Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Beta-Blocker Toxicity Medication

  • Author: Adhi Sharma, MD; Chief Editor: Asim Tarabar, MD  more...
 
Updated: May 02, 2016
 

Medication Summary

Because of the nature of overdoses, definitive evidence-based recommendations are limited. However, commonly used agents include crystalloids, atropine, pressors with catecholamine action, glucagon, and phosphodiesterase inhibitors.

Next

Gastrointestinal Tract Decontaminants

Class Summary

These agents are used to minimize the absorption of ingested compound.

Activated charcoal (Requa Activated Charcoal, EZ-Char, Actidose-Aqua)

 

Although most useful if administered within 4 hours of ingestion, repeated doses may be used, especially with ingestions of sustained-released agents. Limited outcome studies exist, especially when activated charcoal is used more than 1 hour postingestion. No clinical data exist to suggest a benefit of multiple-dose activated charcoal with beta-blockers, even sustained-release preparations.

The dose may be repeated q4h at 0.5 g/kg. Alternate with use of a cathartic; monitor for active bowel sounds.

Previous
Next

Cardiovascular agents

Class Summary

These agents are used for symptomatic bradycardia and/or hypotension. Catecholamines are considered a primary treatment for more severe cases of beta-blocker poisoning.

Atropine IV/IM (Atropine Care, Isopto Atropine)

 

Atropine enhances sinus node automaticity by blocking the effects of acetylcholine at the atrioventricular (AV) node, decreasing refractory time and speeding conduction through the AV node.

Glucagon (GlucaGen)

 

Glucagon is considered the drug of choice for beta-blocker toxicity by many authors. This agent stimulates production of cyclic adenosine monophosphate (cAMP) through nonadrenergic pathways. Result is enhanced myocardial contractility, heart rate, and AV conduction.

An upper dose limit has not been established.

Epinephrine (Adrenalin)

 

Agents with combined alpha- and beta-selective properties may be necessary to maintain blood pressure. A beta-agonist may competitively antagonize the effect of the beta-blocker.

The amount of beta-agonist required might be several orders of magnitude above those recommended in standard Advanced Cardiac Life Support (ACLS) protocols

Dopamine

 

Agents with combined alpha- and beta-selective properties may be necessary to maintain blood pressure. A beta-agonist may competitively antagonize the effect of the beta-blocker.

The amount of beta-agonist required might be several orders of magnitude above those recommended in standard ACLS protocols. In a canine model, the doses of isoproterenol and dopamine had to be increased 15 and 5 times, respectively, in order to effect similar hemodynamic changes that occurred before beta-blockade with 1 mg/kg of propranolol.

Inamrinone

 

Inamrinone produces vasodilation and increases the inotropic state. Tachycardia occurs more commonly with this agent than with dobutamine. Inamrinone may exacerbate myocardial ischemia. Case reports describe it as effective when other agents fail.

Calcium chloride

 

Calcium chloride moderates nerve and muscle performance by regulating the action potential excitation threshold. At high doses, propranolol blocks the calcium channels that may induce asystole, AV block, and depressed myocardial contraction.

Magnesium sulfate

 

Magnesium sulfate acts as antiarrhythmic agent and diminishes the frequency of premature ventricular contractions (PVCs), particularly those secondary to acute ischemia. This agent is used to treat torsade de pointes associated with sotalol intoxication.

Insulin regular human (Novolin, Humulin)

 

High-dose insulin therapy is highly investigational but should be considered when other therapies are failing. Dextrose infusion of 10-75 g/h may be required. Consult a toxicologist if this regimen is considered.

Previous
Next

Benzodiazepines

Class Summary

These agents prevent seizure recurrence and terminate clinical and electrical seizure activity.

Lorazepam (Ativan)

 

Benzodiazepines are considered the treatment of choice for beta-blocker–induced seizures. Of the benzodiazepines, lorazepam has the longest anticonvulsant activity (4-6 h) and is preferred. By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, all levels of CNS, including limbic and reticular formation, may be depressed. It is important to monitor the patient's blood pressure after administering dose. Adjust as needed.

Diazepam (Valium, Diastat)

 

Diazepam depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. It is considered second-line therapy for seizures.

Phenobarbital

 

Phonobarbital may be necessary to control status epilepticus.

Previous
 
Contributor Information and Disclosures
Author

Adhi Sharma, MD Medical Toxicology Consultant, New York City Poison Control Center

Adhi Sharma, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology

Disclosure: Nothing to disclose.

Coauthor(s)

Lemeneh Tefera, MD, FAAEM Attending Physician, Department of Emergency Medicine, Beth Israel Medical Center

Lemeneh Tefera, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Aman Aminzay, MD Attending Physician, Department of Emergency Medicine, Beth Israel Medical Center, Albert Einstein College of Medicine

Aman Aminzay, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Acknowledgements

John G Benitez, MD, MPH, FACMT, FAACT, FACPM, FAAEM, Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH, FACMT, FAACT, FACPM, FAAEM, is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, and Wilderness Medical Society

Disclosure: Nothing to disclose.

David C Lee, MD Research Director, Department of Emergency Medicine, Associate Professor, North Shore University Hospital and New York University Medical School

David C Lee, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of Medscape Reference gratefully acknowledge the medical review of this article by Lada Kokan, MD.

References
  1. Brubacher JR. Beta-Adrenergic Antagonists. In: Hoffman RS, Howland MA, Lewin NA, Nelson LS, Goldfrank LR, eds. Goldfrank’s Toxicologic Emergencies. 10th ed. New York, NY: McGraw-Hill Education; 2015.

  2. Lopes P, Kataky R. Chiral interactions of the drug propranolol and a1-acid-glycoprotein at a micro liquid-liquid interface. Anal Chem. 2012 Mar 6. 84(5):2299-304. [Medline].

  3. Mowry JB, Spyker DA, Brooks DE, McMillan N, Schauben JL. 2014 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 32nd Annual Report. Clin Toxicol (Phila). 2015. 53 (10):962-1147. [Medline]. [Full Text].

  4. Hoot NR, Benitez JG, Palm KH. Hemodynamically unstable: accidental atenolol toxicity?. J Emerg Med. 2013 Sep. 45(3):355-7. [Medline].

  5. InnoPran XL [package insert]. GlaxoSmithKline. May 2, 2016. Available at [Full Text].

  6. Wax PM, Erdman AR, Chyka PA, et al. beta-blocker ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2005. 43(3):131-46. [Medline].

  7. Escajeda JT, Katz KD, Rittenberger JC. Successful treatment of metoprolol-induced cardiac arrest with high-dose insulin, lipid emulsion, and ECMO. Am J Emerg Med. 2015 Aug. 33 (8):1111.e1-4. [Medline].

  8. Position statement and practice guidelines on the use of multi-dose activated charcoal in the treatment of acute poisoning. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. 1999. 37(6):731-51.

  9. Engebretsen KM, Kaczmarek KM, Morgan J, Holger JS. High-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning. Clin Toxicol (Phila). 2011 Apr. 49(4):277-83. [Medline].

  10. Sebe A, Dişel NR, Açıkalın Akpınar A, Karakoç E. Role of intravenous lipid emulsions in the management of calcium channel blocker and β-blocker overdose: 3 years experience of a university hospital. Postgrad Med. 2015 Mar. 127 (2):119-24. [Medline].

  11. Bania TC, Chu J, Perez E, Su M, Hahn IH. Hemodynamic effects of intravenous fat emulsion in an animal model of severe verapamil toxicity resuscitated with atropine, calcium, and saline. Acad Emerg Med. 2007 Feb. 14(2):105-11. [Medline].

  12. Hayes BD, Gosselin S, Calello DP, Nacca N, Rollins CJ, Abourbih D, et al. Systematic review of clinical adverse events reported after acute intravenous lipid emulsion administration. Clin Toxicol (Phila). 2016 Jun. 54 (5):365-404. [Medline].

 
Previous
Next
 
Bradycardia is evident on a rhythm strip from a 48-year-old man who presented to the emergency department after a generalized tonic-clonic seizure. The patient was also hypotensive (82/55 mm Hg). The family reported that he was taking a medication, which proved to be propranolol, for a rapid heart rate. Propranolol is the most common beta-blocker involved in severe beta-blocker poisoning. It is nonselective and has membrane-stabilizing effects that are responsible for CNS depression, seizures, and prolongation of the QRS complex.
Sotalol is associated with the rhythm shown below in both therapeutic doses and toxic ingestions. Sotalol has been used as a class III antiarrhythmic agent to control dangerous ventricular tachydysrhythmias in some individuals. It causes polymorphic ventricular tachycardia (torsade de pointes) in approximately 4% of patients. Rarely, prolongation of the QT interval has been reported with propranolol.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.