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Toxicity, Beta-blocker: Treatment & Medication

Author: Adhi Sharma, MD, Assistant Professor, Department of Emergency Medicine, Mount Sinai School of Medicine; Chairman, Department of Emergency Medicine, Good Samaritan Hospital Medical Center; Medical Toxicology Consultant, New York City Department of Health and Poison Control Center
Coauthor(s): Lemeneh Tefera, MD, FAAEM, Attending Physician, Department of Emergency Medicine, Beth Israel Medical Center; Aman Aminzay, MD, Resident, Department of Emergency Medicine, Beth Israel Medical Center, Albert Einstein College of Medicine
Contributor Information and Disclosures

Updated: Apr 21, 2009

Treatment

Prehospital Care

  • Follow standard protocols for bradycardia, hypotension, and seizures. Cardiac monitoring, oxygen administration, and reliable intravenous access are essential.
  • Activated charcoal
    • No benefit has been shown for prehospital administration of charcoal; the decision to administer activated charcoal should be made in the ED.
    • Ipecac syrup is contraindicated.

Emergency Department Care

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. 

  • Crystalloid: If hypotensive, administer 20 mL/kg of isotonic intravenous fluids and place the patient in the Trendelenburg position. If the patient is unresponsive to these measures, administer pharmacologic therapies as discussed in the following section.
  • The pharmacotherapy of beta-blocker overdose may include a variety of inotropes and chronotropes, such as epinephrine and atropine, for hypotension and bradycardia. These are discussed below in more detail. Please note that the doses of these agents should be titrated to response so that a patient with beta-blocker overdose may require higher doses of these agents than those noted in ACLS protocols. Consultation with a toxicologist can help guide these decisions.
  • Glucagon: Because a glucagon bolus can be diagnostic and therapeutic, the clinician can empirically administer glucagon and check for a response.
  • 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 multiple dose activated charcoal (MDAC) may be useful in reducing bioavailability of nadolol, probably by removal of the drug through the enterohepatic circulation.
  • Benzodiazepines are the drugs of choice if seizures occur.
  • Enhanced elimination: 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 (low lipid solubility, 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.
  • Insulin: In case reports and animal models, high-dose insulin infusion (in combination with glucose administration to maintain serum glucose levels) has been reported to improve outcomes. The mechanism of action is via the positive inotropic effects of insulin. 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.

Consultations

  • 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

Medication

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.

GI decontaminant

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


Activated charcoal (Liqui-Char)

Although most useful if used within 4 h 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 h postingestion. No data exist to suggest a benefit of multiple dose activated charcoal with beta-blockers, even sustained-release preparations.
May repeat the dose q4h at 0.5 g/kg (alternate use of cathartic; monitor for active bowel sounds).

Adult

1 g/kg PO (first dose usually with cathartic), up to 50-100 g

Pediatric

1-2 g/kg PO (<2 y: omit cathartic), up to 15-30 g

May inactivate ipecac syrup if used concomitantly; effectiveness of other medications decreases with coadministration; do not mix with sherbet, milk, or ice cream (decreases absorptive properties)

Documented hypersensitivity; poisoning or overdosage of mineral acids and alkalis; unprotected airway with absent gag reflex

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for active bowel sounds before readministration to minimize risk of charcoal ileus; not very effective in poisonings of ethanol, methanol, and iron salts; induce emesis before administering activated charcoal; after emesis with ipecac, patient may not tolerate activated charcoal for 1-2 h; can administer in early stages of gastric lavage; without sorbitol, gastric lavage returns are black

Cardiovascular agents

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 (Atropair)

Enhances sinus node automaticity by blocking the effects of acetylcholine at the AV node, decreasing refractory time and speeding conduction through the AV node.

Adult

Hypotension: 0.5-1 mg IV with repeated doses at 5-min intervals until desired response
Cardiac arrest: 1 mg IV repeated at 3- to 5-min intervals; minimal dose: 0.5 mg IV
Maximal dose: 0.04 mg/kg IV or 3 mg IV is fully vagolytic

Pediatric

Hypotension: 0.02 mg/kg IV; minimum dose 0.1 mg IV
Cardiac arrest: Maximum single dose of 0.5 mg IV for children and 1 mg for adolescents; may repeat dose once; not to exceed 1 mg for children and 2 mg for adolescents

Coadministration with other anticholinergics have additive effects; pharmacologic effects of atenolol and digoxin may increase; antipsychotic effects of phenothiazines may decrease; tricyclic antidepressants with anticholinergic activity may increase effects

Documented hypersensitivity; thyrotoxicosis; narrow-angle glaucoma; tachycardia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid in Down syndrome or children with brain damage to prevent hyperreactive response; avoid in coronary heart disease, tachycardia, congestive heart failure, cardiac arrhythmias, and hypertension; caution in peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in prostatic hypertrophy, prostatism can have dysuria and may require catheterization


Glucagon

Considered DOC by many. Stimulates production of cAMP through nonadrenergic pathways. Result is enhanced myocardial contractility, heart rate, and AV conduction.
An upper dose limit has not been established.

Adult

3-10 mg IV bolus followed by 2-5 mg/h infusion

Pediatric

150 mcg/kg IV over 1 min; followed 2-5 mg/h infusion

May enhance effects of anticoagulants (although onset may be delayed); monitor prothrombin activity and for signs of bleeding in patients receiving anticoagulants; adjust dose accordingly

Documented hypersensitivity; pheochromocytoma

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Monitor blood glucose levels in hypoglycemic patients until they are asymptomatic; effective in treating hypoglycemia only if sufficient liver glycogen is present; because hepatic glycogen availability is necessary to treat hypoglycemic patients glucagon has virtually no effects in patients with starvation, adrenal insufficiency, or chronic hypoglycemia; nausea may cause increased vagal tone; avoid phenol toxicity by diluting in D5W


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 ACLS protocols

Adult

1 mcg/min IV; titrate to effect

Pediatric

0.1 mcg/kg/min IV; titrate to effect

Guanethidine may increase effect of direct-acting vasopressors, possibly resulting in severe hypertension; TCAs may potentiate pressor response of direct-acting vasopressors; phenytoin, alpha- and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong effects of epinephrine

Documented hypersensitivity; tachyarrhythmias; tachycardia; heart block caused by digitalis intoxication; ventricular arrhythmias, which require inotropic therapy; angina pectoris; uncorrected hypovolemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

By increasing myocardial oxygen requirements while decreasing effective coronary perfusion, may have a deleterious effect on the injured or failing heart; in some patients, presumably with organic disease of the AV node and its branches, may paradoxically worsen heart blocks or precipitate Adams-Stokes attacks; caution in coronary artery disease, coronary insufficiency, diabetes, or hyperthyroidism and sensitivity to sympathomimetic amines; if heart rate >110 BPM, may be advisable to decrease infusion rate or temporarily discontinue infusion


Dopamine (Intropin)

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 propranolol.

Adult

Begin at 2-5 mcg/kg/min IV progressing in 5-10 mcg/kg/min increments prn

Pediatric

Administer as in adults

Guanethidine may increase effect of direct-acting vasopressors, possibly resulting in severe hypertension; TCAs may potentiate pressor response of direct-acting vasopressors; phenytoin, alpha- and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong effects of dopamine

Documented hypersensitivity; tachyarrhythmias; tachycardia; heart block caused by digitalis intoxication; ventricular arrhythmias, which require inotropic therapy; angina pectoris; uncorrected hypovolemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

By increasing myocardial oxygen requirements while decreasing effective coronary perfusion, may have a deleterious effect on the injured or failing heart; in some patients, presumably with organic disease of the AV node and its branches, may paradoxically worsen heart blocks or precipitate Adams-Stokes attacks; caution in coronary artery disease, coronary insufficiency, diabetes, or hyperthyroidism and sensitivity to sympathomimetic amines; if heart rate >110 BPM, may be advisable to decrease infusion rate or temporarily discontinue infusion


Isoproterenol (Isuprel)

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 propranolol.

Adult

2-4 mcg/min IV; titrate to effect

Pediatric

0.1 mcg/kg/min IV; titrate to effect

Guanethidine may increase effect of direct-acting vasopressors, possibly resulting in severe hypertension; TCAs may potentiate pressor response of direct-acting vasopressors

Documented hypersensitivity; tachyarrhythmias; tachycardia; heart block caused by digitalis intoxication; ventricular arrhythmias, which require inotropic therapy; angina pectoris; uncorrected hypovolemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

By increasing myocardial oxygen requirements while decreasing effective coronary perfusion, may have a deleterious effect on the injured or failing heart; in some patients, presumably with organic disease of the AV node and its branches, may paradoxically worsen heart blocks or precipitate Adams-Stokes attacks; caution in coronary artery disease, coronary insufficiency, diabetes, or hyperthyroidism and sensitivity to sympathomimetic amines; if heart rate >110 BPM, may be advisable to decrease infusion rate or temporarily discontinue infusion


Inamrinone - formerly amrinone (Inocor)

Produces vasodilation and increases inotropic state. More likely to cause tachycardia than dobutamine. May exacerbate myocardial ischemia. Case reports describe as effective when other agents fail.

Adult

0.75 mg/kg IV initial, followed by 5-10 mcg/kg/min maintenance infusion; additionally, 0.75 mg/kg may be given 30 min after therapy begins; not to exceed 10 mg/kg/d

Pediatric

Not established
Suggested dosing: 0.75 mg/kg IV initial, followed by 10 mcg/kg/min maintenance infusion; infants may require larger doses

Coadministration with diuretics may result in hypovolemia and decrease in filling pressure; cardiac glycosides have additive effects on inamrinone; admixing with furosemide or dextrose may cause precipitation

Documented hypersensitivity; uncorrected hypovolemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue therapy if symptoms of liver toxicity develop; correct hypokalemia before giving therapy


Calcium chloride

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

Adult

100-1000 mg slow IV push of 10% solution

Pediatric

20-25 mg/kg IV push

Coadministration with digoxin may cause arrhythmias; with thiazides, may induce hypercalcemia; may antagonize effects of calcium channel blockers, atenolol, and sodium polystyrene sulfonate; precipitates with sodium bicarbonate and may be sclerosing to peripheral veins

Ventricular fibrillation not associated with hyperkalemia; digitalis toxicity; hypercalcemia; renal insufficiency; cardiac disease

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Administer slowly (not to exceed 0.5-1 mL/min) to avoid extravasation; hypercalcemia may occur in renal failure; calcium gluconate may be less effective


Magnesium sulfate

Acts as antiarrhythmic agent and diminishes frequency of PVCs, particularly when secondary to acute ischemia. Used to treat torsade de pointes associated with sotalol intoxication.

Adult

2 g IV over 1-2 min, followed by a second 2 g bolus and infusion of 3-20 mg/min in patients not responding to the initial bolus or with recurrence of arrhythmias

Pediatric

25-50 mg/kg diluted to 10 mg/mL for IV infusion over several min

Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade observed with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine

Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

May alter cardiac conduction leading to heart block in digitalized patients; monitor respiratory rate, deep tendon reflex, and renal function when electrolyte is administered parenterally; caution when administering magnesium dose because may produce significant hypertension or asystole; in overdose, calcium gluconate, 10-20 mL IV of 10% solution, can be given as antidote for clinically significant hypermagnesemia


Insulin (Novolin, Humulin)

High-dose insulin therapy with euglycemia was associated with significant improvement in survival, compared with high-dose infusions of epinephrine and glucagon in an anesthetized canine model as well as case series of human overdose. This intriguing therapy is still 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.

Adult

Not established
Suggested dosing: 0.5-1 U/kg/h IV with frequent boluses of dextrose

Pediatric

Not established

Medications that may decrease hypoglycemic effects of insulin include acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid estrogens, ethacrynic acid, calcitonin, oral contraceptives, diazoxide, dobutamine phenothiazines, cyclophosphamide, dextrothyroxine, lithium carbonate, epinephrine, morphine sulfate, and niacin; medications that may increase hypoglycemic effects of insulin include calcium, ACE inhibitors, alcohol, tetracyclines, beta-blockers, lithium carbonate, anabolic steroids, pyridoxine, salicylates, MAOIs, mebendazole, sulfonamides, phenylbutazone, chloroquine, clofibrate, fenfluramine, guanethidine, octreotide, pentamidine, and sulfinpyrazone

Documented hypersensitivity; hypoglycemia; inability to closely monitor serum glucose concentrations

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Investigational; hyperthyroidism may increase renal clearance of insulin and may need more insulin to treat hyperkalemia; hypothyroidism may delay insulin turnover, requiring less insulin to treat hyperkalemia; monitor glucose carefully; dose adjustments of insulin may be necessary in patients with renal and hepatic dysfunction

Benzodiazepines

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, may depress all levels of CNS, including limbic and reticular formation.
Important to monitor patient's blood pressure after administering dose. Adjust prn.

Adult

0.05-0.10 mg/kg IV over 2 min

Pediatric

0.03-0.05 mg/kg IV; not to exceed 4 mg/dose

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs

Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, Parkinson disease, shock, respiratory depression, or glaucoma


Diazepam (Valium)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Is second-line therapy for seizures.

Adult

0.10 mg/kg IV over 2 min; may repeat q5-10min

Pediatric

0.2-0.5 mg/kg/dose IV over 2 min; may repeat q5-15min

Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohols, and MAOIs

Documented hypersensitivity; narrow-angle glaucoma; hypotension

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution with other CNS depressants, low albumin levels, hepatic disease (may increase toxicity), shock, respiratory depression, or glaucoma


Phenobarbital (Barbita, Luminal)

May be necessary to control status epilepticus.

Adult

15-20 mg/kg IV over 20 min

Pediatric

10-20 mg/kg IV; not to exceed 1 mg/kg/min

May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients stabilized on anticoagulants may require dosage adjustments if added to or withdrawn from their regimen); coadministration with alcohol may produce additive CNS effects and death; chloramphenicol, valproic acid, and MAOIs may increase phenobarbital toxicity; rifampin may decrease phenobarbital effects; induction of microsomal enzymes may result in decreased effects of oral contraceptives in women (must use additional contraceptive methods to prevent unwanted pregnancy); menstrual irregularities also may occur

Documented hypersensitivity; severe respiratory disease; marked impairment of liver function; hypotension; nephritic patients

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

In prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; caution in fever, hyperthyroidism, diabetes mellitus, and severe anemia because adverse reactions can occur; caution in myasthenia gravis and myxedema

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References

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Further Reading

Keywords

beta-blocker toxicity, beta-blocker poisoning, beta-blocker overdose, beta-adrenergic antagonist overdose, beta-adrenergic antagonist toxicity, hypertension, postmyocardial infarction, migraine headaches, essential tremors, thyrotoxicosis, glaucoma, anxiety, propranolol, nadolol, timolol, pindolol, acebutolol, labetalol, sotalol, oxprenolol, practolol, esmolol, alprenolol, metoprolol, quinidinelike effects, Vaughan-Williams class I antiarrhythmic effects, QT interval prolongation, prolonged QT interval, multifocal premature ventricular contractions, PVCs, bigeminy, ventricular tachycardia, ventricular fibrillation, torsade de pointes, seizures, hypoglycemia

Contributor Information and Disclosures

Author

Adhi Sharma, MD, Assistant Professor, Department of Emergency Medicine, Mount Sinai School of Medicine; Chairman, Department of Emergency Medicine, Good Samaritan Hospital Medical Center; Medical Toxicology Consultant, New York City Department of Health and Poison Control Center
Adhi Sharma, MD is a member of the following medical societies: American College of Clinical Toxicologists, American College of Emergency Physicians, and 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, Resident, 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.

Medical Editor

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.

Pharmacy Editor

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.

Managing Editor

John G Benitez, MD, MPH, FACMT, FACPM, FAAEM, Associate Professor, Department of Medicine, Clinical Pharmacology Division, Vanderbilt University; Managing Director, Tennessee Poison Center
John G Benitez, MD, MPH, FACMT, FACPM, FAAEM is a member of the following medical societies: 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.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

 
 
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