Carbon monoxide (CO) is a colorless, tasteless, and odorless product of incomplete fuel combustion. It exerts its pathophysiologic effect by its avid binding to hemoglobin, with consequent displacement of oxygen. Tissue hypoxia is worsened by the deleterious effect on oxyhemoglobin dissociation and the direct effects of CO on the cytochrome system. Symptoms of CO poisoning are related to the blood carboxyhemoglobin level, time course of exposure, respiratory rate, age of the patient, and presence of underlying illness. Blood carboxyhemoglobin levels are dependent on the ambient CO level, which, in turn, is determined by the source of CO production and meteorologic and climatic factors.1
The symptoms and signs of CO poisoning are extremely varied. Nonspecific symptoms, eg, headache, nausea, vomiting, fatigue, and malaise, are common. Because of the fixed oxygen needs of the circulatory and nervous systems, cardiovascular and neurologic symptoms are frequent. However, virtually every organ system may be