What are the treatment options for beta blocker toxicity?

Treatment of Beta-Blocker Toxicity

Immediate First-Line Pharmacologic Management

For hypotension due to beta-blocker poisoning, initiate vasopressors immediately and add high-dose insulin euglycemic therapy early, either in conjunction with or for cases refractory to vasopressor support. 1

High-Dose Insulin Euglycemic Therapy (Class 1 Recommendation)

• Administer a bolus of 1 U/kg regular insulin IV, followed by continuous infusion of 1 U/kg/hour, titrated to clinical effect up to 10 U/kg/hour in refractory cases. 1, 2
• High-dose insulin improves cardiac contractility in cardiogenic shock from beta-blocker poisoning and is associated with lower rates of vasoconstrictive complications compared to vasopressor-only therapy. 1
• Co-administer dextrose infusions to maintain euglycemia (typically requiring large volumes). 1, 2
• Monitor and supplement potassium closely, as insulin drives potassium intracellularly and supplementation is typically required. 2
• This therapy should be initiated early in life-threatening cases, not reserved as a last resort. 2

Vasopressor Therapy (Class 1 Recommendation)

• Vasopressors are recommended for hypotension and should be initiated promptly as they are readily available and act quickly. 1
• Choose catecholamines (epinephrine or isoproterenol) as first-line agents based on the type of hemodynamic compromise present. 3
• Multiple vasopressors were associated with mortality benefit in systematic reviews, though often used in combination with other therapies. 3

Second-Line Pharmacologic Interventions

Glucagon (Class 2a Recommendation)

• It is reasonable to use a bolus of glucagon followed by continuous infusion for bradycardia or hypotension. 1
• Glucagon increases contractility and improves hemodynamics through positive inotropic effects independent of beta-receptors. 1, 4
• This is particularly useful when glucagon is available, though evidence shows variable response in case series. 3

Atropine (Class 2b Recommendation)

• It may be reasonable to administer atropine for beta-blocker-induced bradycardia, though evidence shows variable response. 1, 2
• Multiple intravenous boluses were associated with improvement in heart rate and blood pressure in case reports. 3

Electrical Pacing (Class 2b Recommendation)

• It may be reasonable to attempt temporary cardiac pacing for beta-blocker-induced bradycardia refractory to pharmacologic therapy. 1, 2
• Temporary overdrive pacing has particular utility in sotalol toxicity to prevent arrhythmias. 3

Advanced Life Support Measures

VA-ECMO (Class 2a Recommendation)

• It is reasonable to utilize veno-arterial extracorporeal membrane oxygenation for life-threatening beta-blocker poisoning with cardiogenic shock refractory to maximal pharmacological interventions. 1, 2
• VA-ECMO was associated with improved survival in patients with persistent cardiogenic shock in observational studies and case series. 1, 3
• This should be considered early in refractory cases rather than as a terminal intervention. 2

Hemodialysis (Class 2b Recommendation)

• It may be reasonable to use hemodialysis for life-threatening atenolol or sotalol poisoning specifically. 1, 2
• Atenolol has low protein binding (0-5%) and small volume of distribution (1.0-1.2 L/kg), making it amenable to extracorporeal removal. 2
• Evidence suggests hemodialysis may improve elimination in massive overdoses of water-soluble beta-blockers, though survival benefit is not definitively established. 3

Supportive Care and Monitoring

Initial Assessment

• Cardiovascular symptoms typically appear within 2 hours of ingestion for immediate-release formulations, 8 hours for sustained-release, and 12 hours for sotalol. 2
• Contact poison control or medical toxicology immediately, as these cases require treatments most clinicians use infrequently. 2
• Place patients in intensive care with continuous multiparametric monitoring. 4

Metabolic Management

• Treat hypoglycemia with supplemental dextrose as part of standard care. 1
• Monitor for lactic acidosis, variable serum potassium, and hypoxia-hypercapnia from hypoventilation. 4
• Obtain early ECG, as electrocardiographic signs usually appear before clinical signs; QRS enlargement predicts severe ventricular arrhythmia. 4

Critical Pitfalls to Avoid

• Do not wait for laboratory confirmation of beta-blocker levels, as assays are rarely available and correlate poorly with symptoms (except sotalol). 2
• Intravenous lipid emulsion therapy is NOT recommended for life-threatening beta-blocker poisoning (Class 3: No Benefit). 1
• Fatalities are more likely with co-ingestion of other cardioactive drugs such as calcium channel blockers; carefully assess for co-exposures. 2, 5
• Receptor selectivity is lost in overdose, leading to overlapping manifestations among different beta-blockers. 2
• Highly lipophilic agents like propranolol can cause CNS effects including delirium, coma, and seizures. 2
• Sotalol uniquely causes QT prolongation and torsade de pointes due to potassium channel blocking properties. 2

Graduated Treatment Algorithm

Begin with intravenous fluids and vasopressors for hemodynamic instability, add high-dose insulin euglycemic therapy early (not as rescue therapy), consider glucagon as adjunctive therapy, and escalate to VA-ECMO for cases unresponsive to pharmacologic interventions. 3