What is the management of beta blocker toxicity?

Management of Beta Blocker Toxicity

High-dose insulin therapy should be administered for hypotension due to beta-blocker poisoning refractory to or in conjunction with vasopressor therapy. 1

Clinical Manifestations

• Beta blocker toxicity primarily causes hypotension due to bradycardia and reduced cardiac contractility 2
• Some beta blockers can cause additional arrhythmias through sodium or potassium channel blockade 2
• Hypotension may be cardiogénica, vasodilatory, or multifactorial in nature 2
• Hypoglycemia may be present in some cases 2

Treatment Algorithm

First-Line Interventions

• Vasopressors: Recommended for hypotension due to beta-blocker poisoning (Class 1, Level C-LD) 1, 2

  • Readily available and act quickly as initial therapy for beta-blocker induced hypotension 1
  • Choose epinephrine or norepinephrine as first-line agents 3, 4

• High-dose insulin therapy: Recommended for hypotension refractory to or in conjunction with vasopressor therapy (Class 1, Level B-NR) 1, 2

  • Improves inotropy in cardiogenic shock from beta-blocker poisoning 1
  • Associated with lower rates of vasoconstrictive complications than vasopressor-only therapy 1
  • Typical dosing: 1 U/kg bolus followed by 1 U/kg/hour infusion, titrated to clinical effect 2
  • Requires co-administration of dextrose and potassium infusions 2
  • Monitor for hypoglycemia and hypokalemia as common adverse effects 3

Second-Line Interventions

• Glucagon: Reasonable to use a bolus followed by continuous infusion for bradycardia or hypotension (Class 2a, Level C-LD) 1, 2

  • Increases contractility and improves hemodynamics 1, 2
  • Caution: May cause transient increase in pulse and blood pressure in patients taking beta-blockers 5
  • May lose efficacy or produce hypoglycemia in patients taking indomethacin 5

• Atropine: May be reasonable for beta-blocker-induced bradycardia (Class 2b, Level C-LD) 1, 2

  • Limited evidence supports its use in beta-blocker toxicity 6

• Electrical pacing: May be reasonable for beta-blocker-induced bradycardia (Class 2b, Level C-LD) 1, 2

  • Consider for refractory bradycardia, particularly with sotalol toxicity 3, 7

Advanced Interventions

• Extracorporeal life support (VA-ECMO): Reasonable for life-threatening beta-blocker poisoning with cardiogenic shock refractory to pharmacological interventions (Class 2a, Level C-LD) 1, 2

  • May be life-saving for patients with persistent cardiogenic shock refractory to maximal supportive care 1
  • Consider early in severe cases unresponsive to other therapies 3

• Hemodialysis: May be reasonable for life-threatening atenolol or sotalol poisoning (Class 2b, Level C-LD) 1, 2

  • Most effective for water-soluble beta-blockers like atenolol 3

Interventions Not Recommended

• Intravenous lipid emulsion therapy: Not likely to be beneficial for life-threatening beta-blocker poisoning (Class 3: No Benefit, Level C-LD) 1, 2
  • Evidence shows variable response to this therapy 3

Special Considerations

• Supplemental dextrose should be administered to treat associated hypoglycemia 2
• Beta-blocker toxicity is often refractory to conventional vasopressor therapy 2, 4
• ECG monitoring is essential as electrocardiographic signs usually appear before clinical signs 8
• QRS enlargement is a predictor of severe ventricular arrhythmia 8
• Continuous multiparametric monitoring in an intensive care unit setting is required 8, 9

Monitoring Parameters

• Continuous cardiac monitoring for bradycardia and conduction abnormalities 6, 9
• Regular blood pressure measurements 9
• Blood glucose monitoring, especially when using high-dose insulin therapy 2, 3
• Serum potassium levels during insulin therapy 2, 3
• Acid-base status and oxygenation 8

By following this evidence-based approach to beta-blocker toxicity management, clinicians can optimize outcomes in these potentially life-threatening cases.