![]() The primary effect of CN is a blocking of the mitochondrial respiration chain and the formation of intracellular adenosine triphosphate (ATP). CO binds to the reduced form of CCO and CN binds to either the reduced CCO heme (Fe 2+) or oxidized heme (Cu B 2+). The active (O 2-binding) site of CCO is binuclear, consisting of heme a 3 and Cu B. Both CO and CN affect the mitochondria by binding to the enzyme cytochrome- c oxidase a, a3 (CCO), the terminal enzyme complex of the respiratory chain in complex IV. However, where CO impairs the ability of erythrocytes to transfer oxygen, CN binds to erythrocytes but does not affect the oxygen transfer. The similarity between CO and CN is the ability to bind iron ions. Both parkinsonian symptoms and a dystonia syndrome have been observed. ![]() As very few people survive severe CN poisoning, reports of late neurological sequelae are rare.ĬN poisoning in mild degrees is recognized as a cause of permanent neurological disability, ranging from various extrapyramidal syndromes to post-anoxic vegetative states. Autopsy findings include petechial, subarachnoid or subdural haemorrhages. Virtually all patients with severe, acute CN poisoning die immediately. Death is due to respiratory arrest but the heart invariably outlasts respiration and may continue to beat for as long as 3-4 min. In most severe cases the patients symptoms are unconsciousness, convulsions, cardiovascular collapse followed by shock, pulmonary oedema and death. In more severe cases the patient will have dyspnoea, bradycardia, hypotension and arrhythmia. In milder cases of CN poisoning the symptoms are headache, nausea, vertigo, anxiety, altered mental status, tachypnea, hypertension and there may be an odour of bitter almonds in the patients expiration. CN also stimulates the nociceptors, leading to a brief sensation of dryness and burning in the nose and throat. Initially, the symptoms include a brief period of hyperpnoea, due to direct stimulation of the chemo receptors of the carotid and aortic bodies by CN. CN can be distributed in the body within seconds and death can occur within seconds or minutes after a large dose. Since CN is a small lipid soluble molecule and mainly undissociated, distribution and penetration of CN into cells is rapid. HCN is easily absorbed from all routes of exposure. ![]()
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