A 32-year-old man presents to the emergency department after a crack cocaine binge. He has chest pain, blood pressure 190/110 mmHg, heart rate 118/min, and agitation. An intern plans to give intravenous propranolol to control both tachycardia and hypertension. Why should this be avoided?
- A Propranolol precipitates acute kidney injury in cocaine users
- B Propranolol accelerates cocaine metabolism producing toxic metabolites
- C Unopposed alpha-mediated vasoconstriction can worsen hypertension and coronary vasospasm ✓
- D Beta-blockers convert cocaine-induced chest pain into aortic dissection
Explanation
Cocaine produces simultaneous alpha-adrenergic vasoconstriction and beta-adrenergic chronotropic stimulation. Giving a non-selective beta-blocker blocks vasodilatory beta-2 receptors while leaving alpha-1 vasoconstriction unopposed, which can paradoxically raise blood pressure, worsen coronary spasm, and reduce coronary perfusion. First-line treatment is benzodiazepines, which blunt sympathetic outflow, with nitrates added for ischemic chest pain. Propranolol does not alter cocaine metabolism and dissection is not the feared mechanism.
Reference: Goldfrank's Toxicologic Emergencies, 11th ed.
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