Esmolol (Brevibloc)

• 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

• Generic Name: Esmolol hydrochloride
• Brand Names: Brevibloc, generics

Ultra-short-acting cardioselective β1-adrenergic blocker

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

• 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

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):

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

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

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

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

• 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