## Mechanism of Cyanide Toxicity **Key Point:** Cyanide binds irreversibly to the ferric iron (Fe³⁺) in cytochrome c oxidase (Complex IV), the final enzyme in the electron transport chain, preventing electron transfer to oxygen and halting aerobic respiration. ### Why Complex IV? Cytochrome c oxidase catalyzes the transfer of electrons to molecular oxygen, the final step of oxidative phosphorylation. When cyanide binds to the Fe³⁺ center: 1. Electron transport stops 2. ATP production ceases 3. Cells shift to anaerobic metabolism (lactic acidosis) 4. Tissues with high oxygen demand (brain, heart) fail first ### Biochemical Consequence - **Histotoxic hypoxia:** Cells cannot use oxygen despite adequate supply and normal arterial oxygen saturation - Blood remains oxygenated (cherry-red appearance may occur) - Venous O₂ saturation remains high (paradoxical finding) **High-Yield:** The hallmark of cyanide poisoning is **normal PaO₂ and SaO₂ with severe metabolic acidosis and elevated venous oxygen saturation** — a pathognomonic triad. **Clinical Pearl:** This is why pulse oximetry and arterial blood gases may appear reassuring in cyanide poisoning, but the patient is dying from cellular asphyxia.
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