Glucagon Therapy for β-Blocker Overdose

Abstract

Two cases of severe β-blocker overdose are presented that were treated successfully with glucagon therapy. The effects of glucagon in reversing the cardiovascular depression of profound β-blockade, including its mechanism of action, onset and duration of action, dosage and administration, cost and availability, and side effects are reviewed. Medical complications of β-blocker overdose include hypotension, bradycardia, heart failure, impaired atrioventricular conduction, bronchospasm and, occasionally, seizures. Atropine and isoproterenol have been inconsistent in reversing the bradycardia and hypotension of β-blocker overdose. Glucagon increases heart rate and myocardial contractility, and improves atrioventricular conduction. These effects are unchanged by the presence of β-receptor blocking drugs. This suggests that glucagon's mechanism of action may bypass the β-adrenergic receptor site. Because it may bypass the β-receptor site, glucagon can be considered as an alternative therapy for profound β-blocker intoxications. The doses of glucagon required to reverse severe β-blockade are 50 μg/kg iv loading dose, followed by a continuous infusion of 1–15 mg/h, titrated to patient response. Glucagon-treated patients should be monitored for side effects of nausea, vomiting, hypokalemia, and hyperglycemia. The high cost and limited availability of glucagon may be the only factors precluding its future clinical acceptance.