Why does resp. depression cause acidosis, but PE cause alkalosis?

[Poit]

I'm not that great at pulmonary physio. Is it because with PE you get an elevated RR, and w/ resp. depression a drop? If so, why are you able to expel CO2 with PE, but not take in O2? A PE would cause a block in perfusion to the lung, creating a dead space. Since CO2 and O2 are both perfusion limited, it seems like less CO2 would be expelled.

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[AcademicNeurosurgery]

I'm not that great at pulmonary physio. Is it because with PE you get an elevated RR, and w/ resp. depression a drop? If so, why are you able to expel CO2 with PE, but not take in O2? A PE would cause a block in perfusion to the lung, creating a dead space. Since CO2 and O2 are both perfusion limited, it seems like less CO2 would be expelled.

Respiratory depression is due to some extrinsic factor decreasing RR. The RR is decreased by definition. This leads to retention of CO2 -> acidosis.

PE inhibits blood flow to a specific point downstream from the clot resulting in hypoxemia. The body will compensate by increasing RR. Thus, CO2 will blown off - alkalosis.

 

[Dires]

Short and simple:

Respiratory depression: decreased alveolar ventilation = increase CO2 = acidosis

PE: shortness of breath = increased respiratory rate = increased ventilation = decreased CO2 = alkalosis

 

[Poit]

Makes sense. Thanks.