What is the pathophysiology of cyanide asphyxiation from smoke inhalation?

Updated: Oct 15, 2021
  • Author: Keith A Lafferty, MD; Chief Editor: Joe Alcock, MD, MS  more...
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The incomplete combustion of nitrogen-containing materials releases hydrogen CN (HCN), a colorless gas with a bitter almond odor that is detectable by 40% of the population. The burning of cotton generates 130 µg HCN/g; of paper, 1100 µg HCN/g; and of wool, 6300 µg HCN/g. [12] CN is 20 times more toxic than CO and can cause immediate respiratory arrest.

CN directly stimulates chemoreceptors of carotid and aortic bodies, leading to a brief period of hyperpnea. [12] CN is a small lipophilic molecule and a chemical asphyxiant that interferes with cellular metabolism by binding to the ferric ion on cytochrome a3, subsequently halting cellular respiration. Affected cells convert to anaerobic metabolism, and lactic acidosis ensues.

The organs most sensitive to cellular hypoxia are the central nervous system (CNS) and the heart. The CNS reacts to low concentrations of CN by promoting hyperventilation, thereby increasing exposure.

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