## Mechanism of Cyanide Toxicity **Key Point:** Cyanide binds irreversibly to the ferric iron (Fe³⁺) in cytochrome c oxidase (Complex IV) of the electron transport chain, blocking the final step of aerobic respiration. ### Why Complex IV? Cytochrome c oxidase is the terminal enzyme in the electron transport chain. It accepts electrons from cytochrome c and transfers them to oxygen, which is reduced to water. Cyanide's binding to the Fe³⁺ centre prevents this electron transfer, halting the entire chain. ### Consequence: Histotoxic Hypoxia Unlike hypoxemic or circulatory hypoxia, cyanide poisoning causes **histotoxic hypoxia** — oxygen is available in the blood and tissues, but cells cannot utilize it. This is why the arteriovenous oxygen difference (A-V O₂) remains normal or narrow, and tissues become anoxic despite adequate oxygenation. **High-Yield:** The hallmark finding is **bright red venous blood** (high venous O₂ saturation) because tissues cannot extract oxygen. ### Rapid Onset Cyanide acts within seconds to minutes because it blocks the final common pathway of energy production. Even brief exposure can be fatal. **Clinical Pearl:** Cyanide poisoning should be suspected in any patient with sudden collapse, altered consciousness, seizures, or cardiac arrhythmias in an industrial or fire-related setting, especially when venous oxygen saturation is paradoxically high.
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