Beta-Blocker Overdose

Updated 2nd July 2024


  • Most ingestions are benign, exceptions include:
    • overdoses in the elderly and those with decreased cardio-respiratory reserve
    • co-ingestions of other cardiovascularly active agents (especially negative inotropes)
    • severe beta blocker overdoses
  • Two beta-blockers require special consideration:
    • propanolol causes sodium channel blockade
    • sotalol causes potassium efflux blockade


  • competitive antagonism of beta-1 and beta-2 receptors (selectivity may vary with type of beta blocker and dose)
    • decreased production of intracellular cyclic adenosine monophosphate (cAMP)
    • impairs the many metabolic and cardiovascular effects of circulating catecholamines.
    • used in therapeutic doses to decrease heart rate and blood pressure.
    • in overdose causes increasing severe negative effects on chrontropy, dromotropy, and inotropy leading to cardiac failure and cardiogenic shock.
    • Utilising glucose instead of fatty acids which produce less ATP, may exacerbate the cardiac effects.
  • Propranolol also causes sodium channel blockade, widening the QRS and promoting ventricular dysrhythmias and enters the CNS to exert direct toxicity.
  • Sotalol also blocks cardiac potassium efflux channels causing QT prolongation and the risk of torsades de pointes.


  • Rapid absorption (slower if modified release formulation)
  • Peak serum concentration usually 1 – 3h
  • Propranolol is extremely lipophilic
  • Elimination half lives vary and are extended in overdose. Propanol is normally ~12h.



  • onset of effects usually within 1-2 hours
  • onset may be delayed following metoprolol MR ingestion


  • Propanolol >1-2g oral ingestion is likely to cause significant toxicity, with onset <6 hours

Patient factors

  • worse toxicity expected if:
    • elderly
    • cardio-respiratory comorbidities
    • on regular, or co-ingested with, cardiovascularly active agents (especially negative inotropes)

General clinical features

  • CVS: hypotension, negative dromotropy (progress AV block – PR prolongation may be the first sign of beta blocker toxicity) and negative chronotropy (bradycardia), heart failure (including pulmonary oedema), cardiovascular collapse
  • RESP: bronchospasm (e.g. if coexistent asthma)
  • METABOLIC: hypoglycaemia, hyperkalaemia
  • NEURO: stupor, coma (usually secondary to hypotension)

Propanolol (“sodium channel blocker masquerading as a beta blocker”)

  • CVS: QRS prolongation, ventricular arrhythmias, cardiac arrest
  • NEURO: delirium, coma, seizures (usually within first 2 hours)


  • QT prolongation and Torsades des Pointes (TdP)



  • Bradycardia
    • Atropine 0.01 – 0.03 mg/kg IV (temporising)
    • Adrenaline 10-20 mcg bolus (child 0.1 mcg/kg) q2-3 min until adequate perfusion, then consider infusion: e.g. Adrenaline 0.15mg/kg in 50ml D5W at 1-10ml/h IV (0.05 – 0.5 mcg/kg/min).
    • Isoprenaline 1 – 10 micrograms/min IV infusion (0.05-1.0 microgram/kg/min in children) (may exacerbated hypotension through B2 effects, especially if ingestant is B1-specific beta blocker)
    • Electrical pacing – transcutaneous pacing is often ineffective, however transvenous pacing may provide definitive therapy if pharmacological therapy fails
  • Hypotension (requires a graduated approach)
    • 20ml/kg IV crystalloid bolus (beware of pulmonary oedema if considering repeated fluid boluses)
    • Adrenaline first line if bradycardic and hypotensive as described above
    • If refractory to adrenaline, assess for evidence of bradycardia (see above), poor cardiac contractility, and vasodilation
      • Poor cardiac contractility – treat with High dose Insulin Euglycaemic Therapy (HIET) (see High-dose Insulin Euglycaemic Therapy)
        • acts as an inotrope, lacks a chronotropic effect and may cause vasodilation
        • complications of hypoglycaemia and hypokalaemia from HIET may be more likely when used for beta blocker toxicity than when used for calcium channel blocker toxicity.
      • Vasodilation (aka vasoplegia) – treat with noradrenaline, e.g. 0.15mg/kg in 50ml D5W at 1-10ml/h IV (0.05 – 0.5 mcg/kg/min); consider other vasopressors if refractory vasoplegia.
      • If refractory to fluids, catecholamines, and HIET, with evidence of cardiogenic cause of hypotension the consider extracorporeal life support (ECLS). NB. ECLS is not usually appropriate for refractory vasoplegia.
  • Torsades de pointes (due to sotalol)
    • Administer magnesium sulfate 10 mmol (0.05 mmol/kg in children) IV over 15 minutes.
    • Correct hypoxia, hypokalaemia and hypocalcaemia
    • If heart rate is <100 beats/minute commence an isoprenaline infusion IV at 1-10 microgram/min (0.05-2.0 microgram/kg/min in children) or overdrive pacing to maintain heart rate at 100-120 beats/minute.
  • QRS widening and ventricular dysrhythmias (due to propanolol)
    • Suspect impending ventricular dysrhythmias if QRS >120 msec
    • Sodium bicarbonate 2 mmol/kg IV, can be repeated every 1-2 minutes to restore a perfusing rhythm and multiple doses maybe required; can titrate to effect by observing for QRS narrowing
    • Defibrillation can be attempted by may not be effective
    • Intubate and hyperventilate to target pH 7.5 to 7.55 to decrease sodium channel blockade
    • Lignocaine 1.5 mg/kg IV can be considered as a third line agent when the pH is >7.5.
    • Type Ia antidysrhythmic agents (e.g. procainamide) and amiodarone are contraindicated
  • CNS effects
    • Drowsiness is commonly due to cardiovascular effects (e.g. hypotension) with most beta blockers and may respond to correction of hypotension.
    • However, propanolol has direct CNS effects requiring early intubation if progressive obtundation (e.g. GCS <12) or seizures, and hyperventilation to target pH 7.5 to 7.55

Supportive care and monitoring

  • serial monitoring:
    • electrocardiography
    • cardiac output monitoring if severe toxicity (e.g. serial echocardiography, and/or continuous cardiac output monitors)
    • glucose and potassium
  • FASTHUGS IN BED Please (as appropriate)


  • Screening
    • ECG (use QT nomogram if sotalol-induced QT prolongation; see QT interval)
    • paracetamol level
  • Specific investigations (guided by clinical presentation)
    • Serial ECGs and cardiac monitoring for at least 4 hours
    • EUC
    • Echocardiography (especially if persistent hypotension)


  • activated charcoal up to 2 hours post ingestion (4 hours if MR preparation)

Enhance elimination

  • Nil


  • Nil


  • Consult clinical toxicologist if evidence of significant toxicity or predicted by risk assessment
  • Patients who are asymptomatic and have a normal ECG at 6 hours are medically cleared (12 hours if ingestion of MR formulation)
  • Patients with clinical or ECG manifestations require admission to HDU or ICU.
  • Refer for psychiatric assessment if potential deliberate self harm.


  • Glucagon was previously considered an “antidote” for beta blocker toxicity, however a lack of evidence of effectiveness means it is no longer considered standard of care (see Glucagon as an Antidote).
  • Intralipid is often considered a “last ditch measure” for lipid soluble toxicants, however evidence of effectiveness for beta blocker toxicity is lacking (see Intralipid and Lipid Rescue Therapy).



  • Boyd R, Ghosh A. Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. Glucagon for the treatment of symptomatic beta blocker overdose. Emerg Med J. 2003 May;20(3):266-7. PMC1726108.
  • Lavonas EJ, Akpunonu PD, Arens AM, Babu KM, Cao D, Hoffman RS, Hoyte CO, Mazer-Amirshahi ME, Stolbach A, St-Onge M, Thompson TM, Wang GS, Hoover AV, Drennan IR; American Heart Association. 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. Circulation. 2023 Oct 17;148(16):e149-e184. doi: 10.1161/CIR.0000000000001161. Epub 2023 Sep 18. PMID: 37721023. [article]
  • Lauterbach M. Clinical toxicology of beta-blocker overdose in adults. Basic Clin Pharmacol Toxicol. 2019 Aug;125(2):178-186. doi: 10.1111/bcpt.13231. Epub 2019 Apr 15. PMID: 30916882.
  • Rotella JA, Greene SL, Koutsogiannis Z, Graudins A, Hung Leang Y, Kuan K, Baxter H, Bourke E, Wong A. Treatment for beta-blocker poisoning: a systematic review. Clin Toxicol (Phila). 2020 Oct;58(10):943-983. doi: 10.1080/15563650.2020.1752918. Epub 2020 Apr 20. PMID: 32310006.

FOAM and web resources

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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