A 16-year-old girl presents 8 hours after ingesting a large quantity of aspirin tablets. She has tachypnoea, tinnitus, sweating, and vomiting. Arterial blood gas shows pH 7.48, PaCO2 28 mmHg, bicarbonate 20 mEq/L. The primary reason for the initial respiratory alkalosis in salicylate poisoning is:
- A Uncoupling of oxidative phosphorylation causing lactic acidosis with compensatory hyperventilation
- B Salicylate directly stimulates the medullary respiratory centre, increasing ventilation ✓
- C Inhibition of carbonic anhydrase leading to renal bicarbonate loss
- D Pulmonary oedema causing hypoxaemic drive to breathe
Explanation
Salicylates directly stimulate the respiratory centre in the medulla, producing hyperventilation, a fall in PaCO2 and a pure respiratory alkalosis early in poisoning. Uncoupling of oxidative phosphorylation occurs later and produces the metabolic (high anion gap) acidosis seen as toxicity progresses. Carbonic anhydrase inhibition is a property of acetazolamide, not aspirin.
Reference: Katzung's Basic and Clinical Pharmacology, 16th ed.
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