for all you high altituders (pulm question!)

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Fungi121

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You know those questions you HATE because you really have a tough time understanding? Could someone give me a hand? 🙁

Q: Guy who lives at high altitude is found to have a normal arterial O2 content. Why?


A: (Answer is that, compared to a normal person, he's got a high hematocrit, low arterial PO2, and low arterial O2 saturation)

PLEASE feel free to point out where I'm wrong and help me out. My reasoning:

-Arterial O2 content = Hg-bound oxygen + dissolved oxygen, basically (there's that formula but whatevs)

-Arterial PO2 = Basically determined by the environment (Sea level, mountains) and is the dissolved O2

-Arterial O2 sat = % hemoglobin saturation with oxygen

-Hematocrit = % of RBCs in blood

This guy lives at high altitude so you'd expect arterial PO2 to be low, leading to low O2 sat. However, since he LIVES there, you assume some sort of compensation has taken place. Increased hematocrit = increased RBCs which means more hemoglobin binding oxygen = more oxygen bound so the arterial O2 content is elevated...but the arterial PO2 and arterial O2 sat stay the same?

Super karma hugs to whoever can help me out, tell me what to fix, etc....pulm and I are not friends 🙁
 
The arterial PO2 is a function of the partial pressure of oxygen of the air that a person inhales. His high Hct is from the increased EPO his body's putting out and this functions to somewhat ameliorate the tissue hypoxia he's experiencing, but it isn't capable of fixing the underlying decreased FiO2 that the dude is breathing at high altitudes. The equation below helps me visualize the relationship between FiO2, PaO2, and SaO2. It pretty much says that if a person is breathing in air with low partial pressure of O2 (ie like a guy on Everest), then his alveolar, arterial and Hb saturation will all be subsequently affected. Since the body can't change the content of the air its breathing, it reacts by making more RBCs to carry all of the O2 it can snag from the relatively oxygen-deficient air (and this works as an adaptive mechanism, but with more RBCs with relatively less O2 to bind from the air, there will have to be a lower % saturation).

FiO2 --> PAO2 --> PaO2 --> SaO2

Does that kinda make sense?
 
This guy lives at high altitude so you'd expect arterial PO2 to be low, leading to low O2 sat. However, since he LIVES there, you assume some sort of compensation has taken place. Increased hematocrit = increased RBCs which means more hemoglobin binding oxygen = more oxygen bound so the arterial O2 content is elevated...but the arterial PO2 and arterial O2 sat stay the same?

The arterial PO2 is decreased, which subsequently means that the SaO2 is decreased. Total arterial O2 is able to stay the same because there is an increased quantity of Hb.

(Hb x 1.34 x SaO2) + (PaO2 x 0.003)

So, in the equation, PaO2 and SaO2 are decreased (because of PiBond's stream of O2: FiO2 --> PAO2 --> PaO2 --> SaO2), but because the quantity of Hb is increased due to compensation, the total arterial oxygen content is roughly the same as someone at a normal altitude.
 
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