therefore any condition that disrupts this blood supply will cause surfactant concentrations to decline and therefore put the alveolus at risk of collapse as surface tension is allowed to increase.,True,H2O,,,,
ee8fc11f-2fca-4b79-9750-4ac437dfa6c0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"A good illustration of the effect of surfactant is respiratory distress syndrome of the newborn. The underdeveloped lungs of infants born prematurely (at about twenty-eight weeks), cannot produce sufficient surfactant. Alveoli rapidly collapse (known as atelectasis), and pulmonary edema develops because of the excessive surface tension in the alveolar walls.",True,H2O,,,,
3c5eddce-c4de-46f5-8c2f-01e46f8ac050,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,Text,False,Text,,,,
1d7eb45d-b50b-46e4-b36f-f8893a99669b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Levitsky, Michael G. “Chapter 2: Mechanics of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
99723c3d-eec7-47e3-80a2-c9c6a645058b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
bbbb3759-a05d-4d4b-bd25-602b96a32260,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Lung Volumes,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/#chapter-29-section-1,"Widdicombe, John G., and Andrew S. Davis. “Chapter 2.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
f61319a5-ce91-4e77-80d5-4312ab9e6d8d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,Introduction,False,Introduction,,,,
58ee578d-e4b1-4830-84b2-dcc89a8025a1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,Lung Volumes,False,Lung Volumes,,,,
b454bc14-42f4-417b-874e-ab5bb6ca09ef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,First let us look at lung volumes. This trace from a spirometer (figure 3.1) shows the change in lung volume as a patient breathes normally and then performs some specific maneuvers.,True,Lung Volumes,Figure 3.1,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
b454bc14-42f4-417b-874e-ab5bb6ca09ef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,First let us look at lung volumes. This trace from a spirometer (figure 3.1) shows the change in lung volume as a patient breathes normally and then performs some specific maneuvers.,True,Lung Volumes,Figure 3.1,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
b454bc14-42f4-417b-874e-ab5bb6ca09ef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,First let us look at lung volumes. This trace from a spirometer (figure 3.1) shows the change in lung volume as a patient breathes normally and then performs some specific maneuvers.,True,Lung Volumes,Figure 3.1,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
2c62c2d6-7019-4bc8-89b6-9586eb89dc68,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,Let us work through the trace from left to right. The initial part of the trace shows resting or “tidal” breathing. The amount of volume inspired during each breath is referred to as tidal volume.,True,Lung Volumes,,,,
55f3ce1a-c832-4098-ab79-b5a19f792995,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Once a normal expiration is complete, however, the lung is far from empty, and when instructed, this patient (figure 3.1) breathes out as far as they can; this excess that comes out the lung is referred to as the expiratory reserve volume.",True,Lung Volumes,Figure 3.1,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
55f3ce1a-c832-4098-ab79-b5a19f792995,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Once a normal expiration is complete, however, the lung is far from empty, and when instructed, this patient (figure 3.1) breathes out as far as they can; this excess that comes out the lung is referred to as the expiratory reserve volume.",True,Lung Volumes,Figure 3.1,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
55f3ce1a-c832-4098-ab79-b5a19f792995,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Once a normal expiration is complete, however, the lung is far from empty, and when instructed, this patient (figure 3.1) breathes out as far as they can; this excess that comes out the lung is referred to as the expiratory reserve volume.",True,Lung Volumes,Figure 3.1,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
694b8b11-d728-47e8-94bb-30fc8bd40eb0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Even at this point, however, some air remains in the lung, and this is referred to as residual volume. Even with maximal efforts, this volume cannot be exhaled, so at no point can the lung be fully emptied. This also means that residual volume can never be measured with a spirometer.",True,Lung Volumes,,,,
0215b371-b779-49f8-906f-8c5d54fc8878,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Our patient (figure 3.1) returns to normal tidal breathing for two breaths before taking a full breath in, filling the lungs as much as they can. This extra volume into the lung after a normal tidal inspiration is referred to as inspiratory reserve volume. Related to this volume is the inspiratory capacity, which is the volume that can be taken into the lung after a normal expiration; inspiratory capacity is a useful clinical measurement that we will return to when we deal with some disease states.",True,Lung Volumes,Figure 3.1,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
0215b371-b779-49f8-906f-8c5d54fc8878,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Our patient (figure 3.1) returns to normal tidal breathing for two breaths before taking a full breath in, filling the lungs as much as they can. This extra volume into the lung after a normal tidal inspiration is referred to as inspiratory reserve volume. Related to this volume is the inspiratory capacity, which is the volume that can be taken into the lung after a normal expiration; inspiratory capacity is a useful clinical measurement that we will return to when we deal with some disease states.",True,Lung Volumes,Figure 3.1,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
0215b371-b779-49f8-906f-8c5d54fc8878,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Our patient (figure 3.1) returns to normal tidal breathing for two breaths before taking a full breath in, filling the lungs as much as they can. This extra volume into the lung after a normal tidal inspiration is referred to as inspiratory reserve volume. Related to this volume is the inspiratory capacity, which is the volume that can be taken into the lung after a normal expiration; inspiratory capacity is a useful clinical measurement that we will return to when we deal with some disease states.",True,Lung Volumes,Figure 3.1,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.1.png,Figure 3.1: Lung volumes detected by spirometry.
19c6d929-13c4-4910-95d0-939b1056b6a9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Another clinically valuable measurement is vital capacity, which is the volume of air that our patient can move out of the lung after a full inspiration, that is, the total lung capacity, minus the residual volume (remember: residual volume cannot be expelled). Forced vital capacity is a common measure taken in pulmonary function testing, and this is simply the volume that can be expelled from total lung capacity during a forceful expiration. The importance of this maneuver being forced will be dealt with when we look at airway compression (chapter 6).",True,Lung Volumes,,,,
36c04cf7-2774-4d95-aca5-3d2a1fbaf575,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"While the volumes we have just seen measured by spirometry in the pulmonary function lab provide valuable clinical information, we need to now look at some physiological variables that are also critical for our understanding of lung function and disease.",True,Lung Volumes,,,,
a8b7d970-3ac2-480d-881f-0d91a4de2c48,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,Components of Tidal Breathing,False,Components of Tidal Breathing,,,,
b33a7224-bd49-41c6-8edf-178e39001f36,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"As you have seen, the volume of air inspired during a normal breath is tidal volume, and the size of this is dependent on body size, but in the example here is listed as 500 mL (a good approximation). Not all this 500 mL reaches the gas exchange surfaces in the respiratory zone, however, as some never gets further than the conducting zone (i.e., it stays in the anatomical dead space). From chapter 1 we know that this dead space has a volume of 150 mL, so the amount of air reaching the alveoli in the respiratory zone is our tidal volume (500 mL), minus the dead space volume, so alveolar volume is 350 mL.",True,Components of Tidal Breathing,,,,
d0b6f85c-fdda-4cc2-aa23-ac800062ef4b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"This brings us to an important point of clarification. Minute ventilation (denoted as Ve) is the volume of air exchanged in the lung within a minute. This is analogous to cardiac output, the volume of blood pumped by the heart in a minute. As such, minute ventilation is the average tidal volume (VT) multiplied by the number of breaths taken in a minute (RR).",True,Components of Tidal Breathing,,,,
b6b71ac2-cbde-4399-979a-c1fc6536e678,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,Equation 3.1,True,Components of Tidal Breathing,,,,
d149c8d7-b2df-452b-9f7f-cbdba9b453b0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,[latex]Ve = RR \times V_T[/latex],False,[latex]Ve = RR \times V_T[/latex],,,,
72b0d655-1ddd-483d-a7e5-df1cc087b10b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"So if respiratory rate is 10 bpm and tidal volume is 500 mL, minute ventilation is 5,000 mL.",True,[latex]Ve = RR \times V_T[/latex],,,,
98ca5bec-3817-4d70-881e-5b00f2f046ea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,Equation 3.2,True,[latex]Ve = RR \times V_T[/latex],,,,
7bb4c139-48e1-4c7c-9b3f-9a6d7f96778d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"[latex]Ve = 10\:bpm \times 500\:mL = 5,000\:mL\:per\:min[/latex]",False,"[latex]Ve = 10\:bpm \times 500\:mL = 5,000\:mL\:per\:min[/latex]",,,,
2802fae3-a911-45a3-ad5a-460d520394cd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Physiologically more important, however, is the alveolar minute ventilation (VA) that accounts for the “wasted” ventilation that never reached a gas exchange surface but remained in the anatomical dead space. So the calculation for VA is",True,"[latex]Ve = 10\:bpm \times 500\:mL = 5,000\:mL\:per\:min[/latex]",,,,
a88a55b3-4641-44c4-ad8c-b8b33c9366e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,Equation 3.3,True,"[latex]Ve = 10\:bpm \times 500\:mL = 5,000\:mL\:per\:min[/latex]",,,,
b6e9d13b-66f7-46a8-96ab-d475c748289b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,[latex]V_A = RR \times (V_T - V_D)[/latex],False,[latex]V_A = RR \times (V_T - V_D)[/latex],,,,
83f19c6c-8545-41cf-b608-beb9662fc9d5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"where VD is the anatomical dead space (approximately 150 mL). So for our previous example, alveolar minute ventilation is",True,[latex]V_A = RR \times (V_T - V_D)[/latex],,,,
f290546d-1db6-4ff2-9502-7ad5e92f9392,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,Equation 3.4,True,[latex]V_A = RR \times (V_T - V_D)[/latex],,,,
90b7b65e-4e98-422d-be27-d4546b39c8fb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"[latex]V_A = 10 \times (500 - 150\:mL) = 3,500\:mL\:per\:min[/latex]",False,"[latex]V_A = 10 \times (500 - 150\:mL) = 3,500\:mL\:per\:min[/latex]",,,,
d80aeeff-9f7c-4db1-833a-541f295b2ec5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,describing only the volume of air that reached the respiratory zone.,True,"[latex]V_A = 10 \times (500 - 150\:mL) = 3,500\:mL\:per\:min[/latex]",,,,
15f20749-195b-49e7-b409-515e6fc3a7c0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"So far the involvement of anatomical dead space might seem academic, as it remains constant. But let us consider a different breathing pattern (as often occurs in disease states).",True,"[latex]V_A = 10 \times (500 - 150\:mL) = 3,500\:mL\:per\:min[/latex]",,,,
4bfd5164-0c54-46b3-86d5-416544498d58,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"In our example above minute ventilation is 5,000 mL, but accounting for dead space we see that alveolar minute ventilation is 3,500 mL. Now let us consider another breathing pattern—one typical of a patient with restrictive lung disease where tidal volume is reduced and respiratory rate is increased. With a tidal volume of 250 mL and rate of 20, the minute ventilation remains the same, 5,000 mL.",True,"[latex]V_A = 10 \times (500 - 150\:mL) = 3,500\:mL\:per\:min[/latex]",,,,
2bd31da0-3702-4c8e-a1f1-9ac81a1de2e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,Equation 3.5,True,"[latex]V_A = 10 \times (500 - 150\:mL) = 3,500\:mL\:per\:min[/latex]",,,,
d7def146-a3cd-4428-ade2-8ba00513cf9e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"[latex]Ve = 20\:bpm \times 250\:mL = 5,000\:mL\:per\:min[/latex]",False,"[latex]Ve = 20\:bpm \times 250\:mL = 5,000\:mL\:per\:min[/latex]",,,,
ec65e0f1-748c-476b-8a38-004be48f92a5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,But calculating alveolar minute ventilation we see that a greater proportion of the reduced tidal volume is consumed by dead space.,True,"[latex]Ve = 20\:bpm \times 250\:mL = 5,000\:mL\:per\:min[/latex]",,,,
adcda3c4-42b4-4e25-a064-7649f0d193ae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,Equation 3.6,True,"[latex]Ve = 20\:bpm \times 250\:mL = 5,000\:mL\:per\:min[/latex]",,,,
664c157c-f589-4704-8700-a5326c1aae64,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"[latex]V_A = 20 \times (250 - 150\:mL) = 2,000\:mL\:per\:min[/latex]",False,"[latex]V_A = 20 \times (250 - 150\:mL) = 2,000\:mL\:per\:min[/latex]",,,,
b4203cfb-a426-4e85-a9e1-a20f6d5763e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"So despite maintaining the same minute ventilation, the second patient’s alveolar minute ventilation is reduced by 1,500 mL, which is significant given that this is the volume of air going to the gas exchange surfaces.",True,"[latex]V_A = 20 \times (250 - 150\:mL) = 2,000\:mL\:per\:min[/latex]",,,,
a9dda7ba-3e9d-45f0-a679-5c532174a4ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"This partially explains why increases in ventilation are initially achieved by increases in tidal volume; as shown in figure 3.2, as tidal volume increases during exercise intensity (represented by oxygen uptake) until it reaches a plateau. Only when this plateau is reached are further increases in minute ventilation achieved by increasing respiratory rate.",True,"[latex]V_A = 20 \times (250 - 150\:mL) = 2,000\:mL\:per\:min[/latex]",Figure 3.2,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.2.png,Figure 3.2: Changes in breathing tidal volume and respiratory rate with increasing levels of exercise.
a9dda7ba-3e9d-45f0-a679-5c532174a4ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"This partially explains why increases in ventilation are initially achieved by increases in tidal volume; as shown in figure 3.2, as tidal volume increases during exercise intensity (represented by oxygen uptake) until it reaches a plateau. Only when this plateau is reached are further increases in minute ventilation achieved by increasing respiratory rate.",True,"[latex]V_A = 20 \times (250 - 150\:mL) = 2,000\:mL\:per\:min[/latex]",Figure 3.2,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.2.png,Figure 3.2: Changes in breathing tidal volume and respiratory rate with increasing levels of exercise.
a9dda7ba-3e9d-45f0-a679-5c532174a4ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"This partially explains why increases in ventilation are initially achieved by increases in tidal volume; as shown in figure 3.2, as tidal volume increases during exercise intensity (represented by oxygen uptake) until it reaches a plateau. Only when this plateau is reached are further increases in minute ventilation achieved by increasing respiratory rate.",True,"[latex]V_A = 20 \times (250 - 150\:mL) = 2,000\:mL\:per\:min[/latex]",Figure 3.2,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.2.png,Figure 3.2: Changes in breathing tidal volume and respiratory rate with increasing levels of exercise.
0b52994e-6bbb-42ec-99d0-81a0daba39a5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"So why not keep increasing tidal volume? At higher lung volumes the elastic limit of the lung is approached, and it takes more energy (muscular force) to expand, so it is more efficient and the work of breathing is less if the rate of breathing is increased to achieve higher levels of minute ventilation. This brings us to our next topic, lung compliance.",True,"[latex]V_A = 20 \times (250 - 150\:mL) = 2,000\:mL\:per\:min[/latex]",,,,
46052223-9b9f-4feb-9256-5441a822c41d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,Lung Compliance,False,Lung Compliance,,,,
1675ca60-2681-48dd-89bc-8ae38cddc7ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Lung compliance is a description of how easy the lung is to inflate, more specifically, how much volume will change for a given pressure differential. Figure 3.3 shows a typical and normal lung compliance curve. The lower line shows how volume changes as intrapleural pressure becomes more negative (as the chest wall and diaphragm expand the thorax). The upper curve is the compliance of the lung during expiration, and it is clearly different; this is an example of hysteresis, meaning that the relationship depends on direction, and we will see why this exists later.",True,Lung Compliance,Figure 3.3,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
1675ca60-2681-48dd-89bc-8ae38cddc7ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Lung compliance is a description of how easy the lung is to inflate, more specifically, how much volume will change for a given pressure differential. Figure 3.3 shows a typical and normal lung compliance curve. The lower line shows how volume changes as intrapleural pressure becomes more negative (as the chest wall and diaphragm expand the thorax). The upper curve is the compliance of the lung during expiration, and it is clearly different; this is an example of hysteresis, meaning that the relationship depends on direction, and we will see why this exists later.",True,Lung Compliance,Figure 3.3,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
1675ca60-2681-48dd-89bc-8ae38cddc7ad,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Lung compliance is a description of how easy the lung is to inflate, more specifically, how much volume will change for a given pressure differential. Figure 3.3 shows a typical and normal lung compliance curve. The lower line shows how volume changes as intrapleural pressure becomes more negative (as the chest wall and diaphragm expand the thorax). The upper curve is the compliance of the lung during expiration, and it is clearly different; this is an example of hysteresis, meaning that the relationship depends on direction, and we will see why this exists later.",True,Lung Compliance,Figure 3.3,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
ae896baf-73ed-46dc-9c5c-63e610dab01c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,Lung Compliance During Inspiration,False,Lung Compliance During Inspiration,,,,
53888513-8088-4b95-8918-dc85a222952a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"You will notice at low lung volumes the slope of the compliance curve (figure 3.3) is shallower, meaning that it takes a relatively large pressure change to cause an increase in volume. This tells us at low lung volumes the lung is less distensible, or has low compliance.",True,Lung Compliance During Inspiration,Figure 3.3,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
53888513-8088-4b95-8918-dc85a222952a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"You will notice at low lung volumes the slope of the compliance curve (figure 3.3) is shallower, meaning that it takes a relatively large pressure change to cause an increase in volume. This tells us at low lung volumes the lung is less distensible, or has low compliance.",True,Lung Compliance During Inspiration,Figure 3.3,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
53888513-8088-4b95-8918-dc85a222952a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"You will notice at low lung volumes the slope of the compliance curve (figure 3.3) is shallower, meaning that it takes a relatively large pressure change to cause an increase in volume. This tells us at low lung volumes the lung is less distensible, or has low compliance.",True,Lung Compliance During Inspiration,Figure 3.3,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.3.png,Figure 3.3: Lung compliance curve.
e7298108-fb30-4834-b516-cbc894f159aa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"If we start to breathe at a higher lung volume, the slope of the curve is steeper, meaning that for a similar change in pressure there is a greater change in volume (i.e., the lung is more compliant).",True,Lung Compliance During Inspiration,,,,
bde0d9fe-da42-429a-854e-a8577f497cd7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"If we start breathing at a higher lung volume still, closer to total lung capacity, we see the slope of the compliance curve flatten out again, showing that at the lung volumes the compliance of the lung is low.",True,Lung Compliance During Inspiration,,,,
195a87ce-1509-4252-bc4d-cfb67274a63b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"As you might imagine, the normal range for breathing is in the middle range where the slope is steep and the lung compliant. This corresponds to an intrapleural pressure range of −5 to −10 cm H2O, which you should know is the normal range of intrapleural pressures during tidal breathing. This means we normally breathe at a lung volume at which the lung is most compliant and therefore takes less work to inflate.",True,Lung Compliance During Inspiration,,,,
859758a6-f6c7-41f8-bd1b-e1e6f003a8ce,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,H2O,False,H2O,,,,
d9a33a28-aac0-4ad0-8695-9209a7d4ec07,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Too low a lung volume and compliance falls and work of breathing increases, likewise during breathing at high lung volumes, another contributing reason for why tidal volume plateaus during exercise.",True,H2O,,,,
a786d0dc-ef9c-4058-a630-c187c52e0702,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"So now let us look at why compliance is low at high and low lung volumes, starting with the cause of low lung compliance at low volumes.",True,H2O,,,,
ad36f5cf-3749-486e-bbe5-104269cfd2e4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Low compliance at low volumes—Surface tension: The reason why the lung takes more pressure to inflate at low volumes is surface tension. As mentioned in chapter 1 the alveoli have a thin layer of fluid lining their inner surface. As we saw in the pleural space, this causes surface tension. Unlike the surface tension in the pleural space, in the alveoli surface tension is a disadvantage.",True,H2O,,,,
22a022c5-be2d-4ff5-baed-c20c03a580f4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Surface tension is generated as water molecules cluster together to reduce their exposure to the gas in the alveolar space. As they gather together they drag the alveolar wall with them, producing a force that tends to pull the alveolar walls inward. The alveolar pressure opposes this force and should prevent the alveolus from collapsing (figure 3.4).",True,H2O,Figure 3.4,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.4.png,Figure 3.4: Opposing forces of alveolar pressure and surface tension.
22a022c5-be2d-4ff5-baed-c20c03a580f4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Surface tension is generated as water molecules cluster together to reduce their exposure to the gas in the alveolar space. As they gather together they drag the alveolar wall with them, producing a force that tends to pull the alveolar walls inward. The alveolar pressure opposes this force and should prevent the alveolus from collapsing (figure 3.4).",True,H2O,Figure 3.4,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.4.png,Figure 3.4: Opposing forces of alveolar pressure and surface tension.
22a022c5-be2d-4ff5-baed-c20c03a580f4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Surface tension is generated as water molecules cluster together to reduce their exposure to the gas in the alveolar space. As they gather together they drag the alveolar wall with them, producing a force that tends to pull the alveolar walls inward. The alveolar pressure opposes this force and should prevent the alveolus from collapsing (figure 3.4).",True,H2O,Figure 3.4,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.4.png,Figure 3.4: Opposing forces of alveolar pressure and surface tension.
20dc8b7c-a365-40f2-a378-5fca2a131793,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"The relationship between these two opposing forces is described by Laplace’s law that states the outward (alveolar) pressure needed to oppose the inwardly directed tension is proportionate to the tension (obviously), but also inversely related to the radius of the alveolus (i.e., the smaller the radius, the greater the inwardly acting force).",True,H2O,,,,
743e4ce3-1f10-4d1c-964f-111dcc38e88a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"This explains why compliance is low at low lung volumes. At low lung volumes the alveoli are smaller and thus have a smaller radius. Laplace’s law states that with a low radius the pressure needed to overcome the inward force will be greater, explaining why a larger alveolar (outward) pressure is needed to inflate the alveolus from a low starting volume.",True,H2O,,,,
375bdbbe-a736-4215-94f8-647ecbb85f55,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"As lung volume increases, and thus alveolar radius increases, the pressure needed to overcome the inward acting force becomes less and the compliance of the lung increases. This explains why compliance is improved at the normal operating range of lung volumes.",True,H2O,,,,
94234e5d-51b2-444b-a8da-c5d0abff94a7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"This also explains the hysteresis of the compliance curve. During expiration as alveoli are becoming progressively smaller, the inwardly acting force generated by surface tension becomes progressively greater. This phenomenon consequently assists expiration and contributes to expiration being a passive process.",True,H2O,,,,
343d655f-f369-457a-9265-14191657035d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Low compliance at high lung volumes—Elastic limit: At high lung volumes the alveolar radius has increased further, suggesting that compliance should be further improved as the effect of surface tension will be much less. But surface tension is not the only factor involved, and the compliance curve flattens here, meaning a greater pressure is needed to achieve a volume change at high lung volumes. The low compliance at high lung volumes is caused by another phenomenon altogether. At high lung volumes expansion of the lung becomes limited by the elastic limit of the lung, a little like trying to further stretched an already stretch elastic band—it is harder to do.",True,H2O,,,,
511b5013-d2c5-439b-b99b-a0f5c92fa659,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"So with surface tension causing problems at low lung volumes and tissue elastic limit causing problems at high lung volumes, the compliance curve is steepest (i.e., most favorable) in the middle, as mentioned before, which is the operating volume of the lung. These principles are summarized in figure 3.5.",True,H2O,Figure 3.5,Lung Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.5.png,"Figure 3.5: Summary of lung volumes and compliance. At low volumes alveoli are small and subject to greater surface tension forces that generate an inwardly acting force that requires greater alveolar pressure to achieve inflation. At higher lung volumes surface tension is less effective at generating an inward force, so less pressure is required to cause inflation (the lung is more compliant). At very high lung volumes surface tension poses even less of a problem, but the elastic limits of the lung are being reached, and increases in volume require alveolar pressures to overcome elastic recoil."
511b5013-d2c5-439b-b99b-a0f5c92fa659,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"So with surface tension causing problems at low lung volumes and tissue elastic limit causing problems at high lung volumes, the compliance curve is steepest (i.e., most favorable) in the middle, as mentioned before, which is the operating volume of the lung. These principles are summarized in figure 3.5.",True,H2O,Figure 3.5,Lung Volumes,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.5.png,"Figure 3.5: Summary of lung volumes and compliance. At low volumes alveoli are small and subject to greater surface tension forces that generate an inwardly acting force that requires greater alveolar pressure to achieve inflation. At higher lung volumes surface tension is less effective at generating an inward force, so less pressure is required to cause inflation (the lung is more compliant). At very high lung volumes surface tension poses even less of a problem, but the elastic limits of the lung are being reached, and increases in volume require alveolar pressures to overcome elastic recoil."
511b5013-d2c5-439b-b99b-a0f5c92fa659,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"So with surface tension causing problems at low lung volumes and tissue elastic limit causing problems at high lung volumes, the compliance curve is steepest (i.e., most favorable) in the middle, as mentioned before, which is the operating volume of the lung. These principles are summarized in figure 3.5.",True,H2O,Figure 3.5,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/3.5.png,"Figure 3.5: Summary of lung volumes and compliance. At low volumes alveoli are small and subject to greater surface tension forces that generate an inwardly acting force that requires greater alveolar pressure to achieve inflation. At higher lung volumes surface tension is less effective at generating an inward force, so less pressure is required to cause inflation (the lung is more compliant). At very high lung volumes surface tension poses even less of a problem, but the elastic limits of the lung are being reached, and increases in volume require alveolar pressures to overcome elastic recoil."
1cb4fec2-984e-47ac-831e-b8c290829ce7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Improving lung compliance with surfactant: So after that information on how surface tension is a problem for the lung, we now have to look at how it could be so much worse if the lung did not protect itself.",True,H2O,,,,
7fb88962-6bc2-41ed-8eac-76b3f68c6d1b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Despite it having an effect, particularly at low lung volumes, the lung actually reduces the effect of alveolar surface tension by releasing “surfactant,” a molecule that disrupts surface tension. In brief, the surfactant molecule (dipalmitoyl phosphatidylcholine) has a similar structure to the phospholipids that make up cell membranes with a hydrophobic end and a hydrophilic end, allowing it to surround water and repel it at the same time, thus breaking up the interaction between water molecules. So as surfactant significantly reduces surface tension, it thereby increases lung compliance and the risk of alveolar collapse. It also helps keep the air space dry, as excessive surface tension tends to draw water into the space from the capillaries and interstitial spaces.",True,H2O,,,,
9bcf885f-e9b7-4828-88b0-dedc5fdbb313,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,Surfactant is released onto the alveolar inner surface by Type II alveolar cells (recall Type I cells are those making up the alveolar wall). Type II cells produce surfactant at a high rate and thus demand a constant and generous blood flow; therefore any condition that disrupts this blood supply will cause surfactant concentrations to decline and therefore put the alveolus at risk of collapse as surface tension is allowed to increase.,True,H2O,,,,
7f7a5537-199b-4e76-bfd9-97e3fc917b94,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"A good illustration of the effect of surfactant is respiratory distress syndrome of the newborn. The underdeveloped lungs of infants born prematurely (at about twenty-eight weeks), cannot produce sufficient surfactant. Alveoli rapidly collapse (known as atelectasis), and pulmonary edema develops because of the excessive surface tension in the alveolar walls.",True,H2O,,,,
863f12a2-575b-4dbd-ab06-9441136829a3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,Text,False,Text,,,,
8c46a1d8-9602-45f2-b1d0-81163e243c3e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Levitsky, Michael G. “Chapter 2: Mechanics of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
f9ae28fc-f7ac-476a-80d6-4dc0ae4f6413,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
37f82f2a-578f-4444-8f8f-60e93a7b51be,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,3. Lung Volumes and Compliance,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/lung-volumes-and-compliance/,"Widdicombe, John G., and Andrew S. Davis. “Chapter 2.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
5b7cdf1c-6e3e-4689-a4b4-001b0e7d0b85,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"Before we get into the details of how we breathe in, let me make sure we are all on the same page by going right back to basics, so bare with me or skip ahead if you are happy with pressure, volume, and flow.",True,Text,,,,
9e430d7f-a263-41b5-819a-5d6f57a475d3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"To get air to move into the lungs we need to generate a pressure differential; that is the pressure inside the lungs must be lower than the pressure outside (i.e., atmospheric pressure), so that air moves down the pressure gradient into the lungs.",True,Text,,,,
2a56dfa9-1088-4e0d-8a05-7d0dae7eabe3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"The low pressure inside the lungs is generated by increasing lung volume; bigger volume means fewer molecules in the same space, and therefore lower pressure (go back and revisit Boyle’s law if needed).",True,Text,,,,
700a30d9-cdcb-4a22-934d-dbb9221c27e8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"The basis of inspiration is lowering lung pressure below atmospheric pressure, so that atmospheric pressure pushes air down the airways until pressure equilibrates. So the fundamental first step is, how do we increase lung volume?",True,Text,,,,
f0582f89-5080-4d8c-973f-c82797cb93ae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"To understand the mechanics of breathing we have to deal with two concepts: first how the action of the respiratory muscles increases thoracic volume, and second (and more complex) we need to understand the interaction of the lungs and the thoracic wall.",True,Text,,,,
cf71568f-25a9-4c48-880c-f5fdda101c9b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,Let us deal with the respiratory muscles and expansion of the thorax first.,True,Text,,,,
0868332f-60c0-4f17-8a2c-fbadee58d223,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,Changing Thoracic Volume,False,Changing Thoracic Volume,,,,
2e10d819-9c0e-4ff8-97ba-e2aa7cfc6a63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
2e10d819-9c0e-4ff8-97ba-e2aa7cfc6a63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
2e10d819-9c0e-4ff8-97ba-e2aa7cfc6a63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
2e10d819-9c0e-4ff8-97ba-e2aa7cfc6a63,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
8b500a6a-6ed6-49c0-a989-611c6fd54a2f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"It is worth a quick reminder that while controlling a visceral organ and performing a homeostatic function, the diaphragm and the other respiratory muscles are skeletal muscle and have the force-generation characteristics of such. As well as being under reflex control, it can also be controlled voluntarily (such as during speech).",True,Changing Thoracic Volume,,,,
6630b073-10dd-4a89-9b32-1f911273bc20,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
6630b073-10dd-4a89-9b32-1f911273bc20,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
6630b073-10dd-4a89-9b32-1f911273bc20,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
6630b073-10dd-4a89-9b32-1f911273bc20,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
9b4271e3-76cb-47d8-9449-ce65ba432fd8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"When phrenic nerve activity stops, the diaphragm relaxes and returns to its resting dome-like position; this is aided by the recoil of the expanded lung and the decompression of the abdominal contents. The return to the resting position reduces thoracic volume and increases thoracic pressure above atmospheric pressure and air exits the lung down the reversed pressure gradient.",True,Changing Thoracic Volume,,,,
218f33db-878e-4e96-a7ae-8fea0a27b6ff,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"During inspiration the thoracic volume is also increased by the action of the external intercostal muscles. Controlled by the intercostal nerve, contraction of the external intercostals causes the rib cage to rise upward and outward, resulting in an expansion of the thoracic volume in addition to the action of the diaphragm. This action is generated by the oblique positioning of the external intercostals between the ribs, and the sternum and upper ribs are stabilized by simultaneous activation of the scalenus muscles.",True,Changing Thoracic Volume,,,,
a1515008-08ab-4670-a844-d743bdd8e6e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
a1515008-08ab-4670-a844-d743bdd8e6e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
a1515008-08ab-4670-a844-d743bdd8e6e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
a1515008-08ab-4670-a844-d743bdd8e6e5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
26844539-30f0-458f-ba5e-1090747c25a6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"Expiration is generally simpler. The elastic tissue of the lung has been expanded during inspiration, and a little like letting go of a stretch elastic band, the lungs recoil when the inspiratory muscles relax. This recoil reduces lung volume and increases lung pressure above atmospheric pressure and air exits the lung. Depending on the final lung volume achieved during inspiration, recoil of the chest wall may also contribute to expiration.",True,Changing Thoracic Volume,,,,
519a542a-f7b9-46fe-b36b-95775d34ba1b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
519a542a-f7b9-46fe-b36b-95775d34ba1b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
519a542a-f7b9-46fe-b36b-95775d34ba1b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
519a542a-f7b9-46fe-b36b-95775d34ba1b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
ed5b401d-6934-4fba-9f9e-b732881f104c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,How the Lungs Move with the Chest Wall,False,How the Lungs Move with the Chest Wall,,,,
b79578ea-4f17-4d85-a425-ccef0537b748,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"Now having dealt with the expansion of the thoracic cage, we should look at the relationship between the thoracic wall and the lungs and how the lungs and the inside of the thorax are adhered to each other so when the thoracic wall moves the lungs follow.",True,How the Lungs Move with the Chest Wall,,,,
5fcde448-c4dd-4364-9f75-8234b4d7ccea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
5fcde448-c4dd-4364-9f75-8234b4d7ccea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
5fcde448-c4dd-4364-9f75-8234b4d7ccea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
5fcde448-c4dd-4364-9f75-8234b4d7ccea,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
9a164c3c-d73e-457a-8d69-06f6aa3c6a12,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"We have mentioned the pressure inside the lungs, but now we have to think about the pressure inside the pleural space—called intra-pleural pressure. Even at normal, resting lung volumes the elastic tissue in the lungs is already somewhat stretched, so the lungs have a tendency to recoil, pulling inward. The chest wall, alternatively, has a tendency to spring outward. These opposing movements are prevented by the surface tension in the pleural space and cause a negative intrapleural pressure, that is below atmospheric pressure.",True,How the Lungs Move with the Chest Wall,,,,
4f7752a8-2faa-45cb-ab9f-36a375757362,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
4f7752a8-2faa-45cb-ab9f-36a375757362,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
4f7752a8-2faa-45cb-ab9f-36a375757362,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
4f7752a8-2faa-45cb-ab9f-36a375757362,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
be8d9cc7-fde3-4e7d-91dd-b6426638caed,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
be8d9cc7-fde3-4e7d-91dd-b6426638caed,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
be8d9cc7-fde3-4e7d-91dd-b6426638caed,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
be8d9cc7-fde3-4e7d-91dd-b6426638caed,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
00c543a1-17f7-4f9a-b450-3f05758900fe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"This increase in lung volume (and referring back to Boyle’s law, the pressure of a gas tends to decrease as the volume of the container increases) causes a decrease in pressure in the lung. This is reflected in a decrease in alveolar pressure.",True,How the Lungs Move with the Chest Wall,,,,
fdffa40a-6b58-4b16-8891-34463a849827,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,This drop in alveolar pressure generates a pressure differential between the airways and the atmosphere outside—the atmospheric pressure now being greater than the reduced airway pressure causes the flow of air into the airways and toward the alveoli.,True,How the Lungs Move with the Chest Wall,,,,
6f11a9b3-494e-4ff8-8809-20a8917f1621,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"Now let us look at these pressures during expiration. At the end of inspiration the lungs are stretched and the recoil force is high. When the activity of the inspiratory muscles stops, the recoil of the lung is unopposed and the lung recoils (a little like letting go of that stretched elastic band). Therefore, in quiet breathing, the process of breathing out is normally passive and relies on the potential energy stored in the lungs’ elastic tissue.",True,How the Lungs Move with the Chest Wall,,,,
f733002d-db88-4551-bac3-5e617da255e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"As the lung recoils and returns toward its resting position, the intrapleural pressure becomes less negative and the volume decreases, resulting in a rise in alveolar pressure, as described by Boyle’s law. This rise in alveolar pressure means the pressure gradient is reversed, with pressure inside the lung becoming greater than atmospheric pressure. This reversed pressure differential causes the flow of air from the airways toward the outside—and expiration is achieved.",True,How the Lungs Move with the Chest Wall,,,,
72cefa2a-7f84-4d03-a27d-2a7be6d25a22,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"As already mentioned, this is a passive process that relies on lung recoil, and the expiratory muscles remain inactive during quiet breathing. However, when there is a greater ventilatory demand, such as during exercise or lung disease, the respiratory system cannot wait for this passive and relatively slow process to occur, so the expiratory muscles are activated and thoracic volume (and therefore lung volume) is reduced actively much more quickly; this may cause intrapleural pressure to go positive as the thoracic wall actively pushes on the intrapleural space (and the lungs). This positive pleural pressure during active expiration can have significant ramifications in diseased lungs that we will see later on.",True,How the Lungs Move with the Chest Wall,,,,
2a517037-4a55-4c86-b951-3124a9890d41,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,Text,False,Text,,,,
6a7adc1f-816c-4819-9fd2-4cd9c0699dd7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"Levitsky, Michael G. “Chapter 2: Mechanics of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
338eec0f-6210-47e2-815e-4cb6f22fc67a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"West, John B. “Chapter 2: Ventilation—How Gas Gets to the Alveoli.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
2b9193ef-7bb1-481e-ac3e-9f75bc87ed4b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
bc98cf63-9fee-49ed-ade0-f899370c481e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-3,"Widdicombe, John G., and Andrew S. Davis. “Chapter 1.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
a391bacd-d328-448f-855f-6b7a2d2f259d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"Before we get into the details of how we breathe in, let me make sure we are all on the same page by going right back to basics, so bare with me or skip ahead if you are happy with pressure, volume, and flow.",True,Text,,,,
b3506471-d73c-4c5e-a285-37769144e4d0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"To get air to move into the lungs we need to generate a pressure differential; that is the pressure inside the lungs must be lower than the pressure outside (i.e., atmospheric pressure), so that air moves down the pressure gradient into the lungs.",True,Text,,,,
6c4ecb2b-428f-42b2-898e-a05d4d7f1c01,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"The low pressure inside the lungs is generated by increasing lung volume; bigger volume means fewer molecules in the same space, and therefore lower pressure (go back and revisit Boyle’s law if needed).",True,Text,,,,
1e6ce8d1-939e-41ce-9f70-1b19ae81ce42,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"The basis of inspiration is lowering lung pressure below atmospheric pressure, so that atmospheric pressure pushes air down the airways until pressure equilibrates. So the fundamental first step is, how do we increase lung volume?",True,Text,,,,
be7763c0-4550-4f34-a215-f0bbfd3709c7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"To understand the mechanics of breathing we have to deal with two concepts: first how the action of the respiratory muscles increases thoracic volume, and second (and more complex) we need to understand the interaction of the lungs and the thoracic wall.",True,Text,,,,
92752f2f-b37f-444d-a1e2-a0658aacfa15,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,Let us deal with the respiratory muscles and expansion of the thorax first.,True,Text,,,,
e3007da6-dcdf-443d-aa68-84626bcc414c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,Changing Thoracic Volume,False,Changing Thoracic Volume,,,,
1aa92b5b-9374-4c15-b780-d95e2fcbb33e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
1aa92b5b-9374-4c15-b780-d95e2fcbb33e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
1aa92b5b-9374-4c15-b780-d95e2fcbb33e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
1aa92b5b-9374-4c15-b780-d95e2fcbb33e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
6fe3adf6-72f1-4635-b805-ad74cf919475,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"It is worth a quick reminder that while controlling a visceral organ and performing a homeostatic function, the diaphragm and the other respiratory muscles are skeletal muscle and have the force-generation characteristics of such. As well as being under reflex control, it can also be controlled voluntarily (such as during speech).",True,Changing Thoracic Volume,,,,
8d1a1f2e-5703-4a45-ae92-dcd15bef0151,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
8d1a1f2e-5703-4a45-ae92-dcd15bef0151,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
8d1a1f2e-5703-4a45-ae92-dcd15bef0151,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
8d1a1f2e-5703-4a45-ae92-dcd15bef0151,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
e29d6a57-ac20-462a-a86d-689bf9c005f4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"When phrenic nerve activity stops, the diaphragm relaxes and returns to its resting dome-like position; this is aided by the recoil of the expanded lung and the decompression of the abdominal contents. The return to the resting position reduces thoracic volume and increases thoracic pressure above atmospheric pressure and air exits the lung down the reversed pressure gradient.",True,Changing Thoracic Volume,,,,
4f203ea5-9de9-40da-beaa-464bf4cf95b0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"During inspiration the thoracic volume is also increased by the action of the external intercostal muscles. Controlled by the intercostal nerve, contraction of the external intercostals causes the rib cage to rise upward and outward, resulting in an expansion of the thoracic volume in addition to the action of the diaphragm. This action is generated by the oblique positioning of the external intercostals between the ribs, and the sternum and upper ribs are stabilized by simultaneous activation of the scalenus muscles.",True,Changing Thoracic Volume,,,,
c0a17d89-48e8-476d-b15b-82ffb36a790f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
c0a17d89-48e8-476d-b15b-82ffb36a790f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
c0a17d89-48e8-476d-b15b-82ffb36a790f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
c0a17d89-48e8-476d-b15b-82ffb36a790f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
3395b766-18ff-4659-b985-2c549e4f1c5f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"Expiration is generally simpler. The elastic tissue of the lung has been expanded during inspiration, and a little like letting go of a stretch elastic band, the lungs recoil when the inspiratory muscles relax. This recoil reduces lung volume and increases lung pressure above atmospheric pressure and air exits the lung. Depending on the final lung volume achieved during inspiration, recoil of the chest wall may also contribute to expiration.",True,Changing Thoracic Volume,,,,
b5595dc0-d29f-40fe-8b0c-915c4cd5c44c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
b5595dc0-d29f-40fe-8b0c-915c4cd5c44c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
b5595dc0-d29f-40fe-8b0c-915c4cd5c44c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
b5595dc0-d29f-40fe-8b0c-915c4cd5c44c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
146fa6f3-f30a-4d9d-8744-2c7b60849a41,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,How the Lungs Move with the Chest Wall,False,How the Lungs Move with the Chest Wall,,,,
20ae7c4a-11ce-4738-9b32-4297a60925e9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"Now having dealt with the expansion of the thoracic cage, we should look at the relationship between the thoracic wall and the lungs and how the lungs and the inside of the thorax are adhered to each other so when the thoracic wall moves the lungs follow.",True,How the Lungs Move with the Chest Wall,,,,
9df10313-c654-4f74-86d8-94d8b2d486b3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
9df10313-c654-4f74-86d8-94d8b2d486b3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
9df10313-c654-4f74-86d8-94d8b2d486b3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
9df10313-c654-4f74-86d8-94d8b2d486b3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
edd51427-7f26-4048-a0b2-4472ae526511,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"We have mentioned the pressure inside the lungs, but now we have to think about the pressure inside the pleural space—called intra-pleural pressure. Even at normal, resting lung volumes the elastic tissue in the lungs is already somewhat stretched, so the lungs have a tendency to recoil, pulling inward. The chest wall, alternatively, has a tendency to spring outward. These opposing movements are prevented by the surface tension in the pleural space and cause a negative intrapleural pressure, that is below atmospheric pressure.",True,How the Lungs Move with the Chest Wall,,,,
440ca146-3f8f-454e-913c-6e4fa7ce092a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
440ca146-3f8f-454e-913c-6e4fa7ce092a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
440ca146-3f8f-454e-913c-6e4fa7ce092a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
440ca146-3f8f-454e-913c-6e4fa7ce092a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
743005de-ff8b-4125-95e4-cce8cd1d926c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
743005de-ff8b-4125-95e4-cce8cd1d926c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
743005de-ff8b-4125-95e4-cce8cd1d926c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
743005de-ff8b-4125-95e4-cce8cd1d926c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
d7f91585-5178-425d-9c32-cb4853cbbe9c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"This increase in lung volume (and referring back to Boyle’s law, the pressure of a gas tends to decrease as the volume of the container increases) causes a decrease in pressure in the lung. This is reflected in a decrease in alveolar pressure.",True,How the Lungs Move with the Chest Wall,,,,
3e32600f-295a-44b6-827a-e8a7d208102c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,This drop in alveolar pressure generates a pressure differential between the airways and the atmosphere outside—the atmospheric pressure now being greater than the reduced airway pressure causes the flow of air into the airways and toward the alveoli.,True,How the Lungs Move with the Chest Wall,,,,
af5e8d9a-575d-4106-9326-2dd4a801c4b4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"Now let us look at these pressures during expiration. At the end of inspiration the lungs are stretched and the recoil force is high. When the activity of the inspiratory muscles stops, the recoil of the lung is unopposed and the lung recoils (a little like letting go of that stretched elastic band). Therefore, in quiet breathing, the process of breathing out is normally passive and relies on the potential energy stored in the lungs’ elastic tissue.",True,How the Lungs Move with the Chest Wall,,,,
639ef17f-4f0d-4b2a-b605-3ba6a5659a5b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"As the lung recoils and returns toward its resting position, the intrapleural pressure becomes less negative and the volume decreases, resulting in a rise in alveolar pressure, as described by Boyle’s law. This rise in alveolar pressure means the pressure gradient is reversed, with pressure inside the lung becoming greater than atmospheric pressure. This reversed pressure differential causes the flow of air from the airways toward the outside—and expiration is achieved.",True,How the Lungs Move with the Chest Wall,,,,
376679dc-f803-4ed7-a398-380385738ab4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"As already mentioned, this is a passive process that relies on lung recoil, and the expiratory muscles remain inactive during quiet breathing. However, when there is a greater ventilatory demand, such as during exercise or lung disease, the respiratory system cannot wait for this passive and relatively slow process to occur, so the expiratory muscles are activated and thoracic volume (and therefore lung volume) is reduced actively much more quickly; this may cause intrapleural pressure to go positive as the thoracic wall actively pushes on the intrapleural space (and the lungs). This positive pleural pressure during active expiration can have significant ramifications in diseased lungs that we will see later on.",True,How the Lungs Move with the Chest Wall,,,,
a2ecb3a6-7f9b-4de1-bdbc-ed341649c411,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,Text,False,Text,,,,
e2abbfb7-6bef-4d78-8d0f-031418e058cc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"Levitsky, Michael G. “Chapter 2: Mechanics of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
d2740afd-39a8-4197-8713-595f53b2a91b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"West, John B. “Chapter 2: Ventilation—How Gas Gets to the Alveoli.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
c1eaa474-3674-47b9-a326-39a79444abd8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
55ad92db-7bb5-4d1f-b976-b01dc08a5e93,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-2,"Widdicombe, John G., and Andrew S. Davis. “Chapter 1.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
480f35bd-d8fc-4cc3-b4d8-f3470993aeb9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"Before we get into the details of how we breathe in, let me make sure we are all on the same page by going right back to basics, so bare with me or skip ahead if you are happy with pressure, volume, and flow.",True,Text,,,,
56648680-9d34-452a-b3f5-81e050215476,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"To get air to move into the lungs we need to generate a pressure differential; that is the pressure inside the lungs must be lower than the pressure outside (i.e., atmospheric pressure), so that air moves down the pressure gradient into the lungs.",True,Text,,,,
0deeb012-9791-4722-9321-d46e75ad9413,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"The low pressure inside the lungs is generated by increasing lung volume; bigger volume means fewer molecules in the same space, and therefore lower pressure (go back and revisit Boyle’s law if needed).",True,Text,,,,
d57fcd2e-ec4b-4420-9827-10d5233a9815,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"The basis of inspiration is lowering lung pressure below atmospheric pressure, so that atmospheric pressure pushes air down the airways until pressure equilibrates. So the fundamental first step is, how do we increase lung volume?",True,Text,,,,
8b265105-9ea6-458c-822d-7c5ca28c1114,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"To understand the mechanics of breathing we have to deal with two concepts: first how the action of the respiratory muscles increases thoracic volume, and second (and more complex) we need to understand the interaction of the lungs and the thoracic wall.",True,Text,,,,
011a64e4-583c-454a-a3c0-08aedce760bc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,Let us deal with the respiratory muscles and expansion of the thorax first.,True,Text,,,,
b82098af-971a-433b-a686-0eae01dbb939,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,Changing Thoracic Volume,False,Changing Thoracic Volume,,,,
7bd8aae7-ce57-4eb0-885f-0345fad77ada,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
7bd8aae7-ce57-4eb0-885f-0345fad77ada,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
7bd8aae7-ce57-4eb0-885f-0345fad77ada,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
7bd8aae7-ce57-4eb0-885f-0345fad77ada,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
0452cca9-21bd-4d30-a52e-636afff2f612,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"It is worth a quick reminder that while controlling a visceral organ and performing a homeostatic function, the diaphragm and the other respiratory muscles are skeletal muscle and have the force-generation characteristics of such. As well as being under reflex control, it can also be controlled voluntarily (such as during speech).",True,Changing Thoracic Volume,,,,
93a16c27-66a2-48c8-9830-c8e72ca0775f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
93a16c27-66a2-48c8-9830-c8e72ca0775f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
93a16c27-66a2-48c8-9830-c8e72ca0775f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
93a16c27-66a2-48c8-9830-c8e72ca0775f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
2223b428-f2ea-44a7-8a53-9a92196db953,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"When phrenic nerve activity stops, the diaphragm relaxes and returns to its resting dome-like position; this is aided by the recoil of the expanded lung and the decompression of the abdominal contents. The return to the resting position reduces thoracic volume and increases thoracic pressure above atmospheric pressure and air exits the lung down the reversed pressure gradient.",True,Changing Thoracic Volume,,,,
0c62ab3e-7376-45e5-8540-e27cab3d9dc8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"During inspiration the thoracic volume is also increased by the action of the external intercostal muscles. Controlled by the intercostal nerve, contraction of the external intercostals causes the rib cage to rise upward and outward, resulting in an expansion of the thoracic volume in addition to the action of the diaphragm. This action is generated by the oblique positioning of the external intercostals between the ribs, and the sternum and upper ribs are stabilized by simultaneous activation of the scalenus muscles.",True,Changing Thoracic Volume,,,,
aa459fa9-40e0-4f69-aebe-21fc7adfbfd9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
aa459fa9-40e0-4f69-aebe-21fc7adfbfd9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
aa459fa9-40e0-4f69-aebe-21fc7adfbfd9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
aa459fa9-40e0-4f69-aebe-21fc7adfbfd9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
47e27f5b-7ff2-4440-a051-d952235eeb67,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"Expiration is generally simpler. The elastic tissue of the lung has been expanded during inspiration, and a little like letting go of a stretch elastic band, the lungs recoil when the inspiratory muscles relax. This recoil reduces lung volume and increases lung pressure above atmospheric pressure and air exits the lung. Depending on the final lung volume achieved during inspiration, recoil of the chest wall may also contribute to expiration.",True,Changing Thoracic Volume,,,,
9f74e10f-3fad-4ec3-91cd-f6c18c208ee3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
9f74e10f-3fad-4ec3-91cd-f6c18c208ee3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
9f74e10f-3fad-4ec3-91cd-f6c18c208ee3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
9f74e10f-3fad-4ec3-91cd-f6c18c208ee3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
3b78de77-9fed-4ea2-ae55-2309e9f17a06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,How the Lungs Move with the Chest Wall,False,How the Lungs Move with the Chest Wall,,,,
6b3849ec-6b2e-4d6f-ba5c-04d2a659a573,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"Now having dealt with the expansion of the thoracic cage, we should look at the relationship between the thoracic wall and the lungs and how the lungs and the inside of the thorax are adhered to each other so when the thoracic wall moves the lungs follow.",True,How the Lungs Move with the Chest Wall,,,,
3f026c92-b6ae-41f5-bccd-b47a854afbe8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
3f026c92-b6ae-41f5-bccd-b47a854afbe8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
3f026c92-b6ae-41f5-bccd-b47a854afbe8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
3f026c92-b6ae-41f5-bccd-b47a854afbe8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
52ebbdbd-ce91-40d6-b58c-5bf5fd22c923,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"We have mentioned the pressure inside the lungs, but now we have to think about the pressure inside the pleural space—called intra-pleural pressure. Even at normal, resting lung volumes the elastic tissue in the lungs is already somewhat stretched, so the lungs have a tendency to recoil, pulling inward. The chest wall, alternatively, has a tendency to spring outward. These opposing movements are prevented by the surface tension in the pleural space and cause a negative intrapleural pressure, that is below atmospheric pressure.",True,How the Lungs Move with the Chest Wall,,,,
3aca4b21-cf75-4b24-8fa6-9fac9cbf8089,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
3aca4b21-cf75-4b24-8fa6-9fac9cbf8089,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
3aca4b21-cf75-4b24-8fa6-9fac9cbf8089,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
3aca4b21-cf75-4b24-8fa6-9fac9cbf8089,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
393b2744-4e4f-4af9-a3c2-60c1891939c0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
393b2744-4e4f-4af9-a3c2-60c1891939c0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
393b2744-4e4f-4af9-a3c2-60c1891939c0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
393b2744-4e4f-4af9-a3c2-60c1891939c0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
fa25fbab-34dd-4859-af18-428ac050620d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"This increase in lung volume (and referring back to Boyle’s law, the pressure of a gas tends to decrease as the volume of the container increases) causes a decrease in pressure in the lung. This is reflected in a decrease in alveolar pressure.",True,How the Lungs Move with the Chest Wall,,,,
f18783be-55e1-41d3-9c11-b18d9a6985a4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,This drop in alveolar pressure generates a pressure differential between the airways and the atmosphere outside—the atmospheric pressure now being greater than the reduced airway pressure causes the flow of air into the airways and toward the alveoli.,True,How the Lungs Move with the Chest Wall,,,,
42fbbc08-f540-4d04-8b82-e4597250f372,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"Now let us look at these pressures during expiration. At the end of inspiration the lungs are stretched and the recoil force is high. When the activity of the inspiratory muscles stops, the recoil of the lung is unopposed and the lung recoils (a little like letting go of that stretched elastic band). Therefore, in quiet breathing, the process of breathing out is normally passive and relies on the potential energy stored in the lungs’ elastic tissue.",True,How the Lungs Move with the Chest Wall,,,,
2210dbca-b34b-41dc-ba03-a2e61fc4a977,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"As the lung recoils and returns toward its resting position, the intrapleural pressure becomes less negative and the volume decreases, resulting in a rise in alveolar pressure, as described by Boyle’s law. This rise in alveolar pressure means the pressure gradient is reversed, with pressure inside the lung becoming greater than atmospheric pressure. This reversed pressure differential causes the flow of air from the airways toward the outside—and expiration is achieved.",True,How the Lungs Move with the Chest Wall,,,,
70ccbb4a-5f3b-4d20-b83c-3633100de8e0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"As already mentioned, this is a passive process that relies on lung recoil, and the expiratory muscles remain inactive during quiet breathing. However, when there is a greater ventilatory demand, such as during exercise or lung disease, the respiratory system cannot wait for this passive and relatively slow process to occur, so the expiratory muscles are activated and thoracic volume (and therefore lung volume) is reduced actively much more quickly; this may cause intrapleural pressure to go positive as the thoracic wall actively pushes on the intrapleural space (and the lungs). This positive pleural pressure during active expiration can have significant ramifications in diseased lungs that we will see later on.",True,How the Lungs Move with the Chest Wall,,,,
e5fade9d-6fe9-4841-b37f-e41f77599bc1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,Text,False,Text,,,,
1e35d9e5-9f71-4250-8078-d4c1ec719c48,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"Levitsky, Michael G. “Chapter 2: Mechanics of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
53cf7053-67a9-4a92-aec5-0d12ca1aee2d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"West, John B. “Chapter 2: Ventilation—How Gas Gets to the Alveoli.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
183d7f09-34f2-4212-8b8e-cae9125828dc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
1c87494e-769f-4def-95ed-d6bd8af7e06f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/#chapter-27-section-1,"Widdicombe, John G., and Andrew S. Davis. “Chapter 1.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
48133d7d-f663-4cdb-98bf-4c4ed53985ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"Before we get into the details of how we breathe in, let me make sure we are all on the same page by going right back to basics, so bare with me or skip ahead if you are happy with pressure, volume, and flow.",True,Text,,,,
5809b18d-572d-44e5-8229-404d234bdbc3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"To get air to move into the lungs we need to generate a pressure differential; that is the pressure inside the lungs must be lower than the pressure outside (i.e., atmospheric pressure), so that air moves down the pressure gradient into the lungs.",True,Text,,,,
c80e2741-e358-41c0-aa56-eaa02bcd5cf2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"The low pressure inside the lungs is generated by increasing lung volume; bigger volume means fewer molecules in the same space, and therefore lower pressure (go back and revisit Boyle’s law if needed).",True,Text,,,,
d3d3f9a8-72b5-4e38-b0e9-7d5162877cb5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"The basis of inspiration is lowering lung pressure below atmospheric pressure, so that atmospheric pressure pushes air down the airways until pressure equilibrates. So the fundamental first step is, how do we increase lung volume?",True,Text,,,,
11669ca7-3451-4a7f-90fd-f7b80396b5dc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"To understand the mechanics of breathing we have to deal with two concepts: first how the action of the respiratory muscles increases thoracic volume, and second (and more complex) we need to understand the interaction of the lungs and the thoracic wall.",True,Text,,,,
08f5e316-7384-4cb9-8361-c31a542bedcf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,Let us deal with the respiratory muscles and expansion of the thorax first.,True,Text,,,,
44a58e86-e855-445c-9579-6c8e9283a269,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,Changing Thoracic Volume,False,Changing Thoracic Volume,,,,
75a069c3-771f-4569-92fc-8d57c2bc4db7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
75a069c3-771f-4569-92fc-8d57c2bc4db7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
75a069c3-771f-4569-92fc-8d57c2bc4db7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
75a069c3-771f-4569-92fc-8d57c2bc4db7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"The muscle that generates the greatest change in thoracic volume (and thereby the greatest contribution to breathing) is the diaphragm (figure 2.1). Separating the thoracic and abdominal cavities, this sheetlike muscle forms a dome shape in the relaxed state that encroaches into the thorax. This sheet is formed of three sections, the anterior portion originating at the ribs and sternum, and the posterior portion originating on the vertebrae. These are connected by the central portion that is comprised of a tendon sheet.",True,Changing Thoracic Volume,Figure 2.1,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.1.png,Figure 2.1: The diaphragm.
afd807a2-83b9-4a7b-bb59-ed4841a258fc,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"It is worth a quick reminder that while controlling a visceral organ and performing a homeostatic function, the diaphragm and the other respiratory muscles are skeletal muscle and have the force-generation characteristics of such. As well as being under reflex control, it can also be controlled voluntarily (such as during speech).",True,Changing Thoracic Volume,,,,
de8ad201-3e6c-4771-b118-25504812d5df,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
de8ad201-3e6c-4771-b118-25504812d5df,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
de8ad201-3e6c-4771-b118-25504812d5df,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
de8ad201-3e6c-4771-b118-25504812d5df,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"Activation of the phrenic nerve stimulates the diaphragm and generates inspiration. Upon stimulation the contracting diaphragm flattens out, descending toward the abdomen. As it does so the thoracic volume increases, and consequently thoracic pressure falls. When thoracic pressure falls below atmospheric pressure, air moves down the generated pressure gradient and enters the lung. Note that this increase in thoracic volume comes at the expense of the abdominal volume, and abdominal contents can be compressed during inspiration. The diaphragm may descend as much as 10 cm, but a descent of 1 cm is sufficient to provide tidal breathing (figure 2.2).",True,Changing Thoracic Volume,Figure 2.2,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.2.png,Figure 2.2: Diaphragm positional change.
c6badac6-5213-40d9-b99e-26d58bf40144,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"When phrenic nerve activity stops, the diaphragm relaxes and returns to its resting dome-like position; this is aided by the recoil of the expanded lung and the decompression of the abdominal contents. The return to the resting position reduces thoracic volume and increases thoracic pressure above atmospheric pressure and air exits the lung down the reversed pressure gradient.",True,Changing Thoracic Volume,,,,
ee1039df-5e5e-4072-a732-53330f347248,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"During inspiration the thoracic volume is also increased by the action of the external intercostal muscles. Controlled by the intercostal nerve, contraction of the external intercostals causes the rib cage to rise upward and outward, resulting in an expansion of the thoracic volume in addition to the action of the diaphragm. This action is generated by the oblique positioning of the external intercostals between the ribs, and the sternum and upper ribs are stabilized by simultaneous activation of the scalenus muscles.",True,Changing Thoracic Volume,,,,
ff674e65-4bc5-4ab4-88b1-f5d06e9e9acb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
ff674e65-4bc5-4ab4-88b1-f5d06e9e9acb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
ff674e65-4bc5-4ab4-88b1-f5d06e9e9acb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
ff674e65-4bc5-4ab4-88b1-f5d06e9e9acb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"During periods of high ventilatory need (or drive) other muscles can contribute to expansion of the rib cage (figure 2.3). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breath is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.",True,Changing Thoracic Volume,Figure 2.3,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/Inspiration.jpeg,Figure 2.3: Inspiratory muscles of the rib cage.
d3a76807-bb04-4eee-9f75-d61882333f72,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"Expiration is generally simpler. The elastic tissue of the lung has been expanded during inspiration, and a little like letting go of a stretch elastic band, the lungs recoil when the inspiratory muscles relax. This recoil reduces lung volume and increases lung pressure above atmospheric pressure and air exits the lung. Depending on the final lung volume achieved during inspiration, recoil of the chest wall may also contribute to expiration.",True,Changing Thoracic Volume,,,,
48f4a68e-20bb-4525-8e0a-f95bad4b08fe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
48f4a68e-20bb-4525-8e0a-f95bad4b08fe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
48f4a68e-20bb-4525-8e0a-f95bad4b08fe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
48f4a68e-20bb-4525-8e0a-f95bad4b08fe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"So during quiet resting breathing, expiration is passive, relying on the expenditure of the stored, potential energy in the elastic lung tissue. However, when ventilation needs to be increased, such as during exercise, this process is too slow, and this passive process needs some active help in order to increase the rate of breathing. Activation of the internal intercostal muscles draws the rib cage downward to reduce thoracic volume. Thoracic volume is further decreased by contraction of muscles surrounding the abdomen; these increase abdominal pressure and help push the diaphragm upward (figure 2.4).",True,Changing Thoracic Volume,Figure 2.4,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.4.jpeg,Figure 2.4: Expiratory muscles.
48e9efed-f444-4455-96c0-cfaf93f181b4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,How the Lungs Move with the Chest Wall,False,How the Lungs Move with the Chest Wall,,,,
9a19f0b5-98d5-4edb-9c06-55b746d74816,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"Now having dealt with the expansion of the thoracic cage, we should look at the relationship between the thoracic wall and the lungs and how the lungs and the inside of the thorax are adhered to each other so when the thoracic wall moves the lungs follow.",True,How the Lungs Move with the Chest Wall,,,,
22aa073e-8406-4d31-b47d-197fc242b00a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
22aa073e-8406-4d31-b47d-197fc242b00a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
22aa073e-8406-4d31-b47d-197fc242b00a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
22aa073e-8406-4d31-b47d-197fc242b00a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"The inside of the thoracic cavity is lined with a membrane, the parietal pleura. The outside of the lungs are lined with a membrane called the visceral pleura. The space between these membranes, the pleural cavity or pleural space, is filled with pleural fluid (figure 2.5). Normally there is only 5–10 mL of pleural fluid to cover all the lung’s external surface. So the fluid layer and the intra-pleural space is extremely thin. When a thin layer of fluid is trapped between two surfaces it exerts surface tension and holds the two surfaces together; if you’ve ever been doing the washing up and trapped a layer of water between too dinner plates you’ll have noticed its difficult to pry the plates apart. It is similar for the pleural membranes, and it is this surface tension that holds the outside of the lungs to the inside of the thorax. We will deal with surface tension in more detail in a later chapter.",True,How the Lungs Move with the Chest Wall,Figure 2.5,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.5.png,Figure 2.5: The pleural membranes and space.
13dd7ab2-08ca-4717-8671-9b1ba0ba7829,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"We have mentioned the pressure inside the lungs, but now we have to think about the pressure inside the pleural space—called intra-pleural pressure. Even at normal, resting lung volumes the elastic tissue in the lungs is already somewhat stretched, so the lungs have a tendency to recoil, pulling inward. The chest wall, alternatively, has a tendency to spring outward. These opposing movements are prevented by the surface tension in the pleural space and cause a negative intrapleural pressure, that is below atmospheric pressure.",True,How the Lungs Move with the Chest Wall,,,,
1703d102-9c4b-4d08-8ff9-4d36eb1672b6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
1703d102-9c4b-4d08-8ff9-4d36eb1672b6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
1703d102-9c4b-4d08-8ff9-4d36eb1672b6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
1703d102-9c4b-4d08-8ff9-4d36eb1672b6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"We should now consider what happens to intrapleural and airway pressures during the breathing cycle. First, let us look at the pressures and volumes before inspiration begins (figure 2.6). The intrapleural pressure is slightly negative (−5 cm H2O) due to the recoil of the lung and outward spring of the chest wall. Before the breath starts lung volume is considered zero and flow is also zero (i.e., volume has not changed and there is no movement of air in the airways). Alveolar pressure, the pressure inside the lungs, is also zero, really meaning it is equal to atmospheric pressure.",True,How the Lungs Move with the Chest Wall,Figure 2.6,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
8b77fb24-aa82-45e5-99d1-28e598bf5c2f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,How the Lungs Move with the Chest Wall,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
8b77fb24-aa82-45e5-99d1-28e598bf5c2f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,Changing Thoracic Volume,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
8b77fb24-aa82-45e5-99d1-28e598bf5c2f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,Fundamentals of Gas Movement,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
8b77fb24-aa82-45e5-99d1-28e598bf5c2f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"Look at what happens (figure 2.6) when the respiratory muscles are activated to increase thoracic volume and achieve a breath in. As the thoracic wall moves outward and the diaphragm descends, thoracic volume and therefore lung volume increases. More tension is generated in the stretching elastic tissue of the lungs as the lung expands—and just like stretching an elastic band, the recoil force increases, and the stretching lung now pulls back harder on the pleural space. This causes the intrapleural pressure to become even more negative (−8 cm H2O).",True,How the Lungs Move with the Chest Wall,Figure 2.6,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/05/2.6.png,Figure 2.6: The breathing cycle.
923cc88c-e73e-4707-83fa-b827f282e27f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"This increase in lung volume (and referring back to Boyle’s law, the pressure of a gas tends to decrease as the volume of the container increases) causes a decrease in pressure in the lung. This is reflected in a decrease in alveolar pressure.",True,How the Lungs Move with the Chest Wall,,,,
87e34175-5684-4f6e-8fd9-6d7ddcfa35a1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,This drop in alveolar pressure generates a pressure differential between the airways and the atmosphere outside—the atmospheric pressure now being greater than the reduced airway pressure causes the flow of air into the airways and toward the alveoli.,True,How the Lungs Move with the Chest Wall,,,,
29548cfd-d2fa-42d3-91a0-b248ad4ddfe4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"Now let us look at these pressures during expiration. At the end of inspiration the lungs are stretched and the recoil force is high. When the activity of the inspiratory muscles stops, the recoil of the lung is unopposed and the lung recoils (a little like letting go of that stretched elastic band). Therefore, in quiet breathing, the process of breathing out is normally passive and relies on the potential energy stored in the lungs’ elastic tissue.",True,How the Lungs Move with the Chest Wall,,,,
f450756f-e137-4146-95f0-8e17c99c0451,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"As the lung recoils and returns toward its resting position, the intrapleural pressure becomes less negative and the volume decreases, resulting in a rise in alveolar pressure, as described by Boyle’s law. This rise in alveolar pressure means the pressure gradient is reversed, with pressure inside the lung becoming greater than atmospheric pressure. This reversed pressure differential causes the flow of air from the airways toward the outside—and expiration is achieved.",True,How the Lungs Move with the Chest Wall,,,,
21a4bce3-de9e-4e57-9969-474ce6abc221,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"As already mentioned, this is a passive process that relies on lung recoil, and the expiratory muscles remain inactive during quiet breathing. However, when there is a greater ventilatory demand, such as during exercise or lung disease, the respiratory system cannot wait for this passive and relatively slow process to occur, so the expiratory muscles are activated and thoracic volume (and therefore lung volume) is reduced actively much more quickly; this may cause intrapleural pressure to go positive as the thoracic wall actively pushes on the intrapleural space (and the lungs). This positive pleural pressure during active expiration can have significant ramifications in diseased lungs that we will see later on.",True,How the Lungs Move with the Chest Wall,,,,
5342400a-fc6b-49e1-b085-c03d25c35847,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,Text,False,Text,,,,
6c89a2e0-aa10-4879-9cdf-87f8f27db639,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"Levitsky, Michael G. “Chapter 2: Mechanics of Breathing.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
1f88e2a1-e308-47ed-8825-3d0950785a30,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"West, John B. “Chapter 2: Ventilation—How Gas Gets to the Alveoli.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
934ff5a3-71f2-4081-8a01-94261dc0b069,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"West, John B. “Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
b1c746d5-2e98-4505-b01a-281d331c72a4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,2. Mechanics of the Lungs,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/mechanics-of-the-lungs/,"Widdicombe, John G., and Andrew S. Davis. “Chapter 1.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
3c8b34ab-c9f8-4728-8aad-518dd91e7284,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"We will see how blood gases are monitored and maintained through neurochemical control of lung expansion and relaxation to achieve the appropriate level of alveolar ventilation. Factors that affect the degree of gas exchange between the lung and blood will be discussed, along with the coordination of ventilation and perfusion of the lung. Finally, we will see how oxygen and carbon dioxide are transported in the bloodstream to and from tissue and the mechanisms that ensure appropriate delivery and a stable blood gas environment. Before we begin, however, we will look at the functional anatomy of the lung and how the lung is well designed to perform its primary role and defend itself from the external environment.",True,Text,,,,
adc941bc-907d-461e-871c-823b65183d79,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,Defense of the Lung,False,Defense of the Lung,,,,
57f4f53d-d33e-4c7e-873d-33f33788ea22,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
57f4f53d-d33e-4c7e-873d-33f33788ea22,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
57f4f53d-d33e-4c7e-873d-33f33788ea22,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
57f4f53d-d33e-4c7e-873d-33f33788ea22,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
57f4f53d-d33e-4c7e-873d-33f33788ea22,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
57f4f53d-d33e-4c7e-873d-33f33788ea22,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
f288bfbb-d2c9-4f26-bd73-b9cc05195f26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
f288bfbb-d2c9-4f26-bd73-b9cc05195f26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
f288bfbb-d2c9-4f26-bd73-b9cc05195f26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
f288bfbb-d2c9-4f26-bd73-b9cc05195f26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
f288bfbb-d2c9-4f26-bd73-b9cc05195f26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
f288bfbb-d2c9-4f26-bd73-b9cc05195f26,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
696f5302-3baf-4605-87e5-ffa601be665d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
696f5302-3baf-4605-87e5-ffa601be665d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
696f5302-3baf-4605-87e5-ffa601be665d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
696f5302-3baf-4605-87e5-ffa601be665d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
696f5302-3baf-4605-87e5-ffa601be665d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
696f5302-3baf-4605-87e5-ffa601be665d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
fb2d60c5-4916-44d2-9ef3-7f1a3f15d18c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,The Bronchial Tree,False,The Bronchial Tree,,,,
e9c72af1-ff8b-4aae-b16e-1c90f7d65f86,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
e9c72af1-ff8b-4aae-b16e-1c90f7d65f86,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
e9c72af1-ff8b-4aae-b16e-1c90f7d65f86,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
e9c72af1-ff8b-4aae-b16e-1c90f7d65f86,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
e9c72af1-ff8b-4aae-b16e-1c90f7d65f86,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
e9c72af1-ff8b-4aae-b16e-1c90f7d65f86,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
d54cb433-447c-4fc8-a471-77d0133a64ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
d54cb433-447c-4fc8-a471-77d0133a64ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
d54cb433-447c-4fc8-a471-77d0133a64ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
d54cb433-447c-4fc8-a471-77d0133a64ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
d54cb433-447c-4fc8-a471-77d0133a64ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
d54cb433-447c-4fc8-a471-77d0133a64ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
f02e387e-e075-4b37-b9b6-a610e5f32c9b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
f02e387e-e075-4b37-b9b6-a610e5f32c9b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
f02e387e-e075-4b37-b9b6-a610e5f32c9b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
f02e387e-e075-4b37-b9b6-a610e5f32c9b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
f02e387e-e075-4b37-b9b6-a610e5f32c9b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
f02e387e-e075-4b37-b9b6-a610e5f32c9b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
c2a4e335-8cef-43b7-a64e-256d43c36ffb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,Flow in the Airways,False,Flow in the Airways,,,,
7c524b3e-db2b-48a2-bf84-86e51af527a1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"Airflow down the bronchial tree is caused by the generation of a pressure differential when lung volume is expanded by contraction of the respiratory muscles (more on this in chapter 2). Inspired air first enters the airways of the conducting zone, which while having the largest diameter airways also has the fewest; consequently the total cross-sectional area of the conducting zone is relatively low. With a large volume of air passing through a low cross-sectional area, the velocity of air in the conducting zone is high and is moving by “bulk flow” generated by the pressure differential (like water through a hose) until it reaches the terminal bronchioles and the end of the conducting zone.",True,Flow in the Airways,,,,
63a3d858-bef4-4104-bfc5-25dc72d5b028,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"When this air enters the respiratory zone, it slows rapidly. This is due to the enormous total cross-sectional area of the airways in the respiratory zone—while the airways are much narrower here, they are far more numerous. The final transfer of the gases through the respiratory zone is therefore achieved by diffusion; the rate of diffusion is so rapid and the distances so short that concentration differences are abolished within a second.",True,Flow in the Airways,,,,
6a95a121-4333-4cfb-bb85-7dfaf892f9dd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"As an aside, this deceleration of the air at the terminal bronchioles means any particles that have been able to descend this deep are frequently deposited here. This has ramifications for disease and also delivery of inhaled medications.",True,Flow in the Airways,,,,
8b36b6b2-ee9b-4210-95ae-14ea1935c368,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,Primary Objective: Gas Exchange,False,Primary Objective: Gas Exchange,,,,
ba772aac-d906-41ac-a41f-012f852e38ff,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"Gases that have diffused to the respiratory zone find themselves in an ideal environment for gas exchange. We will deal with gas exchange in more detail later (chapter 7), but you should appreciate that the essential components for efficient gas exchange are all present in the lung.",True,Primary Objective: Gas Exchange,,,,
b007a1b0-21ac-42ed-bc9d-b2aab0db116e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"A large surface area is generated by the 500 million alveoli, and while each alveolus only has a diameter of 0.3 mm, collectively they produce a total gas exchange surface of 100 m2—about the surface area of a tennis court.",True,Primary Objective: Gas Exchange,,,,
c0c5c417-5ff6-472c-a25f-5ad889382fc3,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"The membranes that gases transfer across are very thin and pose little opposition. In brief, oxygen entering the alveolus only has to cross the squamous cell of the alveolus wall, a very thin basement membrane, and then the squamous cell of the capillary wall to get into the pulmonary circulation. The total distance can be as low as 0.2 micrometers. This degree of thinness also makes these membranes prone to damage.",True,Primary Objective: Gas Exchange,,,,
389b6c13-b75d-4d7c-b994-a2cd8388bdac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"As well as the alveolus receiving air (that is being ventilated), the other essential component for gas exchange is blood flow. This is provided by the pulmonary circulation and consists of all cardiac output coming from the right heart. The pulmonary circulation forms very dense networks of capillaries surrounding each alveolus, so much so that the alveoli can be imagined as being washed over with blood.",True,Primary Objective: Gas Exchange,,,,
7e4649c8-2ea2-4feb-8341-0aca3e7d30b8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"These characteristics make the lung a highly efficient exchange organ between the environment and the circulation, which is ideal for the transfer of O2 into the bloodstream and, just as importantly, CO2 out. It also allows some drugs to be delivered by inhalation, but also has the potential to allow noxious substances into the bloodstream. Likewise, changes in any of these characteristics of the lung in disease, such as loss of surface area in emphysema or membrane thickening in pulmonary fibrosis, can severely diminish gas exchange.",True,Primary Objective: Gas Exchange,,,,
c4504439-76d3-4abd-9822-b70c3d6d691e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,Text,False,Text,,,,
bb13387c-a557-4bd6-8b04-3e30d6d82916,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"Levitsky, Michael G. “Chapter 1: Function and Structure of the Respiratory System.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
9faee6ea-d9bf-4b11-a3d3-8561cb811717,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"West, John B. “Chapter 1: Structure and Function—How the Architecture of the Lung Subserves Its Function.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
218cbf6e-39c5-4595-a269-e07c1485f153,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-5,"Widdicombe, John G., and Andrew S. Davis. “Chapter 1.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
fc803dbc-b864-4d32-8b3f-9c1acc1ead12,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"We will see how blood gases are monitored and maintained through neurochemical control of lung expansion and relaxation to achieve the appropriate level of alveolar ventilation. Factors that affect the degree of gas exchange between the lung and blood will be discussed, along with the coordination of ventilation and perfusion of the lung. Finally, we will see how oxygen and carbon dioxide are transported in the bloodstream to and from tissue and the mechanisms that ensure appropriate delivery and a stable blood gas environment. Before we begin, however, we will look at the functional anatomy of the lung and how the lung is well designed to perform its primary role and defend itself from the external environment.",True,Text,,,,
efa50d17-5a16-4095-8712-93bc621f07ef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,Defense of the Lung,False,Defense of the Lung,,,,
33c4fb24-ef08-4e0d-a58b-5a7b6d9fa8f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
33c4fb24-ef08-4e0d-a58b-5a7b6d9fa8f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
33c4fb24-ef08-4e0d-a58b-5a7b6d9fa8f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
33c4fb24-ef08-4e0d-a58b-5a7b6d9fa8f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
33c4fb24-ef08-4e0d-a58b-5a7b6d9fa8f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
33c4fb24-ef08-4e0d-a58b-5a7b6d9fa8f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
0f3a9b01-dbb6-47ad-88ac-5701e93dee06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
0f3a9b01-dbb6-47ad-88ac-5701e93dee06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
0f3a9b01-dbb6-47ad-88ac-5701e93dee06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
0f3a9b01-dbb6-47ad-88ac-5701e93dee06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
0f3a9b01-dbb6-47ad-88ac-5701e93dee06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
0f3a9b01-dbb6-47ad-88ac-5701e93dee06,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
9bd640df-4d2c-4766-b5b9-b9d3a7f938ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
9bd640df-4d2c-4766-b5b9-b9d3a7f938ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
9bd640df-4d2c-4766-b5b9-b9d3a7f938ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
9bd640df-4d2c-4766-b5b9-b9d3a7f938ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
9bd640df-4d2c-4766-b5b9-b9d3a7f938ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
9bd640df-4d2c-4766-b5b9-b9d3a7f938ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
20f7c58c-67a0-4c30-bc02-4d9146aa8b2c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,The Bronchial Tree,False,The Bronchial Tree,,,,
816c6864-6fb4-4e06-99fa-0d7b06681b7a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
816c6864-6fb4-4e06-99fa-0d7b06681b7a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
816c6864-6fb4-4e06-99fa-0d7b06681b7a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
816c6864-6fb4-4e06-99fa-0d7b06681b7a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
816c6864-6fb4-4e06-99fa-0d7b06681b7a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
816c6864-6fb4-4e06-99fa-0d7b06681b7a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
ce335dd5-e233-47f3-9306-6a9d5b70f495,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
ce335dd5-e233-47f3-9306-6a9d5b70f495,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
ce335dd5-e233-47f3-9306-6a9d5b70f495,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
ce335dd5-e233-47f3-9306-6a9d5b70f495,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
ce335dd5-e233-47f3-9306-6a9d5b70f495,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
ce335dd5-e233-47f3-9306-6a9d5b70f495,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
9ef35f75-c658-4bd8-bace-08bf5452cc81,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
9ef35f75-c658-4bd8-bace-08bf5452cc81,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
9ef35f75-c658-4bd8-bace-08bf5452cc81,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
9ef35f75-c658-4bd8-bace-08bf5452cc81,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
9ef35f75-c658-4bd8-bace-08bf5452cc81,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
9ef35f75-c658-4bd8-bace-08bf5452cc81,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
c8638430-7b6c-418f-a23f-82c2088d27b6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,Flow in the Airways,False,Flow in the Airways,,,,
cbc9abbd-3570-4eaf-af65-b1e94a1211a5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"Airflow down the bronchial tree is caused by the generation of a pressure differential when lung volume is expanded by contraction of the respiratory muscles (more on this in chapter 2). Inspired air first enters the airways of the conducting zone, which while having the largest diameter airways also has the fewest; consequently the total cross-sectional area of the conducting zone is relatively low. With a large volume of air passing through a low cross-sectional area, the velocity of air in the conducting zone is high and is moving by “bulk flow” generated by the pressure differential (like water through a hose) until it reaches the terminal bronchioles and the end of the conducting zone.",True,Flow in the Airways,,,,
3d7d1b03-79ab-495b-b9df-33daa7a9eddd,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"When this air enters the respiratory zone, it slows rapidly. This is due to the enormous total cross-sectional area of the airways in the respiratory zone—while the airways are much narrower here, they are far more numerous. The final transfer of the gases through the respiratory zone is therefore achieved by diffusion; the rate of diffusion is so rapid and the distances so short that concentration differences are abolished within a second.",True,Flow in the Airways,,,,
41246028-a557-4e02-b71a-c7373994da01,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"As an aside, this deceleration of the air at the terminal bronchioles means any particles that have been able to descend this deep are frequently deposited here. This has ramifications for disease and also delivery of inhaled medications.",True,Flow in the Airways,,,,
b090d5c6-47e2-485a-83d5-2611e7859e4e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,Primary Objective: Gas Exchange,False,Primary Objective: Gas Exchange,,,,
0c324a3b-eb9f-4fb2-b87a-950dacf405fa,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"Gases that have diffused to the respiratory zone find themselves in an ideal environment for gas exchange. We will deal with gas exchange in more detail later (chapter 7), but you should appreciate that the essential components for efficient gas exchange are all present in the lung.",True,Primary Objective: Gas Exchange,,,,
d6b6ef73-360f-4415-a545-cfbfc7b0d3de,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"A large surface area is generated by the 500 million alveoli, and while each alveolus only has a diameter of 0.3 mm, collectively they produce a total gas exchange surface of 100 m2—about the surface area of a tennis court.",True,Primary Objective: Gas Exchange,,,,
56189b48-6ae0-43c4-b613-97a91aa407d1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"The membranes that gases transfer across are very thin and pose little opposition. In brief, oxygen entering the alveolus only has to cross the squamous cell of the alveolus wall, a very thin basement membrane, and then the squamous cell of the capillary wall to get into the pulmonary circulation. The total distance can be as low as 0.2 micrometers. This degree of thinness also makes these membranes prone to damage.",True,Primary Objective: Gas Exchange,,,,
0d6ed9ba-7f88-4487-936d-4a5af454fbfb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"As well as the alveolus receiving air (that is being ventilated), the other essential component for gas exchange is blood flow. This is provided by the pulmonary circulation and consists of all cardiac output coming from the right heart. The pulmonary circulation forms very dense networks of capillaries surrounding each alveolus, so much so that the alveoli can be imagined as being washed over with blood.",True,Primary Objective: Gas Exchange,,,,
fdf31d10-824a-416d-9b67-c4f51e1418da,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"These characteristics make the lung a highly efficient exchange organ between the environment and the circulation, which is ideal for the transfer of O2 into the bloodstream and, just as importantly, CO2 out. It also allows some drugs to be delivered by inhalation, but also has the potential to allow noxious substances into the bloodstream. Likewise, changes in any of these characteristics of the lung in disease, such as loss of surface area in emphysema or membrane thickening in pulmonary fibrosis, can severely diminish gas exchange.",True,Primary Objective: Gas Exchange,,,,
1b6157d4-0da9-48fc-8123-b147a56ea26a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,Text,False,Text,,,,
b79a8067-9d09-493e-a2ce-7c962f8b83de,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"Levitsky, Michael G. “Chapter 1: Function and Structure of the Respiratory System.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
332fc354-2d05-457a-bf82-1271c4552758,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"West, John B. “Chapter 1: Structure and Function—How the Architecture of the Lung Subserves Its Function.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
9a52b8ca-a867-4675-bc03-1543a949cb67,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Flow in the Airways,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-4,"Widdicombe, John G., and Andrew S. Davis. “Chapter 1.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
5435d4f6-be41-472c-96cd-401a57f53782,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"We will see how blood gases are monitored and maintained through neurochemical control of lung expansion and relaxation to achieve the appropriate level of alveolar ventilation. Factors that affect the degree of gas exchange between the lung and blood will be discussed, along with the coordination of ventilation and perfusion of the lung. Finally, we will see how oxygen and carbon dioxide are transported in the bloodstream to and from tissue and the mechanisms that ensure appropriate delivery and a stable blood gas environment. Before we begin, however, we will look at the functional anatomy of the lung and how the lung is well designed to perform its primary role and defend itself from the external environment.",True,Text,,,,
f495618b-0996-4f65-9843-43461bbd65f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,Defense of the Lung,False,Defense of the Lung,,,,
4d6d90d4-bb4c-4fea-945b-9606fa2ade5a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
4d6d90d4-bb4c-4fea-945b-9606fa2ade5a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
4d6d90d4-bb4c-4fea-945b-9606fa2ade5a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
4d6d90d4-bb4c-4fea-945b-9606fa2ade5a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
4d6d90d4-bb4c-4fea-945b-9606fa2ade5a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
4d6d90d4-bb4c-4fea-945b-9606fa2ade5a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
eded1143-b392-494a-9f06-9ec970ad7eae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
eded1143-b392-494a-9f06-9ec970ad7eae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
eded1143-b392-494a-9f06-9ec970ad7eae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
eded1143-b392-494a-9f06-9ec970ad7eae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
eded1143-b392-494a-9f06-9ec970ad7eae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
eded1143-b392-494a-9f06-9ec970ad7eae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
fc6d2f0f-6f2e-476c-8d87-1d08aee95099,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
fc6d2f0f-6f2e-476c-8d87-1d08aee95099,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
fc6d2f0f-6f2e-476c-8d87-1d08aee95099,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
fc6d2f0f-6f2e-476c-8d87-1d08aee95099,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
fc6d2f0f-6f2e-476c-8d87-1d08aee95099,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
fc6d2f0f-6f2e-476c-8d87-1d08aee95099,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
543ebf2c-cf3c-40be-aa4f-a5beda34c761,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,The Bronchial Tree,False,The Bronchial Tree,,,,
d68ae110-9547-49f2-b318-3ae88bedc595,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
d68ae110-9547-49f2-b318-3ae88bedc595,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
d68ae110-9547-49f2-b318-3ae88bedc595,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
d68ae110-9547-49f2-b318-3ae88bedc595,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
d68ae110-9547-49f2-b318-3ae88bedc595,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
d68ae110-9547-49f2-b318-3ae88bedc595,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
57e2f327-2778-4b91-9914-ce917ce49bef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
57e2f327-2778-4b91-9914-ce917ce49bef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
57e2f327-2778-4b91-9914-ce917ce49bef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
57e2f327-2778-4b91-9914-ce917ce49bef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
57e2f327-2778-4b91-9914-ce917ce49bef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
57e2f327-2778-4b91-9914-ce917ce49bef,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
e39e6c7c-bac4-4072-8f3c-682c1a178a96,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
e39e6c7c-bac4-4072-8f3c-682c1a178a96,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
e39e6c7c-bac4-4072-8f3c-682c1a178a96,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
e39e6c7c-bac4-4072-8f3c-682c1a178a96,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
e39e6c7c-bac4-4072-8f3c-682c1a178a96,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
e39e6c7c-bac4-4072-8f3c-682c1a178a96,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
fc3bf5e6-446b-4d56-a4fd-39923d61ec30,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,Flow in the Airways,False,Flow in the Airways,,,,
4d0d8cef-44d5-4505-bacf-3b7365837324,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"Airflow down the bronchial tree is caused by the generation of a pressure differential when lung volume is expanded by contraction of the respiratory muscles (more on this in chapter 2). Inspired air first enters the airways of the conducting zone, which while having the largest diameter airways also has the fewest; consequently the total cross-sectional area of the conducting zone is relatively low. With a large volume of air passing through a low cross-sectional area, the velocity of air in the conducting zone is high and is moving by “bulk flow” generated by the pressure differential (like water through a hose) until it reaches the terminal bronchioles and the end of the conducting zone.",True,Flow in the Airways,,,,
676dacd8-3ba5-4f9a-935b-65a6d7f30002,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"When this air enters the respiratory zone, it slows rapidly. This is due to the enormous total cross-sectional area of the airways in the respiratory zone—while the airways are much narrower here, they are far more numerous. The final transfer of the gases through the respiratory zone is therefore achieved by diffusion; the rate of diffusion is so rapid and the distances so short that concentration differences are abolished within a second.",True,Flow in the Airways,,,,
f9d7a676-a639-480b-b2f3-98d65f2a1e2d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"As an aside, this deceleration of the air at the terminal bronchioles means any particles that have been able to descend this deep are frequently deposited here. This has ramifications for disease and also delivery of inhaled medications.",True,Flow in the Airways,,,,
05c93d10-41d0-4fd6-95cd-4d6622fd0c39,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,Primary Objective: Gas Exchange,False,Primary Objective: Gas Exchange,,,,
8eded5ab-6e19-4b2e-95f6-a7bf2979d339,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"Gases that have diffused to the respiratory zone find themselves in an ideal environment for gas exchange. We will deal with gas exchange in more detail later (chapter 7), but you should appreciate that the essential components for efficient gas exchange are all present in the lung.",True,Primary Objective: Gas Exchange,,,,
1eab8f09-eb1b-4458-b80c-99a7d030aece,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"A large surface area is generated by the 500 million alveoli, and while each alveolus only has a diameter of 0.3 mm, collectively they produce a total gas exchange surface of 100 m2—about the surface area of a tennis court.",True,Primary Objective: Gas Exchange,,,,
6a7a8e32-788f-418d-865e-5d7b6f61c8db,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"The membranes that gases transfer across are very thin and pose little opposition. In brief, oxygen entering the alveolus only has to cross the squamous cell of the alveolus wall, a very thin basement membrane, and then the squamous cell of the capillary wall to get into the pulmonary circulation. The total distance can be as low as 0.2 micrometers. This degree of thinness also makes these membranes prone to damage.",True,Primary Objective: Gas Exchange,,,,
6baf3cc4-810c-4113-846c-818e70c3d3ae,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"As well as the alveolus receiving air (that is being ventilated), the other essential component for gas exchange is blood flow. This is provided by the pulmonary circulation and consists of all cardiac output coming from the right heart. The pulmonary circulation forms very dense networks of capillaries surrounding each alveolus, so much so that the alveoli can be imagined as being washed over with blood.",True,Primary Objective: Gas Exchange,,,,
96d22540-51a3-4e0f-8bcb-d09b859f9525,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"These characteristics make the lung a highly efficient exchange organ between the environment and the circulation, which is ideal for the transfer of O2 into the bloodstream and, just as importantly, CO2 out. It also allows some drugs to be delivered by inhalation, but also has the potential to allow noxious substances into the bloodstream. Likewise, changes in any of these characteristics of the lung in disease, such as loss of surface area in emphysema or membrane thickening in pulmonary fibrosis, can severely diminish gas exchange.",True,Primary Objective: Gas Exchange,,,,
cfab7fc1-b303-4cd0-826e-fdb60c6fad3c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,Text,False,Text,,,,
4277aa9e-10ae-46b0-aa4a-d206ace59390,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"Levitsky, Michael G. “Chapter 1: Function and Structure of the Respiratory System.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
e6890bc7-571a-4051-a082-ecbe9fef8ab7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"West, John B. “Chapter 1: Structure and Function—How the Architecture of the Lung Subserves Its Function.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
52ff52a4-1ff3-4edb-9278-af137b70e469,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Bronchial Tree,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-3,"Widdicombe, John G., and Andrew S. Davis. “Chapter 1.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
e8262229-1286-486d-b35f-e938c1ba0b97,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"We will see how blood gases are monitored and maintained through neurochemical control of lung expansion and relaxation to achieve the appropriate level of alveolar ventilation. Factors that affect the degree of gas exchange between the lung and blood will be discussed, along with the coordination of ventilation and perfusion of the lung. Finally, we will see how oxygen and carbon dioxide are transported in the bloodstream to and from tissue and the mechanisms that ensure appropriate delivery and a stable blood gas environment. Before we begin, however, we will look at the functional anatomy of the lung and how the lung is well designed to perform its primary role and defend itself from the external environment.",True,Text,,,,
a0b43e74-4792-4b4f-a5a5-e1cc2f5a92ab,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,Defense of the Lung,False,Defense of the Lung,,,,
70c1be6e-9c87-4e61-aff6-f85285cb71a0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
70c1be6e-9c87-4e61-aff6-f85285cb71a0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
70c1be6e-9c87-4e61-aff6-f85285cb71a0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
70c1be6e-9c87-4e61-aff6-f85285cb71a0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
70c1be6e-9c87-4e61-aff6-f85285cb71a0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
70c1be6e-9c87-4e61-aff6-f85285cb71a0,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
11b82058-1295-4e5e-8b41-afaf758eede6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
11b82058-1295-4e5e-8b41-afaf758eede6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
11b82058-1295-4e5e-8b41-afaf758eede6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
11b82058-1295-4e5e-8b41-afaf758eede6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
11b82058-1295-4e5e-8b41-afaf758eede6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
11b82058-1295-4e5e-8b41-afaf758eede6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
5235de14-ed87-439d-a8a4-a34379bf3367,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
5235de14-ed87-439d-a8a4-a34379bf3367,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
5235de14-ed87-439d-a8a4-a34379bf3367,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
5235de14-ed87-439d-a8a4-a34379bf3367,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
5235de14-ed87-439d-a8a4-a34379bf3367,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
5235de14-ed87-439d-a8a4-a34379bf3367,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
5d626e62-735d-453c-87f3-fabf0269ead6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,The Bronchial Tree,False,The Bronchial Tree,,,,
8af89c92-23a3-4e99-901e-2fcc0cedde0a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
8af89c92-23a3-4e99-901e-2fcc0cedde0a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
8af89c92-23a3-4e99-901e-2fcc0cedde0a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
8af89c92-23a3-4e99-901e-2fcc0cedde0a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
8af89c92-23a3-4e99-901e-2fcc0cedde0a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
8af89c92-23a3-4e99-901e-2fcc0cedde0a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
20ad5f49-3f24-4469-afc5-b5ad9201cb99,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
20ad5f49-3f24-4469-afc5-b5ad9201cb99,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
20ad5f49-3f24-4469-afc5-b5ad9201cb99,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
20ad5f49-3f24-4469-afc5-b5ad9201cb99,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
20ad5f49-3f24-4469-afc5-b5ad9201cb99,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
20ad5f49-3f24-4469-afc5-b5ad9201cb99,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
9be75446-9c69-463a-baf5-c97422c459d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
9be75446-9c69-463a-baf5-c97422c459d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
9be75446-9c69-463a-baf5-c97422c459d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
9be75446-9c69-463a-baf5-c97422c459d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
9be75446-9c69-463a-baf5-c97422c459d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
9be75446-9c69-463a-baf5-c97422c459d9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
bcd11eaa-c498-4928-87e5-fe3e72d246f4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,Flow in the Airways,False,Flow in the Airways,,,,
5dc6bb9b-dff5-415c-a6a1-578e42a7e33b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"Airflow down the bronchial tree is caused by the generation of a pressure differential when lung volume is expanded by contraction of the respiratory muscles (more on this in chapter 2). Inspired air first enters the airways of the conducting zone, which while having the largest diameter airways also has the fewest; consequently the total cross-sectional area of the conducting zone is relatively low. With a large volume of air passing through a low cross-sectional area, the velocity of air in the conducting zone is high and is moving by “bulk flow” generated by the pressure differential (like water through a hose) until it reaches the terminal bronchioles and the end of the conducting zone.",True,Flow in the Airways,,,,
6920a18b-286d-4df4-b66c-13fce4999c9f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"When this air enters the respiratory zone, it slows rapidly. This is due to the enormous total cross-sectional area of the airways in the respiratory zone—while the airways are much narrower here, they are far more numerous. The final transfer of the gases through the respiratory zone is therefore achieved by diffusion; the rate of diffusion is so rapid and the distances so short that concentration differences are abolished within a second.",True,Flow in the Airways,,,,
0eecdf94-f068-4f57-a99b-43451c6a4205,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"As an aside, this deceleration of the air at the terminal bronchioles means any particles that have been able to descend this deep are frequently deposited here. This has ramifications for disease and also delivery of inhaled medications.",True,Flow in the Airways,,,,
25d6c7fa-b990-4ecc-9bc6-eaf6b2720e79,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,Primary Objective: Gas Exchange,False,Primary Objective: Gas Exchange,,,,
6ca2d108-21e9-47cf-9002-35af9c965346,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"Gases that have diffused to the respiratory zone find themselves in an ideal environment for gas exchange. We will deal with gas exchange in more detail later (chapter 7), but you should appreciate that the essential components for efficient gas exchange are all present in the lung.",True,Primary Objective: Gas Exchange,,,,
9e9c8f87-a3fb-460f-a2d8-0cf4f5e1f5fb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"A large surface area is generated by the 500 million alveoli, and while each alveolus only has a diameter of 0.3 mm, collectively they produce a total gas exchange surface of 100 m2—about the surface area of a tennis court.",True,Primary Objective: Gas Exchange,,,,
e8aec0cf-35b2-4628-88f0-82bb485b5efe,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"The membranes that gases transfer across are very thin and pose little opposition. In brief, oxygen entering the alveolus only has to cross the squamous cell of the alveolus wall, a very thin basement membrane, and then the squamous cell of the capillary wall to get into the pulmonary circulation. The total distance can be as low as 0.2 micrometers. This degree of thinness also makes these membranes prone to damage.",True,Primary Objective: Gas Exchange,,,,
185b321a-bcee-41de-9fc2-0845f6245011,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"As well as the alveolus receiving air (that is being ventilated), the other essential component for gas exchange is blood flow. This is provided by the pulmonary circulation and consists of all cardiac output coming from the right heart. The pulmonary circulation forms very dense networks of capillaries surrounding each alveolus, so much so that the alveoli can be imagined as being washed over with blood.",True,Primary Objective: Gas Exchange,,,,
0be6e9cc-ec01-4960-a94e-80bfa5e2f151,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"These characteristics make the lung a highly efficient exchange organ between the environment and the circulation, which is ideal for the transfer of O2 into the bloodstream and, just as importantly, CO2 out. It also allows some drugs to be delivered by inhalation, but also has the potential to allow noxious substances into the bloodstream. Likewise, changes in any of these characteristics of the lung in disease, such as loss of surface area in emphysema or membrane thickening in pulmonary fibrosis, can severely diminish gas exchange.",True,Primary Objective: Gas Exchange,,,,
cced4a32-b3bb-44c8-8d11-729d0611d818,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,Text,False,Text,,,,
63c86963-ec72-4c04-a402-9cbf7b0ce0a6,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"Levitsky, Michael G. “Chapter 1: Function and Structure of the Respiratory System.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
e8a80ad2-1f9b-4ff8-b764-25fb4973037a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"West, John B. “Chapter 1: Structure and Function—How the Architecture of the Lung Subserves Its Function.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
753dd1a7-5d6d-46f0-b830-ec2d3c758af4,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,Defense of the Lung,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-2,"Widdicombe, John G., and Andrew S. Davis. “Chapter 1.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
a45198e8-51e1-4f33-b3de-e0bf3772a7a2,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"We will see how blood gases are monitored and maintained through neurochemical control of lung expansion and relaxation to achieve the appropriate level of alveolar ventilation. Factors that affect the degree of gas exchange between the lung and blood will be discussed, along with the coordination of ventilation and perfusion of the lung. Finally, we will see how oxygen and carbon dioxide are transported in the bloodstream to and from tissue and the mechanisms that ensure appropriate delivery and a stable blood gas environment. Before we begin, however, we will look at the functional anatomy of the lung and how the lung is well designed to perform its primary role and defend itself from the external environment.",True,Text,,,,
1cc1756f-1196-4ca9-a21a-6405c4a38246,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,Defense of the Lung,False,Defense of the Lung,,,,
a69bf33e-5b4d-4cdf-8568-a06cbf7ba46e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
a69bf33e-5b4d-4cdf-8568-a06cbf7ba46e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
a69bf33e-5b4d-4cdf-8568-a06cbf7ba46e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
a69bf33e-5b4d-4cdf-8568-a06cbf7ba46e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
a69bf33e-5b4d-4cdf-8568-a06cbf7ba46e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
a69bf33e-5b4d-4cdf-8568-a06cbf7ba46e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
c4010747-e41e-4fac-b0d3-9b6b438f9835,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
c4010747-e41e-4fac-b0d3-9b6b438f9835,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
c4010747-e41e-4fac-b0d3-9b6b438f9835,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
c4010747-e41e-4fac-b0d3-9b6b438f9835,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
c4010747-e41e-4fac-b0d3-9b6b438f9835,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
c4010747-e41e-4fac-b0d3-9b6b438f9835,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
32822d31-38c6-4f68-b984-2ac6cfb01892,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
32822d31-38c6-4f68-b984-2ac6cfb01892,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
32822d31-38c6-4f68-b984-2ac6cfb01892,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
32822d31-38c6-4f68-b984-2ac6cfb01892,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
32822d31-38c6-4f68-b984-2ac6cfb01892,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
32822d31-38c6-4f68-b984-2ac6cfb01892,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
39af5008-ef3f-4665-be27-fd825d96e439,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,The Bronchial Tree,False,The Bronchial Tree,,,,
51b882f5-bd8c-4b42-a104-0df812d4fdf5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
51b882f5-bd8c-4b42-a104-0df812d4fdf5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
51b882f5-bd8c-4b42-a104-0df812d4fdf5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
51b882f5-bd8c-4b42-a104-0df812d4fdf5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
51b882f5-bd8c-4b42-a104-0df812d4fdf5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
51b882f5-bd8c-4b42-a104-0df812d4fdf5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
6a2c69cf-a0d8-4f3e-8d76-7184d1f80337,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
6a2c69cf-a0d8-4f3e-8d76-7184d1f80337,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
6a2c69cf-a0d8-4f3e-8d76-7184d1f80337,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
6a2c69cf-a0d8-4f3e-8d76-7184d1f80337,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
6a2c69cf-a0d8-4f3e-8d76-7184d1f80337,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
6a2c69cf-a0d8-4f3e-8d76-7184d1f80337,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
62bd2dc9-b0e4-4846-bdc8-18b5fc0e5a90,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
62bd2dc9-b0e4-4846-bdc8-18b5fc0e5a90,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
62bd2dc9-b0e4-4846-bdc8-18b5fc0e5a90,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
62bd2dc9-b0e4-4846-bdc8-18b5fc0e5a90,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
62bd2dc9-b0e4-4846-bdc8-18b5fc0e5a90,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
62bd2dc9-b0e4-4846-bdc8-18b5fc0e5a90,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
dfa80ba0-4fd5-43f4-bda1-1b91c57638f9,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,Flow in the Airways,False,Flow in the Airways,,,,
bfeafcfd-9d88-4acf-80eb-8a11a17ce2d1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"Airflow down the bronchial tree is caused by the generation of a pressure differential when lung volume is expanded by contraction of the respiratory muscles (more on this in chapter 2). Inspired air first enters the airways of the conducting zone, which while having the largest diameter airways also has the fewest; consequently the total cross-sectional area of the conducting zone is relatively low. With a large volume of air passing through a low cross-sectional area, the velocity of air in the conducting zone is high and is moving by “bulk flow” generated by the pressure differential (like water through a hose) until it reaches the terminal bronchioles and the end of the conducting zone.",True,Flow in the Airways,,,,
f8295541-3f9e-4aa2-a9e1-d0fd48794ed7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"When this air enters the respiratory zone, it slows rapidly. This is due to the enormous total cross-sectional area of the airways in the respiratory zone—while the airways are much narrower here, they are far more numerous. The final transfer of the gases through the respiratory zone is therefore achieved by diffusion; the rate of diffusion is so rapid and the distances so short that concentration differences are abolished within a second.",True,Flow in the Airways,,,,
3f9197ea-25f8-4487-95cc-d9831287643f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"As an aside, this deceleration of the air at the terminal bronchioles means any particles that have been able to descend this deep are frequently deposited here. This has ramifications for disease and also delivery of inhaled medications.",True,Flow in the Airways,,,,
473ecda8-1b10-4cd7-85b2-a6508e0eec4e,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,Primary Objective: Gas Exchange,False,Primary Objective: Gas Exchange,,,,
32e84f76-820e-4e8e-9a71-86e7f7d36dfb,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"Gases that have diffused to the respiratory zone find themselves in an ideal environment for gas exchange. We will deal with gas exchange in more detail later (chapter 7), but you should appreciate that the essential components for efficient gas exchange are all present in the lung.",True,Primary Objective: Gas Exchange,,,,
d3d51863-b2d7-46fe-a02d-593f3900d5f5,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"A large surface area is generated by the 500 million alveoli, and while each alveolus only has a diameter of 0.3 mm, collectively they produce a total gas exchange surface of 100 m2—about the surface area of a tennis court.",True,Primary Objective: Gas Exchange,,,,
cd7cf79e-38e9-4509-884a-b11419d96a36,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"The membranes that gases transfer across are very thin and pose little opposition. In brief, oxygen entering the alveolus only has to cross the squamous cell of the alveolus wall, a very thin basement membrane, and then the squamous cell of the capillary wall to get into the pulmonary circulation. The total distance can be as low as 0.2 micrometers. This degree of thinness also makes these membranes prone to damage.",True,Primary Objective: Gas Exchange,,,,
51a2664c-c2d3-4e19-88fa-ddc6eea2022a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"As well as the alveolus receiving air (that is being ventilated), the other essential component for gas exchange is blood flow. This is provided by the pulmonary circulation and consists of all cardiac output coming from the right heart. The pulmonary circulation forms very dense networks of capillaries surrounding each alveolus, so much so that the alveoli can be imagined as being washed over with blood.",True,Primary Objective: Gas Exchange,,,,
c3733a17-4569-406f-a24e-809b58855dee,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"These characteristics make the lung a highly efficient exchange organ between the environment and the circulation, which is ideal for the transfer of O2 into the bloodstream and, just as importantly, CO2 out. It also allows some drugs to be delivered by inhalation, but also has the potential to allow noxious substances into the bloodstream. Likewise, changes in any of these characteristics of the lung in disease, such as loss of surface area in emphysema or membrane thickening in pulmonary fibrosis, can severely diminish gas exchange.",True,Primary Objective: Gas Exchange,,,,
535bdb6d-79f2-4f95-8c63-00ae41d7f708,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,Text,False,Text,,,,
881efac6-0907-4d65-8744-087b0b64ed31,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"Levitsky, Michael G. “Chapter 1: Function and Structure of the Respiratory System.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
2953f861-7527-4570-a0f1-f3416fc27b9f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"West, John B. “Chapter 1: Structure and Function—How the Architecture of the Lung Subserves Its Function.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
8497120e-dfbe-4f09-b946-781d652b1d02,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,The Components of Lung Function,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/#chapter-5-section-1,"Widdicombe, John G., and Andrew S. Davis. “Chapter 1.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,
a9368aa4-598f-46db-bc92-8ef40241cf70,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"We will see how blood gases are monitored and maintained through neurochemical control of lung expansion and relaxation to achieve the appropriate level of alveolar ventilation. Factors that affect the degree of gas exchange between the lung and blood will be discussed, along with the coordination of ventilation and perfusion of the lung. Finally, we will see how oxygen and carbon dioxide are transported in the bloodstream to and from tissue and the mechanisms that ensure appropriate delivery and a stable blood gas environment. Before we begin, however, we will look at the functional anatomy of the lung and how the lung is well designed to perform its primary role and defend itself from the external environment.",True,Text,,,,
cbcda52b-3972-4e48-96a0-f376a2a7d5a7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,Defense of the Lung,False,Defense of the Lung,,,,
e3e496ee-e7bc-4f77-91d3-a0555c84ca66,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
e3e496ee-e7bc-4f77-91d3-a0555c84ca66,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
e3e496ee-e7bc-4f77-91d3-a0555c84ca66,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
e3e496ee-e7bc-4f77-91d3-a0555c84ca66,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
e3e496ee-e7bc-4f77-91d3-a0555c84ca66,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
e3e496ee-e7bc-4f77-91d3-a0555c84ca66,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"As the only internal organ exposed to the external environment, the lung needs special protection from particles or pathogens that could be transported down the airways with inhaled air. The first line of defense is the nasal cavity, which is lined with a ciliated epithelial, dispersed within which are goblet cells producing mucus (figure 1.2). This mucus forms a sticky layer on top of the epithelial surface and traps inhaled particles, bacteria, or other potential pathogens. The mucus is then moved by the cilia back toward the pharynx where it can be coughed or spat out.",True,Defense of the Lung,Figure 1.2,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
3dd80f0e-c1ec-4d8a-8792-9fc66b674d6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
3dd80f0e-c1ec-4d8a-8792-9fc66b674d6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
3dd80f0e-c1ec-4d8a-8792-9fc66b674d6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
3dd80f0e-c1ec-4d8a-8792-9fc66b674d6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
3dd80f0e-c1ec-4d8a-8792-9fc66b674d6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
3dd80f0e-c1ec-4d8a-8792-9fc66b674d6c,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The inhaled air also must be warmed and humidified before it reaches the gas exchange surfaces, otherwise the relatively cold and dry air would cause evaporation of the thin water layer lining the gas exchange surfaces that is essential for allowing gases to dissolve and diffuse into or out of the pulmonary bloodstream. This warming and humidification is achieved by transfer of heat and water from blood in the highly vascularized nasal cavity (figure 1.3).",True,Defense of the Lung,Figure 1.3,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.3.jpeg,Figure 1.3: Air conditioning. The highly vascularized nasal cavity helps warm and humidify inhaled air before it proceeds toward the lower airways.
05c242ed-7d92-48f1-8be4-ff41629fb850,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
05c242ed-7d92-48f1-8be4-ff41629fb850,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
05c242ed-7d92-48f1-8be4-ff41629fb850,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
05c242ed-7d92-48f1-8be4-ff41629fb850,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
05c242ed-7d92-48f1-8be4-ff41629fb850,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
05c242ed-7d92-48f1-8be4-ff41629fb850,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The second line of defense (which becomes more important when breathing through the mouth) is the lining of the trachea. Again, this is covered with a ciliated epithelium with mucus-producing goblet cells (figure 1.2). As in the nasal cavity, particles and potential pathogens are trapped in the mucus layer and cilia move the mucus up toward the mouth for expulsion. The trachea and larynx also contain sensory nerve endings (rapidly adapting receptors, nicknamed “irritant receptors”) that respond to the arrival of particles on the epithelial surface and initiate the cough reflex and propel the offending particles out of the airway (see more in chapter 17).",True,Defense of the Lung,Figure 1.2,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.2.png,"Figure 1.2: The mucociliary escalator of the airway. The cilia on the apical surface of the pseudostratified epithelium push a layer of mucus (produced by the goblet cells) toward the mouth, carrying pathogens and particulates out of the airway."
cbf435dc-d003-4a3d-bc7e-c5264b98bd6b,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,The Bronchial Tree,False,The Bronchial Tree,,,,
53cb3e4d-7e44-463e-916e-a6fd392c58ec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
53cb3e4d-7e44-463e-916e-a6fd392c58ec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
53cb3e4d-7e44-463e-916e-a6fd392c58ec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
53cb3e4d-7e44-463e-916e-a6fd392c58ec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
53cb3e4d-7e44-463e-916e-a6fd392c58ec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
53cb3e4d-7e44-463e-916e-a6fd392c58ec,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The airways, or bronchial tree (figure 1.4), consist of a series of branching tubes that become narrower and shorter but more numerous as they descend into the lung.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
433451ad-2f4e-4013-b120-74b635391910,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
433451ad-2f4e-4013-b120-74b635391910,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
433451ad-2f4e-4013-b120-74b635391910,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
433451ad-2f4e-4013-b120-74b635391910,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
433451ad-2f4e-4013-b120-74b635391910,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
433451ad-2f4e-4013-b120-74b635391910,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The trachea bifurcates into the primary bronchi, left and right, transporting air into the left and right lungs, respectively. The primary bronchi consequently divide into lobar (or secondary) bronchi, the number of which correspond to the number of lobes in each lung. The lobar bronchi then divide into segmental (or tertiary) bronchi to supply the segments of each lobe. This bifurcation process continues to the terminal bronchioles. This initial section of the bronchial tree is referred to as the conducting zone as its role is to transfer air to the gas exchange surfaces (figure 1.4). As no gas exchange takes place here, these airways constitute the anatomical dead space and have a volume of approximately 150 mL.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
1373e289-42c0-4b8a-827f-95faf741477a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Primary Objective: Gas Exchange,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
1373e289-42c0-4b8a-827f-95faf741477a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Flow in the Airways,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
1373e289-42c0-4b8a-827f-95faf741477a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,The Bronchial Tree,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
1373e289-42c0-4b8a-827f-95faf741477a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,Defense of the Lung,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
1373e289-42c0-4b8a-827f-95faf741477a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,The Components of Lung Function,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
1373e289-42c0-4b8a-827f-95faf741477a,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"Each terminal bronchiole then divides into numerous respiratory bronchioles, the walls of which may contain some alveoli and are therefore capable of some gas exchange; this is the transition to the respiratory zone of the lung and the onset of gas exchange (figure 1.4). The respiratory zone becomes firmly established when terminal bronchioles divide into alveolar ducts that are fundamentally tubes lined with alveoli. These alveolar ducts then terminate in alveolar sacs. The portion of lung distal to each terminal bronchiole forms an anatomical unit called the acinus. Although only a few millimeters long, collectively these acini make up the respiratory zone and form the vast majority of the lung’s volume.",True,The Bronchial Tree,Figure 1.4,1. Fundamentals,https://pressbooks.lib.vt.edu/app/uploads/sites/73/2022/02/1.4.png,Figure 1.4: The bronchial tree. The major airways of the conducting zone (anatomical dead space) are labeled.
12b807b9-5fad-4efb-a1ce-429954be9190,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,Flow in the Airways,False,Flow in the Airways,,,,
656988a7-2de1-4477-b43c-18e0dfc4c9d1,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"Airflow down the bronchial tree is caused by the generation of a pressure differential when lung volume is expanded by contraction of the respiratory muscles (more on this in chapter 2). Inspired air first enters the airways of the conducting zone, which while having the largest diameter airways also has the fewest; consequently the total cross-sectional area of the conducting zone is relatively low. With a large volume of air passing through a low cross-sectional area, the velocity of air in the conducting zone is high and is moving by “bulk flow” generated by the pressure differential (like water through a hose) until it reaches the terminal bronchioles and the end of the conducting zone.",True,Flow in the Airways,,,,
f083150a-9c6f-490c-a8bb-55e7fb686d4f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"When this air enters the respiratory zone, it slows rapidly. This is due to the enormous total cross-sectional area of the airways in the respiratory zone—while the airways are much narrower here, they are far more numerous. The final transfer of the gases through the respiratory zone is therefore achieved by diffusion; the rate of diffusion is so rapid and the distances so short that concentration differences are abolished within a second.",True,Flow in the Airways,,,,
d22a21eb-7b01-4fc7-85e2-83ab95ef3f9d,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"As an aside, this deceleration of the air at the terminal bronchioles means any particles that have been able to descend this deep are frequently deposited here. This has ramifications for disease and also delivery of inhaled medications.",True,Flow in the Airways,,,,
ca24c015-9c6a-4553-876d-8a0739e25086,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,Primary Objective: Gas Exchange,False,Primary Objective: Gas Exchange,,,,
187e2721-1b01-42de-aabe-132a482c32a7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"Gases that have diffused to the respiratory zone find themselves in an ideal environment for gas exchange. We will deal with gas exchange in more detail later (chapter 7), but you should appreciate that the essential components for efficient gas exchange are all present in the lung.",True,Primary Objective: Gas Exchange,,,,
47bc2fed-18e0-41f9-8313-b7dd6ce12c1f,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"A large surface area is generated by the 500 million alveoli, and while each alveolus only has a diameter of 0.3 mm, collectively they produce a total gas exchange surface of 100 m2—about the surface area of a tennis court.",True,Primary Objective: Gas Exchange,,,,
5474f4da-4944-4605-8b8c-1543d57154b7,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"The membranes that gases transfer across are very thin and pose little opposition. In brief, oxygen entering the alveolus only has to cross the squamous cell of the alveolus wall, a very thin basement membrane, and then the squamous cell of the capillary wall to get into the pulmonary circulation. The total distance can be as low as 0.2 micrometers. This degree of thinness also makes these membranes prone to damage.",True,Primary Objective: Gas Exchange,,,,
0d24af8a-1a59-4778-ad6d-187f26425952,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"As well as the alveolus receiving air (that is being ventilated), the other essential component for gas exchange is blood flow. This is provided by the pulmonary circulation and consists of all cardiac output coming from the right heart. The pulmonary circulation forms very dense networks of capillaries surrounding each alveolus, so much so that the alveoli can be imagined as being washed over with blood.",True,Primary Objective: Gas Exchange,,,,
3bbc7f5d-fcd0-475d-abd1-46b6ce03a061,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"These characteristics make the lung a highly efficient exchange organ between the environment and the circulation, which is ideal for the transfer of O2 into the bloodstream and, just as importantly, CO2 out. It also allows some drugs to be delivered by inhalation, but also has the potential to allow noxious substances into the bloodstream. Likewise, changes in any of these characteristics of the lung in disease, such as loss of surface area in emphysema or membrane thickening in pulmonary fibrosis, can severely diminish gas exchange.",True,Primary Objective: Gas Exchange,,,,
dad445ef-5c22-42c2-914a-dbd878ba0637,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,Text,False,Text,,,,
94420486-6ef8-4509-9c0e-0990a05fcab8,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"Levitsky, Michael G. “Chapter 1: Function and Structure of the Respiratory System.” In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.",True,Text,,,,
974e3555-9c0f-42ad-85c5-04c1e45c3fdf,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"West, John B. “Chapter 1: Structure and Function—How the Architecture of the Lung Subserves Its Function.” In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.",True,Text,,,,
8df2e4a7-ac2c-4188-aec7-cffedbc6e4ac,https://pressbooks.lib.vt.edu/pulmonaryphysiology/,1. Fundamentals,https://pressbooks.lib.vt.edu/pulmonaryphysiology/chapter/chapter-1/,"Widdicombe, John G., and Andrew S. Davis. “Chapter 1.” In Respiratory Physiology. Baltimore: University Park Press, 1983.",True,Text,,,,