PaO2 in severe anemia

[MudPhud20XX]

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So Kaplan physio explains that both polycythemia and anemia do not affect PaO2 b/c they only affect the oxygen transported by hemoglobin not the oxygen dissolved in plasma.

However, in case of severe anemia, theoretically wouldn't you observe slight increased PaO2? Since the oxygen molecules will be forced to be dissolved in plasma? Considering normal PaO2 is around 95, it may go up a bit like 97-98 mmHg right? (not exceeding 100 mmHg since it will still need to be equilibrated with the alveolar oxygen pressure.)

Also, in CO poisoning, since PaO2 doesn't change, how would you be able to make a diagnosis? Kaplan says P50 value will be helpful but doesn't explain the reason. Under normal circumstance, P50 occurs around PO2 = 26 mmHg, which is actually a lot lower than the PvO2 which is around 40 mmHg, so how do we clinically make a diagnosis using P50 value?

Many thanks in advance.

 

[bulldogmed]

So Kaplan physio explains that both polycythemia and anemia do not affect PaO2 b/c they only affect the oxygen transported by hemoglobin not the oxygen dissolved in plasma.

However, in case of severe anemia, theoretically wouldn't you observe slight increased PaO2? Since the oxygen molecules will be forced to be dissolved in plasma? Considering normal PaO2 is around 95, it may go up a bit like 97-98 mmHg right? (not exceeding 100 mmHg since it will still need to be equilibrated with the alveolar oxygen pressure.)

Also, in CO poisoning, since PaO2 doesn't change, how would you be able to make a diagnosis? Kaplan says P50 value will be helpful but doesn't explain the reason. Under normal circumstance, P50 occurs around PO2 = 26 mmHg, which is actually a lot lower than the PvO2 which is around 40 mmHg, so how do we clinically make a diagnosis using P50 value?

Many thanks in advance.

From Costanzo's Physiology, p. 209
"Dissolved O2 is free in solution and accounts for approximately 2% of the total O2 content of blood. Recall that dissolved O2 is the only form of O2 that produces a partial pressure, which in turn, drives O2 diffusion. (In contrast, O2 bound to hemoglobin does not contribute to its partial pressure in blood.)"

Having a decrease in hgb (the definition of anemia) is not going to significantly alter the amount of dissolved O2 in plasma. You're talking about a decrease in proteins in a solution increasing or decreasing a solubility of a gas. That's not going to happen on the order of changes involved in anemia.

 

[Memyself123]

can u pls help i have the same question as to why pO2 will not increase if there is less hb because i guess pO2 is at the crossroads of 2 equilibriums one with hb and the other with air in the lungs so it should be affected eitherways

when u said in your ans "" not significantly altered"" did that mean small change or no change at all?

 

[zmiller5000]

So Kaplan physio explains that both polycythemia and anemia do not affect PaO2 b/c they only affect the oxygen transported by hemoglobin not the oxygen dissolved in plasma.

However, in case of severe anemia, theoretically wouldn't you observe slight increased PaO2? Since the oxygen molecules will be forced to be dissolved in plasma? Considering normal PaO2 is around 95, it may go up a bit like 97-98 mmHg right? (not exceeding 100 mmHg since it will still need to be equilibrated with the alveolar oxygen pressure.)

Also, in CO poisoning, since PaO2 doesn't change, how would you be able to make a diagnosis? Kaplan says P50 value will be helpful but doesn't explain the reason. Under normal circumstance, P50 occurs around PO2 = 26 mmHg, which is actually a lot lower than the PvO2 which is around 40 mmHg, so how do we clinically make a diagnosis using P50 value?

Many thanks in advance.

-PaO2 is ONLY dependent on the solubility of oxygen in blood and the ability of the lungs to ventilate and exchange gas. The presence or absence of hemoglobin will not change that.
-w/r to carbon monoxide poisoning, PaO2 is rarely the first test you will do because it requires an arterial blood draw. Carbon monoxide poisoning does cause a decrease in O2 saturation that is NOT accompanied by physical evidence of cyanosis (because the hemoglobin is not empty..it has been filled with carbon monoxide instead). You would use a h/x of possible exposure to carbon monoxide i.e. fire or suicide attempt coupled with decreased O2 saturation. If ABGs are obtained, and the PaO2 is normal..this is even more suggestive of carbon monoxide poisoning. Now it gets complicated if a patient was say in a fire and had both damage to the lungs (resulting in decreased PaO2 and lower O2 sat) and possible carbon monoxide exposure. I am not totally sure how the patient would be worked up at that point, but you will probably assume some degree of carbon monoxide exposure and treat empirically.