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J07: Beta Blockers

Mike Sugimoto

Updated:

Reviewed:

Introduction

Beta blockers are widely used in the management of an extensive range of clinical problems, including hypertension, heart failure, migraine headaches, tremor, and aortic dissection. Although overdoses of these medications, either accidental or otherwise, occur infrequently, beta blocker toxicity associated with significant morbidity and mortality. The primary mechanism for beta blocker toxicity is through the adrenergic blocking action of these medications. Some beta blockers, such as sotalol, propranolol, and acebutalol, have significant pro-arrhythmic tendencies.

Essentials

As with all poisoning or overdoses, manage the airway and ensure adequate oxygenation and ventilation while a more comprehensive history is obtained
Search for and treat reversible causes: do not overlook other causes of the patient’s symptoms
Prehospital management of beta blocker overdose is limited, and specific therapies should only be undertaken in consultation with CliniCall. Rapid transport is indicated for virtually all patients.

General Information

Consider the possibility of co-ingestion of other drugs in patients who are suspected of beta blocker toxicity, particularly calcium channel blockers, digoxin, clonidine, and cholinergic agents.
Beta blocker toxicity is generally more severe in individuals with a pre-existing cardiovascular history.
Patients who have overdosed on beta blocking drugs typically become symptomatic within two hours, with virtually all becoming symptomatic within six hours.
The most common symptoms are bradycardia and hypotension. Myocardial depression and cardiogenic shock can develop in severe cases. Ventricular dysrhythmias are more common with propranolol and sotalol. Mental status changes, such as confusion, delirium, seizures, and unconsciousness, can occur at virtually any point.
Respiratory depression has been reported. Bronchospasm and hypoglycemia, produced by the beta blockade, can complicate management.
Possible electrocardiogram changes include PR elongation, QRS prolongation, and any bradydysrhythmia.

Interventions

First Responder (FR) Interventions

Protect the airway and ensure adequate oxygenation and ventilation
- → B01: Airway Management
Provide supplemental oxygen as required
- → A07: Oxygen and Medication Administration

Emergency Medical Responder (EMR) & All License Levels Interventions

Provide supplemental oxygen to maintain SpO₂ ≥ 94%
- → A07: Oxygen and Medication Administration
Measure capillary blood glucose levels
Initiate transport and consider ACP intercept

Primary Care Paramedic (PCP) Interventions

Consider vascular access and fluid bolus. Target systolic blood pressure of 90 mmHg or better. Do not give more that 2 L of fluid.
- → D03: Vascular Access

Correct hypoglycemia if present:
- → E01: Hypoglycemia and Hyperglycemia

Advanced Care Paramedic (ACP) Interventions

Obtain and interpret 12-lead ECG
- → PR16: 12 Lead ECG

Treat bradycardia:
- → C02: Bradycardia
- Atropine. Note that atropine may not reverse bradycardia, or offer only partial recovery
- Transcutaneous pacing may be required, and may be ineffective

Manage seizures:
- MIDAZOLam
- See CPG F02: Seizures for additional details.
If airway management is required, aggressively attempt to limit peri-procedural hypotension.
→ PR18: Anesthesia Induction
→ PR23: Awake Intubation

Consultation with CliniCall (1-833-829-4099) is mandatory for any of the following therapies:

Consider glucagon: 5 mg slow IV push if available.
Correct ventricular arrhythmias:
- Consider calcium chloride.
- Consider sodium bicarbonate in wide complex dysrhythmias.
- Consider magnesium sulfate (particularly in cases of sotalol-induced ventricular dysrhythmia)
- Consider EPINEPHrine infusion, escalating in consultation with CliniCall. Note that higher dose rates may be required to overcome competitive inhibition.

Evidence Based Practice

Overdose-Poisoning

References

Barrueto F. Beta blocker poisoning. In UptoDate. 2020. [Link]