The influence of the haldane effect on alveolar CO2 tension equilibrated with mixed venous blood in man.

Abstract

When blood in the pulmonary capillary is oxygenated in hypercapnic air, PCO2 in the red cell has been thought to exceed alveolar PCO2 due to the Haldane effect, inducing outward CO2 diffusion. As long as the inward CO2 diffusion and, consequently, HCO3- formation are prevented in the red cell, the CO2 gain in plasma is reduced down to the level predicted from a CO2 dissociation curve of separated plasma. Therefore, if the direction of the CO2 diffusion is not reversed during the contact time, the virtual venous PCO2 (PEq), where the CO2 loss due to the Haldane effect is balanced with the gain due to the venoalveolar PCO2 gradient, becomes higher than the oxygenated venous PCO2 in proportion to the CO2 difference between the true and separated plasma. In order to verify the validity of the above assumption, the PEq value was measured in normo- and hypercapnia by using the Defares' extrapolation method in six normal subjects. The results obtained revealed that the PEq estimated in hypercapnia was obviously higher than that in normocapnia. The above difference was significantly greater in normoxia than in hypoxia. Furthermore, it agreed fairly well with the theoretical difference presumed by taking the difference in CO2 content between separated and true plasma and the R. Q. effect on the alveolar gas volume into account, suggesting that the inward CO2 diffusion following the oxygenation reaction could be disregarded in normoxic hypercapnia.