Affinity of carbon monoxide to hemoglobin increases at low oxygen fractions.

Following systemic inflammation, the lung induces an isoenzyme of heme oxygenase (HO-1), catalyzing carbon monoxide (CO) production through breakdown of heme molecules. However, it is still debated why the paradoxical arterio-venous carboxyhemoglobin (COHb) difference occurs only during critical illness but not in healthy volunteers. To elucidate whether oxygen fractions at (sub-)physiologic ranges alter the affinity of CO to hemoglobin (Hb), we performed an in vitro laboratory experiment, in which we exposed venous blood samples to fixed CO-doses at incrementing oxygen fractions (FiO2). ANOVA demonstrated that the affinity of CO (200 and 400 ppm) to Hb progressively increased with an FiO2 from 0% to 15%, whereas at higher oxygen tensions this effect vanished. This might explain why the arterio-venous COHb difference found in critically ill patients is not reproducible in healthy adults, since the latter ones are characterized by higher venous oxygen saturations.