Contribution of the Haldane effect to the rise of arterial Pco2 in hypoxic patients breathing oxygen.

Arterial (PaCO2), alveolar (PACO2), mixed expired (PECO2) CO2 pressures, CO2 production (VCO2) as well as arterial O2 saturation (SaO2) were measured on 20 severely hypoxic and hypercapnic patients breathing air (A) and 100% O2 (HO). On HO, mean PaCO2 increased to 56.6 torr from 50.8 torr on A, whereas there was no significant change in PACO2 (38.3 on A, 38.6 on HO), so that the arterial-alveolar gradient (aADCO2) increased from 12.5 to 18.0 torr. PECO2 remained essentially the same. There was a statistically significant correlation between the increase in PaCO2 on HO and the arterial unsaturation (100 - SaO2) on A and also between PaCO2 on A and its increment on HO. When the rise in PaCO2 and aADCO2 were estimated which resulted from the shift in the Co2 dissociation curve due to complete oxygenation of hemoglobin on HO (Haldane effect), 78% of the observed change in PaCO2 could be accounted for. The deadspace/tidal volume ratio (VD/VT) increased from 0.59 on A to 0.64 and 87% of this difference could be attributed to the Haldane effect. The results emphasize the importance of considering this effect when interpreting alterations in PaCO2, aADCO2 and VD/VT on transition from air to hyperoxia, particularly in patients with severe hypoxemia and hypercapnia.