A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 58-year-old man is rushed to the ER in the middle of the night with severe chest pain. He arrives in the ER short of breath, sweating, and looking terrified. His blood pressure is noted to be 250/140, and he is immediately administered nitroprusside. His blood pressure is controlled, but he soon develops confusion and lactic acidosis. Which of the following are potential side effects of nitroprusside administration?
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A
CoughIncorrect. Cough is a classic ACE inhibitor side effect (bradykinin accumulation), not associated with nitroprusside.
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B
HyperkalemiaIncorrect. Hyperkalemia is associated with potassium-sparing diuretics, ACE inhibitors, and ARBs — not nitroprusside.
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C
HypoventilationIncorrect. Hypoventilation isn't a typical nitroprusside effect — it tends to cause tachycardia/reflex hypotension.
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D
Cyanide toxicityCorrect. Nitroprusside releases cyanide upon metabolism; prolonged/high-dose use causes cyanide toxicity with confusion and lactic acidosis.
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E
MethemoglobinemiaIncorrect. Methemoglobinemia is associated with nitrate/nitrite exposure (and topical anesthetics such as benzocaine), producing chocolate-brown blood and cyanosis unresponsive to oxygen; nitroprusside characteristically causes cyanide rather than methemoglobin toxicity.
↑ Tap an answer to reveal the reasoning
Answer: D. Sodium nitroprusside is a potent, fast-acting vasodilator used IV for hypertensive emergencies. It dissociates in the bloodstream to release nitric oxide (causing vasodilation) and cyanide. Cyanide is normally detoxified by the liver to thiocyanate using sulfur donors (rhodanese with thiosulfate) and excreted renally. With prolonged or high-dose infusion — especially in patients with renal or hepatic dysfunction — cyanide accumulates faster than it can be cleared, producing cyanide toxicity.
Cyanide blocks cytochrome c oxidase (complex IV) in the mitochondrial electron transport chain, preventing oxygen utilization. This causes inability of tissues to extract oxygen, anaerobic metabolism, and lactic acidosis (a tell-tale sign), plus altered mental status, tachycardia, and ultimately cardiovascular collapse.
The patient here developed confusion and lactic acidosis after nitroprusside — characteristic of cyanide toxicity. Treatment includes stopping the drug and administering hydroxocobalamin (binds cyanide to form cyanocobalamin, renally excreted) or sodium thiosulfate (provides sulfur for endogenous detoxification by rhodanese) and sodium nitrite (induces methemoglobinemia, which binds cyanide).
**Why each option:**
**A.** Cough is a classic ACE inhibitor side effect (bradykinin accumulation), not associated with nitroprusside.
**B.** Hyperkalemia is associated with potassium-sparing diuretics, ACE inhibitors, and ARBs — not nitroprusside.
**C.** Hypoventilation isn't a typical nitroprusside effect — it tends to cause tachycardia/reflex hypotension.
**D.** Correct. Nitroprusside releases cyanide upon metabolism; prolonged/high-dose use causes cyanide toxicity with confusion and lactic acidosis.