Management of cardiovascular instability resulting from calcium channel antagonist (CCB) or beta-adrenergic receptor antagonist (BB) poisoning follows similar principles. We report an overdose involving nebivolol in a polydrug ingestion resulting in cardiac arrest, successfully treated with IFE and a very HDI infusion. This would be congruent with the lipid sink theory of IFE mechanism. We hypothesize that after the administration of IFE the epinephrine was able to exert its effect on receptors previously occupied with the nebivolol. He was discharged with baseline neurologic function. With subsequent hypotension, vasopressors were withheld in favor of HDI and supportive care. His care included IFE infusion along with HDI bolus and infusion with doses as high as 21.8 units/kg/h. Spontaneous circulation returned 30 s after a 100 mL bolus of 20% IFE, and the patient then became briefly hypertensive and tachycardic with heart rate and blood pressure measured as high as 123/min and 251/162 mmHg, respectively. Standard resuscitation including epinephrine had no effect. Over the subsequent 4 h, he became bradycardic and hypotensive and developed bradyasystolic cardiac arrest. The initial ECG showed sinus rhythm with a QTc of 483 ms and a QRS of 112 ms. He had a heart rate of 71/min and a blood pressure of 98/61 mmHg. We report a nebivolol-induced cardiac arrest in the setting of a polydrug ingestion, successfully resuscitated with intravenous fat emulsion (IFE) and high-dose insulin (HDI).Ī 48-year-old man was brought to the emergency department after ingesting nebivolol and ethanol, along with possibly diazepam and cocaine. Nebivolol, a beta blocker with 3-10 times more beta1 cardioselectivity than metoprolol, has caused hypotension and bradycardia in overdose.
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