Cyanide Poisoning

The primary mechanism of action is two fold:

• High-pressure oxygen forces more oxygen into the bloodstream, helping to counteract the cellular oxygen blockade caused by cyanide. Cyanide prevents cells from using oxygen by disrupting mitochondrial electron transport, so increasing oxygen delivery can help bypass this inhibition.

• HBOT enhances the conversion of cyanide to less toxic compounds. Specifically, it promotes the activity of the enzyme rhodanese, which converts cyanide to thiocyanate, a much less harmful substance that can be easily excreted by the kidneys.

While HBOT is not the sole treatment for cyanide poisoning, it plays a crucial supportive role in managing the metabolic crisis caused by cyanide toxicity. It is particularly valuable in severe cases where rapid intervention is critical to preventing cellular damage and potential organ failure.