Acute aortic syndromes/acute aortic dissection (off-label use):
Note: Manage patients on an emergency basis (including operative assessment) by first controlling pain with IV opioids and heart rate (target <60 beats per minute) with a parenteral beta blocker (eg, esmolol) while targeting systolic blood pressure of 100 to 120 mm Hg (or lowest tolerated pressure without compromising perfusion). If systolic blood pressure remains elevated after heart rate is consistently <60 beats per minute with beta-blockade, may consider adding a parenteral vasodilator (ie, nitroprusside or nicardipine). Invasive blood pressure monitoring, preferably via arterial line, in a critical care unit is recommended for appropriate dose titration (ACC/AHA [Whelton 2018]; ACCF/AHA [Hiratzka 2010]).
IV: Initial: 500 mcg/kg loading dose over 1 minute, followed by a continuous infusion of 25 to 50 mcg/kg/minute. Titrate infusion by 25 to 50 mcg/kg/minute every 5 minutes as needed to achieve target heart rate and blood pressure; for more rapid blood pressure control, may consider a repeat loading dose (eg, 500 mcg/kg) before every up titration; maximum continuous infusion dose: 300 mcg/kg/minute (ACC/AHA [Whelton 2018]; Marik 2007; Marik 2011; Peixoto 2019; Varon 2008).
Atrial fibrillation/flutter, acute ventricular rate control:
Note: Avoid in patients with decompensated heart failure; for unstable patients, electrical cardioversion is preferred (AHA/ACC/HRS [January 2014]; AHA [Panchal 2020].
Rapid titration with bolus doses: IV: Initial: 500 mcg/kg loading dose over 1 minute followed by a continuous infusion of 50 mcg/kg/minute; reassess clinical response after 4 minutes and if ventricular rate is not controlled, administer a second bolus of 500 mcg/kg and increase infusion to 100 mcg/kg/minute; reassess clinical response after 4 minutes and if ventricular rate is not controlled, administer a third (and final) bolus of 500 mcg/kg and increase infusion to 150 mcg/kg/minute; reassess clinical response after 4 minutes and if ventricular rate is not controlled, increase infusion to a maximum continuous infusion dose of 200 mcg/kg/minute (without a bolus dose).
Slow titration without bolus doses: IV: Initial: 50 mcg/kg/minute; titrate as needed based on clinical response every 30 minutes in increments of 50 mcg/kg/minute up to a maximum continuous infusion dose of 200 mcg/kg/minute.
Electroconvulsive therapy (off-label use): IV: 1,000 mcg/kg administered 1 minute prior to induction of anesthesia (Weinger 1991).
Hypertensive emergency (off-label use):
Note: In general, reduce mean arterial blood pressure gradually by ~10% to 20% over the first hour, then by an additional 5% to 15% over the next 23 hours, unless there is a compelling indication for more rapid blood pressure and heart rate control (eg, acute aortic dissection) Invasive blood pressure monitoring is recommended for appropriate dose titration (ACC/AHA [Whelton 2018]; Elliot 2022a).
IV: Initial: 250 to 500 mcg/kg loading dose over 1 minute, followed by a continuous infusion of 25 to 50 mcg/kg/minute. Titrate infusion by 25 to 50 mcg/kg/minute every 5 minutes as needed to achieve target blood pressure while maintaining adequate heart rate; for more rapid blood pressure control, may consider a repeat loading dose (eg, 250 to 500 mcg/kg) before every up-titration; maximum continuous infusion dose: 300 mcg/kg/minute (ACC/AHA [Whelton 2018]; Elliot 2022b; Marik 2007; Marik 2011; Peixoto 2019; Varon 2008).
Intraoperative and postoperative tachycardia and/or hypertension:
Immediate control: IV: Initial bolus: 1,000 mcg/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).
Gradual control: IV: Initial bolus: 500 mcg/kg over 1 minute, followed by a 50 mcg/kg/minute infusion for 4 minutes. 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 300 mcg/kg/minute; may administer an optional loading dose equal to the initial bolus (500 mcg/kg over 1 minute) prior to each increase in infusion rate.
For control of tachycardia, doses >200 mcg/kg/minute provide minimal additional effect. For control of postoperative hypertension, as many as one-third of patients may require higher doses (250 to 300 mcg/kg/minute) to control blood pressure; the safety of doses >300 mcg/kg/minute has not been studied.
Intubation (off-label use): IV: 1,000 to 2,000 mcg/kg given 1.5 to 3 minutes prior to intubation (Kindler 1996; Levitt 2001; Ugur 2007).
Supraventricular tachycardia or noncompensatory sinus tachycardia:
IV: Loading dose (optional): 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 (manufacturer’s labeling).
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) up to 300 mcg/kg/minute (ACC/AHA/HRS [Page 2016]; manufacturer’s labeling).
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 500 mcg/kg loading dose may be administered, prior to increasing to an infusion rate of 150 mcg/kg/minute. The infusion rate may be increased further in 50 mcg/kg/minute increments, with or without bolus doses, up to a maximum infusion rate of 300 mcg/kg/minute (ACC/AHA/HRS [Page 2016]; manufacturer’s labeling).
Thyroid storm (alternative agent) (off-label use):
Note: For control of adrenergic symptoms until thyroid storm has resolved (ATA [Ross 2016]). Administer while under continuous cardiac monitoring; may be used if it is uncertain that a beta-blocker will be tolerated since after discontinuation, duration of action is very short. Avoid use in patients with decompensated low-output heart failure (systolic dysfunction) (ATA [Ross 2016]; Choudhury 1998; Modarresi 2020; Nayak 2006; Woeber 1992).
IV: 250 to 500 mcg/kg loading dose, followed by a continuous infusion of 50 to 100 mcg/kg/minute; adjust dose based on heart rate and BP. Use in combination with other appropriate agents (ATA [Ross 2016]; Brunette 1991; Ross 2022).
Ventricular tachycardia (off-label use): IV: 500 mcg/kg bolus followed by 50 mcg/kg/minute (AHA/ACC/HRS [Al-Khatib 2017]).
Guidelines for transfer to oral therapy (beta-blocker, calcium channel blocker):
Infusion should be reduced by 50% thirty 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 for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
No dosage adjustment necessary. Not removed by hemo- or peritoneal dialysis. Supplemental dose is not necessary.
No dosage adjustment necessary.
(For additional information see "Esmolol: Pediatric drug information")
Note: Dose must be titrated to individual response and tolerance.
Hypertensive emergency/urgency: Infants, Children, and Adolescents: Continuous IV infusion: 100 to 500 mcg/kg/minute infusion (NHBPEP Working Group 2004); another approach is to initiate therapy with a bolus of 100 to 500 mcg/kg over 1 minute, followed by an infusion of 25 to 100 mcg/kg/minute; titrating as needed up to 500 mcg/kg/minute (Chandar 2012; Temple 2000).
Postoperative hypertension: Limited data available; large effective dose range reported: Infants and Children: Initial IV bolus: 100 to 500 mcg/kg, followed by continuous IV infusion: Initial rate: 100 to 500 mcg/kg/minute; titrate to effect; range of effective doses: 125 to 1,000 mcg/kg/minute (Tabbutt 2008a; Tabbutt 2008b; Wiest 1998). Dosing based on several trials. In the largest trial, patients (n=118, weight ≥2.5 kg, age <6 years, mean age: ~18 months) experiencing hypertension after coarctation of aorta repair received a median maximum dose of 521 mcg/kg/minute (Tabbutt 2008b); the need for coadministration of nitroprusside infusion increased with patient age (age ≤30 days: 27%; age >30 days to <2 years: 54%; age 2 to 6 years: 69%). In a smaller trial (n=20, age range: 1 month to 12 years, median age: 25.6 months), patients experiencing hypertension after heart surgery (including 10 with coarctation of the aorta) required a higher mean effective dose of 700 mcg/kg/minute. In this trial, infants were initiated at 100 mcg/kg/minute, then titrated by 50 mcg/kg/minute every 10 minutes; patients with aortic coarctation repair required a significantly higher dose (mean: 830 ± 153 mcg/kg/minute) than patients with repair of other congenital heart defects (mean: 570 ± 230 mcg/kg/minute) (Wiest 1998).
Supraventricular tachycardia (SVT): Limited data available: Children and Adolescents: Initial IV bolus: 100 to 500 mcg/kg over 1 minute followed by a continuous IV infusion: Initial rate: 25 to 100 mcg/kg/minute, titrate in 25 to 50 mcg/kg/minute increments; usual maintenance dose: 50 to 500 mcg/kg/minute (Park 2014); doses up to 1,000 mcg/kg/minute have been reported (Trippel 1991). One electrophysiologic study assessing esmolol-induced beta-blockade (n=20, age range: 2 to 16 years) used an initial dose of 600 mcg/kg over 2 minutes followed by an infusion of 200 mcg/kg/minute; the infusion was titrated upward by 50 to 100 mcg/kg/minute every 5 to 10 minutes until a reduction >10% in heart rate or mean blood pressure occurred. Mean dose required: 550 mcg/kg/minute with a range of 300 to 1,000 mcg/kg/minute (Trippel 1991).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Infants, Children, and Adolescents: No dosage adjustment necessary. Not removed by hemo- or peritoneal dialysis; supplemental dose is not necessary (Aronoff 2007; Flaherty 1989).
There are no specific pediatric recommendations; based on experience in adult patients, no dosage adjustment required.
Refer to adult dosing.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous, as hydrochloride:
Brevibloc: 100 mg/10 mL (10 mL)
Brevibloc in NaCl: 2000 mg (100 mL); 2500 mg (250 mL)
Generic: 2000 mg (100 mL); 2500 mg (250 mL)
Solution, Intravenous, as hydrochloride [preservative free]:
Brevibloc in NaCl: 2000 mg (100 mL); 2500 mg (250 mL) [latex free, pvc free]
Brevibloc Premixed: 2500 mg (250 mL) [latex free, pvc free]
Brevibloc Premixed DS: 2000 mg (100 mL) [latex free, pvc free]
Generic: 2000 mg (100 mL); 2500 mg (250 mL); 100 mg/10 mL (10 mL); 2500 mg/250 mL (250 mL); 2000 mg/100 mL (100 mL)
Yes
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous, as hydrochloride:
Brevibloc: 2500 mg (250 mL); 100 mg/10 mL (10 mL)
IV: Loading doses may be administered over 30 seconds to 1 minute depending on how urgent the need for effect. 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).
Vesicant; ensure proper needle or catheter placement prior to and during infusion; avoid extravasation.
Extravasation management: If extravasation occurs, stop infusion immediately and disconnect (leave cannula/needle in place); gently aspirate extravasated solution (do NOT flush the line); remove needle/cannula; elevate extremity.
Parenteral: IV: Commercially available concentrations (10 mg/mL and 20 mg/mL) are iso-osmotic and can be used for direct IV use; loading doses (eg, Adults: 500 mcg/kg) may be administered over 30 seconds to 1 minute depending on how urgent the need for effect. Do not introduce additives into the premixed bags. Medication port of premixed bag should be used to withdraw only the initial bolus; do not use medication port to withdraw additional bolus doses (sterility cannot be assured).
Vesicant; ensure proper needle or catheter placement prior to and during infusion; avoid extravasation. If extravasation occurs, stop infusion immediately and disconnect (leave cannula/needle in place); gently aspirate extravasated solution (do NOT flush the line); remove needle/cannula; elevate extremity.
Note: Premixed solutions available.
IV infusion: 2500 mg in 250 mL (concentration: 10,000 mcg/mL) or 2000 mg in 100 mL (concentration: 20,000 mcg/mL) of D5W or NS
Note: Premixed solutions available.
IV infusion: 10 mg/mL, 20 mg/mL
Intraoperative and postoperative tachycardia and/or hypertension: Treatment of intraoperative and postoperative tachycardia and/or hypertension
Sinus tachycardia: Treatment of noncompensatory sinus tachycardia
Supraventricular tachycardia and atrial fibrillation/flutter: Control of ventricular rate in patients with supraventricular tachycardia or atrial fibrillation/flutter
Acute aortic syndromes/acute aortic dissection; Electroconvulsive therapy (attenuation of adrenergic response); Hypertensive emergency; Intubation (attenuation of adrenergic response); Thyroid storm; Ventricular tachycardia
Esmolol may be confused with Osmitrol.
Brevibloc may be confused with Brevital, Bumex, Buprenex.
The Institute for Safe Medication Practices (ISMP) includes this medication among its list of drugs which have a heightened risk of causing significant patient harm when used in error.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
>10%: Cardiovascular: Asymptomatic hypotension (25%), symptomatic hypotension (12%)
1% to 10%:
Cardiovascular: Peripheral ischemia (1%)
Central nervous system: Dizziness (≤3%), drowsiness (3%), headache (2%), agitation (≤2%), confusion (≤2%)
Gastrointestinal: Nausea (7%), vomiting (1%)
Local: Infusion site reaction (8%; including inflammation and induration)
<1%, postmarketing, and/or case reports: Abdominal distress, abnormality in thinking, angioedema, anxiety, bradycardia, constipation, coronary artery vasospasm, depression, dyspepsia, flushing, heart block, hyperkalemia, increased heart rate (moderate increase above pretreatment levels 30 minutes after discontinuation), infusion site irritation, local thrombophlebitis (at infusion site), local tissue necrosis (at infusion site), pallor, paresthesia, psoriasis, renal tubular acidosis (hyperkalemic), seizure, severe bradycardia, sinus pause, skin blister (at infusion site), syncope, urinary retention, urticaria, voice disorder, xerostomia
Hypersensitivity to esmolol or any component of the formulation; severe sinus bradycardia; heart block greater than first degree (except in patients with a functioning artificial ventricular pacemaker); sick sinus syndrome; cardiogenic shock; decompensated heart failure; IV administration of calcium channel blockers (eg, verapamil) in close proximity to esmolol (ie, while cardiac effects of other drug are still present); pulmonary hypertension
Documentation of allergenic cross-reactivity for beta-blockers is limited. However, because of similarities in chemical structure and/or pharmacologic actions, the possibility of cross-sensitivity cannot be ruled out with certainty.
Canadian labeling: Additional contraindications (not in US labeling): Patients requiring inotropic agents and/or vasopressors to maintain cardiac output and systolic blood pressure; hypotension; right ventricular failure secondary to pulmonary hypertension; untreated pheochromocytoma
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.
• Extravasation: Vesicant; ensure proper needle or catheter placement prior to and during infusion. Avoid extravasation. Extravasation can lead to skin necrosis and sloughing; avoid infusions into small veins or through a butterfly catheter.
• Hyperkalemia: Esmolol has been associated with elevations in serum potassium and development of hyperkalemia especially in patients with risk factors (eg, kidney impairment); monitor serum potassium during therapy.
• Hypotension: Can commonly occur; patients need close blood pressure monitoring. If an unacceptable drop in blood pressure occurs, reduction in dose or discontinuation may reverse hypotension (usually within 30 minutes).
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: Can cause bradycardia including sinus pause, heart block, severe bradycardia, and cardiac arrest. Consider preexisting conditions such as first degree AV block, sick sinus syndrome, or other conduction disorders before initiating; use is contraindicated in patients with sick sinus syndrome or second- or third-degree AV block (except in patients with a functioning artificial ventricular pacemaker).
• Diabetes: Use with caution in patients with diabetes mellitus; may potentiate hypoglycemia and/or mask signs and symptoms.
• Heart failure: Use with caution in patients with compensated heart failure and monitor for a worsening of the condition. Use is contraindicated in patients with decompensated heart failure.
• Kidney impairment: Use with caution in patients with kidney impairment; active metabolite retained.
• Myasthenia gravis: Use with caution in patients with myasthenia gravis.
• Peripheral vascular disease (PVD) and Raynaud disease: Can precipitate or aggravate symptoms of arterial insufficiency in patients with PVD and Raynaud 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.
• 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.
Special populations:
• Older patients: Bradycardia may be observed more frequently in 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: Use esmolol with caution in patients with hypertension associated with hypothermia; monitor vital signs closely and titrate esmolol slowly.
• Hypovolemic patients: Avoid use in patients with hypovolemia; treat hypovolemia first, otherwise, use of esmolol may attenuate reflex tachycardia and further increase the risk of hypotension.
None known.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.
Acetylcholinesterase Inhibitors: May enhance the bradycardic effect of Beta-Blockers. Risk C: Monitor therapy
Alfuzosin: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
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 C: Monitor therapy
Alpha2-Agonists: May enhance the AV-blocking effect of Beta-Blockers. Sinus node dysfunction may also be enhanced. Beta-Blockers may enhance the rebound hypertensive effect of Alpha2-Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. Management: Closely monitor heart rate during treatment with a beta blocker and clonidine. Withdraw beta blockers several days before clonidine withdrawal when possible, and monitor blood pressure closely. Recommendations for other alpha2-agonists are unavailable. Risk D: Consider therapy modification
Amifostine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Amifostine. Management: When used at chemotherapy doses, hold blood pressure lowering medications for 24 hours before amifostine administration. If blood pressure lowering therapy cannot be held, do not administer amifostine. Use caution with radiotherapy doses of amifostine. Risk D: Consider therapy modification
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
Amphetamines: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy
Antidiabetic Agents: Beta-Blockers (Beta1 Selective) may enhance the hypoglycemic effect of Antidiabetic Agents. 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
Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may enhance the hypotensive effect of Antipsychotic Agents (Second Generation [Atypical]). Risk C: Monitor therapy
Barbiturates: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Benperidol: May enhance the hypotensive effect of Blood Pressure Lowering Agents. 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
Bradycardia-Causing Agents: May enhance the bradycardic effect of other Bradycardia-Causing Agents. Risk C: Monitor therapy
Brigatinib: May diminish the antihypertensive effect of Antihypertensive Agents. Brigatinib may enhance the bradycardic effect of Antihypertensive Agents. Risk C: Monitor therapy
Brimonidine (Topical): May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Bromperidol: May diminish the hypotensive effect of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may enhance the hypotensive effect of Bromperidol. Risk X: Avoid combination
Bupivacaine: Beta-Blockers may increase the serum concentration of Bupivacaine. Risk C: Monitor therapy
Calcium Channel Blockers (Nondihydropyridine): May enhance the bradycardic effect of Esmolol. Management: Administration of IV verapamil or diltiazem together with esmolol is contraindicated if one agent is given while the effects of the other are still present. Canadian esmolol labeling specifies that use within 24 hours is contraindicated. Risk D: Consider therapy modification
Cannabis: Beta-Blockers may enhance the adverse/toxic effect of Cannabis. Specifically, the risk of hypoglycemia may be increased. Risk C: Monitor therapy
Ceritinib: Bradycardia-Causing Agents may enhance the bradycardic effect of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Risk D: Consider therapy modification
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. Risk C: Monitor therapy
Dexmethylphenidate: May diminish the therapeutic effect of Antihypertensive Agents. Risk C: Monitor therapy
Diazoxide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. 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. Beta-Blockers may enhance the negative inotropic effect of Disopyramide. Risk C: Monitor therapy
DOBUTamine: Beta-Blockers may diminish the therapeutic effect of DOBUTamine. 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. Increase monitoring for clinical response and adverse effects. Risk D: Consider therapy modification
DULoxetine: Blood Pressure Lowering Agents may enhance the hypotensive effect of DULoxetine. Risk C: Monitor therapy
EPHEDrine (Systemic): Beta-Blockers may diminish the therapeutic effect of EPHEDrine (Systemic). Risk C: Monitor therapy
EPINEPHrine (Nasal): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of EPINEPHrine (Nasal). Risk C: Monitor therapy
EPINEPHrine (Oral Inhalation): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of EPINEPHrine (Oral Inhalation). Risk C: Monitor therapy
Epinephrine (Racemic): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of Epinephrine (Racemic). Risk C: Monitor therapy
EPINEPHrine (Systemic): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of EPINEPHrine (Systemic). Risk C: Monitor therapy
Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates): Beta-Blockers may enhance the vasoconstricting effect of Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates). Risk C: Monitor therapy
Etilefrine: May enhance the bradycardic effect of Beta-Blockers. Beta-Blockers may diminish the therapeutic effect of Etilefrine. Risk C: Monitor therapy
Etofylline: Beta-Blockers may diminish the therapeutic effect of Etofylline. Risk X: Avoid combination
Fexinidazole: Bradycardia-Causing Agents may enhance the arrhythmogenic effect of Fexinidazole. Risk X: Avoid combination
Fingolimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Fingolimod. Management: Consult with the prescriber of any bradycardia-causing agent to see if the agent could be switched to an agent that does not cause bradycardia prior to initiating fingolimod. If combined, perform continuous ECG monitoring after the first fingolimod dose. Risk D: Consider therapy modification
Flunarizine: May enhance the therapeutic effect of Antihypertensive Agents. Risk C: Monitor therapy
Grass Pollen Allergen Extract (5 Grass Extract): Beta-Blockers may enhance the adverse/toxic effect of Grass Pollen Allergen Extract (5 Grass Extract). More specifically, Beta-Blockers may inhibit the ability to effectively treat severe allergic reactions to Grass Pollen Allergen Extract (5 Grass Extract) with epinephrine. Some other effects of epinephrine may be unaffected or even enhanced (e.g., vasoconstriction) during treatment with Beta-Blockers. Management: Consider alternatives to either grass pollen allergen extract (5 grass extract) or beta-blockers in patients with indications for both agents. Canadian product labeling specifically lists this combination as contraindicated. Risk D: Consider therapy modification
Herbal Products with Blood Pressure Increasing Effects: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy
Herbal Products with Blood Pressure Lowering Effects: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Hypotension-Associated Agents: Blood Pressure Lowering Agents may enhance the hypotensive effect of Hypotension-Associated Agents. Risk C: Monitor therapy
Isoproterenol: Beta-Blockers may diminish the therapeutic effect of Isoproterenol. Risk C: Monitor therapy
Ivabradine: Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. Risk C: Monitor therapy
Lacosamide: Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. Risk C: Monitor therapy
Levodopa-Containing Products: Blood Pressure Lowering Agents may enhance the hypotensive effect of Levodopa-Containing Products. Risk C: Monitor therapy
Lidocaine (Systemic): Beta-Blockers may increase the serum concentration of Lidocaine (Systemic). Risk C: Monitor therapy
Loop Diuretics: May enhance the hypotensive effect of Antihypertensive Agents. Risk C: Monitor therapy
Lormetazepam: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Mavacamten: Beta-Blockers may enhance the adverse/toxic effect of Mavacamten. Specifically, negative inotropic effects may be increased. 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 C: Monitor therapy
Methoxyflurane: May enhance the hypotensive effect of Beta-Blockers. Risk C: Monitor therapy
Methylphenidate: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy
Midodrine: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Mivacurium: Beta-Blockers may enhance the therapeutic effect of Mivacurium. Risk C: Monitor therapy
Molsidomine: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Morphine (Systemic): May increase the serum concentration of Esmolol. Risk C: Monitor therapy
Naftopidil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Nicergoline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Nicorandil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
NIFEdipine: May enhance the hypotensive effect of Beta-Blockers. NIFEdipine may enhance the negative inotropic effect of Beta-Blockers. Risk C: Monitor therapy
Nitroprusside: Blood Pressure Lowering Agents may enhance the hypotensive effect of Nitroprusside. Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents: May diminish the antihypertensive effect of Beta-Blockers. Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents (Topical): May diminish the therapeutic effect of Beta-Blockers. Risk C: Monitor therapy
Obinutuzumab: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Management: Consider temporarily withholding blood pressure lowering medications beginning 12 hours prior to obinutuzumab infusion and continuing until 1 hour after the end of the infusion. Risk D: Consider therapy modification
Ozanimod: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Pentoxifylline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Pholcodine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Pholcodine. Risk C: Monitor therapy
Phosphodiesterase 5 Inhibitors: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Ponesimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Ponesimod. Management: Avoid coadministration of ponesimod with drugs that may cause bradycardia when possible. If combined, monitor heart rate closely and consider obtaining a cardiology consult. Do not initiate ponesimod in patients on beta-blockers if HR is less than 55 bpm. Risk D: Consider therapy modification
Prostacyclin Analogues: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Quinagolide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Reserpine: May enhance the hypotensive effect of Beta-Blockers. Risk C: Monitor therapy
Rivastigmine: May enhance the bradycardic effect of Beta-Blockers. Risk X: Avoid combination
Siponimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. If combined, consider obtaining a cardiology consult regarding patient monitoring. Risk D: Consider therapy modification
Succinylcholine: Beta-Blockers may enhance the neuromuscular-blocking effect of Succinylcholine. Risk C: Monitor therapy
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
Tasimelteon: Beta-Blockers may diminish the therapeutic effect of Tasimelteon. Management: Consider avoiding nighttime administration of beta-blockers during tasimelteon therapy due to the potential for reduced tasimelteon efficacy. Risk D: Consider therapy modification
Theophylline Derivatives: Beta-Blockers (Beta1 Selective) may diminish the bronchodilatory effect of Theophylline Derivatives. Risk C: Monitor therapy
Tofacitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
White Birch Allergen Extract: Beta-Blockers may enhance the adverse/toxic effect of White Birch Allergen Extract. Specifically, beta-blockers may reduce the effectiveness of beta-agonists that may be required to treat systemic reactions to white birch allergen extract. Risk X: Avoid combination
Exposure to esmolol may cause fetal bradycardia which may continue after esmolol is discontinued. If maternal use of a beta-blocker is needed, fetal growth should be monitored during pregnancy and the newborn should be monitored for 48 hours after delivery for bradycardia, hypoglycemia, and respiratory depression (ESC [Regitz-Zagrosek 2018]).
Esmolol is a short-acting beta-blocker and not indicated for the chronic treatment of hypertension; however, use may be considered as an alternative agent for hypertensive emergencies in pregnancy (ACOG 2019; ESC [Cífková 2020]). Agents other than esmolol may be preferred for the treatment of supraventricular tachycardia, atrial fibrillation, atrial flutter, and ventricular tachycardia in pregnancy. Consult current guidelines for indication specific recommendations (ACC/AHA/HRS [Page 2016]; ESC [Regitz-Zagrosek 2018]).
It is not known if esmolol is present in breast milk.
Due to the potential for serious adverse reactions in the breastfed infant, the manufacturer recommends a decision be made whether to discontinue breastfeeding or the drug, considering the importance of treatment to the mother. The short half-life and the fact that it is not intended for chronic use should limit any potential exposure to the breastfeeding infant.
Blood pressure, MAP, heart rate, continuous ECG, respiratory rate, IV site; serum potassium (especially with kidney impairment); consult individual institutional policies and procedures
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
Onset of action: Beta-blockade: IV: 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:
Children ≥2.5 years and Adolescents ≤16 years: 2 ± 1.4 L/kg (range: 0.5 to 3.6 L/kg) (Wiest 1991)
Adults: 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:
Children ≥18 months and Adolescents ≤16 years: Variable; mean range: 2.7 to 4.8 minutes (reported full range: 0.2 to 9.9 minutes) (Cuneo 1994; Tabbutt 2008; Wiest 1991; Wiest 1998)
Adults: Esmolol: 9 minutes; Acid metabolite: 3.7 hours; elimination of metabolite decreases with end-stage kidney disease
Excretion: Urine (~73% to 88% as acid metabolite, <2% unchanged drug)
Solution (Brevibloc in NaCl Intravenous)
2000 mg/100 mL (per mL): $2.16
2500 mg/250 mL (per mL): $0.72
Solution (Brevibloc Intravenous)
100 mg/10 mL (per mL): $2.56
Solution (Brevibloc Premixed DS Intravenous)
2000 mg/100 mL (per mL): $1.92
Solution (Brevibloc Premixed Intravenous)
2500 mg/250 mL (per mL): $0.72
Solution (Esmolol HCl Intravenous)
100 mg/10 mL (per mL): $0.88 - $1.89
2000 mg/100 mL (per mL): $1.55
2500 mg/250 mL (per mL): $0.57
Solution (Esmolol HCl-Sodium Chloride Intravenous)
2000 mg/100 mL (per mL): $1.91 - $5.44
2500 mg/250 mL (per mL): $0.67 - $2.02
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