USMLE Question about DVT/respiratory alkalosis

[teotuf]

So in the setting of DVT, I understand that there would be hypoxemia due to V/Q mismatch, which would then lead to hyperventilation. But why would there be respiratory alkalosis??? If oxygen can't get in due to V/Q mismatch, why is CO2 able to get out? (e.g. to me, the PaO2 and PaCO2 should be inversely correlated, if O2 can't get in, then CO2 can't get out).

I'm specifically referring to QID 6578 on UWSA1 for those with access to that.

Thanks guys

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[NeuroLAX]

I hope my understanding is correct, but I believe it is due to the fact that the respiratory center only responds to CO2/decreased pH, so a build up of CO2 will cause hyperventilation. Hyperventilation causes CO2 to go down... less acid --> respiratory alkalosis. Just because you have a PE doesn't mean you can't exchange gases at all. Now, if we are talking about a saddle embolus... then you have a huge problem.

 

[teotuf]

I hope my understanding is correct, but I believe it is due to the fact that the respiratory center only responds to CO2/decreased pH, so a build up of CO2 will cause hyperventilation. Hyperventilation causes CO2 to go down... less acid --> respiratory alkalosis. Just because you have a PE doesn't mean you can't exchange gases at all. Now, if we are talking about a saddle embolus... then you have a huge problem.

So we did a little research on this, and apparently acidosis vs alkalosis depends on the size of the embolus as you suggested. Small PE would result in alkalosis (still able to compensate through perfusion), and something like saddle PE would result in acidosis (lack of perfusion). But we couldn't find anything on the associated PaO2 values for small PE.

What I don't understand is how you can get a respiratory alkalosis with severely decreased PaO2. Where would you be able to blow off CO2 successfully to result in alkalosis, while at the same time NOT able to get O2 in and still resulting in hypoxemia???

The correct answer in the question was high pH, low PaCO2, low Pa O2, so I'm still not quite able to rationalize that...

 

[teotuf]

Okay, so apparently did a little more digging and came up with the answer:

Apparently CO2 is PERFUSION limited (i.e. PACO2 = PaCO2 under most circumstances, and not subject to V/Q mismatch), but O2 is DIFFUSION limited (i.e. subject to V/Q mismatch). It is this mismatch that allows CO2 to get out and still limiting the O2 from getting in. Apparently I never learned this piece of crucial information anywhere...

 

[GadRads]

Okay, so apparently did a little more digging and came up with the answer:

Apparently CO2 is PERFUSION limited (i.e. PACO2 = PaCO2 under most circumstances, and not subject to V/Q mismatch), but O2 is DIFFUSION limited (i.e. subject to V/Q mismatch). It is this mismatch that allows CO2 to get out and still limiting the O2 from getting in. Apparently I never learned this piece of crucial information anywhere...

CO2 is perfusion-limited, and O2 is also generally thought to be perfusion-limited, except in cases (such as intense exercise) where the O2 gradient between alveoli and capillary blood doesn't dissipate as readily. By lack of gradient dissipation during exercise I mean there is no equilibration, which is almost similar to CO (carbon monoxide).

To answer your initial question (which is a good question by the way, and it took a little while to think about it): CO2 gets out because CO2 diffuses at a faster rate than O2. This physicochemical property is due to Graham's law of diffusion and the added effect of the carbonic anhydrase system. http://hyperphysics.phy-astr.gsu.edu/hbase/kinetic/henry.html

CO2 has 20X the diffusion of rate of O2 due to higher solubility even though it has greater molecular weight. Secondly, in the lungs, the increased O2 pressures favor H+ loss from Hb, and the now higher Cl- in the RBC is exchanged with HCO3-, bringing HCO3- into the cell. Carbonic anhydrase now breaks down carbonic acid (H2CO3) to generate CO2. This is the combination of the Haldane effect and HCO3-/Cl- shift. If you think about this, you will be able to see how this solubility of CO2 as HCO3- favors a faster diffusion rate of CO2 over O2. The extent of CO2 blown out is also controlled by respiratory centers.

 

[GadRads]

What I don't understand is how you can get a respiratory alkalosis with severely decreased PaO2. Where would you be able to blow off CO2 successfully to result in alkalosis, while at the same time NOT able to get O2 in and still resulting in hypoxemia???

The correct answer in the question was high pH, low PaCO2, low Pa O2, so I'm still not quite able to rationalize that...

In line with my previous post, with hyperventilation the PaO2 will increase and PaCO2 will decrease, but the change in PaCO2 will be greater. My guess is that the PaO2 does not increase high enough to get back to normal. So it appears a normal functioning lung is more important for increasing PaO2 than for reducing PaCO2. CO2 diffuses so well that it manages to get by on scraps.

 

[teotuf]

In line with my previous post, with hyperventilation the PaO2 will increase and PaCO2 will decrease, but the change in PaCO2 will be greater. My guess is that the PaO2 does not increase high enough to get back to normal. So it appears a normal functioning lung is more important for increasing PaO2 than for reducing PaCO2. CO2 diffuses so well that it manages to get by on scraps.

Yup! Unless you have something like a saddle embolus that takes out both lungs - then the perfusion drops to next to nothing, and even CO2 can't get out.

So basically, PE leads to hypoxemia, which then leads to hyperventilation. Hyperventilation, depending on the SIZE of the PE, results in respiratory ALKALOSIS (small PE), or respiratory ACIDOSIS and failure (saddle embolus).

Another interesting thing is that the central chemoreceptor is not the main driving force here. If the patient does indeed have respiratory alkalosis, since the central chemoreceptor responds to pH/CO2, he should not be hyperventilating anymore. But since he IS hyperventilating, while at the same time still has alkalosis, the chemoreceptor has to be responding to hypoxemia and not acidosis.

 

[GadRads]

Yup! Unless you have something like a saddle embolus that takes out both lungs - then the perfusion drops to next to nothing, and even CO2 can't get out.

So basically, PE leads to hypoxemia, which then leads to hyperventilation. Hyperventilation, depending on the SIZE of the PE, results in respiratory ALKALOSIS (small PE), or respiratory ACIDOSIS and failure (saddle embolus).

Another interesting thing is that the central chemoreceptor is not the main driving force here. If the patient does indeed have respiratory alkalosis, since the central chemoreceptor responds to pH/CO2, he should not be hyperventilating anymore. But since he IS hyperventilating, while at the same time still has alkalosis, the chemoreceptor has to be responding to hypoxemia and not acidosis.

I agree. The driver will be low O2 tension sensed by the carotid bodies.