Hydrogen Cyanide Poisoning

Cyanide reversibly inhibit cytochrome oxidase. In cases of cyanide poisoning, the venous blood is bright red because the oxygen has not been used. It acts as a cellular asphixiant. By binding to cytochrome oxidase, it prevents the use of oxygen incellular metabolism. The central nervous system is particularly sensitive to the toxic effects of HCN.

Initial symptoms may be confused with carbon monoxide poisoning. These include excitement, eye irritation, headache, confusion, dizziness, nausea, vomiting, and weakness. As HCN poisoning progresses, titanic spasms, lockjaw, convulsions, hallucinations, loss of consciousness, and coma may occur.

Definitive diagnosis have to occur in a hospital setting. Measurement of carboxyhemoglobin and blood cyanide concentrations will help to differentiate between CO and HCN poisoning.

Hydrogen cyanide is realeased during combustion of materials such polyurethane, nylon, and acrylonitrile. Firefighters are at great rick of exposure to this compound.

Hydrogen cyanide (hydrocyanic acid, HCN) is a highly poisonous compound found widely in nature. It is released from cyanogenic glycosides by the action of ß-glucosidase (e.g. emulsin) and oxinitrilase groups of enzymes. A number of plants, especially those containing cyanogenic glycosides, can metabolize HCN, usually by the reaction with serine (C3H7NO3) or cysteine (C3H7NO2S) to form cyanoalanine.