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why would pulm. embolism cause resp alkalosis and not resp acidosis? i just missed this on uworld and the explanation wasn't given properly
pulm embolism
- Thread starter ctizzle13498
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you get respiratory acidosis when CO2 accumulates in your blood due to various causes, but think always in something that prevents air from exiting the lung, such as hypoventilation or obstruction
well, in pulmonary embolism you don't have any problem with air circulation, you have problems with perfusion of the lung. If you can't perfuse your lung well you'll get hypoxia and hypercapnia and it leads to hyperventilation which leads to hypocapnia which leads to alkalosis.
sorry if I wasn't clear enough lol
well, in pulmonary embolism you don't have any problem with air circulation, you have problems with perfusion of the lung. If you can't perfuse your lung well you'll get hypoxia and hypercapnia and it leads to hyperventilation which leads to hypocapnia which leads to alkalosis.
sorry if I wasn't clear enough lol
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if you aren't perfusing your lung well, then how does the hyperventilation lead to hypocapnia/alkalosis?
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^ Was wondering about that. Here's what I found:
In patients with acute PE, total dead space increases because lung units continue to be ventilated despite diminished or absent perfusion. Complete obstruction of a pulmonary artery by an embolus causes an increase in anatomic dead space. In contrast, incomplete obstruction of a pulmonary artery increases physiological dead space, ie, ratios of ventilation to perfusion increase. Increased dead space impairs the efficient elimination of carbon dioxide. However, medullary chemoreceptors sense any increase in arterial PCO2, and they will increase the total minute ventilation, thereby lowering the arterial PCO2 to normal and often below normal. Thus, most patients with PE present with a lower than normal arterial PCO2 and respiratory alkalosis because of an increased total minute ventilation. Limited data suggest that the increased total minute ventilation occurs because of reflex stimulation of irritant and juxta capillary sensors in the lung.
http://circ.ahajournals.org/content/108/22/2726.full
So, overcompensation.
In patients with acute PE, total dead space increases because lung units continue to be ventilated despite diminished or absent perfusion. Complete obstruction of a pulmonary artery by an embolus causes an increase in anatomic dead space. In contrast, incomplete obstruction of a pulmonary artery increases physiological dead space, ie, ratios of ventilation to perfusion increase. Increased dead space impairs the efficient elimination of carbon dioxide. However, medullary chemoreceptors sense any increase in arterial PCO2, and they will increase the total minute ventilation, thereby lowering the arterial PCO2 to normal and often below normal. Thus, most patients with PE present with a lower than normal arterial PCO2 and respiratory alkalosis because of an increased total minute ventilation. Limited data suggest that the increased total minute ventilation occurs because of reflex stimulation of irritant and juxta capillary sensors in the lung.
http://circ.ahajournals.org/content/108/22/2726.full
So, overcompensation.
