Successful Treatment of Metoprolol-Induced Cardiac Arrest With High-Dose Insulin, Lipid Emulsion, and ECMO

beta-Adrenergic antagonist toxicity causes cardiovascular collapse often refractory to standard therapy. Alternative therapies include high-dose insulin, lipid emulsion, and venoarterial extracorporeal membrane oxygenation (VA-ECMO). A 47-year-old man ingested 10 g of metoprolol tartrate in a suicide attempt. Upon emergency department presentation, he was comatose, bradycardic, and hypotensive. Glucagon (14 mg IV) and vasopressor/inotropic support (epinephrine 0.1 mu g/[kg min], dobutamine 10 mu g/[kg min]) were administered. Despite these therapies, he developed cardiac arrest for 55 minutes, requiring epinephrine (5 mg IV) and vasopressin (40 U IV) with multiple episodes of return of spontaneous circulation. Additional vasopressor administration (vasopressin 0.04 U/min, norepinephrine 0.5 mu g/[kg min]) did not improve his hemodynamics. High-dose insulin (250 U IV) and 20% lipid emulsion (100 mL bolus with 200 mL/30 min infusion) were administered, and VA-ECMO was initiated with hemodynamic improvement. His postarrest neurologic examination demonstrated lack of brainstem reflexes and cortical motor response. He awoke 11.5 hours after time of ingestion. Venoarterial extracorporeal membrane oxygenation was discontinued at hospital day 3, and the patient was discharged on hospital day 10 with excellent neurologic recovery. A serum metoprolol level measured 25,000 ng/mL (therapeutic 20-340 ng/mL). High-dose insulin has been shown to be beneficial in beta-adrenergic antagonist cardiotoxicity. Lipid emulsion is thought to act as a lipid extractor, lowering serum and tissue levels. Venoarterial extracorporeal membrane oxygenation was used with the above therapies, restoring organ perfusion and allowing intrinsic drug metabolism and elimination. High-dose insulin, lipid emulsion, and VA-ECMO should be considered for refractory cardiac arrest secondary to beta-adrenergic antagonist toxicity such as metoprolol.