V/Q mismatch and Hypoxia in PE

[nm825]

I don't really understand why PE causes hypoxia physiologically.

Here's what I have:

1) PE decreases Q as some alveoli thereby increasing V/Q (dead space).

2) Blood then gets shunted from the blocked vessels to the open vessels. Healthy aveoli see twice as much blood. This means the Q for the healthy alveoli is elevated, thereby decreasing V/Q in the healthy alveoli.

The dead space results in hypercapnia and subsequent hyperventilation to bring PaCO2 levels down to normal. If you're hyperventilating, why then are you hypoxemic? If you're taking rapid/deep breaths, aren't you bringing more oxygen in? Shouldn't this be able to saturate the blood?

Secondly, I'm trying to understand why V/Q mismatch elevated the A-a gradient. The only think I can think of is that in the dead space alveoli PAO2=~140 and PACO2=~0. Averaging the overly-ventilated alveoli with normal alveoli results in an overall elevated PA02 compared to normal. At the same time, you're hypoxemic so overall PaO2 is going to be low. This results in an increased A-a gradient. Is this thinking right?

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[Doctorlife]

The problem is the blood clot prevents a certain amount of oxygen from getting into the alveoli. So yea, you are breathing more, but not sufficient. There's a mismatch. There should be a certain amount of air crossing into the alveoli matched with a certain amount of blood crossing over into the capillaries. But this clot is throwing that equation off, the mismatch. So the body tries to compensate by breathing more but there is still a clot and thus there is still a mismatch. No matter how much you try to breath you still wont have the same match as you would without the clot.