Obstructive Lung Disease Hypoxemia and Dyspnea sequence - USMLE Forums
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Old 04-08-2011
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Lungs Obstructive Lung Disease Hypoxemia and Dyspnea sequence

Can someone please explain why does Chronic Bronchitis have early-onset hypoxemia and late-onset dyspnea and vice versa with Emphysema?
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Old 04-08-2011
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emphysema is destruction of alvoelar wall septa...two or more alveoli may coalese to form one...now when the air enters during inspiration, it fills up this enlarged alveoli. due to pressure situations within the alveoli, the terminal bronchiole gets plugged and this air cannot escape. now when the patient tries to inspire, the plugged in bronchiole is opened due to the pressure but this new air cannot get into the alveoli due to the air from thr previous breath.thus with every breath patient gets more breathless.
Try this...inspire maximally and dont exhale. now try to inspire again!! can't do it?? this is exactly the case with emphysematous patients leading to dysnea..
chronic bronchitis is inflammation of airways. in the early stages there is not enough hypoxemia to cause dypnea....
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Old 05-02-2012
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To understand this you need to get some concepts straight:

Hypoxemia (dec in Po2 , and ass with cyanosi), is not the same as Hypoxia (dec O2 delivery to the tissues, including chemoreceptors and hence dyspnea)

now V/Q MISMATCH will cause hypoxemia, but if the Q is still adequate there will be no tissue hypoxia and henca dyspnea.

in emphysema, there is parallel destruction of alveolar wall and capillaries so there is tissue hypoxia ( hence early dyspnea) but no V/Q mismatch and hence no early cyanosis. The opposite is true with Chronic bronchitis : there is a VQ mismatch bec excess mucus causes plugging of bronchioles and dead space, so ....cyanosis, however, there is late onset dyspnea because hypoxia does not occur except when hypoxemia is too low.

This is from FA 2011 p 508, with some Goljian explanations from audio. Please correct me if i correlated something wrong
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Old 05-02-2012
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Quote:
Originally Posted by donofitaly View Post
Can someone please explain why does Chronic Bronchitis have early-onset hypoxemia and late-onset dyspnea and vice versa with Emphysema?
In emphysema hyperinflated lungs limit the air entry as previously mentioned (dyspnea) but theres no CO2 retention that is why hypoxemia develops late in the disease

In chronic bronchitis hyperinflation is not as severe as in emphysema and does not compromise air entry but the CO2 retention causes alveolar PAO2 to fall causing hypoxemia (pao2=pio2-paco2/R)
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Patients with chronic bronchitis suffer from early-onset hypoxemia and late-onset dyspnea, while those with emphysema suffer from late-onset hypoxemia and early-onset dyspnea. Also, an increase in CO2 in alveoli occurs in chronic bronchitis, whereas normal or decreased CO2 characterizes emphysema.
Now, the reason chronic bronchitis is characterized by hypercarbia is that it causes hypoventilation (the hallmark of which is an increased carbon dioxide, with the hypoxemia or low partial pressure of oxygen). Since emphysema affects the parenchyma/alveoli, diffusion impairment causes its hypoxemia (the hallmark of hypoxemia caused by diffusion impairment is normal or decreased carbon dioxide, since hypoxemia stimulates ventilation; btw diffusion impairment of oxygen doesn't affect carbon dioxide diffusion as much because carbon dioxide is much more soluble than oxygen, i.e. if someone has impaired diffusion of carbon dioxide, he probably has very low levels of oxygen that are inadequate for survival).

So, now you know carbon dioxide increases in chronic bronchitis and decreases in emphysema. The effect of this is that cardiac output will increase (or normal according to some research papers) in chronic bronchitis and decrease in emphysema. Why you may ask? The reason is that increased carbon dioxide (in chronic bronchitis) will stimulate peripheral chemoreceptors (carotid and aortic bodies), leading to hyperventilation. This hyperventilation stimulates the mechanoreceptors of the lung, and the resultant sympathetic activity stimulates an increase in heart rate and hence cardiac output. Due to the increased cardiac output, perfusion of the lung increases to keep the oxygen content (=dissolved oxygen + oxygen bound to hemoglobin; dissolved oxygen contributes to partial pressure and hence affects hypoxemia but oxyhemoglobin does not affect the degree of hypoxemia, which is defined as a decrease in partial pressure of oxygen in blood) constant by increasing the hemoglobin that reaches the lung per second, i.e. increased oxyhemoglobin due to cardiac output and decreased dissolved oxygen due to hypoventilation=constant oxygen content). Since oxygen content does not decrease in the early stages of chronic bronchitis, there is no hypoxia and hence no dyspnea in early chronic bronchitis. However, since dissolved oxygen decreases in chronic bronchitis and hence partial pressure of oxygen decreases in the early stages due to hypoventilation, hypoxemia develops in the early stages of chronic bronchitis.

So, now you know why an increase in carbon dioxide in chronic bronchitis leads to increased cardiac output, normal perfusion, and no early dyspnea and why hypoxemia is early due to hypoventilation. Apply these concepts to emphysema to understand why the opposite occurs.
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