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

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Abstract
When blood in the pulmonary capillary is oxygenated in hypercapnic air, PCO2 [CO2 partial pressure] in the red cell apparently exceeds 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. 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. To verify the validity of this assumption, PEq value was measured in normo- and hypercapnia by using the Defares'' extrapolation method in 6 normal subjects. Peq estimated in hypercapnia was > than that in normocapnia. This difference was significantly greater in normoxia than in hypoxia, and 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. [respiratory quotient] effect on the alveolar gas volume into account, suggesting that the inward CO2 diffusion following the oxygenation reaction could be disregarded in normoxic hypercapnia.