Cyanide poisoning blocks Complex IV (cytochrome c oxidase) of the mitochondrial electron transport chain. Which arterial blood gas pattern is expected in a patient with severe cyanide toxicity?

• A Decreased PaO2, increased PaCO2, metabolic acidosis — type 2 respiratory failure pattern
• B Normal PaO2, decreased PaCO2, metabolic alkalosis due to impaired CO2 production
• C Decreased PaO2 and PaCO2, metabolic acidosis — pattern of pulmonary shunting
• D Normal PaO2, elevated venous PO2, high-anion-gap metabolic acidosis with elevated lactate ✓

Explanation

Cyanide inhibits cytochrome oxidase, preventing mitochondrial O2 utilisation. Pulmonary gas exchange is unaffected, so PaO2 is normal and blood is fully saturated. However, since tissues cannot extract oxygen, venous PO2 is paradoxically elevated (oxygen-rich venous blood). Cells are forced into anaerobic glycolysis, generating lactic acid and causing a high-anion-gap metabolic acidosis with elevated serum lactate. Clinically, the combination of normal SpO2, elevated venous O2 saturation, and high lactate in a 'cherry-red' patient in circulatory collapse strongly suggests cyanide poisoning.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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