A patient with hypertensive emergency receives IV sodium nitroprusside infusion for 72 hours and develops metabolic acidosis, confusion, and seizures. Blood gas shows elevated lactate with a narrowed arteriovenous oxygen difference. The underlying mechanism is:
- A Methemoglobinemia reducing oxygen delivery
- B Accumulation of cyanide released during metabolism, poisoning cytochrome oxidase and blocking tissue oxygen utilization ✓
- C Thiocyanate-induced hypothyroidism
- D Reflex coronary steal causing global ischemia
Explanation
Nitroprusside is metabolized by red cells and tissues to release nitric oxide and cyanide ions; cyanide is normally converted to thiocyanate by rhodanese in the liver and excreted renally. With high doses, prolonged infusion, hepatic insufficiency, or renal failure, free cyanide accumulates and inhibits cytochrome oxidase, causing histotoxic hypoxia with lactic acidosis. Thiocyanate accumulation causes a different, slower toxicity.
Reference: Katzung's Basic and Clinical Pharmacology, 16th ed.
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