THE MERCK MANUAL: The Merck Manual of Diagnosis and Therapy
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Esmolol Drug Information Provided by Lexi-Comp

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Pronunciation

(ES moe lol)

Generic Available (U.S.)

Yes: Excludes infusion

Index Terms

  • Esmolol Hydrochloride

Brand Names: U.S.

  • Brevibloc

Brand Names: Canada

  • Brevibloc®

Pharmacologic Category

  • Antiarrhythmic Agent, Class II
  • Beta Blocker, Beta-1 Selective

Pharmacologic Category Synonyms

  • Class II Antiarrhythmic Agent
  • Vaughan-Williams Class II Antiarrhythmic
  • Adrenergic Blocking Agent, Beta-1 Selective

Use: Labeled Indications

Treatment of supraventricular tachycardia (SVT) and atrial fibrillation/flutter (control ventricular rate); treatment of intraoperative and postoperative tachycardia and/or hypertension; treatment of noncompensatory sinus tachycardia

Use: Unlabeled

Children: SVT and postoperative hypertension

Adults: Arrhythmia/rate control during acute coronary syndrome (eg, acute myocardial infarction, unstable angina), aortic dissection, intubation, thyroid storm, pheochromocytoma, electroconvulsive therapy

Pregnancy Risk Factor

C

Pregnancy Considerations

Adverse events were not observed in animal reproduction studies; therefore, esmolol is classified as pregnancy category C. In a cohort study, an increased risk of cardiovascular defects was observed following maternal use of beta-blockers during pregnancy. Intrauterine growth restriction (IUGR), small placentas, as well as fetal/neonatal bradycardia, hypoglycemia, and/or respiratory depression have been observed following in utero exposure to beta-blockers as a class. Adequate facilities for monitoring infants at birth should be available. Untreated chronic maternal hypertension and pre-eclampsia are also associated with adverse events in the fetus, infant, and mother. Esmolol is a short-acting beta-blocker and not intended for the chronic treatment of hypertension in pregnancy. Esmolol has been evaluated for use during intubation as an agent to offset the exaggerated pressor response observed in pregnant women with hypertension undergoing surgery.

Lactation

Excretion in breast milk unknown/use with caution

Breast-Feeding Considerations

It is not known if esmolol is excreted into breast milk. The manufacturer recommends that caution be exercised when administering esmolol to nursing women. The short half-life and the fact that it is not intended for chronic use should limit any exposure to the nursing infant.

Contraindications

Sinus bradycardia; heart block greater than first degree (except in patients with a functioning artificial pacemaker); cardiogenic shock; uncompensated cardiac failure

Warnings/Precautions

Concerns related to adverse effects:

• Anaphylactic reactions: Use caution with history of severe anaphylaxis to allergens; patients taking beta-blockers may become more sensitive to repeated challenges. Treatment of anaphylaxis (eg, epinephrine) in patients taking beta-blockers may be ineffective or promote undesirable effects.

• Hypotension: Can commonly occur; patients need close blood pressure monitoring.

• Skin necrosis: Extravasation can lead to skin necrosis and sloughing.

Disease-related concerns:

• Bronchospastic disease: In general, patients with bronchospastic disease should not receive beta-blockers; however, esmolol, with B1 selectivity, has been used cautiously with close monitoring.

• Conduction abnormality: Consider pre-existing conditions such as sick sinus syndrome before initiating.

• Diabetes: Use with caution in patients with diabetes mellitus; may potentiate hypoglycemia and/or mask signs and symptoms.

• Heart failure (HF): Use with caution in patients with compensated heart failure and monitor for a worsening of the condition.

• Myasthenia gravis: Use with caution in patients with myasthenia gravis.

• Peripheral vascular disease (PVD) and Raynaud's disease: Can precipitate or aggravate symptoms of arterial insufficiency in patients with PVD and Raynaud's disease. Use with caution and monitor for progression of arterial obstruction.

• Pheochromocytoma (untreated): Adequate alpha-blockade is required prior to use of any beta-blocker.

• Renal impairment: Use with caution in patients with renal impairment; active metabolite retained.

• Thyroid disease: May mask signs of hyperthyroidism (eg, tachycardia). If hyperthyroidism is suspected, carefully manage and monitor; abrupt withdrawal may exacerbate symptoms of hyperthyroidism or precipitate thyroid storm.

Concurrent drug therapy issues:

• Calcium channel blockers: Use with caution in patients on concurrent verapamil or diltiazem; bradycardia or heart block can occur.

• Cardiac glycosides: Use with caution in patients receiving digoxin; bradycardia or heart block can occur.

• Inhaled anesthetic agents: Use with caution in patients receiving inhaled anesthetic agents known to depress myocardial contractility.

Special populations:

• Elderly: Bradycardia may be observed more frequently in elderly patients (>65 years of age); dosage reductions may be necessary.

Other warnings/precautions:

• Abrupt withdrawal: Beta-blocker therapy should not be withdrawn abruptly (particularly in patients with CAD), but gradually tapered to avoid acute tachycardia, hypertension, and/or ischemia. Severe exacerbation of angina, ventricular arrhythmias, and myocardial infarction (MI) have been reported following abrupt withdrawal of beta-blocker therapy. Temporary but prompt resumption of beta-blocker therapy may be indicated with worsening of angina or acute coronary insufficiency.

• Hypertension associated with hypothermia: Do not use in the treatment of hypertension associated with vasoconstriction related to hypothermia.

Adverse Reactions

>10%:

Cardiovascular: Asymptomatic hypotension (dose related: 25% to 38%), symptomatic hypotension (dose related: 12%)

Miscellaneous: Diaphoresis (10%)

1% to 10%:

Cardiovascular: Peripheral ischemia (1%)

Central nervous system: Dizziness (3%), somnolence (3%), confusion (2%), headache (2%), agitation (2%), fatigue (1%)

Gastrointestinal: Nausea (7%), vomiting (1%)

Local: Pain on injection (8%), infusion site reaction

<1% (Limited to important or life-threatening): Abdominal discomfort, abnormal thinking, acne, alopecia, anorexia, anxiety, bradycardia, bronchospasm, chest pain, CHF, constipation, depression, dyspepsia, dyspnea, edema, erythema, exfoliative dermatitis, fever, flushing, heart block, lightheadedness, midscapular pain, nasal congestion, pallor, paresthesia, pruritus, pulmonary edema, rigors, seizure, severe bradycardia/asystole (rare), skin discoloration, skin irritation, skin necrosis (from extravasation), syncope, taste perversion, thrombophlebitis, urinary retention, vision change, weakness, wheezing, xerostomia

Metabolism/Transport Effects

None known.

Drug Interactions

Acetylcholinesterase Inhibitors: May enhance the bradycardic effect of Beta-Blockers. Risk C: Monitor therapy

Alpha-/Beta-Agonists (Direct-Acting): Beta-Blockers may enhance the vasopressor effect of Alpha-/Beta-Agonists (Direct-Acting). Epinephrine used as a local anesthetic for dental procedures will not likely cause clinically relevant problems. Management: Cardioselective beta-blockers and lower doses of epinephrine may confer a more limited risk. Patients who may require acute subcutaneous epinephrine (e.g., bee sting kits) should probably avoid beta blockers. Exceptions: Dipivefrin. Risk D: Consider therapy modification

Alpha1-Blockers: Beta-Blockers may enhance the orthostatic hypotensive effect of Alpha1-Blockers. The risk associated with ophthalmic products is probably less than systemic products. Risk D: Consider therapy modification

Alpha2-Agonists: Beta-Blockers may enhance the rebound hypertensive effect of Alpha2-Agonists. This effect can occur when the alpha2-agonist is abruptly withdrawn. Exceptions: Apraclonidine; Brimonidine. Risk D: Consider therapy modification

Amifostine: Antihypertensives may enhance the hypotensive effect of Amifostine. Management: When amifostine is used at chemotherapy doses, antihypertensive medications should be withheld for 24 hours prior to amifostine administration. If antihypertensive therapy can not be withheld, amifostine should not be administered. Risk D: Consider therapy modification

Aminoquinolines (Antimalarial): May decrease the metabolism of Beta-Blockers. Risk C: Monitor therapy

Amiodarone: May enhance the bradycardic effect of Beta-Blockers. Possibly to the point of cardiac arrest. Amiodarone may increase the serum concentration of Beta-Blockers. Risk C: Monitor therapy

Anilidopiperidine Opioids: May enhance the bradycardic effect of Beta-Blockers. Anilidopiperidine Opioids may enhance the hypotensive effect of Beta-Blockers. Risk C: Monitor therapy

Antihypertensives: May enhance the hypotensive effect of other Antihypertensives. Risk C: Monitor therapy

Antipsychotic Agents (Phenothiazines): May enhance the hypotensive effect of Beta-Blockers. Beta-Blockers may decrease the metabolism of Antipsychotic Agents (Phenothiazines). Antipsychotic Agents (Phenothiazines) may decrease the metabolism of Beta-Blockers. Risk C: Monitor therapy

Barbiturates: May decrease the serum concentration of Beta-Blockers. Risk C: Monitor therapy

Beta2-Agonists: Beta-Blockers (Beta1 Selective) may diminish the bronchodilatory effect of Beta2-Agonists. Of particular concern with nonselective beta-blockers or higher doses of the beta1 selective beta-blockers. Risk C: Monitor therapy

Bupivacaine: Beta-Blockers may increase the serum concentration of Bupivacaine. Risk C: Monitor therapy

Calcium Channel Blockers (Dihydropyridine): May enhance the hypotensive effect of Beta-Blockers. Bradycardia and signs of heart failure have also been reported. Risk C: Monitor therapy

Calcium Channel Blockers (Nondihydropyridine): May enhance the hypotensive effect of Beta-Blockers. Bradycardia and signs of heart failure have also been reported. Calcium Channel Blockers (Nondihydropyridine) may increase the serum concentration of Beta-Blockers. Exceptions: Bepridil [Off Market]. Risk C: Monitor therapy

Cardiac Glycosides: Beta-Blockers may enhance the bradycardic effect of Cardiac Glycosides. Risk C: Monitor therapy

Cholinergic Agonists: Beta-Blockers may enhance the adverse/toxic effect of Cholinergic Agonists. Of particular concern are the potential for cardiac conduction abnormalities and bronchoconstriction. Management: Administer these agents in combination with caution, and monitor for conduction disturbances. Avoid methacholine with any beta blocker due to the potential for additive bronchoconstriction. Risk C: Monitor therapy

Diazoxide: May enhance the hypotensive effect of Antihypertensives. Risk C: Monitor therapy

Dipyridamole: May enhance the bradycardic effect of Beta-Blockers. Risk C: Monitor therapy

Disopyramide: May enhance the bradycardic effect of Beta-Blockers. Risk C: Monitor therapy

Dronedarone: May enhance the bradycardic effect of Beta-Blockers. Dronedarone may increase the serum concentration of Beta-Blockers. This likely applies only to those agents that are metabolized by CYP2D6. Management: Use lower initial beta-blocker doses; adequate tolerance of the combination, based on ECG findings, should be confirmed prior to any increase in beta-blocker dose. Risk D: Consider therapy modification

Fingolimod: Beta-Blockers may enhance the bradycardic effect of Fingolimod. Risk C: Monitor therapy

Floctafenine: May enhance the adverse/toxic effect of Beta-Blockers. Risk X: Avoid combination

Herbs (Hypertensive Properties): May diminish the antihypertensive effect of Antihypertensives. Risk C: Monitor therapy

Herbs (Hypotensive Properties): May enhance the hypotensive effect of Antihypertensives. Risk C: Monitor therapy

Hypotensive Agents: May enhance the adverse/toxic effect of other Hypotensive Agents. Risk C: Monitor therapy

Insulin: Beta-Blockers may enhance the hypoglycemic effect of Insulin. Risk C: Monitor therapy

Lidocaine: Beta-Blockers may increase the serum concentration of Lidocaine. Risk C: Monitor therapy

Lidocaine (Systemic): Beta-Blockers may decrease the metabolism of Lidocaine (Systemic). Risk C: Monitor therapy

Lidocaine (Topical): Beta-Blockers may decrease the metabolism of Lidocaine (Topical). Risk C: Monitor therapy

MAO Inhibitors: May enhance the orthostatic hypotensive effect of Orthostatic Hypotension Producing Agents. Risk C: Monitor therapy

Mepivacaine: Beta-Blockers may increase the serum concentration of Mepivacaine. Risk C: Monitor therapy

Methacholine: Beta-Blockers may enhance the adverse/toxic effect of Methacholine. Risk X: Avoid combination

Methylphenidate: May diminish the antihypertensive effect of Antihypertensives. Risk C: Monitor therapy

Midodrine: Beta-Blockers may enhance the bradycardic effect of Midodrine. Risk C: Monitor therapy

Nonsteroidal Anti-Inflammatory Agents: May diminish the antihypertensive effect of Beta-Blockers. Risk C: Monitor therapy

Pentoxifylline: May enhance the hypotensive effect of Antihypertensives. Risk C: Monitor therapy

Phosphodiesterase 5 Inhibitors: May enhance the antihypertensive effect of Antihypertensives. Risk C: Monitor therapy

Propafenone: May increase the serum concentration of Beta-Blockers. Propafenone possesses some independent beta blocking activity. Risk C: Monitor therapy

Prostacyclin Analogues: May enhance the hypotensive effect of Antihypertensives. Risk C: Monitor therapy

QuiNIDine: May decrease the metabolism of Beta-Blockers. Risk C: Monitor therapy

Reserpine: May enhance the hypotensive effect of Beta-Blockers. Risk C: Monitor therapy

Rifamycin Derivatives: May decrease the serum concentration of Beta-Blockers. Exceptions: Rifabutin. Risk C: Monitor therapy

RiTUXimab: Antihypertensives may enhance the hypotensive effect of RiTUXimab. Risk D: Consider therapy modification

Sulfonylureas: Beta-Blockers may enhance the hypoglycemic effect of Sulfonylureas. Cardioselective beta-blockers (eg, acebutolol, atenolol, metoprolol, and penbutolol) may be safer than nonselective beta-blockers. All beta-blockers appear to mask tachycardia as an initial symptom of hypoglycemia. Ophthalmic beta-blockers are probably associated with lower risk than systemic agents. Risk C: Monitor therapy

Theophylline Derivatives: Beta-Blockers (Beta1 Selective) may diminish the bronchodilatory effect of Theophylline Derivatives. Management: Monitor for reduced theophylline efficacy during concomitant use with any beta-blocker. Beta-1 selective agents are less likely to antagonize theophylline than nonselective agents, but selectivity may be lost at higher doses. Risk C: Monitor therapy

Yohimbine: May diminish the antihypertensive effect of Antihypertensives. Risk C: Monitor therapy

Storage

Clear, colorless to light yellow solution which should be stored at 25°C (77°F); excursions permitted to 15°C to 30°C (59°F to 86°F); do not freeze. Protect from excessive heat.

Compatibility

Stable in D5LR, D51/2NS, D5NS, D5W, D5R, D5W with KCl 40 mEq/L, LR, 1/2NS, NS, sodium bicarbonate (5%)

Y-site administration: Compatible: Alcohol (ethyl), amikacin, aminophylline, amiodarone, ampicillin, atracurium, bivalirudin, butorphanol, calcium chloride, cefazolin, ceftazidime, chloramphenicol, cimetidine, cisatracurium, clindamycin, dexmedetomidine, diltiazem, dopamine, doripenem, enalaprilat, erythromycin lactobionate, famotidine, fenoldopam, fentanyl, gentamicin, heparin, hetastarch in lactated electrolyte injection (Hextend®), hydrocortisone sodium succinate, insulin (regular), labetalol, linezolid, magnesium sulfate, methyldopate, metronidazole, micafungin, midazolam, morphine, nafcillin, nicardipine, nitroglycerin, nitroprusside, norepinephrine, pancuronium, penicillin G potassium, piperacillin, polymyxin B sulfate, potassium chloride, potassium phosphates, propofol, ranitidine, remifentanil, sodium acetate, streptomycin, sulfamethoxazole/trimethoprim, tacrolimus, terbutaline, tobramycin, vancomycin, vecuronium. Incompatible: Amphotericin B cholesteryl sulfate complex, furosemide, pantoprazole, warfarin.

Mechanism of Action

Class II antiarrhythmic: Competitively blocks response to beta1-adrenergic stimulation with little or no effect of beta2-receptors except at high doses, no intrinsic sympathomimetic activity, no membrane stabilizing activity

Pharmacodynamics/Kinetics

Onset of action: Beta-blockade: I.V.: 2-10 minutes (quickest when loading doses are administered)

Duration of hemodynamic effects: 10-30 minutes; prolonged following higher cumulative doses, extended duration of use

Distribution: Vd: Esmolol: ~3.4 L/kg; Acid metabolite: ~0.4 L/kg

Protein binding: Esmolol: 55%; Acid metabolite: 10%

Metabolism: In blood by red blood cell esterases; forms acid metabolite (negligible activity; produces no clinically important effects) and methanol (does not achieve concentrations associated with methanol toxicity)

Half-life elimination: Adults: Esmolol: 9 minutes; Acid metabolite: 3.7 hours; elimination of metabolite decreases with end-stage renal disease

Excretion: Urine (~73% to 88% as acid metabolite, <2% unchanged drug)

Dosage

I.V.:

Children:

SVT (unlabeled use): A limited amount of information regarding esmolol use in pediatric patients is currently available. Some centers have utilized doses of 100-500 mcg/kg given over 1 minute for control of supraventricular tachycardias.

Postoperative hypertension (unlabeled use): Loading doses of 500 mcg/kg/minute over 1 minute with maximal doses of 50-250 mcg/kg/minute (mean: 173 mcg/kg/minute) have been used in addition to nitroprusside to treat postoperative hypertension after coarctation of aorta repair.

Adults:

Intraoperative tachycardia and/or hypertension (immediate control): Initial bolus: 80 mg (~1 mg/kg) over 30 seconds, followed by a 150 mcg/kg/minute infusion, if necessary. Adjust infusion rate as needed to maintain desired heart rate and/or blood pressure, up to 300 mcg/kg/minute.

For control of postoperative hypertension, as many as one-third of patients may require higher doses (250-300 mcg/kg/minute) to control blood pressure; the safety of doses >300 mcg/kg/minute has not been studied.

Supraventricular tachycardia (SVT), gradual control of postoperative tachycardia/hypertension: Loading dose: 500 mcg/kg over 1 minute; follow with a 50 mcg/kg/minute infusion for 4 minutes; response to this initial infusion rate may be a rough indication of the responsiveness of the ventricular rate.

Infusion may be continued at 50 mcg/kg/minute or, if the response is inadequate, titrated upward in 50 mcg/kg/minute increments (increased no more frequently than every 4 minutes) to a maximum of 200 mcg/kg/minute.

To achieve more rapid response, following the initial loading dose and 50 mcg/kg/minute infusion, rebolus with a second 500 mcg/kg loading dose over 1 minute, and increase the maintenance infusion to 100 mcg/kg/minute for 4 minutes. If necessary, a third (and final) 500 mcg/kg loading dose may be administered, prior to increasing to an infusion rate of 150 mcg/kg/minute. After 4 minutes of the 150 mcg/kg/minute infusion, the infusion rate may be increased to a maximum rate of 200 mcg/kg/minute (without a bolus dose).

Acute coronary syndromes (when relative contraindications to beta-blockade exist; unlabeled use): 500 mcg/kg over 1 minute; follow with a 50 mcg/kg/minute infusion; if tolerated and response inadequate, may titrate upward in 50 mcg/kg/minute increments every 5-15 minutes to a maximum of 300 mcg/kg/minute (Mitchell, 2002); an additional bolus (500 mcg/kg over 1 minute) may be administered prior to each increase in infusion rate (Mooss, 1994)

Electroconvulsive therapy (unlabeled use): 1 mg/kg administered 1 minute prior to induction of anesthesia (Weinger, 1991)

Intubation (unlabeled use): 1-2 mg/kg I.V. given 1.5-3 minutes prior to intubation (Kindler, 1996)

Thyrotoxicosis or thyroid storm (unlabeled use): 50-100 mcg/kg/minute (Bahn, 2011)

Guidelines for transfer to oral therapy (beta-blocker, calcium channel blocker):

Infusion should be reduced by 50% 30 minutes following the first dose of the alternative agent

Manufacturer suggests following the second dose of the alternative drug, patient's response should be monitored and if control is adequate for the first hour, esmolol may be discontinued.

Dosage adjustment in renal impairment: Dialysis: Not removed by hemo- or peritoneal dialysis; supplemental dose is not necessary.

Administration: I.V.

Infusion into small veins or through a butterfly catheter should be avoided (can cause thrombophlebitis). Medication port of premixed bags should be used to withdraw only the initial bolus, if necessary (not to be used for withdrawal of additional bolus doses).

Administration: I.V. Detail

Infusions must be administered with an infusion pump. Decrease or discontinue infusion if hypotension, congestive heart failure occur.

pH: 4.5-5.5

Monitoring Parameters

Blood pressure, MAP, heart rate, continuous ECG, respiratory rate, I.V. site

Patient Education

Esmolol is administered in emergencies; patient education should be appropriate to the situation.

Geriatric Considerations

Due to alterations in the beta-adrenergic autonomic nervous system, beta-adrenergic blockade may result in less hemodynamic response than seen in younger adults. Studies indicate that despite decreased sensitivity to the chronotropic effects of beta-blockade with age, there appears to be an increased myocardial sensitivity to the negative inotropic effect during stress (ie, exercise). Controlled trials have shown the overall response rate for propranolol to be only 20% to 50% in elderly populations. Therefore, all beta-adrenergic blocking drugs may result in a decreased response as compared to younger adults.

Anesthesia and Critical Care Concerns/Other Considerations

This agent is also used to blunt sympathetic response during intubation, in “at-risk” patients such as those with coronary artery disease (CAD), angina, uncontrolled hypertension, and hyperthyroidism. Esmolol may lose cardio-selection (beta1 specificity) at higher doses. It should be used with caution in patients with bronchospastic pulmonary disease and diabetes.

Cardiovascular Considerations

Coronary Artery Bypass Graft (CABG) Surgery: In patients undergoing CABG, the use of beta-blockers has consistently demonstrated a reduction in the incidence of postoperative atrial fibrillation (POAF). The 2011 ACCF/AHA CABG guidelines recommend the administration of beta-blockers (not specified) for at least 24 hours prior to CABG in all patients unless a contraindication exists. Beta-blockade should be reinstituted as soon as possible after the surgery and prescribed to all CABG patients who do not have contraindications at the time of hospital discharge. Patients who are at high risk of developing POAF who have contraindications to beta-blockade may receive preoperative amiodarone instead. The use of preoperative beta-blockers has also demonstrated a reduction of in-hospital mortality (especially in patients with and LVEF>30%). Beta-blockers also reduce perioperative myocardial ischemia therefore strengthening the need for perioperative administration. In patients who cannot tolerate oral beta-blockade, the use of I.V. beta-blockers (eg, esmolol, metoprolol) is reasonable (Hillis, 2011).

Dental Health: Effects on Dental Treatment

Esmolol is a cardioselective beta-blocker. Local anesthetic with vasoconstrictor can be safely used in patients medicated with esmolol. Nonselective beta-blockers (ie, propranolol, nadolol) enhance the pressor response to epinephrine, resulting in hypertension and bradycardia; this has not been reported for esmolol. Many nonsteroidal anti-inflammatory drugs, such as ibuprofen and indomethacin, can reduce the hypotensive effect of beta-blockers after 3 or more weeks of therapy with the NSAID. Short-term NSAID use (ie, 3 days) requires no special precautions in patients taking beta-blockers.

Dental Health: Vasoconstrictor/Local Anesthetic Precautions

No information available to require special precautions

Mental Health: Effects on Mental Status

May cause drowsiness, confusion, fatigue, or depression

Mental Health: Effects on Psychiatric Treatment

Barbiturates may decrease effects of esmolol

Nursing: Physical Assessment/Monitoring

Requires continuous cardiac, hemodynamic, and infusion site monitoring (to prevent extravasation). Taper dosage slowly when discontinuing. Advise patients with diabetes to monitor glucose levels closely; beta-blockers may alter glucose tolerance.

Oncology: Vesicant

Vesicant

Dosage Forms

Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product

Infusion, premixed in NS, as hydrochloride [preservative free]:

Brevibloc: 2000 mg (100 mL) [20 mg/mL; double strength]

Brevibloc: 2500 mg (250 mL) [10 mg/mL]

Injection, solution, as hydrochloride [preservative free]: 10 mg/mL (10 mL)

Brevibloc: 10 mg/mL (10 mL)

Brevibloc: 20 mg/mL (5 mL [DSC]) [double strength]

References

Angaran DM, Schultz NJ, and Tschida VH, "Esmolol Hydrochloride: An Ultrashort-Acting, Beta-Adrenergic Blocking Agent," Clin Pharm, 1986, 5(4):288-303.

Anderson JL, Adams CD, Antman EM, et al, "ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction) Developed in Collaboration With the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine," J Am Coll Cardiol, 2007, 50(7):e1-e157.

Antman EM, Anbe SC, Alpert JS, et al, "ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction - Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction)," Circulation, 2004, 110(5):588-636.

Bahn RS (Chair), Burch HB, Cooper DS, et al, “Hyperthyroidism and Other Causes of Thyrotoxicosis: Management Guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists,” Thyroid, 2011, 21(6):593-646.

Blomström-Lundqvist C, Scheinman MM, Aliot EM, et al, “ACC/AHA/ESC Guidelines for the Management of Patients With Supraventricular Arrhythmias--Executive Summary. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias),” Circulation, 2003, 108(15):1871-909.

Brunette DD and Rothong C, "Emergency Department Management of Thyrotoxic Crisis With Esmolol," Am J Emerg Med, 1991, 9(3):232-4.

Chobanian AV, Bakris GL, Black HR, et al, "The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 Report," JAMA, 2003, 289(19):2560-71.

Cuneo BF, Zales VR, Blahunka PC, et al, "Pharmacodynamics and Pharmacokinetics of Esmolol, A Short-Acting Beta-Blocking Agent in Children," Pediatr Cardiol, 1994, 15(6):296-301.

Erstad BL and Barletta JF, "Treatment of Hypertension in the Perioperative Patient," Ann Pharmacother, 2000, 34(1):66-79.

Fuster V, Ryden LE, Cannom DS, et al, "ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation-Executive Summary. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation). Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society," J Am Coll Cardiol, 2006, 48(4):854-906.

Gorczynski RJ, "Basic Pharmacology of Esmolol," Am J Cardiol, 1985, 56(11):3F-13F.

Gray RJ, "Managing Critically Ill Patients With Esmolol: An Ultra-Short Acting Beta-Adrenergic Blocker," Chest, 1988, 93(2):398-403.

Hillis LD, Smith PK, Anderson JL, et al, “2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines,” Circulation, 2011, 124(23):2610-42.

Kindler CH, Schumacher PG, Schneider MC, et al, "Effects of Intravenous Lidocaine and/or Esmolol on Hemodynamic Responses to Laryngoscopy and Intubation: A Double-Blind, Controlled Clinical Trial," J Clin Anesth, 1996, 8(6):491-6.

Lang DM, "Anaphylactoid and Anaphylactic Reactions. Hazards of Beta-Blockers," Drug Saf, 1995, 12(5):299-304.

Lowenthal DT, Porter RS, Saris SD, et al, "Clinical Pharmacology, Pharmacodynamics and Interactions With Esmolol," Am J Cardiol, 1985, 56(11):14F-18F.

Luyt D, Dance M, Litmanovich H, et al, "Esmolol in the Treatment of Severe Tachycardia in Neonatal Tetanus," Anaesth Intensive Care, 1994, 22(3):303-4.

Miller A and White S, "Survival Following Massive Intravenous Esmolol Overdose," Clin Toxicol, 1995, 33(5):490-1.

Mitchell RG, Stoddard MF, Ben-Yehuda O, et al, "Esmolol in Acute Ischemic Syndromes," Am Heart J, 2002, 144(5):E9.

Mooss AN, Hilleman DE, Mohiuddin SM, et al, "Safety of Esmolol in Patients With Acute Myocardial Infarction Treated With Thrombolytic Therapy Who Had Relative Contraindications to Beta-Blocker Therapy," Ann Pharmacother, 1994, 28(6):701-3.

National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents, "The Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents," Pediatrics, 2004, 114(2 Suppl):555-76.

Skanes AC, Healey JS, Cairns JA, et al, “Focused 2012 Update of the Canadian Cardiovascular Society Atrial Fibrillation Guidelines: Recommendations for Stroke Prevention and Rate/Rhythm Control,” Can J Cardiol, 2012, 28(2):125-36.

Trippel DL, Wiest DB, and Gillette PC, "Cardiovascular and Antiarrhythmic Effects of Esmolol in Children," J Pediatr, 1991, 119(1):142-7.

Vincent RN, Click LA, Williams HM, et al, "Esmolol As an Adjunct in the Treatment of Systemic Hypertension After Operative Repair of Coarctation of the Aorta," Am J Cardiol, 1990, 65(13):941-3.

Wann SL, Curtis AB, January CT, et al, "2011 ACCF/AHA/HRS Focused Update on the Management of Patients With Atrial Fibrillation (Updating the 2006 Guideline): A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines," Circulation, 2011, 123 (1):104-23.

Weinger MB, Partridge BL, Hauger R, et al, "Prevention of the Cardiovascular and Neuroendocrine Response to Electroconvulsive Therapy: I. Effectiveness of Pretreatment Regimens on Hemodynamics," Anesth Analg, 1991, 73(5):556-62.

Wiest DB, "Esmolol: A Review of Its Therapeutic Efficacy and Pharmacokinetic Characteristics," Clin Pharmacokinet, 1995, 28(3):190-202.

Wiest DB, Garner SS, and Childress LM, "Stability of Esmolol Hydrochloride in 5% Dextrose Injection," Am J Health Syst Pharm, 1995, 52(7):716-8.

Wiest DB, Trippel DL, Gillette PC, et al, "Pharmacokinetics of Esmolol in Children," Clin Pharmacol Ther, 1991, 49(6):618-23.

International Brand Names

  • Ai Luo (CL)
  • Breviblo (PK)
  • Brevibloc (AR, AT, AU, BE, BR, CH, CZ, DK, ES, FI, FR, GB, GR, HK, HN, HU, IE, IT, KP, MX, NL, NO, NZ, PL, SE, TH, TR, TW, UY)
  • Escord (IN)

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Last full review/revision March 2012

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