What is the pathophysiology of cyanide poisoning?
Cyanide ions block the mitochondrial enzyme cytochrome oxidase, which leads to reduced aerobic metabolism. Glycolysis continues, however, resulting in a buildup of pyruvate, which is converted to lactic acid. The end result is a combined intracellular shortage of ATP and lactic acidosis. The brain’s high metabolic rate accounts for its disproportionate vulnerability to cyanide. What is the clinical presentation of cyanide toxicity? The manifestations of cyanide intoxication are dose-dependent. Low to intermediate levels of exposure produce non-specific symptoms such as headache, vertigo, nausea, and vomiting. With higher levels of exposure, patients exhibit depressed mental status, seizures, and increased respirations. Very high levels of exposure result in abrupt loss of consciousness, respiratory depression, and cardiac arrest. Patients with intermediate-level toxicity may worsen several hours after exposure and display a faltering mental status. Results of a physical examination of
