ion (Fe3+ ) and cobalt; in the body, the reaction of hydroxocobalamin with cyanide yields cyanocobalamin, or vitamin B12 The ability of the body to metabolize small quantities of cyanide, given sufficient time, accounts for the dependence of cyanide toxicity on conditions of concentration and exposure time The same amount of cyanide that will kill when given over a few minutes may be successfully metabolized by the body if administered over several hours Doses of cyanide large enough to overwhelm normal metabolism inhibit electron transport of the mitochondrial cytochrome chain The inactivation of this enzyme site results in cellular anoxia and a decreased arteriovenous oxygen difference (from inability of cells to use delivered oxygen), increased lactic acid (from accelerated glycolysis under anaerobic conditions), and metabolic acidosis Clinical Manifestations Clinical manifestations of cyanide poisoning relate to cellular anoxia; thus the heart and brain are most severely affected High concentrations of cyanide vapor initially produce tachypnea, hyperpnea, and hypertension within 10 to 15 seconds Anoxic injury to the CNS and myocardium soon follow, with unconsciousness and seizures (30 seconds after exposure), opisthotonus, trismus, facial muscle spasm, decerebrate posturing, bradycardia, dysrhythmias, hypotension, and eventually cardiac arrest (as early as to minutes after exposure) Exposure to low concentrations of vapor produces nonspecific effects such as headache, light-headedness, nausea, and ataxia “Classic” signs of cyanide poisoning are said to include severe dyspnea without cyanosis, flushing from increased oxygen content venous blood, and a bitter almond odor to breath and body fluids Noteworthy laboratory abnormalities in cyanide poisoning include an abnormally high mixed venous oxygen saturation with a resultant decreased arteriovenous oxygen content difference (one of the most useful laboratory indicators of cyanide poisoning), a high anion gap metabolic acidosis, and hyperlactatemia Both cyanide and nerve-agent casualties can collapse suddenly, stop breathing, and convulse Gasping, normal or dilated pupil size (as opposed to miosis), pink skin (instead of cyanosis), and normal secretions (as opposed to increased secretions) may lead to a clinical diagnosis of cyanide over nerve agent, but none of these signs is pathognomic The similarities between cyanide and nerve-agent casualties may be more apparent than the differences Management