BOTH .

[a_person1234567]

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[DoctorG2020]

I must be stupid or something, because I've been having such a hard time understanding this even though I've read so much about it. I understand why you get hypoxemia with shunting. That's because you're getting mixing of deoxygenated blood with oxygenated blood, and I think I understand why you don't get hypoxemia with dead space. It's because you don't get this mixing and the partial pressure in the arterial will equilibrate with the lung, so you get normal oxygen saturation. What I don't understand is why there is more CO2 in the blood with dead space if you're getting oxygen exchange. If more oxygen is going into the blood why can't more CO2 go out of the blood and be expired out? Why can't the CO2 in the lungs equilibrate with the CO2 in the blood vessels?

So, I like to think of this using the terms "contributory vessels" (not obstructed) vs. "non-contributory vessels" (vessels that are obstructed). Because the non-contributory vessels are blocked and not exchanging gasses, they have no effect on oxygen saturation (no oxygen getting to them for exchange in or out). Thus, there is no hypoxemia because the other contributory vessels are well ventilated and perfused - leading to equilibrium as you said.

However, because the non-contributory vessels are plugged before reaching the alveoli (but still have blood in them with high CO2), the CO2 from these vessels cannot be extracted leading to hypercapnia. The contributory vessels are still extracting CO2 (but at a maximum rate) and cannot extract CO2 at a rate high enough to offset the increased in CO2 on the obstructed side.