Gas-to-blood PCO2 differences during severe hypercapnia.
Five anesthetized dogs were made severely hypercapnic by stepwise addition of CO2 to their inspired air. Blood PCO2 levels greater than 400 Torr were reached. During hypercapnia, the steady-state end-tidal PCO2 (PaCO2) was always higher than the simultaneous measured arterial PCO2 (PaCO2). The mean ratio PaCO2/PACO2 was 0.861 +/- 0.01. These results are consistent with the predictions of the Charged Membrane Hypothesis, that gas-to-blood PCO2 differences should be directly proportional to the blood H+ activity. The results cannot be explained by delayed equilibration of CO2 between plasma and red blood cells. The latter hypothesis predicts that, under the conditions of these experiments, the PCO2 of arterial blood should be higher than the PCO2 of end-tibal gas. The blood HCO3- during hypercapnia did not increase as much as would be predicted if the blood were exposed to CO2 in vitro. This may reflect movement of blood HCO3- generated by the buffering of carbonic acid into intracellular compartments during hypercapnia.
D000136:Acid-Base Equilibrium; D000818:Animals; D001639:Bicarbonates / Q000097:blood*; D002021:Buffers; D002245:Carbon Dioxide / Q000097:blood; D002255:Carbonic Acid / Q000097:blood; D004285:Dogs; D006935:Hypercapnia / Q000378:metabolism*; D012119:Respiration
D001639:Bicarbonates; D002021:Buffers; D002245:Carbon Dioxide; D002255:Carbonic Acid