Beta-Blocker Toxicity

Beta-blocker toxicity is a life-threatening poisoning emergency characterized by the classic triad of bradycardia, hypotension, and hypoglycemia, resulting from direct antagonism of β-adrenergic receptors. Certain agents carry unique risks: propranolol (sodium channel blockade → seizures, wide QRS, ventricular dysrhythmias), sotalol (potassium channel blockade → QT prolongation, torsades de pointes), and labetalol/carvedilol (α₁-antagonism → vasodilatory shock). [1-3]

• Agent, dose, formulation (immediate-release vs. sustained-release — SR formulations can delay peak toxicity by several hours) [4]
• Time of ingestion — critical for decontamination decisions and anticipating clinical trajectory
• Intentional vs. accidental — suicidal intent, access to other medications
• Co-ingestants — calcium channel blockers, other antihypertensives, sedatives, alcohol significantly worsen outcomes [5]
• Symptoms: dizziness, lightheadedness, syncope, dyspnea, wheezing, altered mentation, seizures
• Progression: rapid deterioration possible, especially with propranolol or sotalol [1][3]

• Hemodynamic instability: SBP <90 mmHg, HR <50 bpm refractory to atropine
• Altered mental status / coma — suggests severe toxicity or CNS-penetrating agent (propranolol) [3][6]
• Seizures — hallmark of propranolol toxicity from sodium channel blockade [1]
• Wide QRS complex (>120 ms) — propranolol; signals impending ventricular dysrhythmia [3]
• QT prolongation — sotalol; risk of torsades de pointes [2]
• Cardiogenic shock / cardiac arrest — refractory to standard vasopressors [7]
• Bronchospasm — particularly in patients with reactive airway disease [8]
• Hypoglycemia — especially in children and diabetic patients [1]

Treatments (graduated approach per AHA 2025 Guidelines): [1-2]

Medications to avoid

• Intravenous lipid emulsion (ILE) — expert consensus advises against routine use; reports of abrupt cardiac arrest after administration in oral β-blocker overdose [1-2]
• Atropine in heart transplant patients — can cause paradoxical heart block or sinus arrest [9]

• NPO if hemodynamically unstable or airway compromise anticipated
• Dextrose supplementation is essential when using high-dose insulin therapy — D10W infusion to prevent hypoglycemia [1][9]
• No specific dietary triggers; not applicable in the acute setting

• Cardiovascular: chest pain, palpitations, syncope, presyncope
• Neurologic: altered mentation, seizures, drowsiness, coma
• Respiratory: dyspnea, wheezing, bronchospasm
• GI: nausea, vomiting
• Endocrine: symptoms of hypoglycemia (diaphoresis, tremor, confusion — may be masked by β-blockade)
• Psychiatric: suicidal ideation assessment if intentional ingestion

• Collateral from EMS, family, pharmacy: confirm agent, dose, timing, pill count, access to other medications
• Suicide note or prior attempts — psychiatric risk stratification
• Medication list — co-prescribed CCBs, digoxin, clonidine, or other AV-nodal blocking agents dramatically increase risk [5]
• Family history is generally not relevant in the acute toxicologic setting

• Intentional overdose — higher doses, co-ingestants, delayed presentation
• Sustained-release formulations — delayed and prolonged toxicity [4]
• Specific agents: propranolol and sotalol carry highest morbidity/mortality due to additional channel-blocking properties [1][3]
• Co-ingestion with CCBs, other antihypertensives, sedatives, or alcohol [5]
• Underlying cardiac disease — pre-existing conduction abnormalities, heart failure
• Renal impairment — impaired clearance of water-soluble agents (atenolol, sotalol, nadolol) [1]
• Pediatric patients — more susceptible to hypoglycemia, though severe toxicity from unintentional single-pill exposure in children <6 years is uncommon [1]

• Calcium channel blocker overdose — similar presentation (bradycardia + hypotension); CCB toxicity more often causes hyperglycemia (vs. hypoglycemia in BB toxicity); may have more prominent vasodilatory shock [2-3]
• Digoxin toxicity — bradycardia, AV block, but classically with hyperkalemia and characteristic dysrhythmias (bidirectional VT, regularized atrial fibrillation)
• Clonidine / central α₂-agonist overdose — bradycardia, hypotension, miosis, CNS depression
• Organophosphate poisoning — bradycardia with cholinergic toxidrome (SLUDGE/DUMBELS)
• Acute MI / cardiogenic shock — bradycardia and hypotension from non-toxicologic cause
• Hyperkalemia — bradycardia, conduction delays
• Hypothyroidism / myxedema coma — bradycardia, hypotension, altered mentation

Key distinguishing feature: Hypoglycemia in the setting of bradycardia + hypotension strongly favors β-blocker over CCB toxicity. [2-3]

• Prior overdose attempts or psychiatric history
• Baseline cardiac conduction disease (sick sinus syndrome, AV block)
• Heart failure — prone to significant hemodynamic instability [7]
• Reactive airway disease / COPD — increased bronchospasm risk
• Diabetes — baseline hypoglycemia risk, β-blockade masks tachycardic response
• Renal/hepatic impairment — affects drug clearance

• Vitals: Bradycardia (often <50 bpm), hypotension (SBP <90), may have hypothermia
• Cardiovascular: Diminished heart sounds, S3 gallop if CHF, JVD
• Neurologic: Altered mental status ranging from lethargy to coma; seizures (propranolol); miosis possible
• Respiratory: Wheezing/bronchospasm, respiratory depression in severe cases
• Skin: Cool, clammy, diaphoretic (though diaphoresis may be blunted)
• Capillary refill: Prolonged — indicator of poor perfusion
• Point-of-care glucose: Check immediately — hypoglycemia is common and treatable [2][8]

• Point-of-care glucose — hypoglycemia is common and must be treated immediately [2]
• BMP — electrolytes (K⁺, Ca²⁺, Mg²⁺), renal function, glucose
• Lactate — marker of end-organ hypoperfusion [3]
• VBG/ABG — assess for metabolic acidosis
• Troponin — evaluate for myocardial injury
• Acetaminophen, salicylate, ethanol levels — rule out co-ingestants [3]
• Digoxin level — if on digoxin or if digoxin toxicity is in the differential
• Serial glucose and potassium — mandatory during high-dose insulin therapy (q15–30 min initially) [1]
• Beta-blocker serum levels are generally not clinically useful and not widely available

• Chest X-ray — evaluate for pulmonary edema / cardiogenic shock
• Bedside echocardiography (POCUS) — assess LV function, guide inotropic therapy; can differentiate cardiogenic vs. vasodilatory shock [4]
• CT head — if altered mental status or seizures with unclear etiology
• Advanced imaging is generally unnecessary; diagnosis is clinical

• Bedside echocardiography — most valuable adjunct; guides hemodynamic management (cardiogenic vs. distributive shock) [4]
• Activated charcoal — consider if presentation within 1–2 hours of ingestion and airway is protected; whole-bowel irrigation may be considered for sustained-release formulations [4][9]
• Poison Control Center consultation — recommended for all significant ingestions
• Toxicology consultation — for refractory cases or unclear ingestions

ECG is essential and should be obtained immediately and repeated serially. [3][9]

• Sinus bradycardia — most common finding
• First-, second-, or third-degree AV block — from AV nodal suppression
• QRS widening (>120 ms) — propranolol (sodium channel blockade); treat with sodium bicarbonate [1][3]
• QT prolongation — sotalol (potassium channel blockade); risk of torsades de pointes [2][9]
• Junctional or idioventricular escape rhythms — in severe toxicity
• Ventricular tachycardia / ventricular fibrillation — terminal event

The following figure illustrates the progressive ECG changes seen with sodium channel blocker toxicity, relevant to propranolol overdose:

The ACC/AHA/HRS Acute Bradycardia Algorithm provides a structured approach to managing drug-induced bradycardia:

Beta-blocker toxicity is a clinical diagnosis based on history of exposure plus the characteristic findings of bradycardia, hypotension, and hypoglycemia. [2-3] Severity stratification:

• Mild: Asymptomatic bradycardia, normotensive, alert
• Moderate: Symptomatic bradycardia, mild hypotension responsive to fluids/atropine
• Severe/Life-threatening: Refractory hypotension, cardiogenic shock, seizures, cardiac arrest, AV block, wide QRS, QT prolongation [1]

Key pearl: Hypotension in β-blocker toxicity is often refractory to vasopressor therapy due to receptor blockade, necessitating non-adrenergic strategies (high-dose insulin, glucagon, ECMO). [2][7]

A 10-year German poison center analysis of 2,967 cases found that single-substance β-blocker exposures in adults had no fatalities; deaths occurred with co-ingestions (e.g., bisoprolol + verapamil). [5]

Initial Stabilization (first minutes)

• ABCs, continuous cardiac monitoring, 2 large-bore IVs
• Check point-of-care glucose immediately
• IV crystalloid bolus for hypotension
• Atropine 0.5–1 mg IV for symptomatic bradycardia (often insufficient) [9]

Escalation for hemodynamic instability

• Vasopressors (norepinephrine or epinephrine) — first-line for hypotension; readily available and fast-acting [1-2]
• High-dose insulin — 1 U/kg IV bolus → 1–10 U/kg/h infusion with D10W; AHA recommends early initiation for life-threatening toxicity; monitor glucose q15–30 min and K⁺ q1h [1-2]
• Glucagon — 2–10 mg IV bolus → 1–15 mg/h infusion; anticipate vomiting (protect airway); tachyphylaxis limits prolonged use [1][11]
• IV calcium — calcium chloride 2 g or calcium gluconate 6 g; infusion titrated to blood pressure [1]

Agent-specific interventions

• Propranolol (wide QRS): Sodium bicarbonate 1–2 mEq/kg IV bolus; target serum pH 7.45–7.55 [1]
• Sotalol (QT prolongation): IV magnesium; overdrive pacing for torsades; avoid further QT-prolonging agents [1][9]

Refractory shock

• VA-ECMO — initiate cannulation process early if not responding to maximal pharmacotherapy; may be lifesaving [1-2]
• Hemodialysis — consider for water-soluble agents (atenolol, sotalol, nadolol) with renal impairment [1]

GI decontamination

• Activated charcoal (1 g/kg, max 50 g) if within 1–2 hours of ingestion and airway protected [4][9]
• Whole-bowel irrigation (PEG solution) for sustained-release formulations [4]

• ICU admission: Any patient with hemodynamic instability, altered mental status, dysrhythmias, or requiring vasopressors/antidotes [3]
• Monitored bed / observation: Asymptomatic patients with immediate-release formulations should be observed for a minimum of 6 hours; sustained-release formulations require at least 12–24 hours of monitoring given delayed peak toxicity [4]
• Discharge: Only after prolonged observation with stable vitals, normal ECG, normal glucose, and no symptoms; psychiatric evaluation mandatory if intentional ingestion
• Consult triggers: Toxicology, cardiology (for refractory dysrhythmias or ECMO consideration), psychiatry (for intentional ingestions)

• Psychiatric follow-up is mandatory for all intentional ingestions prior to discharge
• Medication reconciliation — ensure safe prescribing, limit pill quantities, consider medication lock boxes
• Return immediately for: recurrent dizziness, lightheadedness, syncope, chest pain, palpitations, shortness of breath, confusion, or seizures
• Expected recovery: Most patients with isolated β-blocker overdose recover fully with supportive care; co-ingestions carry higher mortality risk [5]
• Primary care follow-up within 1–2 days for medication review and safety planning
• Poison Control (1-800-222-1222) — available 24/7 for ongoing guidance

1. Part 10: Adult and Pediatric Special Circumstances of Resuscitation: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. — Cao D, Arens AM, Chow SL, et al. Circulation. 2025.

2. 2023 American Heart Association Focused Update on the Management of Patients With Cardiac Arrest or Life-Threatening Toxicity Due to Poisoning: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. — Lavonas EJ, Akpunonu PD, Arens AM, et al. Circulation. 2023.

3. Pearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity. — Suarez F, Koyfman A, Long B. The Journal of Emergency Medicine. 2026.

4. Calcium Channel Antagonist and Beta-Blocker Overdose: Antidotes and Adjunct Therapies. — Graudins A, Lee HM, Druda D. British Journal of Clinical Pharmacology. 2016.

5. Clinical Toxicology of Beta-Blocker Overdose in Adults. — Lauterbach M. Basic & Clinical Pharmacology & Toxicology. 2019.

6. Effectiveness of Treatments for Propranolol Toxicity: A Systematic Review of Current Approaches and Evidence. — Hu Y, Mujahid K, Ahsan A, et al. European Journal of Clinical Pharmacology. 2026.

7. FDA Drug Label. — Updated date: 2023-03-31. Food and Drug Administration.

8. FDA Drug Label. — Updated date: 2025-04-17. Food and Drug Administration.

9. Drug-Induced Arrhythmias: A Scientific Statement From the American Heart Association. — Tisdale JE, Chung MK, Campbell KB, et al. Circulation. 2020.

10. Treatment for Beta-Blocker Poisoning: A Systematic Review. — Rotella JA, Greene SL, Koutsogiannis Z, et al. Clinical Toxicology. 2020.

11. 2018 ACC/­AHA/­HRS Guideline on The evaluation and Management Of patients With Bradycardia and Cardiac conduction Delay: A Report of the American College of Cardiology/­American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. — Writing Committee Members, Kusumoto FM, Schoenfeld MH, et al. Heart Rhythm. 2019.

12. The Electrocardiogram in the Poisoned Patient. — Steven H. Mitchell, Christopher P. Holstege, William J. Brady The Electrocardiagram in Emergency and Acute Care. 2023.

13. 2018 ACC/­AHA/­HRS Guideline on The Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: Executive Summary: A Report of the American College of Cardiology/­American Heart Association Task Force on Clinical Practice Guidelines, and the Heart Rhythm Society. — Kusumoto FM, Schoenfeld MH, Barrett C, et al. Journal of the American College of Cardiology. 2019.