Pathophysiology
Clinical meaning
Carbon monoxide (CO) binds hemoglobin with 200-250x greater affinity than oxygen, forming carboxyhemoglobin (COHb). This displaces oxygen from heme binding sites and causes a left shift of the oxyhemoglobin dissociation curve, impairing oxygen release to tissues. CO also binds myoglobin (causing cardiac dysfunction) and mitochondrial cytochrome c oxidase (blocking oxidative phosphorylation). The resulting cellular hypoxia triggers anaerobic metabolism with lactic acidosis. Inflammatory cascades from CO-induced oxidative stress cause lipid peroxidation in the CNS, contributing to delayed neurological sequelae (DNS) appearing 2-40 days post-exposure.