ACUTE carbon monoxide poisoning accounts for approximately 3,500 accidental or suicidal deaths per year in the United States. Many are preventable by medical management based on physiologic understanding.
Carbon monoxide poisoning and its mechanism have been known since Claude Bernard reported in 1857 that this gas caused death by hypoxia, consequent on its reversible combination with hemoglobin.1 The equilibrium reactions were well described by Haldane in 1895.2 Excellent reviews are available.3,4The effects of CO in concentrations encountered clinically are based entirely on its combination with hemoglobin, displacement of oxygen, and consequent disruption of the O2 transport system. Carbon monoxide competes with O2 for binding sites on the hemoglobin molecule, and carboxyhemoglobin (COHb) is without practical function as a carrier of O2. Because affinity of CO for hemoglobin is 230 to 270 times as great as that of O2, the latter is