Overview
Beta-Blocker Overdose
Topic Overview
Summary
Beta-blocker overdose causes bradycardia, hypotension, and cardiogenic shock through blockade of cardiac β1-receptors. Lipophilic agents (propranolol) also cause CNS effects (seizures, coma) and sodium channel blockade (QRS widening). Treatment is supportive with atropine, high-dose glucagon (first-line specific antidote), IV fluids, vasopressors, and in severe cases, high-dose insulin euglycaemic therapy (HIET) or lipid emulsion. Pacing may be required.
Key Facts
- Mechanism: β1-receptor blockade → ↓heart rate, ↓contractility, ↓conduction
- Features: Bradycardia, hypotension, cardiogenic shock
- Propranolol: Also causes seizures, QRS widening (sodium channel blockade)
- First-line: Glucagon (bypasses β-receptor via cAMP)
- Refractory: High-dose insulin, lipid emulsion, extracorporeal support
Clinical Pearls
Glucagon works by bypassing the β-receptor — directly increases cAMP
Propranolol is most dangerous — lipophilic, membrane stabilising, causes seizures
Check glucose — β-blockers mask hypoglycaemia symptoms
Why This Matters Clinically
Beta-blocker overdose can cause refractory cardiogenic shock. Standard resuscitation may fail; specific therapies (glucagon, HIET) are life-saving.
Visual Summary
Visual assets to be added:
- Beta-blocker mechanism of action
- ECG changes in BB overdose
- Glucagon mechanism
- BB overdose management algorithm
Epidemiology
Incidence
- Common medication; increasing use
- Overdose accounts for significant ED presentations
- Mortality 2-5% in severe cases
Demographics
- Adults on beta-blockers (accidental or intentional)
- Elderly at higher risk of complications
Common Agents
| Agent | Properties |
|---|---|
| Propranolol | Non-selective; lipophilic; membrane stabilising — most dangerous |
| Atenolol | β1-selective; hydrophilic |
| Metoprolol | β1-selective; lipophilic |
| Bisoprolol | β1-selective |
| Sotalol | Non-selective + class III antiarrhythmic (QT prolongation) |
| Carvedilol | Non-selective + α-blockade |
Pathophysiology
Mechanism
- β1-receptor blockade in heart
- ↓Heart rate (negative chronotropy)
- ↓Contractility (negative inotropy)
- ↓AV conduction (negative dromotropy)
- → Bradycardia, hypotension, cardiogenic shock
Additional Effects
| Effect | Agents |
|---|---|
| CNS depression, seizures | Lipophilic (propranolol, metoprolol) |
| Sodium channel blockade | Propranolol (QRS widening) |
| QT prolongation | Sotalol |
| Hypoglycaemia | Masked symptoms; impaired gluconeogenesis |
| Bronchospasm | Non-selective agents in asthmatics |
Why Glucagon Works
- Activates adenylyl cyclase independently of β-receptor
- Increases intracellular cAMP
- Improves heart rate and contractility
Clinical Presentation
Symptoms
Signs
Timing
Red Flags
| Finding | Significance |
|---|---|
| HR under 40 | Severe toxicity |
| Hypotension unresponsive to fluids | Cardiogenic shock |
| Wide QRS | Propranolol — sodium channel blockade |
| Seizures | Propranolol — severe |
| QT prolongation | Sotalol — torsades risk |
Dizziness
Common presentation.
Weakness
Common presentation.
Confusion
Common presentation.
Syncope
Common presentation.
Seizures (propranolol)
Common presentation.
Clinical Examination
Vital Signs
- Bradycardia (often severe)
- Hypotension
- Reduced respiratory rate
Cardiovascular
- Weak pulse
- Hypoperfusion signs
- Pulmonary oedema
Neurological
- Reduced GCS
- Seizures
Investigations
Blood Tests
| Test | Finding |
|---|---|
| Glucose | May be low (or masked hypoglycaemia) |
| Potassium | May be elevated (reduced cellular uptake) |
| Lactate | Elevated in shock |
| U&E | Baseline |
ECG
| Finding | Agent |
|---|---|
| Bradycardia | All |
| AV block | All |
| Wide QRS | Propranolol |
| Prolonged QT | Sotalol |
Other
- Paracetamol, salicylate levels (co-ingestion)
- Echo if cardiogenic shock
Classification & Staging
By Severity
| Severity | Features |
|---|---|
| Mild | Bradycardia, minor hypotension |
| Moderate | Symptomatic bradycardia, significant hypotension |
| Severe | Cardiogenic shock, seizures, cardiac arrest |
By Agent
- Hydrophilic (atenolol) — mainly cardiovascular
- Lipophilic (propranolol) — cardiovascular + CNS
Management
Initial Resuscitation
| Action | Details |
|---|---|
| Airway | Protect if reduced GCS |
| Oxygen | |
| IV access | Large bore |
| Monitor | Continuous ECG, BP |
| Check glucose | Treat hypoglycaemia |
Decontamination
- Activated charcoal: Consider if within 1 hour
Specific Antidotes
Atropine:
- 0.5-1 mg IV boluses
- Often ineffective in severe toxicity
Glucagon (First-Line Specific Therapy):
- 5-10 mg IV bolus
- Infusion 2-5 mg/hr if response
- Often causes vomiting — protect airway
High-Dose Insulin Euglycaemic Therapy (HIET):
- 1 unit/kg bolus
- Infusion 0.5-1 unit/kg/hr
- Maintain glucose over 8
- Potassium monitoring essential
Sodium Bicarbonate:
- For QRS widening (propranolol)
- 50-100 mmol IV boluses
- Target narrow QRS
IV Lipid Emulsion (Intralipid):
- For lipophilic agents (propranolol)
- 1.5 mL/kg 20% lipid IV bolus
- Infusion 0.25 mL/kg/min
Vasopressors
- Noradrenaline, adrenaline if needed
- May require high doses
Pacing
- Temporary pacing if refractory bradycardia
Extracorporeal Support
- ECMO/VA-ECMO for refractory cardiogenic shock
- Consider early in severe cases
Complications
Cardiac
- Cardiogenic shock
- Asystole
- Death
Metabolic
- Hypoglycaemia
- Hyperkalaemia
Neurological
- Seizures (propranolol)
- Hypoxic brain injury
Prognosis & Outcomes
Prognosis
- Good if treated early and aggressively
- Mortality 2-5% in severe cases
- Higher with propranolol
Factors Affecting Outcome
- Agent ingested
- Time to treatment
- Access to advanced therapies (ECMO)
Evidence & Guidelines
Key Guidelines
- TOXBASE (UK National Poisons Information Service)
- AACT/EAPCCT Position Statement on Beta-Blocker Poisoning
Key Evidence
- Glucagon is effective but limited supply
- HIET is increasingly used for refractory shock
- Lipid emulsion for lipophilic agents
Patient & Family Information
What is Beta-Blocker Overdose?
Beta-blockers are heart medication. Taking too many can dangerously slow the heart and lower blood pressure.
Symptoms
- Feeling faint or dizzy
- Very slow heartbeat
- Confusion
- Collapse
Treatment
- Medication to speed up the heart (glucagon, other drugs)
- Fluids and sometimes a pacemaker
- Intensive care monitoring
Resources
References
Key Reviews
- Graudins A, et al. Treatment of beta-blocker and calcium channel blocker overdose. Br J Clin Pharmacol. 2016;81(3):453-461. PMID: 26551696
- Shepherd G, Klein-Schwartz W. High-dose insulin therapy for calcium-channel blocker and beta-blocker overdose. Pharmacotherapy. 2014;34(7):748-763. PMID: 24643836
Guidelines
- TOXBASE. Beta-Blocker Poisoning Management. 2023.