Carbon Monoxide/Cyanide

Abstract

Carbon monoxide (CO) poisoning is the leading cause of both accidental and intentional poisoning deaths in the United States. Carbon monoxide produces its toxic effects primarily by reducing the oxygen availability to tissues (anoxic anoxia) in two ways: CO binding to hemoglobin (Hb) reduces the amount of Hb available to carry oxygen to tissues and prevents the release of some of the oxygen from Hb binding sites at the low oxygen tension present in the tissues (leftward shift in the oxygen-Hb dissociation curve). The signs and symptoms of CO intoxication are relatively nonspecific; treatment of CO poisoning is primarily supportive. Evaluation of the extent of CO exposure is based on a determination of the percentage of Hb bound with CO (%COHb) in the blood. Fatalities due to CO exposure are typically characterized by %COHb >50%. The presence of a bright cherry-red coloration of the blood, fingernails, mucous membranes, and skin may indicate CO poisoning. Cyanide is a fast-acting, lethal poison, with death occurring within minutes after inhalation and more slowly following oral ingestion. Cyanide inhibits the electron transport process of cellular respiration at the cytochrome c oxidase step, binding to the heme ion of cytochrome c oxidase. Hydrogen cyanide (HCN) is more rapidly absorbed than salts of cyanide. Detoxification of cyanide to thiocyanate occurs via two enzyme systems: rhodanese and beta-mercaptopyruvate-cyanide sulfurtransferase. The onset of symptoms in cyanide poisoning is dependent on the type of exposure; HCN vapor acts more quickly than cyanide salts. The signs and symptoms of cyanide poisoning are relatively nonspecific, with rapid onset of coma, metabolic acidosis, and symptoms of anoxia without cyanosis as noteworthy indicators. Cyanide deaths have occurred from both accidental and intentional exposure. The findings at autopsy are generally nonspecific. Blood cyanide concentrations of 2–3 mg/L are consistent with death in the absence of other findings.