(ES moe lol)
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
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 effects of other drug are still present); pulmonary hypertension
Canadian labeling: Additional contraindications (not in U.S. 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
U.S. labeling:
Intraoperative and postoperative tachycardia and/or hypertension: IV:
Immediate control: Initial bolus: 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)
Gradual control: Initial bolus: 0.5 mg/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 (0.5 mg/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 (250-300 mcg/kg/minute) to control blood pressure; the safety of doses >300 mcg/kg/minute has not been studied.
Supraventricular tachycardia (SVT) or noncompensatory sinus tachycardia: IV: Loading dose (optional): 0.5 mg/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 0.5 mg/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) 0.5 mg/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).
Note: If a loading dose is not administered, a continuous infusion at a fixed dose reaches steady-state in ~30 minutes. In general, the usual effective dose is 50-200 mcg/kg/minute; doses as low as 25 mcg/kg/minute may be adequate. Maintenance infusions may be continued for up to 48 hours.
Acute coronary syndromes (when relative contraindications to beta-blockade exist; off-label use): IV: 0.5 mg/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 (0.5 mg/kg over 1 minute) may be administered prior to each increase in infusion rate (Mooss, 1994)
Electroconvulsive therapy (off-label use): IV: 1 mg/kg administered 1 minute prior to induction of anesthesia (Weinger, 1991)
Intubation (off-label use): IV: 1-2 mg/kg given 1.5-3 minutes prior to intubation (Kindler 1996; Levitt 2001; Ugur 2007)
Thyrotoxicosis or thyroid storm (off-label use): IV: 50-100 mcg/kg/minute (Bahn, 2011)
Canadian labeling: Note: Not recommended for use >24 hours.
Perioperative tachycardia and/or hypertension: IV:
Associated with intubation: Bolus: 1.5 mg/kg (maximum dose: 100 mg) over 30 seconds given 1-2 minutes prior to intubation.
Intraoperative/postoperative tachycardia and/or hypertension: Initial bolus: 1.5 mg/kg (maximum dose: 100 mg) over 30 seconds, followed by 150 mcg/kg/minute infusion. Adjust infusion rate as needed to maintain desired heart rate or blood pressure (up to 300 mcg/kg/minute).
Atrial fibrillation/atrial flutter: IV:
Loading dose: 0.5 mg/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, rebolus with a second 0.5 mg/kg loading dose over 1 minute, and increase the maintenance infusion to 100 mcg/kg/minute for 4 minutes. If necessary, repeat same procedure (ie, 0.5 mg/kg loading dose and increase maintenance infusion by 50 mcg/kg/minute for 4 minutes) until target heart rate or safety end point (eg, hypotension) begins to occur then omit subsequent loading dose and decrease dosing increment of maintenance infusion to ≤25 mcg/kg/minute or alternatively, the manufacturer labeling suggests that the titration interval may be extended from 5 minutes to 10 minutes. If safety endpoints are exceeded discontinue infusion and when appropriate, resume infusion at reduced dose.
Note: In general, the usual effective dose is 50-200 mcg/kg/minute; doses as low as 25 mcg/kg/minute may be adequate.
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, patients response should be monitored and if control is adequate for the first hour, esmolol may be discontinued.
Refer to adult dosing.
No dosage adjustment necessary. Not removed by hemo- or peritoneal dialysis. Supplemental dose is not necessary.
No dosage adjustment necessary.
IV: Loading doses (eg, 0.5 mg/kg) 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.
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. Stable for at least 24 hours (under refrigeration or at controlled room temperature) at a final concentration of 10 mg/mL in D5W, D5LR, D5R, D51/2NS, D5NS, LR, 1/2NS, or NS.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous, as hydrochloride:
Brevibloc: 10 mg/mL (10 mL)
Brevibloc in NaCl: 2000 mg (100 mL); 2500 mg (250 mL)
Generic: 10 mg/mL (10 mL)
Solution, Intravenous, as hydrochloride [preservative free]:
Generic: 10 mg/mL (10 mL); 100 mg/10 mL (10 mL)
Stable in D5LR, D51/2NS, D5NS, D5W, D5R, D5W with KCl 40 mEq/L, LR, 1/2NS, NS
Y-site administration: Incompatible with amphotericin B cholesteryl sulfate complex, furosemide, lansoprazole, pantoprazole, warfarin.
Acetylcholinesterase Inhibitors: May enhance the bradycardic effect of Beta-Blockers. Monitor therapy
Alfuzosin: May enhance the hypotensive effect of Blood Pressure Lowering Agents. 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. Some beta-adrenoceptor mediated effects of Alpha-/Beta-Agonists (Direct-Acting), including anti-anaphylactic effects of epinephrine, may be diminished by Beta-Blockers. 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. 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. 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. Exceptions: Apraclonidine. Consider therapy modification
Amifostine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Amifostine. Management: When amifostine is used at chemotherapy doses, blood pressure lowering medications should be withheld for 24 hours prior to amifostine administration. If blood pressure lowering therapy cannot be withheld, amifostine should not be administered. Consider therapy modification
Aminoquinolines (Antimalarial): May decrease the metabolism of Beta-Blockers. 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. Monitor therapy
Amphetamines: May diminish the antihypertensive effect of Antihypertensive Agents. Monitor therapy
Anilidopiperidine Opioids: May enhance the bradycardic effect of Beta-Blockers. Anilidopiperidine Opioids may enhance the hypotensive effect of Beta-Blockers. 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. Monitor therapy
Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may enhance the hypotensive effect of Antipsychotic Agents (Second Generation [Atypical]). Monitor therapy
Barbiturates: May decrease the serum concentration of Beta-Blockers. Monitor therapy
Barbiturates: May enhance the hypotensive effect of Blood Pressure Lowering Agents. 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. Monitor therapy
Bradycardia-Causing Agents: May enhance the bradycardic effect of other Bradycardia-Causing Agents. Monitor therapy
Bretylium: May enhance the bradycardic effect of Bradycardia-Causing Agents. Bretylium may also enhance atrioventricular (AV) blockade in patients receiving AV blocking agents. Monitor therapy
Brimonidine (Topical): May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy
Bupivacaine: Beta-Blockers may increase the serum concentration of Bupivacaine. 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. Consider therapy modification
Cardiac Glycosides: Beta-Blockers may enhance the bradycardic effect of Cardiac Glycosides. 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. Avoid combination
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. Monitor therapy
Diazoxide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy
Dipyridamole: May enhance the bradycardic effect of Beta-Blockers. Monitor therapy
Disopyramide: May enhance the bradycardic effect of Beta-Blockers. Beta-Blockers may enhance the negative inotropic effect of Disopyramide. 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. Consider therapy modification
DULoxetine: Blood Pressure Lowering Agents may enhance the hypotensive effect of DULoxetine. Monitor therapy
Ergot Derivatives: Beta-Blockers may enhance the vasoconstricting effect of Ergot Derivatives. Exceptions: Nicergoline. Consider therapy modification
Fingolimod: Esmolol may enhance the bradycardic effect of Fingolimod. Avoid combination
Floctafenine: May enhance the adverse/toxic effect of Beta-Blockers. Avoid combination
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. Consider therapy modification
Herbs (Hypertensive Properties): May diminish the antihypertensive effect of Antihypertensive Agents. Monitor therapy
Herbs (Hypotensive Properties): May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy
Hypotension-Associated Agents: Blood Pressure Lowering Agents may enhance the hypotensive effect of Hypotension-Associated Agents. Monitor therapy
Insulin: Beta-Blockers may enhance the hypoglycemic effect of Insulin. Monitor therapy
Ivabradine: Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. Monitor therapy
Lacosamide: Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. Monitor therapy
Levodopa: Blood Pressure Lowering Agents may enhance the hypotensive effect of Levodopa. Monitor therapy
Lidocaine (Systemic): Beta-Blockers may increase the serum concentration of Lidocaine (Systemic). Monitor therapy
Lidocaine (Topical): Beta-Blockers may increase the serum concentration of Lidocaine (Topical). Monitor therapy
Mepivacaine: Beta-Blockers may increase the serum concentration of Mepivacaine. Monitor therapy
Methacholine: Beta-Blockers may enhance the adverse/toxic effect of Methacholine. Avoid combination
Methylphenidate: May diminish the antihypertensive effect of Antihypertensive Agents. Monitor therapy
Midodrine: Beta-Blockers may enhance the bradycardic effect of Midodrine. Monitor therapy
Molsidomine: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy
Morphine (Systemic): May increase the serum concentration of Esmolol. Monitor therapy
Naftopidil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy
Nicergoline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy
Nicorandil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy
NIFEdipine: May enhance the hypotensive effect of Beta-Blockers. NIFEdipine may enhance the negative inotropic effect of Beta-Blockers. Monitor therapy
Nitroprusside: Blood Pressure Lowering Agents may enhance the hypotensive effect of Nitroprusside. Monitor therapy
Nonsteroidal Anti-Inflammatory Agents: May diminish the antihypertensive effect of Beta-Blockers. 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. Consider therapy modification
Pentoxifylline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy
Phosphodiesterase 5 Inhibitors: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy
Propafenone: May increase the serum concentration of Beta-Blockers. Propafenone possesses some independent beta blocking activity. Monitor therapy
Prostacyclin Analogues: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy
Quinagolide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy
Regorafenib: May enhance the bradycardic effect of Beta-Blockers. Monitor therapy
Reserpine: May enhance the hypotensive effect of Beta-Blockers. Monitor therapy
Rifamycin Derivatives: May decrease the serum concentration of Beta-Blockers. Exceptions: Rifabutin. Monitor therapy
Rivastigmine: May enhance the bradycardic effect of Beta-Blockers. Avoid combination
Ruxolitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Management: Ruxolitinib Canadian product labeling recommends avoiding use with bradycardia-causing agents to the extent possible. Monitor therapy
Succinylcholine: Esmolol may enhance the neuromuscular-blocking effect of Succinylcholine. 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. 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. Monitor therapy
Tofacitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Monitor therapy
Yohimbine: May diminish the antihypertensive effect of Antihypertensive Agents. Monitor therapy
Blood pressure, MAP, heart rate, continuous ECG, respiratory rate, IV site; serum potassium (especially with renal impairment); consult individual institutional policies and procedures
>10%: Cardiovascular: Decreased blood pressure (20% to 50%), asymptomatic hypotension (dose related: 25%), symptomatic hypotension (dose related: 12%)
1% to 10%:
Cardiovascular: Peripheral ischemia (1%)
Central nervous system: Dizziness (3%), drowsiness (3%), agitation (2%), confusion (2%), headache (2%)
Gastrointestinal: Nausea (7%), vomiting (1%)
Local: Infusion site reaction (8%; including inflammation, irritation, and severe reactions associated with extravasation [eg, blistering, necrosis, thrombophlebitis])
<1% (Limited to important or life-threatening): Abdominal distress, abnormality in thinking, angioedema, anorexia, anxiety, arterial spasm (coronary), asystole (rare), bradycardia, bronchospasm, cardiac failure (decompensated), constipation, depression, dizziness, dyspepsia, flushing, heart block, hyperkalemia, pallor, paresthesia, psoriasis, renal tubular acidosis, seizure, severe bradycardia (rare), syncope, urinary retention, urticaria, xerostomia
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, renal 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 (HF): 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.
- Myasthenia gravis: Use with caution in patients with myasthenia gravis.
- Peripheral vascular disease (PVD) and Raynauds 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. Canadian labeling contraindicates use in this patient population.
- 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 (may be fatal). Use is contraindicated when IV calcium channel blockers have been administered in close proximity to esmolol (ie, while effects of other drug are still present).
- Cardiac glycosides: Use with caution in patients receiving digoxin; bradycardia or heart block can occur.
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: 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.
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Adverse events were observed in some animal reproduction studies. Esmolol has been shown to cause fetal bradycardia. Adverse fetal/neonatal events have also been observed with the chronic use of beta-blockers during pregnancy; however, esmolol is a short-acting beta-blocker and not indicated for chronic use. Esmolol is approved for the treatment of supraventricular tachycardia (SVT); however, other agents are preferred in pregnant women (ACC/AHA/HRS [Page 2015]).
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
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
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)
Urine (~73% to 88% as acid metabolite, <2% unchanged drug)
Beta-blockade: IV: 2-10 minutes (quickest when loading doses are administered)
Hemodynamic effects: 10-30 minutes; prolonged following higher cumulative doses, extended duration of use
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 renal disease
Esmolol: 55%; Acid metabolite: 10%
- Discuss specific use of drug and side effects with patient as it relates to treatment. (HCAHPS: During this hospital stay, were you given any medicine that you had not taken before? Before giving you any new medicine, how often did hospital staff tell you what the medicine was for? How often did hospital staff describe possible side effects in a way you could understand?)
- Patient may experience nausea. Have patient report immediately to prescriber signs of high potassium (abnormal heartbeat, confusion, dizziness, passing out, weakness, shortness of breath, numbness or tingling feeling), signs of DVT (edema, warmth, numbness, change in color, or pain in the extremities), severe dizziness, passing out, shortness of breath excessive weight gain, swelling of arms or legs, confusion, bradycardia, arrhythmia, burning or numbness feeling, seizures, or injection site burning, redness, pain, edema, or severe irritation (HCAHPS).
- Educate patient about signs of a significant reaction (eg, wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat). Note: This is not a comprehensive list of all side effects. Patient should consult prescriber for additional questions.
Intended Use and Disclaimer: Should not be printed and given to patients. This information is intended to serve as a concise initial reference for healthcare professionals to use when discussing medications with a patient. You must ultimately rely on your own discretion, experience and judgment in diagnosing, treating and advising patients.