Beta Blocker Overdose
“Propranonlol is a sodium channel blocker masked as a beta blocker”
Beta Blocker Overdose: Understanding the Physiology and Management
Pharmacodynamics / Kinetics: How Beta Blockers Work Normally
To understand the effects of beta blocker overdose, we first need to revisit how these drugs function under normal circumstances. The sympathetic nervous system—our fight-or-flight mechanism—primes the body for action. It increases blood flow to vital organs, dilates airways and pupils, and enhances energy release.
This system is activated when the hypothalamus detects a stressor and signals through the splanchnic nerves to the adrenal glands. These glands secrete adrenaline and noradrenaline directly into the bloodstream, binding to adrenergic receptors on target organs.
α1 receptors cause vasoconstriction and glycogenolysis.
α2 receptors regulate norepinephrine release.
β1 receptors increase heart rate, contractility, and renin release—driving the renin-angiotensin-aldosterone system (RAAS).
β2 receptors promote bronchodilation and vasodilation to skeletal muscle.
β3 receptors stimulate lipolysis in adipose tissue.
For the purposes of beta blocker toxicity, it’s the β-receptors that are most relevant, as these are the sites of action being blocked.
What Happens in a Beta Blocker Overdose?
In overdose, beta blockers competitively inhibit β1 and β2 receptors, suppressing cyclic adenosine monophosphate (cAMP) production and blunting catecholamine effects. While therapeutic blockade reduces myocardial stress in heart failure, overdose causes bradycardia, hypotension, and cardiogenic shock.
Lipophilic agents such as propranolol can cross the blood-brain barrier, leading to central nervous system effects including hypoglycaemia, seizures, and reduced consciousness. Co-ingestion with calcium channel blockers significantly worsens cardiovascular collapse, while bronchospasm may complicate management in asthmatics [1][2][3].
History and Clinical Features
History-taking should identify the specific beta blocker ingested, as agents vary in toxicity. For example, sotalol has class III antiarrhythmic properties and can prolong the QT interval, predisposing to torsades de pointes for up to 48 hours post-ingestion [4][5].
Key assessment steps include:
Airway: secure if consciousness is impaired; consider activated charcoal within 1 hour of ingestion.
Breathing: manage bronchospasm with bronchodilators, though salbutamol may be less effective.
Circulation: treat hypotension with fluids; bradycardia with atropine and, if unresponsive, adrenaline under updated JRCALC guidance.
Disability: manage hypoglycaemia and seizures with benzodiazepines.
Advanced options may include pacing (with limited evidence), VA-ECMO, or experimental interventions such as REBOA for medical cardiac arrest.
Sodium Channel Blockade
Propranolol is unique in having sodium channel blocking properties in addition to beta blockade. This can progress from bradycardia and AV block to QRS widening, QT prolongation, and eventual cardiovascular collapse. Sodium bicarbonate is indicated in cases of cardiac arrest, QRS prolongation, or ventricular arrhythmias [6].
Management Strategies
Managing beta blocker overdose is challenging because of the combined cardiovascular, metabolic, and neurological effects. The approach requires structured resuscitation, thoughtful use of antidotes, and readiness to escalate to advanced therapies.
🔹 Initial Priorities: A–E Approach
Airway: If the patient has a reduced conscious level, secure the airway early to prevent aspiration. Activated charcoal can be considered within one hour of ingestion, provided the airway is protected.
Breathing: Bronchospasm may occur due to β2 receptor blockade. Treat with nebulised salbutamol and ipratropium, though effectiveness may be reduced. Add corticosteroids as supportive therapy.
Circulation: Hypotension and bradycardia are the hallmark features. Start with IV fluids to increase preload via the Frank-Starling mechanism. If bradycardia persists, give atropine (500 mcg IV, repeatable). For atropine-resistant cases, follow updated JRCALC guidance—adrenaline 50 mcg IV boluses every 3–5 minutes, titrated with no maximum dose.
🔹 Adrenaline Infusion
For refractory hypotension or bradycardia, adrenaline infusions are effective but often require very high doses. Titrate carefully, and consider a syringe driver for controlled delivery. Be mindful that the β-blockade reduces receptor availability, meaning higher doses than usual may be necessary.
🔹 Glucagon
Glucagon bypasses β-receptor blockade by directly stimulating adenylate cyclase, increasing intracellular calcium. This can restore contractility and improve cardiac output.
Dose: 5–10 mg IV bolus over 1–2 minutes, followed by infusion if beneficial.
Challenges: Supply is often limited (e.g., HART teams may carry only small amounts), and high doses are required for effect. It also frequently induces vomiting, which complicates care in patients with unprotected airways.
🔹 High-Dose Insulin Euglycaemic Therapy (HIET)
Insulin has potent inotropic effects independent of β-receptors, enhancing myocardial carbohydrate metabolism and calcium influx. In severe overdose with shock, HIET is increasingly recognised as a key therapy.
Administer insulin infusion with concurrent dextrose to maintain normal glucose levels.
HIET is particularly beneficial in patients with acidosis or those unresponsive to catecholamines.
Preparation and administration are logistically challenging, so early communication with ED and critical care teams is vital.
🔹 Sodium Bicarbonate
For QRS widening, arrhythmias, or cardiac arrest due to sodium channel blockade (notably with propranolol), give 100 mL of 8.4% sodium bicarbonate IV as a rapid bolus. Repeat as needed if QRS remains prolonged or arrhythmias persist, aiming for a pH < 7.5. In cases of torsades de pointes, magnesium sulfate should be added alongside bicarbonate.
🔹 Calcium Salts
Although evidence is limited, calcium gluconate may help counteract hypotension, particularly when propranolol-induced calcium channel blockade is suspected. Caution is needed, as it cannot be administered through the same line as sodium bicarbonate due to precipitation risk.
🔹 Advanced Therapies
Transcutaneous pacing: Generally of limited effectiveness, but may be attempted if pharmacological measures fail. Capture thresholds may be higher in acidotic patients.
VA-ECMO: An option in refractory cardiogenic shock or cardiac arrest, depending on local availability.
REBOA: Emerging research suggests potential benefit in medical cardiac arrest to improve coronary perfusion, though this remains experimental.
🔹 Seizure and Hypoglycaemia Management
Seizures should be treated with IV benzodiazepines as per standard protocols.
Hypoglycaemia is a common complication due to impaired gluconeogenesis; monitor closely and correct with IV glucose.
🔹 Resuscitation in Cardiac Arrest
In the event of arrest, standard ALS applies, but with persistence. Beta blocker overdoses can have surprisingly good outcomes after prolonged resuscitation if interventions such as sodium bicarbonate or HIET are introduced. Resuscitation should be prolonged unless futility is established with senior clinical input.
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References:
Beta-blocker toxicity – LITFL Life in the Fast Lane • LITFL
Beta-blocker overdose – NCBI Bookshelf NCBI
Beta blocker toxicity – Medscape EM Sim Cases
TOXBASE: Propranolol Life in the Fast Lane • LITFL
Beta blocker overdose – EM3 EM Sim Cases
Sodium bicarbonate in toxicology – PMC NCBI+1
DrugBank: Amiodarone Life in the Fast Lane • LITFL
High-dose insulin therapy – Utah Poison Control Life in the Fast Lane • LITFL
Glucagon as an antidote – LITFL Life in the Fast Lane • LITFL
Low and slow poisoning – Emergency Medicine Cases EM Sim Cases
JRCALC Algorithm G0200-72 Life in the Fast Lane • LITFL
TOXBASE: Metoprolol NCBI
(Duplicate) TOXBASE: Propranolol — this is already in item 4 above.
TOXBASE: High-Dose Insulin Euglycaemic Therapy – Adults Only NCBI
“PMC9536162” article NCBI