![]() This generally occurs in one of two ways: Hypoxemia occurs when blood somehow passes from the right ventricle into the left ventricle without being fully oxygenated. These problems typically run together, but under certain situations they can become divorced. The key to understanding this is thinking about oxygenation and CO2 clearance separately. understanding the paradox of happy hypoxemia However, COVID is causing us to re-think how to manage this physiology. This isn’t anything especially new – we have occasionally seen this since time immemorial. The logic behind this equation is basically just, if there's more CO2 in the alveolar air, there's less space for oxygen.Happy hypoxemia is severe hypoxemia (poorly responsive to supplemental oxygen) without dyspnea. PAo2 = PIo2 – Paco2/R (it's on pg 668 on FA 2020) since the CO2 is going up, that means the amount of oxygen in the alveoli is going down, which means less oxygen to get into the arterial blood. In this case you have low vent, high perfusion, so therefore you can't get enough of that CO2 out. In this case, the reason you have low oxygen is cause CO2 is highly ventilation dependent. If you had a partial obstruction then you'd have a V/Q mismatch between 0 and 1 which you can solve with oxygen administration by just making sure whatever oxygen does make it past the obstruction is high% and would fully saturate whatever blood it can interface with.ĭead space is when you don't have perfusion, there is no reflex constriction of the alveoli to move ventilation to better perfused areas. Therefore this blood will go to oxygenated areas. These areas that are hypoxic (low ventilation) have reflex vasoconstriction to prevent blood from entering these areas ( i think this is what you were referring to in your dead space explanation). It's almost like that blood went straight from the right ventricle to a random vein in the body and rejoined with the blood in the left atrium since there's no ventilation in those alveoli! If you have shunt in the lungs with a complete airway obstruction for example, then the blood going to those non-ventilated parts will have low oxygenation and then mix with the oxygenated blood in the left atrium, lowering the %O2sat. If you have eisenmengers with a VSD/ASD, the deoxygenated blood is mixing with the oxygenated blood after the point that you can even pick up anymore oxygen so now you're left with oxygen with lower sat than before. And I just used the PaCo2 concentration formula to sort of explain it to myself but I'm not fully convinced.Īhhh i think you may be having some things mixed upĭead space is when you don't have perfusionįor shunt, just imagine the easiest scenario where you have right to left shunt that's not even in the lung and then we'll transport it into the lung. Help would be much much appreciated if anyone can explain this please! I've been stuck on this since days. ![]() In that case, more importantly, what happens to all that CO2 in that blood? If that disappeared too we shouldn't get any hypercapnia at all! So in a pure dead space scenario, which I assume is only hypothetical, what's happening to that desaturated Hb? Do we just assume that it disappears? Which is what happens in Pulm Embolism as you said. Because it doesn't reach the arterial side, it doesn't mix with the normally saturated Hb coming from the normal alveoli, and so doesn't affect the overall saturation of arterial blood or PaO2.īut then realistically all that blood has to go somewhere right? It should land up going to the normally ventilated alveoli and decrease the V/Q ratio there because its increasing Q, blood flow. Ryan explains it in his video is that pure dead space doesn't cause hypoxemia because the desaturated Hb thats going to the dead space alveoli never reaches the arterial side of the circulation, since there's a block in the vessel. Yeah, but why does dead space only affect CO2? Since Q goes up, V/Q goes down - that's V/Q mistmach which causes hypoxemia. Areas of lung that are perfused in PE have very high blood flow (Q) since blood cannot go through all normal channels due to clot. Hypoxemia occurs in PE due to V/Q mismatch. Also there is hypoxemia in PE, but not because of the dead space (because dead space doesn't case low O2). This is because patients hyperventilate to keep Co2 normal despite dead space. There is dead space, but usually not hypercapnia. Leaves more CO2 behind in the blood so CO2 rises. Air goes in and out without picking up CO2. Dead space is ventilated but not perfused. Net result: oxygen fails to improve O2.ĭead space: Has nothing to do with O2, only CO2. So oxygen does not help because it can't get to shunt areas (no ventilation) and it can get to non-shunt areas which are already fully oxygenated. Non-shunted areas are fully oxygenated (100%). In a shunt, blood good from right heart to left heart without passing ventilated areas (i.e., does not pick up oxygen).
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