Abstract An understanding of the physiology of acute carbon monoxide (CO) poisoning remains incomplete. This study describes a novel approach—considering a CO cycle driven by CO inhalation which includes: alveolar CO uptake → the transport to peripheral tissues → an increase in the P CO and COHb in peripheral capillary blood → and a return of COHb to the lungs. Unlike earlier models, this model allows evaluation of how COHb changes will affect physiological events at different sites in this cycle. We calculated increases in the P CO and the COHb at these sites during constant breathing of different CO concentrations, using an approach that emphasizes the importance of the rate of the replacement reaction (CO + oxyhemoglobin (O 2 Hb) ↔ COHb + oxygen (O 2 )) in the physiology of CO poisoning. Key findings include: (i) how interactions between inhaled CO, COHb recirculating back to alveolar capillaries, and alveolar capillary P CO back‐pressure regulate pulmonary CO uptake; (ii) how a decrease in the arterial O 2 Hb evokes an amplification of the P CO in blood entering peripheral tissues; (iii) that hemoglobin's R‐to‐T allosteric shifts influence CO delivery to peripheral tissues; and (iv) a clearer characterization of how tissue P CO is increased during CO exposures.
Coburn et al. (Wed,) studied this question.