Beta Blocker Overdose — Glucagon and High Dose Insulin

Key Points

• Beta-blocker overdose classically causes bradycardia, conduction block, myocardial depression, hypotension, and cardiogenic shock.
• Agent-specific properties matter: propranolol can cause seizures and sodium-channel blockade, while sotalol can cause marked QT prolongation and torsades.
• Vasopressors are recommended for life-threatening hypotension.
• Glucagon bolus followed by infusion is reasonable for symptomatic bradycardia or hypotension.
• High-dose insulin should be used for hypotension refractory to vasopressors.
• High-dose insulin requires frequent glucose and potassium monitoring and dextrose support.
• Hemodialysis can be considered for severe atenolol, nadolol, or sotalol poisoning.
• VA-ECMO is a rescue option for otherwise refractory cardiogenic shock.

Algorithm

1. Assess airway, breathing, circulation, neurologic status, and glucose; place the patient on continuous ECG monitoring.
2. Identify the beta blocker, formulation, amount, timing, renal function, and potential coingestants.
3. Obtain serial ECGs, glucose, electrolytes, renal function, lactate, and acid-base testing; use bedside echocardiography for significant shock.
4. Give cautious fluids when indicated and attempt atropine for symptomatic bradycardia while preparing definitive toxicologic therapy.
5. Start vasopressors promptly for persistent hypotension.
6. Give glucagon bolus followed by infusion for significant symptomatic bradycardia or hypotension when appropriate.
7. Initiate high-dose insulin with glucose and potassium surveillance when hypotension remains refractory to vasopressors.
8. Treat propranolol sodium-channel blockade with sodium bicarbonate and sotalol-associated torsades with magnesium and appropriate rhythm management.
9. Consider dialysis for severe atenolol, nadolol, or sotalol poisoning and VA-ECMO for refractory cardiogenic shock.
10. Admit significant symptomatic or extended-release poisoning to intensive monitored care.

Clinical Synopsis & Reasoning

Beta-blocker poisoning reduces sympathetic support of heart rate, atrioventricular conduction, contractility, and renin release. Severe cases present with sinus bradycardia, AV block, hypotension, cardiogenic shock, altered mental status, seizures, pulmonary edema, or cardiac arrest. The clinical phenotype varies considerably by agent. Propranolol is lipophilic and also blocks cardiac sodium channels in overdose, increasing seizure and wide-complex dysrhythmia risk. Sotalol blocks potassium channels and can markedly prolong the QT interval, producing torsades de pointes. Atenolol, nadolol, and sotalol have properties that make extracorporeal removal more feasible than highly lipophilic or protein-bound beta blockers.

Hypoglycemia can occur, particularly in children and in severe poisoning, while adults may have normal glucose. A careful history should establish the exact beta blocker, immediate versus extended-release preparation, dose, time, renal function, and coingestants. Calcium channel blockers, digoxin, clonidine, and sedatives can produce overlapping bradycardia and shock. Serial ECGs are essential because conduction and repolarization abnormalities can evolve.

Shock is usually cardiogenic but may have vasodilatory components, especially with carvedilol or labetalol because of alpha-1 antagonism. Bedside echocardiography can demonstrate impaired contractility and guide escalation. Management is time-sensitive because prolonged hypotension leads to acidosis and multiorgan injury, which further reduces responsiveness to therapy.

Treatment Strategy & Disposition

Stabilize the airway, oxygenation, ventilation, and circulation; establish IV or IO access; provide continuous ECG monitoring; and contact a poison center or medical toxicologist. Give cautious isotonic fluid if preload deficiency is plausible, but avoid excessive fluid in myocardial depression. Atropine can be attempted for symptomatic bradycardia but is frequently inadequate. Vasopressors should be started promptly for hypotension. Epinephrine is useful when both chronotropy and inotropy are needed, while norepinephrine can support vascular tone in mixed shock.

The 2025 AHA guideline states that a glucagon bolus followed by continuous infusion is reasonable for symptomatic bradycardia or hypotension in life-threatening beta-blocker poisoning. Glucagon increases intracellular cyclic AMP through a receptor pathway independent of beta receptors. Nausea and vomiting are common, so airway protection and antiemetic planning matter. Response can be incomplete or transient and should not delay other therapies.

High-dose insulin with euglycemia therapy should be administered for hypotension refractory to vasopressor therapy. High-dose insulin can improve myocardial inotropy and substrate utilization. Frequent glucose and potassium measurements are mandatory, with dextrose supplementation to maintain safe glucose. Hypokalemia during therapy generally reflects intracellular shift rather than total-body depletion, so replacement must be individualized. Intravenous calcium may be reasonable as an adjunct, especially when the ingestion may involve a CCB or when severe cardiotoxicity persists.

Agent-specific treatment matters. Propranolol-associated wide QRS or ventricular dysrhythmia from sodium-channel blockade can be treated with sodium bicarbonate. Sotalol-associated torsades requires magnesium, correction of electrolytes, and overdrive strategies as clinically appropriate. Hemodialysis may be reasonable in life-threatening poisoning from atenolol, nadolol, or sotalol. VA-ECMO should be considered for refractory cardiogenic shock despite maximal pharmacologic therapy. The benefit of intravenous lipid emulsion is uncertain and it should not be used routinely.

Epidemiology / Risk Factors

• Beta blockers are widely prescribed for cardiovascular disease, migraine, tremor, anxiety-related symptoms, and other indications.
• Severe toxicity is more likely after large intentional ingestion, sustained-release products, significant coingestion, or exposure to agents with membrane-stabilizing or potassium-channel effects.
• Young children may develop clinically important toxicity after relatively small exposures and require poison-center-directed risk assessment.
• Renal impairment increases concern for agents such as atenolol, nadolol, and sotalol.
• Coingestion with calcium channel blockers can produce especially severe bradycardic shock.

Investigations

Key Adjuncts

Pharmacology

Prognosis / Complications

• Most patients recover fully if perfusion is supported until the drug is cleared.
• Refractory shock, severe acidosis, cardiac arrest, and prolonged hypoperfusion are associated with worse outcomes.
• Extended-release preparations and long half-life agents can require prolonged ICU support.
• Propranolol-associated seizures and wide-complex dysrhythmia signal severe poisoning but are reversible with aggressive management.
• Mechanical circulatory support can bridge otherwise fatal cardiogenic shock to recovery in selected patients.

Patient Education / Counseling

• After intentional ingestion, ensure psychiatric assessment and a medication-safety plan before discharge.
• Explain that delayed deterioration can occur after sustained-release preparations even when early vital signs appear reassuring.
• Review all medications and supplements to identify interacting cardioactive drugs.
• Advise secure storage of cardiovascular medications, particularly in homes with children.
• Do not restart a beta blocker after a serious overdose without a coordinated treatment plan.
• Provide emergency and poison-center instructions for future ingestion concerns.

Notes

The most important distinction from CCB overdose is that glucagon has a clearer guideline-supported role in severe beta-blocker poisoning, while high-dose insulin remains essential when shock is refractory to vasopressors. Agent-specific electrophysiology also matters substantially, especially propranolol sodium-channel blockade and sotalol QT prolongation.

The 2025 AHA recommendations discourage a simplistic antidote sequence. Severe poisoning often requires vasopressors, glucagon, high-dose insulin, electrolyte correction, and escalation planning in parallel.

References

1. American Heart Association 2025 Guidelines: Life-Threatening Beta-Blocker Poisoning — Link