Six hours after ingesting an unknown quantity of enteric-coated aspirin tablets, a young woman shows tachypnoea, tinnitus and fever. Arterial blood gas shows pH 7.48, PaCO2 25 mmHg, bicarbonate 18 mEq/L. This early pattern of salicylate toxicity represents:
- A Respiratory acidosis due to medullary depression
- B Pure metabolic acidosis with compensatory hypoventilation
- C Mixed respiratory alkalosis from direct medullary stimulation with metabolic acidosis from uncoupled oxidative phosphorylation ✓
- D Normal anion gap acidosis from renal tubular bicarbonate wasting alone
Explanation
Salicylates directly stimulate the respiratory centre producing hyperventilation and respiratory alkalosis, while simultaneously uncoupling oxidative phosphorylation, driving anaerobic metabolism, lactate accumulation and high anion gap metabolic acidosis. Early in adults the respiratory component dominates, matching this gas. Medullary depression with respiratory acidosis occurs late and after massive doses, which is why option A describes the terminal rather than the early phase.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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