Cyanide binds to Fe3+ in heme-containing proteins. This inhibits the terminal cytochrome complex IV of the electron transport chain. The blocklock of complex IV by cyanide depletes ATP culminating in cell death. Oxygen is unable to reoxidize the reduced cytochrome a3. Thus, cellular respiration is inhibited, as well as ATP production, in essence depriving the cells, tissue, and, ultimately, the whole body of oxygen. Hypoxia evolves into metabolic acidosis and decreased oxygen saturation. The extent of lactic acidosis indicates the severity of the cyanide poisoning. In a collapsed individual, plasma lactate is an indicator of cyanide poisoning. In severe cyanide poisonings, up to 98% of the cyanide in the bloodstream is tightly bound to red blood cells. The ancillary response is myocardial depression and decline in cardiac output. Bradycardia, hypotension, and cardiac arrhythmia then develop into VF and cardiovascular collapse.
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