V/Q mismatch

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seminoma

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New MS2 here, but I think I have a good general understanding so hopefully it won't be hard to explain this to me.

Ventilation defects (atelectasis) don't resolve with administration of O2 (for what I think are obvious reasons).

Perfusion defects (PE) do resolve with O2 administration. I thought that O2 exchange is normally perfusion limited, so to me it seems counterintuitive that giving high PiO2 would show improvement in a patient with perfusion defect.

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There is a caveat. O2 exchange is perfusion limited under normal conditions. If you have a perfusion defect, what that means is that blood is unevenly distributed across the pulmonary capillary tree (due to embolism, etc) but it does not mean that less blood flows through the lungs (remember circulation is a closed circuit). So what you have is more blood flowing through the capillary beds that are still open. There are 2 implications for this:

1) In order to circulate the same amount of cardiac output through fewer capillary beds, blood flow in those beds must be faster. The result is that the margin that you have for o2 exchange to be perfusion limited is decreased

2) The alveoli has to oxygenate more blood than normal. Which could mean blood that flows through later sees a lower oxygen content in the alveoli and hence smaller oxygen gradient for gas exchange, resulting in poor oxygenation.

If the patient has no other co-morbid conditions (such as pulmonary fibrosis or other problems of O2 exchange), #1 is a minor factor. #2 will cause the overall oxygen content of blood returning from the lungs to be lower and is the main cause of the lower SaO2 in pulmonary venous blood. To treat #2 (and also #1), you increase the FIO2 so that there's more oxygen in the remaining perfused alveoli so that all blood flowing past can be adequately oxygenated.
 
if you have a problem where only 50% of the air is going through then you change it from 21% oxygen (normal air) to 42% oxygen.

perfusion problem solved.
 
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