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For further information, see CMDT Part 38-24: Beta-Adrenergic Blockers Poisoning

Key Features

  • The most toxic β-blocker is propranolol

    • It competitively blocks β1- and β2-adrenoceptors

    • Has direct membrane-depressant and CNS effects

Clinical Findings

  • Hypotension and bradycardia are common with mild or moderate intoxication

  • Cardiac depression from more severe poisoning is often unresponsive to conventional β-adrenergic stimulants such as dopamine and norepinephrine

  • With propranolol and other lipid-soluble drugs, seizures and coma may occur

  • Propranolol, oxprenolol, acebutolol, and alprenolol

    • Have membrane-depressant effects

    • Can cause conduction disturbance (wide QRS interval) similar to tricyclic antidepressant overdose


  • Diagnosis is clinical

  • Routine toxicology screening does not usually include β-blockers


  • Activated charcoal

    • Administer 60–100 g orally or via gastric tube, mixed in aqueous slurry

    • Repeated doses may be given

  • Attempts to treat bradycardia or heart block with atropine (0.5–2 mg intravenously), isoproterenol (2–20 mcg/min by intravenous infusion, titrated to the desired heart rate), or an external transcutaneous cardiac pacemaker are often ineffective, and specific antidotal treatment may be necessary

  • For persistent bradycardia and hypotension, give glucagon, 5–10 mg intravenously, followed by infusion of 1–5 mg/h

  • High-dose insulin (0.5–1 unit/kg/h intravenously) along with glucose supplementation has also been used to reverse severe cardiotoxicity

  • Membrane-depressant effects (wide QRS interval) may respond to boluses of sodium bicarbonate (50–100 mEq intravenously) as for tricyclic antidepressant poisoning

  • Intravenous lipid emulsion (Intralipid 20%, 1.5 mL/kg) has been used successfully in severe propranolol overdose

  • Extracorporeal membrane oxygenation (ECMO) should be considered for refractory shock

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