Beta-adrenergic antagonist (ie, beta-blocker) toxicity can produce clinical manifestations including bradycardia, hypotension, arrhythmias, hypothermia, hypoglycemia, and seizures (see the images below). The presentation may range from asymptomatic to shock.
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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. Th....
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Sotalol is associated with the rhythm shown below in both therapeutic doses and toxic ingestions. Sotalol has been used as a class III antiarrhythmic ....
Beta-blockers have been in use for nearly 50 years. In addition to their traditional role in treating hypertension and other cardiovascular disorders, beta-blockers are also used for additional purposes such as migraine headaches, hyperthyroidism, glaucoma, anxiety, and various other disorders. As a result of their expanded use, the incidence of overdose with these agents has also increased.
Beta-blocker toxicity in children usually results from exposure to an adult's unattended medications. Beta-blocker toxicity in adults usually results from a suicide attempt or an accidental overdose of a routine medication.
Understanding the direct and indirect effects of beta-receptor blockade is crucial to rapid identification and appropriate treatment of beta-blocker toxicity. Beta-blockers act as competitive inhibitors of catecholamines, exerting their effects at both central and peripheral receptors. Blockade of beta-receptors results in decreased production of intracellular cyclic adenosine monophosphate (cAMP) with a resultant blunting of multiple metabolic and cardiovascular effects of circulating catecholamines.
Beta1-receptor blockade reduces heart rate, blood pressure, myocardial contractility, and myocardial oxygen consumption. Beta2-receptor blockade inhibits relaxation of smooth muscle in blood vessels, bronchi, the gastrointestinal system, and the genitourinary tract. In addition, beta-adrenergic receptor antagonism inhibits both glycogenolysis and gluconeogenesis, which may result in hypoglycemia.
Other than the direct effects of the beta-adrenoreceptor blockade, toxicity may result from other mechanisms, including sodium and calcium channel blockade, centrally mediated cardiac depression, and alteration of cardiac myocyte energy metabolism.[1]
Numerous beta-blockers are available; these agents comprise a heterogeneous drug family with varying toxicologically relevant characteristics. An understanding of these different characteristics is helpful for understanding the clinical presentations with particular agents and for guiding therapy.
Nonselective activity
Propranolol was the first beta-blocker to enter widespread use; much of the clinical and overdose experience that exists with beta-blockers was provided by case reports and clinical studies of this drug. Propranolol is a nonselective beta-blocker, demonstrating equal affinity for both beta1- and beta2-receptors. Other nonselective beta-blockers include nadolol, timolol, and pindolol. Nonselective beta-blockers exert a wider variety of extracardiac manifestations.
Intrinsic sympathomimetic activity
Some beta-blockers, such as pindolol and acebutolol, also have beta-agonist properties. Although their agonist property is weaker than that of catecholamines, they are capable of stimulating beta-receptors, especially when catecholamine levels are low. Of note, acebutolol has been reported to be particularly lethal in overdose.
Membrane-stabilizing activity
Beta-blockers, such as propranolol, labetalol, and pindolol, can have membrane-stabilizing activity (MSA; eg, the quinidine-like effects of the class IA antidysrhythmic effects). MSA blocks myocyte sodium channels. This property, usually not evident at therapeutic doses, may significantly contribute to toxicity by prolonging QRS duration and impairing cardiac conduction. Seizures are more commonly observed in drugs with MSA. Beta-blockers with MSA are associated with the largest proportion of fatalities.
Lipid solubility
Lipid solubility is higher in agents such as propranolol and carvedilol, but lower in agents such as atenolol and nadolol. It may influence the degree of central nervous system (CNS) effects and utility of hemodialysis or hemoperfusion.[2]
High lipid solubility leads to a larger volume of distribution and better CNS penetration. Lipophilic beta-blockers are primarily metabolized by the liver. Propranolol is among these, and its active metabolite (4-OH propranolol) prolongs its biological activity. Conversely, hydrophilic beta-blockers have a small volume of distribution and are eliminated essentially unchanged by the kidneys; this property allows hydrophilic beta-blockers to be removed by hemodialysis.
QT-interval prolongation
The electrophysiologic effects of sotalol deserve special consideration. Unlike other beta-blockers, sotalol has antidysrhythmic properties consistent with the type III antidysrhythmic agents. Class III agents prolong the action potential duration and the effective refractory period of AV and atrioventricular myocytes, which can lengthen the QT-interval duration and result in polymorphic ventricular tachycardia (ie, torsade de pointes). Ventricular dysrhythmias associated with sotalol toxicity can occur up to 48 hours postingestion.
Propranolol is the most toxic beta-blocker and the most frequently used in suicide attempts worldwide. The 2016 Annual Report of the American Association of Poison Control Centers' (AAPCC) National Poison Data System reported 11,010 single exposures to beta-blockers. Of the reported exposures, 3076 were in children younger than 6 years, and 6633 were in adults 21 years of age and older. Approximately 82 of exposures were unintentional.[3]
Prognosis is largely dependent on the initial response to therapy (6-12 h postingestion) as drug levels are likely to have peaked at this time. In addition, beta-blockers that are lipid soluble and have marked antidysrhythmic (ie, quinidine-like) effects are more lethal (eg, propranolol, sotalol, oxprenolol).
Underlying cardiac or pulmonary disease places the patient at increased risk for poor outcome.
The outcome is significantly worse when these agents are co-ingested with psychotropic or cardioactive drugs. This is true even if the amount of beta-blocker ingested is relatively small. The co-ingestants that most markedly worsen prognosis include calcium channel blockers, cyclic antidepressants, and neuroleptics. These co-ingestions are the most important factor associated with the development of cardiovascular morbidity and mortality.
After co-ingestions, the next most significant factor associated with major morbidity and mortality is exposure to a beta-blocker with membrane-stabilizing activity.
In 2016, the AAPCC reported the following numbers of outcomes in 11,010 cases of beta-blocker exposure[3] :
Ideally, the clinician should determine the specific beta-blocker involved, the quantity, and the time of the overdose. Unfortunately, these details are often not immediately available. When a history of intentional overdose is lacking, beta-blocker toxicity can go unrecognized as a cause of bradycardia and hypotension.
Information regarding the patient's underlying medical condition may be a clinical clue to the possibility of an overdose.
Hoot et al note the risk of chronic beta-blocker toxicity in patients with impaired clearance. They report such a case in a young woman with end-stage renal disease requiring peritoneal dialysis who was receiving antihypertensive treatment with atenolol, which unlike most beta-blockers is excreted primarily by the kidney, and which is poorly cleared by peritoneal dialysis. She presented with sudden onset of abdominal pain and hemodynamic instability with hypotension and relative bradycardia.[4]
Initial evaluation
The initial evaluation of a comatose patient should include consideration of an occult overdose. If a patient is bradycardic and hypotensive, the clinician should consider a beta-blocker or calcium channel blocker overdose. Other associated symptoms may include hypothermia, hypoglycemia, and seizures. Hypoglycemia is relatively uncommon, but it is described in patients with unstable diabetes and in children; beta-blocking drugs may cause hypoglycemia by inhibiting glycogenolysis.
Myocardial conduction delays with decreased contractility typify the acute beta-blocker ingestion.
Cardiac output may diminish with resulting hypotension from bradycardia and negative inotropy. Hypotension due to the beta2-receptor blockade can be profound and jeopardize myocardial perfusion, creating a downward spiral of events.
Beta-blockers that are not sustained-release formulations are all rapidly absorbed from the gastrointestinal tract. The first critical signs of overdose can appear 20 minutes postingestion but are more commonly observed within 1-2 hours. In all clinically significant beta-blocker overdoses, symptoms develop within 6 hours.
Although the half-life of these compounds is usually short (2-12 h), half-lives in the overdose patient may be prolonged because of a depressed cardiac output, reduced blood flow to the liver and kidneys, or because of the formation of active metabolites.
Saturation kinetics prolong elimination at the type of high plasma concentrations that typically occur with overdose. Delayed absorption from long-acting preparations can significantly increase the apparent elimination half-life. Thus, prolonged effects (>72 h) after massive overdoses are not uncommon.
Asymptomatic intoxication occurs mainly in healthy persons with tolerance to these drugs who ingest beta-blockers that lack membrane-stabilizing effects or have a partial agonist effect (eg, pindolol). Individual sensitivity to beta-blockade may be significantly reduced in those patients who have tolerated therapeutic doses of up to 4 g of propranolol daily and in patients who have sustained deliberate overdoses of both practolol and propranolol without serious adverse effects.
Conversely, circulatory collapse may occur in patients with preexisting cardiac failure when sympathetic drive is inhibited by even a small dose of a particular beta-blocker.
Intermediate toxicity results in a moderate drop in blood pressure (systolic BP >80 mm Hg) and/or bradycardia (heart rate < 60 bpm).
Bradycardia
Bradycardia with associated hypotension and shock (systolic BP < 80 mm Hg, heart rate < 60 bpm) defines severe beta-blocker toxicity. Patients with severe toxicity often manifest extracardiac manifestations of intoxication. Bradycardia, by itself, is not necessarily helpful as a warning sign because slowing of the heart rate and damping of tachycardia in response to stress is observed at therapeutic doses.
Although case reports have documented hypotension in the absence of bradycardia, blood pressure usually does not fall before the onset of bradycardia. Bradycardia may be isolated or accompanied by mild conduction disturbances.
CNS symptoms
A depressed level of consciousness and seizures may occur as a result of cellular hypoxia from poor cardiac output, a direct CNS effect caused by sodium channel blocking, or even as a result of hypoglycemia. The lipid-soluble agents have increased distribution into the brain, and these agents are associated with severe CNS toxicity.
Patients who have taken lipid-soluble beta-blockers, such as propranolol, frequently present with seizures after an overdose. Seizures are generalized and may be multiple but are usually brief, lasting seconds to minutes. Seizures occasionally have been reported after therapeutic use of esmolol and with overdose of alprenolol, metoprolol, and oxprenolol. Seizures are far more common after propranolol overdose.
Coma may be prolonged, depending on the half-life of the agent involved and the coexisting morbidity.
Long-term beta-blocker use has been linked with an acute reversible syndrome characterized by disorientation for time and place, short-term memory loss, emotional lability, a slightly clouded sensorium, and decreased performance on neuropsychometrics.[5] For example, severe memory impairment developed in an 81-year-old woman taking propranolol 20 mg 3 times per day (note that the half-life of propranolol is longer in the elderly and in females). Effects were associated with an elevated propranolol blood level (163 mcg/L) and resolved after discontinuation of the drug.
Bronchospasm
Bronchospasm is a rare complication of beta-blocker therapy or overdose but is more likely in patients who already have bronchospastic disease. Sudden fatality following administration of therapeutic doses of beta-blocker has been reported in four patients with asthma. Pulmonary edema had been reported to occur as a result of cardiac failure. Respiratory arrest has also been described with beta-blocker intoxication, especially with propranolol, and is thought to be secondary to a central drug effect.
Perform a fingerstick glucose test, because beta-blockers may be associated with hypoglycemia, especially in patients with diabetes and in children. Also measure serum electrolytes, because hypokalemia may contribute to cardiac arrhythmias. Co-ingestions or concomitant medical conditions may alter other serum electrolytes, so these should be monitored closely, especially in patients with seizures or altered mental status. Measure cardiac enzymes to rule out myocardial infarction in any hemodynamically unstable patient.
Blood gas (arterial or venous) analysis may be helpful for managing metabolic acidosis from seizures or cardiogenic shock or rare cases of severe bronchospasm, respiratory acidosis, or hypoxia. Acidosis from poor cardiac perfusion may be manifested by low serum bicarbonate.
In a severe overdose that impairs myocardial contraction, chest radiographs may show evidence of pulmonary edema.
Electrocardiographic (ECG) results after beta-blocker overdose may include the following:
Progressively worsening sinus bradycardia
Increased PR intervals
Loss of atrial activity
Atrioventricular junctional rhythm
Widening of the QRS complex
Atrioventricular block
Idioventricular rhythm
Asystole
A prolonged QT interval has been observed after sotalol overdose. Ventricular fibrillation and ventricular tachycardia are uncommon because of the antidysrhythmic effects of most beta-blockers, with the exception of sotalol.
The goal of therapy in beta-blocker toxicity is to restore perfusion to critical organ systems by increasing cardiac output. This may be accomplished by improving myocardial contractility, increasing heart rate, or both.
Because of the potential for rapid deterioration, only asymptomatic patients who have been observed for a period of 6 hours should be considered stable for transfer. If intensive care monitoring or therapy is not available, transfer the unstable patient to the closest facility with the necessary capabilities for care, including a medical toxicologist.
Follow standard protocols for bradycardia, hypotension, and seizures. Cardiac monitoring, oxygen administration, and reliable intravenous access are essential.
Prehospital administration of charcoal is indicated when there are no contraindications and the patient is alert and cooperative. If there is any alteration of mental status or concern that the patient may have a precipitous change in status, it is advisable to withhold charcoal.[6]
If the patient is hypotensive, administer 20 mL/kg of isotonic intravenous fluids and place the patient in the Trendelenburg position. If the patient does not respond to these measures, the following interventions may be considered:
Inotropes and chronotropes
Glucagon
Gastric decontamination
Benzodiazepines (in patients with seizures)
Hemodialysis
Cardiac pacing/cardiopulmonary resuscitation
High-dose insulin
Extracorporeal membrane oxygenation (ECMO)[7]
The pharmacotherapy of beta-blocker overdose may include a variety of inotropes and chronotropes, such as epinephrine and atropine, for hypotension and bradycardia (see Medication). Doses of these agents should be titrated to response; consequently, a patient with beta-blocker overdose may require higher doses of these agents than those noted in Advanced Cardiac Life Support (ACLS) protocols. Consultation with a toxicologist can help guide these decisions.
Glucagon can enhance myocardial contractility, heart rate, and atrioventricular conduction; many authors consider it the drug of choice for beta-blocker toxicity. Because a glucagon bolus can be diagnostic and therapeutic, the clinician can empirically administer glucagon and check for a response. An upper dose limit has not been established.
For gastric decontamination, gastric lavage (with appropriate protection of the airway) is preferred over emesis because of the rapid absorption and occasionally precipitous onset of toxicity that may place the patient at risk for aspiration. Gastric lavage may be beneficial if the patient presents to the ED within 1-2 hours of ingestion.
Volunteer studies have indicated that multi-dose activated charcoal (MDAC) may be useful in reducing bioavailability of nadolol and sotalol, probably by removal of the drug through the enterohepatic circulation. However, the American Academy of Clinical Toxicology found insufficient clinical data to support or exclude the use of MDAC in such cases.[8]
Hemodialysis
Hemodialysis may be useful in severe cases of atenolol overdoses because atenolol is less than 5% protein bound and 40-50% is excreted unchanged in urine. Nadolol, sotalol, and atenolol, which have low lipid solubility and low protein binding, reportedly are removed by hemodialysis. Acebutolol is dialyzable. Propranolol, metoprolol, and timolol are not removed by hemodialysis. Consider hemodialysis or hemoperfusion only when treatment with glucagon and other pharmacotherapy fails.
Cardiac pacing/cardiopulmonary resuscitation
Cardiac pacing may be effective in increasing the rate of myocardial contraction. Electrical capture is not always successful and, if capture does occur, blood pressure is not always restored. Reserve cardiac pacing for patients unresponsive to pharmacologic therapy or for those with torsade de pointes unresponsive to magnesium. Multiple case reports describe complete neurologic recovery, even with profound hypotension, if a cardiac rhythm can be sustained.
Resuscitation should, therefore, be aggressive and prolonged. Some have postulated the possibility of a protective effect on the CNS from the membrane-stabilizing effects of drugs such as propranolol.
High-dose insulin
In case reports and animal models, high-dose insulin infusion has been reported to improve outcomes in beta-blocker poisoning, as well as in calcium-channel blocker poisoning. The mechanism of action is via the positive inotropic effects of insulin.
The optimal regimen is still to be determined. The currently recommended regimen is a 1 U/kg of an insulin bolus followed by continuous infusion of 1-10 U/kg/h, but boluses of up to 10 U/kg and continuous infusions as high as 22 U/kg/h have been used with good outcomes and minimal adverse events.[9]
After consultation with a medical toxicologist, this treatment should be considered for overdoses that are refractory to crystalloids, glucagon, and catecholamine infusions. Of note, because of the risk of iatrogenic hypoglycemia and hypokalemia, the clinician must be particularly vigilant in monitoring these patients' serum glucose and potassium levels.
Monitoring
Monitoring must be conducted regularly during high-dose insulin therapy and for up to 24 hours after its discontinuation. Dextrose supplementation is typically required to maintain euglycemia.[9]
Simple methods of monitoring include repeat physical examinations, serial electrocardiograms, and continuous measurement of urinary output after placement of a Foley catheter.
End points of therapy may include the following:
Heart rate >60 beats per minute
Blood pressure >90 mm Hg systolic
Evidence of good organ perfusion (improved mentation or urine output)
The best invasive monitoring methods for patients with severe toxicity are early insertion of an arterial blood pressure catheter and central venous pressure readings.
Intravenous fat emulsion (IFE) therapy is increasingly used as a treatment adjunct for beta-blocker toxicity. However, any consideration of its use is recommended only in consultation with a toxicologist familiar with the administration of IFE as an antidote.
IFE has traditionally been used as a component of parenteral nutrition therapy. More recently, animal models as well as in case reports demonstrated that IFE was effective in the treatment of local anesthetic toxicity and subsequently of beta-blocker toxicity.[10, 11, 7, 12] It has been postulated that the IFE provides a "lipid sink" for fat-soluble drugs, removing them from the target organs.
However, acute IFE administration has been associated with a range of adverse effects, including acute kidney injury, cardiac arrest, ventilation perfusion mismatch, acute lung injury, venous thromboembolism, hypersensitivity, fat embolism, fat overload syndrome, pancreatitis, extracorporeal circulation machine circuit obstruction, allergic reaction, and increased susceptibility to infection. The adverse effects seem to be proportional to the rate of infusion as well as the total dose received.[12]
Regional poison control center and/or a medical toxicologist
Critical care consultation to assist in the management and subsequent admission
Nephrologist, in rare instances when hemodialysis may be necessary
Psychiatric consultation for any patients who report self-harm or where self-harm is suspected
Patients who initially present without symptoms and who remain asymptomatic can be safely discharged after an observation period of 6 hours. Increased caution is necessary with children and patients who have ingested a sustained-release product. In these cases, admission to the hospital for 24 hours is recommended.
To avoid recurrent complications, adjust dosages or change medications for patients who have experienced adverse drug reactions due to combination therapy with calcium channel blockers or impaired metabolism caused by renal or hepatic dysfunction. These changes should be made in concert with the patient's primary care physician.
If there is any suspicion of suicidality and if the patient is medically clear of any toxic overdose, the disposition planning should be made in concert with the consulting psychiatrist.
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.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
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
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
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.
These agents are used for symptomatic bradycardia and/or hypotension. Catecholamines are considered a primary treatment for more severe cases of beta-blocker poisoning.
Clinical Context:
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.
Clinical Context:
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.
What are the clinical manifestations of beta-blocker toxicity?Why has the incidence of beta-blocker toxicity been on the increase?What causes beta-blocker toxicity in children?What is the mechanism of action associated with beta-blockers?What is the pathophysiology of beta-receptors in beta-blocker toxicity?What are mechanisms of beta-blocker toxicity?Why is understanding the characteristics of different beta-blockers important in the management beta-blocker toxicity?What are nonselective beta-blockers?Why is the beta-blocker toxicity of acebutolol particularly lethal in overdose?What is the role of membrane-stabilizing activity in beta-blocker toxicity?What is the role of lipid solubility in beta-blocker toxicity?What are the electrophysiologic effects of sotalol in beta-blocker toxicity?What is the incidence of beta-blocker toxicity?What is the prognosis of beta-blocker toxicity?What are the possible outcomes of beta-blocker toxicity?What should be the focus of history in the evaluation of beta-blocker toxicity?What are the symptoms of beta-blocker toxicity?What are the indications of myocardial conduction in beta-blocker toxicity?What is the effect of beta-blocker toxicity on cardiac output?How quickly do symptoms of beta-blocker toxicity develop?What causes and increase in the half-life of beta-blockers during an overdose?Why are prolonged effects of beta-blocker toxicity common?What are the indications of asymptomatic beta-blocker toxicity?Which factors increase the risk of circulatory collapse in beta-blocker toxicity?What is the significance of a moderate drop in blood pressure in beta-blocker toxicity?What are the signs of bradycardia in beta-blocker toxicity?What are the CNS symptoms of beta-blocker toxicity?How are seizures characterized in beta-blocker toxicity?How is a coma characterized in beta-blocker toxicity?What are the symptoms of long-term beta-blocker use in beta-blocker toxicity?What is the respiratory symptoms of beta-blocker toxicity?What are the differential diagnoses for Beta-Blocker Toxicity?What is included in the initial workup of beta-blocker toxicity?What is the role of blood gas in the workup of beta-blocker toxicity?What is the role of chest radiographs in the workup of beta-blocker toxicity?Which electrocardiographic (ECG) results suggest beta-blocker toxicity?What is the goal of therapy for beta-blocker toxicity?When is transfer indicated for the treatment of beta-blocker toxicity?What is included in prehospital care for beta-blocker toxicity?When is prehospital administration of charcoal indicated in the treatment of beta-blocker toxicity?What is the role of ipecac syrup in the treatment of beta-blocker toxicity?What is included in emergency department (ED) care of beta-blocker toxicity in patients who are hypotensive?What are the drug treatment options for beta-blocker toxicity in the emergency department (ED)?What is the role of glucagon in the emergency department (ED) treatment of beta-blocker toxicity?What is the role of gastric decontamination in the treatment of beta-blocker toxicity?What is the role of charcoal in the treatment of beta-blocker toxicity?What is the role of hemodialysis in the treatment of beta-blocker toxicity?What is the role of cardiac pacing in the treatment of beta-blocker toxicity?What is the role of cardiac resuscitation in the treatment of beta-blocker toxicity?What is the role of high-dose insulin in the treatment of beta-blocker toxicity?What is the optimal regimen for high-dose insulin in the treatment of beta-blocker toxicity?What are the indications for high-dose insulin in the treatment of beta-blocker toxicity?What monitoring is required during high-dose insulin therapy for beta-blocker toxicity?What monitoring is performed during treatment of beta-blocker toxicity?What are the end points of therapy for beta-blocker toxicity?What invasive monitoring methods are used during the treatment of severe beta-blocker toxicity?What is the role of IV fat emulsion (IFE) in the treatment of beta-blocker toxicity?How is IV fat emulsion (IFE) used to treat beta-blocker toxicity?What are the adverse effects of IV fat emulsion (IFE) to treat beta-blocker toxicity?Which specialist consultations are needed for the treatment of beta-blocker toxicity?How long should patients with beta-blocker toxicity remain asymptomatic before discharge?What steps are taken to avoid recurrent complications of beta-blocker toxicity?When is a psychiatric consultation indicated in the treatment of beta-blocker toxicity?Which medications are used to the treat beta-blocker toxicity?Which medications in the drug class Anticonvulsants, Barbiturates are used in the treatment of Beta-Blocker Toxicity?Which medications in the drug class Benzodiazepines are used in the treatment of Beta-Blocker Toxicity?Which medications in the drug class Cardiovascular agents are used in the treatment of Beta-Blocker Toxicity?Which medications in the drug class Gastrointestinal Tract Decontaminants are used in the treatment of Beta-Blocker Toxicity?
Adhi Sharma, MD, Medical Toxicology Consultant, New York City Poison Control Center
Disclosure: Nothing to disclose.
Coauthor(s)
Aman Aminzay, MD, Attending Physician, Department of Emergency Medicine, Beth Israel Medical Center, Albert Einstein College of Medicine
Disclosure: Nothing to disclose.
Lemeneh Tefera, MD, FAAEM, Attending Physician, Department of Emergency Medicine, Beth Israel Medical Center
Disclosure: Nothing to disclose.
Chief Editor
Gil Z Shlamovitz, MD, FACEP, Associate Professor of Clinical Emergency Medicine, Keck School of Medicine of the University of Southern California; Chief Medical Information Officer, Keck Medicine of USC
Disclosure: Nothing to disclose.
Additional Contributors
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
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.
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.
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.
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.
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