A 22-year-old woman presents after ingesting an unknown quantity of enteric-coated aspirin several hours ago. She has tinnitus, nausea, fever, and deep hyperpnoea. Arterial blood gas shows pH 7.48, PaCO2 28 mmHg, bicarbonate 21 mEq/L. The early hyperventilation in salicylate poisoning results from:

• A Metabolic acidosis stimulating peripheral chemoreceptors
• B Uncoupling of oxidative phosphorylation in carotid body cells
• C Salicylate-induced pulmonary oedema causing hypoxaemia
• D Direct stimulation of the medullary respiratory centre by salicylate ✓

Explanation

Salicylates directly stimulate the medullary respiratory centre, producing tachypnoea and hypocapnia, so the earliest acid-base disturbance is respiratory alkalosis. Uncoupling of oxidative phosphorylation occurs later, driving anaerobic metabolism and the classic mixed picture of respiratory alkalosis plus high anion gap metabolic acidosis seen in adults. Peripheral chemoreceptor stimulation and pulmonary oedema are not the primary drivers of the initial hyperventilation. Enteric coating delays absorption, so salicylate levels may rise hours after ingestion.

Reference: Katzung Basic and Clinical Pharmacology, 15th ed.

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Written and medically reviewed by the StethoPrep medical team.