Esmolol
- Dosing Information
- Esmolol is administered by continuous intravenous infusion with or without a loading dose. Additional loading doses and/or titration of the maintenance infusion (step-wise dosing) may be necessary based on desired ventricular response.
- In the absence of loading doses, continuous infusion of a single concentration of esmolol reaches pharmacokinetic and pharmacodynamic steady-state in about 30 minutes.
- The effective maintenance dose for continuous and step-wise dosing is 50 to 200 mcg per kg per minute, although doses as low as 25 mcg per kg per minute have been adequate. Dosages greater than 200 mcg per kg per minute provide little added heart rate lowering effect, and the rate of adverse reactions increases.
- Maintenance infusions may be continued for up to 48 hours.
- Dosing Information
- In this setting it is not always advisable to slowly titrate to a therapeutic effect. Therefore two dosing options are presented:  immediate control and gradual control.
- Administer 1 mg per kg as a bolus dose over 30 seconds followed by an infusion of 150 mcg per kg per min if necessary.
- Adjust the infusion rate as required to maintain desired heart rate and blood pressure. Refer to Maximum Recommended Doses below.
- Administer 500 mcg per kg as a bolus dose over 1 minute followed by a maintenance infusion of 50 mcg per kg per min for 4 minutes.
- Depending on the response obtained, continue dosing as outlined for supraventricular tachycardia. Refer to Maximum Recommended Doses below.
- For the treatment of tachycardia, maintenance infusion dosages greater than 200 mcg per kg per min are not recommended; dosages greater than 200 mcg per kg per min provide little additional heart rate-lowering effect, and the rate of adverse reactions increases.
- For the treatment of hypertension, higher maintenance infusion dosages (250-300 mcg per kg per min) may be required. The safety of doses above 300 mcg per kg per minute has not been studied.
- After patients achieve adequate control of the heart rate and a stable clinical status, transition to alternative antiarrhythmic drugs may be accomplished.
- When transitioning from esmolol to alternative drugs, the physician should carefully consider the labeling instructions of the alternative drug selected and reduce the dosage of esmolol as follows:
- Thirty minutes following the first dose of the alternative drug, reduce the esmolol infusion rate by one-half (50%).
- After administration of the second dose of the alternative drug, monitor the patients response and if satisfactory control is maintained for the first hour, discontinue the esmolol infusion.
- Esmolol injection is available in a pre-mixed bag and ready-to-use vial. Esmolol is not compatible with Sodium Bicarbonate (5%) solution (limited stability) or furosemide (precipitation).
- Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit.
Premixed Bag
- The medication port is to be used solely for withdrawing an initial bolus from the bag.
- Use aseptic technique when withdrawing the bolus dose.
- Do not add any additional medications to the bag.
Ready-to-Use Vial
- The Ready-to-use Vial may be used to administer a loading dosage by hand-held syringe while the maintenance infusion is being prepared.
- Developed by: AHA/ACC/HRS
- IV bolus of 500 mcg/kg administered over 1 min followed by IV infusion of 50300 mcg/kg/min
- Dosing Information
- Initial dose of 500 mcg/kg/min over 1 minute, then a titrated infusion to a dose of 50 to 300 mcg/kg/min administered over 4 minutes.
- Dosing Information
- 1 mg/kg bolus followed by 250 mcg/kg/min in association with propofol.
- Dosing Information
- 80 mg IV
- Dosing Information
- 100 mg bolus into the aortic root administered followed by a 10 to 15 mg/min infusion as many times as required.
- Dosing Information
- 10 mg/mL.
- Dosing Information
- Initial dose of 500 mcg/kg administered over 1 minute, then 50 mcg/kg/min and titrated up to a maximum of 200 mcg/kg/min in 50 mcg/kg/min increments every 4 minutes.
- Severe sinus bradycardia:  May precipitate or worsen bradycardia resulting in cardiogenic shock and cardiac arrest.
- Heart block greater than first degree:  Second- or third-degree atrioventricular block may precipitate or worsen bradycardia resulting in cardiogenic shock and cardiac arrest.
- Sick sinus syndrome:  May precipitate or worsen bradycardia resulting in cardiogenic shock and cardiac arrest.
- Decompensated heart failure:  May worsen heart failure.
- Cardiogenic shock:  May precipitate further cardiovascular collapse and cause cardiac arrest.
- IV administration of cardiodepressant calcium channel blockers (e.g., verapamil) and esmolol in close proximity (i.e., while cardiac effects from the other are still present); fatal cardiac arrests have occurred in patients receiving esmolol and intravenous verapamil.
- Pulmonary hypertension:  May precipitate cardiorespiratory compromise.
- Hypersensitivity reactions, including anaphylaxis to esmolol or any of the inactive ingredients of the product (cross-sensitivity between beta blockers is possible).
Hypotension can occur at any dose but is dose-related. Patients with hemodynamic compromise or on interacting medications are at particular risk. Severe reactions may include loss of consciousness, cardiac arrest, and death. For control of ventricular heart rate, maintenance doses greater than 200 mcg per kg per min are not recommended. Monitor patients closely, especially if pretreatment blood pressure is low. In case of an unacceptable drop in blood pressure, reduce or stop esmolol injection. Decrease of dose or termination of infusion reverses hypotension, usually within 30 minutes.
Bradycardia, including sinus pause, heart block, severe bradycardia, and cardiac arrest have occurred with the use of esmolol injection. Patients with first-degree atrioventricular block, sinus node dysfunction, or conduction disorders may be at increased risk. Monitor heart rate and rhythm in patients receiving esmolol.
If severe bradycardia develops, reduce or stop esmolol.
Beta blockers, like esmolol injection, can cause depression of myocardial contractility and may precipitate heart failure and cardiogenic shock. At the first sign or symptom of impending cardiac failure, stop esmolol and start supportive therapy.
Monitor vital signs closely and titrate esmolol slowly in the treatment of patients whose blood pressure is primarily driven by vasoconstriction associated with hypothermia.
Patients with reactive airways disease should, in general, not receive beta blockers. Because of its relative beta1 selectivity and titratability, titrate esmolol to the lowest possible effective dose. In the event of bronchospasm, stop the infusion immediately; a beta2 stimulating agent may be administered with appropriate monitoring of ventricular rates.
In patients with hypoglycemia, or diabetic patients (especially those with labile diabetes) who are receiving insulin or other hypoglycemic agents, beta blockers may mask tachycardia occurring with hypoglycemia, but other manifestations such as dizziness and sweating may not be masked.
Concomitant use of beta blockers and antidiabetic agents can enhance the effect of antidiabetic agents (blood glucoselowering).
Infusion site reactions have occurred with the use of esmolol injection. They include irritation, inflammation, and severe reactions (thrombophlebitis, necrosis, and blistering), in particular when associated with extravasation. Avoid infusions into small veins or through a butterfly catheter.
If a local infusion site reaction develops, use an alternative infusion site and avoid extravasation.
Beta blockers may exacerbate anginal attacks in patients with Prinzmetals angina because of unopposed alpha receptormediated coronary artery vasoconstriction. Do not use nonselective beta blockers.
If esmolol is used in the setting of pheochromocytoma, give it in combination with an alpha-blocker, and only after the alpha-blocker has been initiated. Administration of beta-blockers alone in the setting of pheochromocytoma has been associated with a paradoxical increase in blood pressure from the attenuation of beta-mediated vasodilation in skeletal muscle.
In hypovolemic patients, esmolol injection can attenuate reflex tachycardia and increase the risk of hypotension.
In patients with peripheral circulatory disorders (including Raynauds disease or syndrome, and peripheral occlusive vascular disease), esmolol may aggravate peripheral circulatory disorders.
Severe exacerbations of angina, myocardial infarction, and ventricular arrhythmias have been reported in patients with coronary artery disease upon abrupt discontinuation of beta blocker therapy. Observe patients for signs of myocardial ischemia when discontinuing esmolol.
Heart rate increases moderately above pretreatment levels 30 minutes after esmolol discontinuation.
Beta blockers, including esmolol, have been associated with increases in serum potassium levels and hyperkalemia. The risk is increased in patients with risk factors such as renal impairment. Intravenous administration of beta blockers has been reported to cause potentially life-threatening hyperkalemia in hemodialysis patients. Monitor serum electrolytes during therapy with esmolol.
Beta blockers, including esmolol, have been reported to cause hyperkalemic renal tubular acidosis. Acidosis in general may be associated with reduced cardiac contractility.
Beta-adrenergic blockade may mask certain clinical signs (e.g., tachycardia) of hyperthyroidism. Abrupt withdrawal of beta blockade might precipitate a thyroid storm; therefore, monitor patients for signs of thyrotoxicosis when withdrawing beta blocking therapy.
When using beta blockers, patients at risk of anaphylactic reactions may be more reactive to allergen exposure (accidental, diagnostic, or therapeutic).
Patients using beta blockers may be unresponsive to the usual doses of epinephrine used to treat anaphylactic or anaphylactoid reactions.
- Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in clinical practice.
- The following adverse reaction rates are based on use of esmolol in clinical trials involving 369 patients with supraventricular tachycardia and over 600 intraoperative and postoperative patients enrolled in clinical trials. Most adverse effects observed in controlled clinical trial settings have been mild and transient. The most important and common adverse effect has been hypotension. Deaths have been reported in post-marketing experience occurring during complex clinical states where esmolol was presumably being used simply to control ventricular rate
- Confusional state and agitation (~2%)
- Anxiety, depression and abnormal thinking (<1%)
- Headache (~ 2%)
- Paresthesia, syncope, speech disorder, and lightheadedness  (<1%)
- Convulsions (<1%), with one death
- Peripheral ischemia (~1%)
- Pallor and flushing (<1%)
- Vomiting (~1%)
- Dyspepsia, constipation, dry mouth, and abdominal discomfort (<1%)
- Urinary retention (<1%)

# Cardiac Disorders
- Cardiac arrest, Coronary arteriospasm

# Skin and Subcutaneous Tissue Disorders
- Angioedema, Urticaria, Psoriasis
- Digitalis glycosides:  Concomitant administration of digoxin and esmolol leads to an approximate 10% to 20% increase of digoxin blood levels at some time points. Digoxin does not affect esmolol pharmacokinetics. Both digoxin and beta blockers slow atrioventricular conduction and decrease the heart rate. Concomitant use increases the risk of bradycardia.
- Anticholinesterases:  esmolol prolonged the duration of succinylcholine-induced neuromuscular blockade and moderately prolonged clinical duration and recovery index of mivacurium.
- Antihypertensive agents clonidine, guanfacine, or moxonidine:  Beta blockers also increase the risk of clonidine-, guanfacine-, or moxonidine-withdrawal rebound hypertension. If, during concomitant use of a beta blocker, antihypertensive therapy needs to be interrupted or discontinued, discontinue the beta blocker first, and the discontinuation should be gradual.
- Calcium channel antagonists:  In patients with depressed myocardial function, use of esmolol with cardiodepressant calcium channel antagonists (e.g., verapamil) can lead to fatal cardiac arrests.
- Sympathomimetic drugs:  Sympathomimetic drugs having beta-adrenergic agonist activity will counteract effects of esmolol.
- Vasoconstrictive and positive inotropic agents:  Because of the risk of reducing cardiac contractility in presence of high systemic vascular resistance, do not use esmolol to control tachycardia in patients receiving drugs that are vasoconstrictive and have positive inotropic effects, such as epinephrine, norepinephrine, and dopamine.
- Teratogenicity studies in rats at intravenous dosages of esmolol hydrochloride up to 3000 mcg/kg/min (10 times the maximum human maintenance dosage) for 30 minutes daily produced no evidence of maternal toxicity, embryotoxicity or teratogenicity, while a dosage of 10,000 mcg/kg/min produced maternal toxicity and lethality. In rabbits, intravenous dosages up to 1000 mcg/kg/min for 30 minutes daily produced no evidence of maternal toxicity, embryotoxicity or teratogenicity, while 2500 mcg/kg/min produced minimal maternal toxicity and increased fetal resorptions.
- Monitor patients closely, especially if pretreatment blood pressure is low. In case of an unacceptable drop in blood pressure, reduce or stop esmolol injection. Decrease of dose or termination of infusion reverses hypotension, usually within 30 minutes.
- Monitor heart rate and rhythm in patients receiving esmolol.
- In patients with intraoperative and postoperative tachycardia and/or hypertension monitor vital signs closely and titrate smolol slowly in the treatment of patients whose blood pressure is primarily driven by vasoconstriction associated with hypothermia.
- Monitor serum electrolytes during therapy with esmolol.
- Monitor patients for signs of thyrotoxicosis when withdrawing beta blocking therapy.
- Dextrose (5%) Injection, USP
- Dextrose (5%) in Lactated Ringers Injection
- Dextrose (5%) in Ringers Injection
- Dextrose (5%) and Sodium Chloride (0.45%) Injection, USP
- Dextrose (5%) and Sodium Chloride (0.9%) Injection, USP
- Lactated Ringers Injection, USP
- Potassium Chloride (40 mEq/liter) in Dextrose (5%) Injection, USP
- Sodium Chloride (0.45%) Injection, USP
- Sodium Chloride (0.9%) Injection, USP
Overdoses of esmolol can cause cardiac and central nervous system effects. These effects may precipitate severe signs, symptoms, sequelae, and complications (for example, severe cardiac and respiratory failure, including shock and coma), and may be fatal. Continuous monitoring of the patient is required.
Cardiac effects
- Bradycardia,atrioventricular block (1st -, 2nd -, 3rd degree), junctional rhythms, intraventricular conduction delays, decreased cardiac contractility,hypotension, cardiac failure (including cardiogenic shock), cardiac arrest/asystole, and pulseless electrical activity.
Central nervous system
- Respiratory depression,seizures, sleep and mood disturbances, fatigue, lethargy, and coma.
- In addition, bronchospasm, mesenteric ischemia, peripheral cyanosis, hyperkalemia, and hypoglycemia (especially in children) may occur.
- Because of its approximately 9-minute elimination half-life, the first step in the management of toxicity should be to discontinue the esmolol infusion. Then, based on the observed clinical effects, consider the following general measures.
- Consider intravenous administration of atropine or another anticholinergic drug or cardiac pacing.
- Consider intravenous administration of a diuretic or digitalis glycoside. In shock resulting from inadequate cardiac contractility, consider intravenous administration of dopamine, dobutamine, isoproterenol, or inamrinone. Glucagon has been reported to be useful.
- Consider intravenous administration of fluids or vasopressor agents such as dopamine or norepinephrine.
- Consider intravenous administration of a beta 2 stimulating agent or a theophylline derivative.
- Massive accidental overdoses of esmolol have resulted from dilution errors. The use of esmolol premixed injection may reduce the potential for dilution errors. Some of these overdoses have been fatal while others resulted in permanent disability. Bolus doses in the range of 625 mg to 2.5 g (12.5-50 mg/kg) have been fatal. Patients have recovered completely from overdoses as high as 1.75 g given over one minute or doses of 7.5 g given over one hour for cardiovascular surgery. The patients who survived appear to be those whose circulation could be supported until the effects of esmolol resolved.
Its elimination half-life after intravenous infusion is approximately 9 minutes. esmolol inhibits the beta1 adrenergic receptors located chiefly in cardiac muscle, but this preferential effect is not absolute and at higher doses it begins to inhibit beta2 adrenergic receptors located chiefly in the bronchial and vascular musculature.
()-Methyl p- hydrocinnamate hydrochloride and has the following structure:
Esmolol hydrochloride has the empirical formula C16H26NO4Cl and a molecular weight of 331.8. It has one asymmetric center and exists as an enantiomeric pair.
Esmolol hydrochloride is a white to off-white crystalline powder. It is a relatively hydrophilic compound which is very soluble in water and freely soluble in alcohol. Its partition coefficient (octanol/water) at pH 7.0 is 0.42 compared to 17.0 for propranolol.
All esmolol presentations are clear, colorless to light yellow, sterile, nonpyrogenic, iso-osmotic solutions of esmolol hydrochloride in sodium chloride. The formulations for esmolol premixed injection, esmolol double strength injection, and esmolol injection are described in the table below:
The calculated osmolarity of esmolol premixed injection and esmolol double strength injection is 312 mOsmol/L. The 250 mL and 100 mL bags are non-latex, non-PVC INTRAVIA bags with dual PVC ports. The INTRAVIA bags are manufactured from a specially designed multilayer plastic (PL 2408). Solutions in contact with the plastic container leach out certain chemical compounds from the plastic in very small amounts; however, biological testing was supportive of the safety of the plastic container materials.
In human electrophysiology studies, esmolol produced effects typical of a beta blocker: a decrease in the heart rate, increase in sinus cycle length, prolongation of the sinus node recovery time, prolongation of the AH interval during normal sinus rhythm and during atrial pacing, and an increase in antegrade Wenckebach cycle length.
In patients undergoing radionuclide angiography, esmolol, at dosages of 200 mcg/kg/min, produced reductions in heart rate, systolic blood pressure, rate pressure product, left and right ventricular ejection fraction and cardiac index at rest, which were similar in magnitude to those produced by intravenous propranolol (4 mg). During exercise, esmolol produced reductions in heart rate, rate pressure product and cardiac index which were also similar to those produced by propranolol, but esmolol produced a significantly larger fall in systolic blood pressure. In patients undergoing cardiac catheterization, the maximum therapeutic dose of 300 mcg/kg/min of esmolol produced similar effects and, in addition, there were small, clinically insignificant increases in the left ventricular end diastolic pressure and pulmonary capillary wedge pressure. At 30 minutes after the discontinuation of esmolol infusion, all of the hemodynamic parameters had returned to pretreatment levels.
The relative cardioselectivity of esmolol was demonstrated in 10 mildly asthmatic patients. Infusions of esmolol 100, 200 and 300 mcg/kg/min produced no significant increases in specific airway resistance compared to placebo. At 300 mcg/kg/min, esmolol produced slightly enhanced bronchomotor sensitivity to dry air stimulus. These effects were not clinically significant, and esmolol was well tolerated by all patients. Six of the patients also received intravenous propranolol, and at a dosage of 1 mg, two experienced significant, symptomatic bronchospasm requiring bronchodilator treatment. One otherpropranolol-treated patient also experienced dry air-induced bronchospasm. No adverse pulmonary effects were observed in patients with COPD who received therapeutic dosages of esmolol for treatment of supraventricular tachycardia (51 patients) or in perioperative settings (32 patients).
Using an appropriate loading dose, steady-state blood levels of esmolol for dosages from 50-300 mcg/kg/min are obtained within five minutes. Steady-state is reached in about 30 minutes without the loading dose. Steady-state blood levels of esmolol increase linearly over this dosage range and elimination kinetics are dose-independent over this range. Steady-state blood levels are maintained during infusion but decrease rapidly after termination of the infusion. Because of its short half-life, blood levels of esmolol can be rapidly altered by increasing or decreasing the infusion rate and rapidly eliminated by discontinuing the infusion.
Consistent with the high rate of blood-based metabolism of esmolol, less than 2% of the drug is excreted unchanged in the urine. Within 24 hours of the end of infusion, the acid metabolite of esmolol in urine accounts for approximately 73-88% of the dosage.
Metabolism of esmolol results in the formation of the corresponding free acid and methanol. The acid metabolite has been shown in animals to have negligible activity and in normal volunteers its blood levels do not correspond to the level of beta blockade. The acid metabolite has an elimination half-life of about 3.7 hours and is excreted in the urine with a clearance approximately equivalent to the glomerular filtration rate. After a 4 hour maintenance infusion of 150 mcg/kg, the plasma concentrations of esmolol are similar in subjects with normal renal function and in patients with ESRD on dialysis. The half-life of the acid metabolite of esmolol, which is primarily excreted unchanged by the kidney, is increased about 12-fold to 48 hours in patients with ESRD. The peak concentrations of the acid metabolite are doubled in ESRD.
Methanol blood levels, monitored in subjects receiving esmolol for up to 6 hours at 300 mcg/kg/min and 24 hours at 150 mcg/kg/min, approximated endogenous levels and were less than 2% of levels usually associated with methanol toxicity.
Esmolol has been shown to be 55% bound to human plasma protein, while the acid metabolite is only 10% bound.
In two multicenter, randomized, double-blind, controlled comparisons of esmolol injection with placebo and propranolol, maintenance doses of 50 to 300 mcg/kg/min of esmolol were found to be more effective than placebo and about as effective as propranolol, 3-6 mg given by bolus injections, in the treatment of supraventricular tachycardia, principally atrial fibrillation and atrial flutter. The majority of these patients developed their arrhythmias postoperatively. About 60-70% of the patients treated with esmolol developed either a 20% reduction in heart rate, a decrease in heart rate to less than 100 bpm, or, rarely, conversion to normal sinus rhythm and about 95% of these patients did so at a dosage of 200 mcg/kg/min or less. The average effective dosage of esmolol was approximately 100 mcg/kg/min in the two studies. Other multicenter baseline-controlled studies gave similar results. In the comparison with propranolol, about 50% of patients in both the esmolol and propranolol groups were on concomitant digoxin. Response rates were slightly higher with both beta blockers in the digoxin-treated patients.
In all studies significant decreases of blood pressure occurred in 20-50% of patients, identified either as adverse reaction reports by investigators, or by observation of systolic pressure less than 90 mmHg or diastolic pressure less than 50 mmHg. The hypotension was symptomatic (mainly hyperhidrosis or dizziness) in about 12% of patients, and therapy was discontinued in about 11% of patients, about half of whom were symptomatic. Hypotension was more common with esmolol (53%) than with propranolol (17%). The hypotension was rapidly reversible with decreased infusion rate or after discontinuation of therapy with esmolol. For both esmolol and propranolol, hypotension was reported less frequently in patients receiving concomitant digoxin.
NDC 10019-055-61, 2500 mg / 250 mL (10 mg/mL) Ready-to-use INTRAVIA Bags
- BREVIBLOC DOUBLE STRENGTH PREMIXED Injection
NDC 10019-075-87, 2000 mg / 100 mL (20 mg/mL) Ready-to-use INTRAVIA Bags
- BREVIBLOC Injection
NDC 10019-115-01, 100 mg / 10 mL (10 mg/mL) Ready-to-use Vials, Package of 25
- Each bag contains no preservative. Once drug has been withdrawn from ready-to-use bag, the bag should be used within 24 hours, with any unused portion discarded.
- Do not use plastic containers in series connections. Such use could result in an embolism due to residual air being drawn from the primary container before administration of the fluid from the secondary container is completed.
- Do not remove unit from overwrap until ready to use. Do not use if overwrap has been previously opened or damaged. The overwrap is a moisture barrier. The inner bag maintains sterility of the solution. Tear overwrap at notch and remove premixed bag. Some opacity of the plastic due to moisture absorption during the sterilization process may be observed. This is normal and does not affect the solution quality or safety. The opacity will diminish gradually.
- Check for minute leaks by squeezing the inner bag firmly. If leaks are found, discard solution, as sterility may be impaired. Do not use unless the solution is clear (colorless to light yellow) and the seal is intact.
- The most common adverse reactions are symptomatic hypotension (hyperhidrosis, dizziness), and asymptomatic hypotension.
- Esmolol HCl
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