Esmolol (Brevibloc) | Medication Reference

Bedside Snapshot

Ultra-Short Half-Life: ~9 minutes; onset within 1–2 minutes, steady effect after a few minutes of infusion changes; offset within 10–20 minutes of stopping → highly titratable and forgiving
Primary Uses: Rapid control of heart rate and blood pressure in critical care; rate control in SVT/AF with RVR; shear stress reduction in aortic dissection or acute aortopathies (HR and dP/dt control)
Typical Adult Dosing: Loading bolus 500–1,000 mcg/kg IV over 1 minute, then infusion 50–200 mcg/kg/min, titrated to effect. Lower starting doses in frail, shocky, or severely LV-dysfunctional patients
β1-Selectivity: Cardioselective at typical doses (β1 > β2), but selectivity decreases at high doses, potentially affecting bronchial β2 receptors
Major Risks: Hypotension, bradycardia, AV block, acute heart failure decompensation, bronchospasm in reactive airway disease
Key Advantage: Ideal when you want β-blockade but aren't sure how the patient will tolerate it—if they crash, turning it off works relatively quickly compared to metoprolol/labetalol

Brand & Generic Names

Generic Name: Esmolol hydrochloride
Brand Names: Brevibloc, generics

Medication Class

Ultra-short-acting cardioselective β1-adrenergic blocker

Pharmacology

Mechanism of Action:

Competitively blocks β1-adrenergic receptors in the heart, reducing the effects of catecholamines (epinephrine, norepinephrine) on the sinoatrial (SA) and atrioventricular (AV) nodes and myocardium
Results in negative chronotropy (↓ heart rate), negative inotropy (↓ contractility), and negative dromotropy (slowed AV conduction)
Cardioselective at typical doses (β1 > β2), but selectivity decreases at high doses, potentially affecting bronchial β2 receptors and peripheral vasculature
By reducing HR and contractility, esmolol lowers myocardial oxygen demand and shear stress on the aortic wall—a key goal in aortic dissection management

Pharmacokinetics:

Onset: 1–2 minutes after IV bolus; peak effect within about 5 minutes of infusion rate change
Distribution: Small volume of distribution; highly water soluble; ~55% protein bound
Metabolism: Rapidly hydrolyzed by erythrocyte esterases to an inactive metabolite; metabolism is not dependent on liver or kidney function
Elimination: Half-life about 9 minutes; hemodynamic effects dissipate within 10–20 minutes of stopping the infusion
Special Considerations: No major dose adjustment required for renal or hepatic impairment, but clinical tolerance (BP, HR, HF) should guide titration

Indications

Rapid control of ventricular rate in supraventricular tachycardias (e.g., AF with RVR, atrial flutter, AVNRT) when β-blockade is appropriate
Management of aortic dissection or other acute aortopathies to reduce HR and dP/dt before or along with vasodilators (e.g., nicardipine, clevidipine)
Short-term control of perioperative or post-op hypertension/tachycardia, especially in cardiac and neuro cases
Adjunct in managing catecholamine surge states (e.g., thyroid storm, pheochromocytoma crisis after alpha blockade, certain tox states) under specialist guidance

Dosing & Administration

Available Forms:

Premixed bags: commonly 2,000 mg in 100 mL (20 mg/mL) or 2,500 mg in 250 mL (10 mg/mL)
Vials: e.g., 100 mg/10 mL (10 mg/mL) for bolus dosing or custom infusions
Infusions are typically run in mcg/kg/min using a pump; double-check concentration and pump settings to avoid decimal errors

Adult Dosing (IV):

Indication / Phase	Dose	Route / Duration	Notes
Initial loading bolus (typical)	500 mcg/kg IV	Over 1 minute	May follow with infusion; lower doses (250 mcg/kg) in frail patients
Second loading bolus (if needed)	500 mcg/kg IV	Over 1 minute	Can repeat if initial response inadequate and BP tolerates
Maintenance infusion – usual range	50–200 mcg/kg/min	Continuous IV infusion	Titrate q5–10 min based on HR/BP
Aortic dissection / severe HTN with tachycardia	500–1,000 mcg/kg bolus, then 50–100 mcg/kg/min	Continuous IV infusion	Goal HR often <60–70 bpm before starting vasodilator
AF with RVR (hemodynamically stable)	500 mcg/kg bolus, then 50–200 mcg/kg/min	Continuous IV infusion	Titrate to HR and BP; can repeat bolus if needed
No bolus strategy (fragile patients)	25–50 mcg/kg/min	Continuous IV infusion	Slowly uptitrate q5–10 min, watching BP/HR
Maximum recommended infusion rate	300 mcg/kg/min	Continuous IV infusion	Above 200 mcg/kg/min limited by bradycardia/hypotension
Transition to longer-acting β-blocker	Give oral β-blocker, then taper esmolol	—	Overlap while adjusting oral dose to avoid rebound

Contraindications

Contraindications:

Sinus bradycardia (clinically significant) or sick sinus syndrome without a pacemaker
Second- or third-degree AV block without a pacemaker
Cardiogenic shock, decompensated heart failure with pulmonary edema (unless used in very controlled settings)
Severe bronchospastic disease (e.g., active asthma exacerbation) where β-blockade could worsen bronchospasm
Known hypersensitivity to esmolol or formulation components

Major Precautions:

Baseline hypotension or marginal perfusion states: even small decreases in HR/contractility can precipitate shock
Use cautiously in patients with HF with reduced EF—helpful for rate control but can worsen output if pushed too far
Diabetes: β-blockers can mask tachycardic response to hypoglycemia; monitor glucose and clinical signs
Bronchospasm/COPD: relatively β1-selective but can still provoke bronchospasm at higher doses
Concurrent nodal-blocking agents (diltiazem, verapamil, digoxin, amiodarone) increase risk of bradycardia and heart block

Hypotension Risk: Baseline hypotension or marginal perfusion states—even small decreases in HR/contractility can precipitate shock. Monitor BP continuously.

Bradycardia & Heart Block: Can cause symptomatic bradycardia or high-grade AV block, especially with concurrent nodal-blocking agents. Continuous ECG monitoring required.

Adverse Effects

Common:

Hypotension (most common)
Bradycardia
Dizziness, fatigue
Nausea

Serious:

Symptomatic bradycardia or high-grade AV block, potentially requiring atropine or pacing
Cardiogenic shock or acute decompensated heart failure
Bronchospasm in susceptible individuals (asthma/COPD)
Severe hypotension with end-organ hypoperfusion

Special Populations

Elderly Patients:

Start with lower bolus doses (250 mcg/kg) or no-bolus strategy
Begin infusion at 25–50 mcg/kg/min and titrate cautiously
Higher risk of hypotension and bradycardia

Renal Impairment:

No specific dose adjustment required (metabolized by RBC esterases, not kidneys)
Clinical tolerance (BP, HR) should guide titration

Hepatic Impairment:

No specific dose adjustment required (metabolized by RBC esterases, not liver)
Clinical tolerance (BP, HR) should guide titration

Pregnancy:

Category C: Limited human data; use only if benefit justifies potential risk
May cause fetal bradycardia; monitor fetal heart rate when used in pregnancy

Lactation:

Unknown if excreted in breast milk; use caution

Monitoring

Clinical Monitoring:

Continuous ECG monitoring for bradycardia, pauses, and AV block
Frequent or continuous blood pressure monitoring, especially during initiation and titration
Clinical signs of perfusion: mental status, urine output, skin perfusion, lactate if indicated
Heart failure signs: JVD, pulmonary edema, rising oxygen requirements when treating tachyarrhythmias in HFrEF
Reassessment after each dose adjustment; be ready to reduce or stop infusion rapidly if hypotension or bradycardia develops

Clinical Pearls

Forgiving Pharmacokinetics: Because of its short half-life, esmolol is very forgiving—if the patient doesn't tolerate β-blockade, you can back off and usually see improvement within 10–20 minutes.

Aortic Dissection Protocol: In aortic dissection, prioritize HR control with esmolol (or another β-blocker) before adding vasodilators like nicardipine or clevidipine to avoid reflex tachycardia.

AF with Borderline BP: In AF with RVR and borderline BP, small esmolol boluses with cautious infusion titration can sometimes achieve rate control where diltiazem would be too vasodilatory.

Transition Strategy: When you find a stable HR/BP response, transition to longer-acting oral β-blockers (e.g., metoprolol, carvedilol) and taper off the esmolol to avoid rebound.

Bronchospasm Risk: Remember that esmolol, despite β1 selectivity, can still provoke bronchospasm at higher doses—have bronchodilators and an alternative strategy ready in asthmatic/COPD patients.

Decimal Error Prevention: Double-check concentration and pump settings—esmolol is dosed in mcg/kg/min, and decimal errors can lead to dangerous over- or under-dosing.

References

1. Lexicomp. (2024). Esmolol: Drug information. Wolters Kluwer.
2. Hiratzka, L. F., Bakris, G. L., Beckman, J. A., et al. (2010). 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease. Circulation, 121(13), e266–e369. https://doi.org/10.1161/CIR.0b013e3181d4739e
3. January, C. T., Wann, L. S., Calkins, H., et al. (2019). 2019 AHA/ACC/HRS focused update on atrial fibrillation. Circulation, 140(2), e125–e151. https://doi.org/10.1161/CIR.0000000000000665
4. Nuttall, G. A., Butterworth, J. F., Legault, C., et al. (2006). Efficacy and safety of esmolol in the treatment of supraventricular tachyarrhythmias: A multicenter, double-blind, randomized trial versus placebo. American Heart Journal, 151(5), 1049–1054. https://doi.org/10.1016/j.ahj.2005.06.023
5. Sum, C. Y., Yacobi, A., Kartzinel, R., et al. (1983). Kinetics of esmolol, an ultra-short-acting beta blocker, and of its major metabolite. Clinical Pharmacology & Therapeutics, 34(4), 427–434. https://doi.org/10.1038/clpt.1983.185