A Case of Beta Blocker and Calcium Channel Blocker Overdose Requiring High Dose Insulin Therapy

Document Type

Conference Proceeding

Publication Date

5-2026

Publication Title

American Journal of Respiratory and Critical Care Medicine

Abstract

Beta Blockers and calcium channel blockers (CCB) are used to treat various conditions including cardiovascular diseases, hypertension, arrhythmias. Beta blockers produce their effects by binding to various beta receptors and inhibiting their effects. CCB exert effects by blocking the inward movement of calcium by binding to voltage-gated calcium channels in the heart, smooth muscle, and pancreas. Beta blocker and CCB overdose present with a constellation of symptoms including bradycardia, hypotension, altered mentation, respiratory compromise, and cardiogenic shock. Initial focus involves assessing airway, breathing, and circulation. Treatment options include intravenous fluids, atropine in non severe cases, glucagon due to its positive chronotropic and inotropic effects, calcium to promote calcium in flux, and vasopressors for refractory hypotension. If patients fail to respond to this therapy, high-dose insulin can be used by augmenting cardiac contractility. Other treatment options for refractory CCB overdose include methylene blue which acts as an adjunct to vasopressors and intravenous lipid emulsion which can sequester lipophilic drugs. We discuss a case of an 85 year old male with a past medical history of depression, hypertension, hyperlipidemia, chronic obstructive pulmonary disease, benign prostatic hyperplasia presenting with presumed CCB and beta blocker overdose. Initial vital signs included HR 36 bpm, BP 86/50, RR 16, Temperature 36 celsius, Spo2 100% . Labs demonstrated a creatinine of 1.86 and unremarkable complete blood count, hepatic function panel, lactic acid, troponins, creatine kinase. ECG showed sinus bradycardia with 1st degree AV Block and chest xray no acute process. The patient was given 1mg of Atropine x2, 2 liters of normal saline, 3 grams of calcium gluconate, started on IV normal saline 75 cc/hr, and Epinephrine 0.32 mcg/kg/min. Poison control was contacted and due to minimal improvement in vital signs, norepinephrine 0.01-0.5 mcg/kg/min was initiated, pushes of calcium gluconate and glucagon were attempted, and dopamine 2-20 mcg/kg/ min was started. Patient remained hypotensive and bradycardic and care was escalated to include glucagon 10mg/hr, high dose insulin 0.5-10 units/kg/hr, D10 uptitrated to D50 infusion, vasopressin 0.04 units/min, phenylephrine 0.1-3 mcg/kg/min, and methylene blue 84mg with a MAP goal of > 60. Vital signs began to improve and the patient was weaned off dopamine, phenylephrine, vasopressin, norepinephrine and remained on epinephrine, insulin drip, and D50 infusion. Family was present and goals of care were discussed.

Volume

212

Issue

S1

First Page

S3795

Last Page

S3795

DOI

10.1093/ajrccm/aamag162.5056

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