Whole body oxygen utilization during acute carbon monoxide poisoning and isocapneic nitrogen hypoxia.

Carbon monoxide (CO) poisoning occurs frequently in victims of enclosed space fires, resulting in the formation of carboxyhemoglobin (COHb). Based on in vitro studies it has been suggested that CO poisoning causes a left shift of the oxyhemoglobin dissociation curve, decreasing peripheral oxygen extraction and exacerbating hypoxic injury. Formation of carboxycytochrome oxidase has also been postulated to act as a toxin by blocking cellular oxygen utilization. The effects of in vitro CO poisoning were evaluated in studies of 12 anesthetized, paralyzed dogs ventilated at 150 cc/kg/min. Six were subjected to CO poisoning by ventilation with a 0.5% CO in air inspirate. Six were ventilated with a mixture of air and nitrogen (N2) to produce a similar decrement of arterial oxyhemoglobin (aO2Hb) saturation. Arterial and mixed venous blood gases, thermal dilution cardiac output, and spectrophotometric arterial and mixed venous O2Hb and COHb saturation were measured. Oxygen consumption (VO2) and extraction (EXT) were calculated from these measurements and the CO and N2 groups were compared by ANOVA and Wilcoxon sign rank test as oxyhemoglobin was progressively decreased. There were no significant differences in VO2 or O2 EXT in these two sets of animals subjected to equivalent reductions of arterial oxyhemoglobin despite the fact that CO poisoning was the mode of desaturation in one group. These findings suggest that CO poisoning is primarily a hypoxic lesion caused by replacement of O2Hb by COHb. Effects predicted from in vitro studies may not be manifest in vivo due to physiologic responses active in the whole organism. This may have implications for the resuscitation of CO-injured patients.