Why is mixed venous O2 saturation *decreased* with hyperventilation?

[Foot Fetish]

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[Ismet]

Why are you assuming that O2 consumption and CO are unchanged?

 

[Foot Fetish]

Why are you assuming that O2 consumption and CO are unchanged?

Just because the instructor wrote that into the problem. I realize that, in reality, someone who is hyperventilating would likely also be tachycardic and thus have some increase in cardiac output.

 

[*brobro*]

My guess is that it is likely due to the increased inspiratory effort creating increased oxygen consumption. The local environment around the muscles of inspiration will be very acidic and oxygen deprived causing increased o2 consumption and a shift of the curve to the right. Then the diaphragm, intercostals, SCM, etc. will dump all that deoxygenated blood proximally into the venous system.

I didn't double check my facts here but hopefully this is correct enough that it will lead you down the right path?

 

[SurfingDoctor]

Can't explain the physiology perse because the interferences don't make sense. You can't have a change in venous saturation without changes in cardiac output or oxygen extraction (and therefore, consumption). These are all related to the Fick Principle:


VO2 (Oxygen Consumption) = Cardiac Output x Hgb x (SaO2 - SvO2)

You can see, in order for VO2 to be the same with a fixed CO, you can't have any change in the difference between the saturation of the arterial and venous systems.

I suppose if you had abnormal hemoglobin or a super high left shift of the Hgb disassociation curve (like in the setting of CO-Hgb) but in that case, the oxygen never leaves the Hgb, so the SvO2 is higher, not lower (in reference to the calculated value, not measured value)