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Carvedilol

Medically reviewed by Drugs.com. Last updated on May 14, 2020.

Pronunciation

(KAR ve dil ole)

Dosage Forms

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Capsule Extended Release 24 Hour, Oral, as phosphate:

Coreg CR: 10 mg, 20 mg, 40 mg, 80 mg

Generic: 10 mg, 20 mg, 40 mg, 80 mg

Tablet, Oral:

Coreg: 3.125 mg, 6.25 mg, 12.5 mg, 25 mg

Generic: 3.125 mg, 6.25 mg, 12.5 mg, 25 mg

Brand Names: U.S.

  • Coreg
  • Coreg CR

Pharmacologic Category

  • Antihypertensive
  • Beta-Blocker With Alpha-Blocking Activity

Pharmacology

As a racemic mixture, carvedilol has nonselective beta-adrenoreceptor and alpha-adrenergic blocking activity. No intrinsic sympathomimetic activity has been documented. Associated effects in hypertensive patients include reduction of cardiac output, exercise- or beta-agonist-induced tachycardia, reduction of reflex orthostatic tachycardia, vasodilation, decreased peripheral vascular resistance (especially in standing position), decreased renal vascular resistance, reduced plasma renin activity, and increased levels of atrial natriuretic peptide. In CHF, associated effects include decreased pulmonary capillary wedge pressure, decreased pulmonary artery pressure, decreased heart rate, decreased systemic vascular resistance, increased stroke volume index, and decreased right atrial pressure (RAP).

Absorption

Rapid and extensive, but with large first pass effect; first pass effect is stereoselective with R(+) enantiomer achieving plasma concentrations 2 to 3 times higher than S(-) enantiomer; delayed with food

Distribution

Vd: 115 L; distributes into extravascular tissues

Metabolism

Extensively (98%) hepatic, via CYP2D6, 2C9, 3A4, 2C19, 1A2, and 2E1 (2% excreted unchanged); metabolized predominantly by aromatic ring oxidation and glucuronidation; oxidative metabolites undergo conjugation via glucuronidation and sulfation; three active metabolites (4-hydroxyphenyl metabolite is 13 times more potent than parent drug for beta-blockade, however, active metabolites achieve plasma concentrations of only 1/10 of those for carvedilol); first-pass effect; plasma concentrations in the elderly and those with cirrhotic liver disease are 50% and 4 to 7 times higher, respectively. Metabolism is subject to genetic polymorphism; CYP2D6 poor metabolizers have a 2- to 3-fold higher plasma concentration of the R(+) enantiomer and a 20% to 25% increase in the S(-) enantiomer compared to extensive metabolizers.

Excretion

Primarily feces; urine (<2%, unchanged)

Onset of Action

Antihypertensive effect: Alpha-blockade: Within 30 minutes; Beta-blockade: Within 1 hour. Peak antihypertensive effect: ~1 to 2 hours

Time to Peak

Extended release: ~5 hours

Half-Life Elimination

Infants and Children 6 weeks to 3.5 years (n=8): 2.2 hours (Läer 2002)

Children and Adolescents 5.5 to 19 years (n=7): 3.6 hours (Läer 2002)

Adults 7 to 10 hours; some have reported lower values: Adults 24 to 37 years (n=9): 5.2 hours (Läer 2002)

R(+)-carvedilol: 5 to 9 hours

S(-)-carvedilol: 7 to 11 hours

Protein Binding

>98%, primarily to albumin

Special Populations: Renal Function Impairment

Plasma concentrations may be higher (40% to 50% in moderate to severe renal impairment).

Special Populations: Hepatic Function Impairment

Severe hepatic impairment (cirrhosis) patients have a 4- to 7-fold increase in concentrations.

Special Populations: Elderly

Plasma levels are about 50% higher

Special Populations Note

Heart failure: AUC and Cmax increased up to 100%.

Use: Labeled Indications

Heart failure with reduced ejection fraction, including left ventricular dysfunction following myocardial infarction: Treatment of mild to severe chronic heart failure of ischemic or cardiomyopathic origin or left ventricular dysfunction following myocardial infarction (clinically stable with left ventricular ejection fraction ≤40%).

Hypertension: Management of hypertension. Note: Beta-blockers are not recommended as first-line therapy (ACC/AHA [Whelton 2018]).

Off Label Uses

Angina, chronic stable

Based on the 2012 American College of Cardiology Foundation (ACCF)/American Heart Association (AHA) guideline for the diagnosis and management of patients with stable ischemic heart disease, a beta-blocker is recommended, in the absence of contraindications, for the treatment of chronic stable angina.

Atrial fibrillation/flutter, maintenance of ventricular rate control

Data from a randomized, double-blind, placebo-controlled trial support the use of carvedilol (with or without digoxin) in the management of atrial fibrillation in patients with heart failure [Khand 2003].

Based on the 2014 AHA/American College of Cardiology (ACC)/Heart Rhythm Society guideline for the management of patients with atrial fibrillation, the use of beta-blockers for ventricular rate control in patients with atrial fibrillation is effective and recommended for this condition, especially in patients with heart failure.

Myocardial infarction, early treatment and secondary prevention

According to the 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction and the 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes, an oral beta-blocker should be initiated within the first 24 hours unless the patient has signs of heart failure, evidence of a low-output state, an increased risk for cardiogenic shock, or other contraindications.

Variceal hemorrhage prophylaxis, primary

Data from clinical trials support the use of carvedilol for primary prophylaxis of variceal hemorrhage [Bañares 2002], [Bhardwaj 2017], [Reiberger 2013], [Tripathi 2009].

Based on the 2017 American Association for the Study of Liver Diseases guidelines on the management of portal hypertensive bleeding in cirrhosis, use of carvedilol is an effective and recommended option for primary prophylaxis of variceal hemorrhage.

Contraindications

Serious hypersensitivity to carvedilol or any component of the formulation; decompensated cardiac failure requiring intravenous inotropic therapy; bronchial asthma or related bronchospastic conditions; second- or third-degree AV block, sick sinus syndrome, and severe bradycardia (except in patients with a functioning artificial pacemaker); cardiogenic shock; severe hepatic impairment

Documentation of allergenic cross-reactivity for drugs alpha/beta adrenergic blocking agents 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): Severe hypotension; primary obstructive valvular heart disease; mental incapacity (eg, severe Alzheimer disease, alcoholism, drug abuse), unless closely supervised by an appropriate caregiver.

Dosing: Adult

Angina, chronic stable (off-label use):

Note: For vasospastic angina, beta-blockers are not recommended; other agents (eg, calcium channel blockers, nitrates) are preferred. For nonvasospastic angina, guidelines recommend titrating dose to a resting heart rate of 55 to 60 beats per minute (ACCF/AHA [Fihn 2012]), while other experts recommend a target of 60 to 70 beats per minute (Kannam 2019).

Immediate release: Oral: Initial: 12.5 mg twice daily; increase dose as tolerated to desired effect; usual dosage range: 25 to 50 mg twice daily (Hauf-Zachariou 1997; Weiss 1998).

Atrial fibrillation/flutter, maintenance of ventricular rate control (off-label use):

Note: Initiate cautiously in patients with concomitant heart failure. Avoid in patients with decompensated heart failure; electrical cardioversion preferred in these patients (AHA/ACC/HRS [January 2014]; AHA [Neumar 2010]).

Immediate release: Oral: Usual dosage range: 3.125 to 25 mg twice daily (AHA/ACC/HRS [January 2014]).

Heart failure with reduced ejection fraction, including left ventricular dysfunction following myocardial infarction:

Note: Initiate only in stable patients. In hospitalized patients, volume status should be optimized and IV diuretics, vasodilators, and inotropic agents successfully discontinued. Use caution when initiating in patients with New York Heart Association class IV symptoms or recent heart failure exacerbation (particularly in those who required inotropes during their hospital stay) (ACCF/AHA [Yancy 2013]; Meyer 2019).

Immediate release: Oral: Initial: 3.125 mg twice daily for 2 weeks, then up-titrate gradually (eg, doubling the dose every ≥2 weeks) to the recommended or maximum tolerated dose while monitoring for signs and symptoms of heart failure (ACC/AHA [Yancy 2017]; ACCF/AHA [Yancy 2013]; Packer 1996; Packer 2001).

Maximum recommended dose:

≤85 kg: 25 mg twice daily.

>85 kg: 50 mg twice daily.

Extended release: Oral: Initial: 10 mg once daily for 2 weeks, then up-titrate gradually (eg, doubling the dose every ≥2 weeks) to the maximum tolerated dose while monitoring for signs and symptoms of heart failure; maximum dose: 80 mg/day (ACC/AHA [Yancy 2017]; ACCF/AHA [Yancy 2013]).

Hypertension (alternative agent):

Note: Not recommended in the absence of specific comorbidities (eg, arrhythmia ischemic heart disease, heart failure with reduced ejection fraction) (ACC/AHA [Whelton 2018]).

Immediate release: Oral: Initial: 6.25 mg twice daily; titrate in ≥1-week intervals as needed based on patient response; usual dosage range: 6.25 to 25 mg twice daily; maximum dose: 50 mg/day (ACC/AHA [Whelton 2018]).

Extended release: Oral: Initial: 20 mg once daily; titrate in ≥1-week intervals as needed based on patient response; usual dosage range: 20 to 80 mg/day; maximum dose: 80 mg/day (ACC/AHA [Whelton 2018]).

Myocardial infarction, early treatment and secondary prevention (alternative agent) (off-label use):

Note: An oral beta-blocker is recommended within the first 24 hours for most patients (ACCF/AHA [O'Gara 2013]). Patients who do not receive a beta-blocker within 24 hours of myocardial infarction due to contraindications should be reevaluated for secondary prevention at a later date. The optimal duration of therapy is unknown; some experts treat for a minimum of 3 years and continue longer for patients with high-risk features (eg, cardiogenic shock, heart failure, chronic kidney disease) at initial presentation (Rosenson 2019).

Immediate release: Oral: Initial: 3.125 to 6.25 mg twice daily; titrate dose based on heart rate and blood pressure as tolerated up to 25 mg twice daily (Dargie 2001).

Variceal hemorrhage prophylaxis, primary (alternative agent) (off-label use):

Immediate release: Oral: Initial: 3.125 mg twice daily or 6.25 mg once daily; titrate according to resting heart rate (target 55 to 60 beats per minute) while maintaining blood pressure (eg, systolic blood pressure ≥90 mm Hg) to a maximum dose of 6.25 mg twice daily (AASLD [Garcia-Tsao 2017]; Bañares 2002; Bhardwaj 2017; Reiberger 2013; Sanyal 2019; Tripathi 2009).

Conversion from immediate release to extended release (Coreg CR):

Current dose IR tablets 3.125 mg twice daily: Convert to ER capsules 10 mg once daily.

Current dose IR tablets 6.25 mg twice daily: Convert to ER capsules 20 mg once daily.

Current dose IR tablets 12.5 mg twice daily: Convert to ER capsules 40 mg once daily.

Current dose IR tablets 25 mg twice daily: Convert to ER capsules 80 mg once daily.

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Geriatric

Refer to adult dosing. Consider lower initial doses and titrate to response (ACCF/AHA [Aronow 2011]).

Dosing: Pediatric

Note: Immediate release and extended release products are not interchangeable on a mg:mg basis due to pharmacokinetic differences. Individualize dosage for each patient; monitor patients closely during initiation and upwards titration of dose; reduce dosage for hypotension or bradycardia (adolescents ≥ 18 years: 55 bpm; younger patients may alternate target). Pharmacokinetic data suggests a faster carvedilol elimination in young pediatric patients (< 3.5 years) which may require more frequent dosing (3 times daily) and a higher target dose per kg (Laer, 2002; Shaddy, 2007).

Heart failure: Prior to initiating therapy, other CHF medications should be stabilized and fluid retention minimized.

Infants, Children, and Adolescents ≤ 17 years: Limited data available, efficacy results variable; optimal dose not established: Oral: Immediate release tablets: Initial: Reported mean: 0.075-0.08 mg/kg/dose twice daily; titrate as tolerated; may increase dose by typically 50% every 2 weeks; usual reported maintenance (target) dose range: 0.3-0.75 mg/kg/dose twice daily; the usual titration time to reach target dose was 11-14 weeks (Bruns, 2001; Rusconi, 2004); maximum daily dose: 50 mg/day. Dosing based on two retrospective analyses of a total 70 pediatric patients (age range: 3 months to 19 years) which showed improvement in left ventricular function and heart failure symptoms (67% to 68% of patients showed improvement in NYHA class). However, in a large, a multicenter, double-blind, placebo-controlled, dose-finding trial in 161 pediatric patients (treatment group: n=103, median age range: 33-43 months), a lower target dose range of 0.2-0.4 mg/kg/dose twice daily did not result in a statistical difference in composite clinical end point scores compared to placebo; the authors suggested multiple factors for negative efficacy findings including that the study may have been underpowered due to unexpected, high improvement of the placebo-arm; a subset analysis suggests ventricular morphology may play a role in efficacy (Shaddy, 2007).

Adolescents ≥18 years:

Immediate release tablets: Oral: Initial: 3.125 mg twice daily for 2 weeks; if tolerated, may increase to 6.25 mg twice daily. May double the dose every 2 weeks to the highest dose tolerated by patient.

Maximum recommended dose:

Mild to moderate heart failure:

<85 kg: 25 mg twice daily

>85 kg: 50 mg twice daily

Severe heart failure: 25 mg twice daily

Extended release capsules: Oral: Initial: 10 mg once daily for 2 weeks; if tolerated, may double the dose (eg, 20 mg, 40 mg) every 2 weeks up to 80 mg once daily; maintain on lower dose if higher dose is not tolerated

Hypertension: Adolescents ≥18 years:

Immediate release tablets: Oral: Initial: 6.25 mg twice daily; if tolerated, dose should be maintained for 1-2 weeks, then increased to 12.5 mg twice daily; maximum daily dose: 50 mg/day

Extended release capsules: Oral: Initial: 20 mg once daily; if tolerated, dose should be maintained for 1-2 weeks, then increased to 40 mg once daily if necessary; maximum daily dose: 80 mg/day

Left ventricular dysfunction following MI: Adolescents ≥ 18 years: Note: Initiate only after patient is hemodynamically stable and fluid retention has been minimized.

Immediate release tablets: Oral: Initial: 3.125-6.25 mg twice daily; increase dosage incrementally (eg, from 6.25 to 12.5 mg twice daily) at intervals of 3-10 days, as tolerated, to a target dose of 25 mg twice daily

Extended release capsules: Oral: Initial: 10-20 mg once daily; increase dosage incrementally at intervals of 3-10 days, as tolerated, to a target dose of 80 mg once daily

Conversion from immediate release to extended release (Coreg CR®): Adolescents ≥ 18 years:

Current dose immediate release tablets 3.125 mg twice daily: Convert to extended release capsules 10 mg once daily

Current dose immediate release tablets 6.25 mg twice daily: Convert to extended release capsules 20 mg once daily

Current dose immediate release tablets 12.5 mg twice daily: Convert to extended release capsules 40 mg once daily

Current dose immediate release tablets 25 mg twice daily: Convert to extended release capsules 80 mg once daily

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Extemporaneously Prepared

A 1.25 mg/mL carvedilol oral suspension may be made with tablets and one of two different vehicles (Ora-Blend or 1:1 mixture of Ora-Sweet and Ora-Plus). Crush five 25 mg tablets in a mortar and reduce to a fine powder; add 15 mL of purified water and mix to a uniform paste. Mix while adding chosen vehicle in incremental proportions to almost 100 mL; transfer to a calibrated amber bottle, rinse mortar with vehicle, and add quantity of vehicle sufficient to make 100 mL. Label “shake well”. Stable for 84 days when stored in amber prescription bottles at room temperature (Loyd, 2006).

Carvedilol oral liquid suspensions (0.1 mg/mL and 1.67 mg/mL) made from tablets, water, Ora-Plus, and Ora-Sweet were stable for 12 weeks when stored in glass amber bottles at room temperature (25°C). Use one 3.125 mg tablet for the 0.1 mg/mL suspension or two 25 mg tablets for the 1.67 mg/mL suspension; grind the tablet(s) and compound a mixture with 5 mL of water, 15 mL Ora-Plus, and 10 mL Ora-Sweet. Final volume of each suspension: 30 mL; label “shake well” (data on file, GlaxoSmithKline, Philadelphia, PA: DOF #132 [Note: Manufacturer no longer disseminates this document]).

Loyd A Jr, “Carvedilol 1.25 mg/mL Oral Suspension,” Int J Pharm Compounding, 2006, 10(3):220.

Administration

Oral: Administer with food to minimize the risk of orthostatic hypotension. Extended-release capsules and its contents should not be crushed, chewed, or divided. Capsules may be opened and its contents sprinkled on applesauce for immediate use.

Dietary Considerations

Should be taken with food to minimize the risk of orthostatic hypotension.

Storage

Coreg: Store at <30°C (<86°F). Protect from moisture.

Coreg CR: Store at 25°C (77°F); excursions permitted to 15°C to 30°C (59°F to 86°F). Protect from light.

Drug Interactions

Acetylcholinesterase Inhibitors: May enhance the bradycardic effect of Beta-Blockers. Monitor therapy

Afatinib: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Afatinib. Management: If combined, administer the P-gp inhibitor simultaneously with, or after, the dose of afatinib. Monitor closely for signs and symptoms of afatinib toxicity and if the combination is not tolerated, reduce the afatinib dose by 10 mg. Consider therapy modification

Ajmaline: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Alfuzosin: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Aliskiren: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Aliskiren. 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. 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. 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. 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

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

Benperidol: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Beta2-Agonists: Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Beta2-Agonists. Avoid combination

Betrixaban: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Betrixaban. Management: Decrease adult betrixaban dose to an initial single dose of 80 mg followed by 40 mg once daily if combined with a P-gp inhibitor. Avoid concomitant use of betrixaban and P-gp inhibitors in patients with severe renal impairment (CrCL less than 30 mL/min). Consider therapy modification

Bilastine: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Bilastine. Avoid combination

Bradycardia-Causing Agents: May enhance the bradycardic effect of other Bradycardia-Causing Agents. Monitor therapy

Brigatinib: May diminish the antihypertensive effect of Antihypertensive Agents. Brigatinib may enhance the bradycardic effect of Antihypertensive Agents. Monitor therapy

Brimonidine (Topical): May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Bromperidol: Blood Pressure Lowering Agents may enhance the hypotensive effect of Bromperidol. Bromperidol may diminish the hypotensive effect of Blood Pressure Lowering Agents. Avoid combination

Bupivacaine: Beta-Blockers may increase the serum concentration of Bupivacaine. Monitor therapy

Calcium Channel Blockers (Nondihydropyridine): May enhance the hypotensive effect of Beta-Blockers. Bradycardia and signs of heart failure have also been reported. Calcium Channel Blockers (Nondihydropyridine) may increase the serum concentration of Beta-Blockers. Monitor therapy

Cardiac Glycosides: Beta-Blockers may enhance the bradycardic effect of Cardiac Glycosides. Monitor therapy

Celiprolol: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Celiprolol. 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. 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. Monitor therapy

Cimetidine: May increase the serum concentration of Carvedilol. Monitor therapy

Cobicistat: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Colchicine: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Colchicine. Colchicine distribution into certain tissues (e.g., brain) may also be increased. Management: Colchicine is contraindicated in patients with impaired renal or hepatic function who are also receiving a P-gp inhibitor. In those with normal renal and hepatic function, reduce colchicine dose as directed. See interaction monograph for details. Consider therapy modification

CycloSPORINE (Systemic): P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of CycloSPORINE (Systemic). Monitor therapy

CYP2C9 Inhibitors (Moderate): May increase the serum concentration of Carvedilol. Specifically, concentrations of the S-carvedilol enantiomer may be increased. Monitor therapy

CYP2D6 Inhibitors (Moderate): May increase the serum concentration of Carvedilol. Monitor therapy

CYP2D6 Inhibitors (Strong): May increase the serum concentration of Carvedilol. Monitor therapy

Dabigatran Etexilate: P-glycoprotein/ABCB1 Inhibitors may increase serum concentrations of the active metabolite(s) of Dabigatran Etexilate. Monitor therapy

Dexmethylphenidate: May diminish the therapeutic effect of Antihypertensive Agents. Monitor therapy

Diazoxide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Digoxin: May enhance the bradycardic effect of Carvedilol. Carvedilol may increase the serum concentration of Digoxin. 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

DOXOrubicin (Conventional): P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of DOXOrubicin (Conventional). Avoid combination

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. Consider therapy modification

DULoxetine: Blood Pressure Lowering Agents may enhance the hypotensive effect of DULoxetine. Monitor therapy

Edoxaban: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Edoxaban. Monitor therapy

EPINEPHrine (Nasal): Beta-Blockers (with Alpha-Blocking Properties) may diminish the therapeutic effect of EPINEPHrine (Nasal). Monitor therapy

EPINEPHrine (Oral Inhalation): Beta-Blockers (with Alpha-Blocking Properties) may diminish the therapeutic effect of EPINEPHrine (Oral Inhalation). Monitor therapy

Epinephrine (Racemic): Beta-Blockers (with Alpha-Blocking Properties) may diminish the therapeutic effect of Epinephrine (Racemic). Monitor therapy

EPINEPHrine (Systemic): Beta-Blockers (with Alpha-Blocking Properties) may diminish the therapeutic effect of EPINEPHrine (Systemic). Monitor therapy

Ergot Derivatives: Beta-Blockers may enhance the vasoconstricting effect of Ergot Derivatives. Management: Avoid coadministration of beta-blockers and ergot derivatives whenever possible. If concomitant use cannot be avoided, monitor patients closely for evidence of excessive peripheral vasoconstriction. Consider therapy modification

Etofylline: Beta-Blockers may diminish the therapeutic effect of Etofylline. Avoid combination

Etoposide: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Etoposide. Monitor therapy

Etoposide Phosphate: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Etoposide Phosphate. Monitor therapy

Everolimus: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Everolimus. Monitor therapy

Fexinidazole [INT]: Bradycardia-Causing Agents may enhance the arrhythmogenic effect of Fexinidazole [INT]. Avoid combination

Fingolimod: Beta-Blockers may enhance the bradycardic effect of Fingolimod. Management: Avoid the concomitant use of fingolimod and beta-blockers if possible. If coadministration is necessary, patients should have overnight continuous ECG monitoring conducted after the first dose of fingolimod. Monitor patients for bradycardia. Consider therapy modification

Floctafenine: May enhance the adverse/toxic effect of Beta-Blockers. Avoid combination

Glecaprevir and Pibrentasvir: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Glecaprevir and Pibrentasvir. 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. 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

Insulins: Beta-Blockers may enhance the hypoglycemic effect of Insulins. 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

Lapatinib: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Lapatinib. Monitor therapy

Lefamulin: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Lefamulin. Management: Avoid concomitant use of lefamulin tablets with P-glycoprotein/ABCB1 inhibitors. If concomitant use is required, monitor for lefamulin adverse effects. Consider therapy modification

Levodopa-Containing Products: Blood Pressure Lowering Agents may enhance the hypotensive effect of Levodopa-Containing Products. 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

Lormetazepam: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Lumacaftor and Ivacaftor: May decrease the serum concentration of CYP2C9 Substrates (High Risk with Inhibitors or Inducers). Lumacaftor and Ivacaftor may increase the serum concentration of CYP2C9 Substrates (High Risk with Inhibitors or Inducers). Monitor therapy

Lumefantrine: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). 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. Monitor therapy

Methoxyflurane: May enhance the hypotensive effect of Beta-Blockers. Monitor therapy

Methylphenidate: May diminish the antihypertensive effect of Antihypertensive Agents. Monitor therapy

Midodrine: May enhance the bradycardic effect of Bradycardia-Causing Agents. Monitor therapy

Molsidomine: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Morphine (Systemic): P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Morphine (Systemic). Monitor therapy

Nadolol: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Nadolol. Monitor therapy

Naftopidil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Naldemedine: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Naldemedine. Monitor therapy

Naloxegol: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Naloxegol. 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

Nonsteroidal Anti-Inflammatory Agents (Topical): May diminish the therapeutic 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

PAZOPanib: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of PAZOPanib. Avoid combination

Peginterferon Alfa-2b: May decrease the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Peginterferon Alfa-2b may increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Pentoxifylline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Pholcodine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Pholcodine. 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

Ranolazine: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Ranolazine. Monitor therapy

Regorafenib: May enhance the bradycardic effect of Beta-Blockers. Monitor therapy

Reserpine: May enhance the hypotensive effect of Beta-Blockers. Monitor therapy

RifAMPin: May decrease the serum concentration of Carvedilol. Monitor therapy

Rifamycin Derivatives: May decrease the serum concentration of Beta-Blockers. Monitor therapy

RifAXIMin: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of RifAXIMin. Monitor therapy

Rimegepant: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Rimegepant. Avoid combination

RisperiDONE: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of RisperiDONE. Monitor therapy

Rivastigmine: May enhance the bradycardic effect of Beta-Blockers. Avoid combination

RomiDEPsin: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of RomiDEPsin. Monitor therapy

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

Saquinavir: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Saquinavir. Monitor therapy

Silodosin: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Silodosin. Monitor therapy

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. Consider therapy modification

Sirolimus: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Sirolimus. Management: Avoid concurrent use of sirolimus with P-glycoprotein (P-gp) inhibitors when possible and alternative agents with lesser interaction potential with sirolimus should be considered. Monitor for increased sirolimus concentrations/toxicity if combined. Consider therapy modification

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

Tacrolimus (Systemic): P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Tacrolimus (Systemic). Monitor therapy

Talazoparib: Carvedilol may increase the serum concentration of Talazoparib. Management: If concurrent use cannot be avoided, reduce talazoparib dose to 0.75 mg once daily. When carvedilol is discontinued, increase the talazoparib dose to the dose used before initiation of carvedilol after 3 to 5 times the half-life of carvedilol. Consider therapy modification

Tegaserod: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Tegaserod. Monitor therapy

Teniposide: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Teniposide. Monitor therapy

Terlipressin: May enhance the bradycardic effect of Bradycardia-Causing Agents. Monitor therapy

Theophylline Derivatives: Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Theophylline Derivatives. Monitor therapy

Tofacitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Monitor therapy

Tolvaptan: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Tolvaptan. Monitor therapy

Topotecan: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Topotecan. Avoid combination

Ubrogepant: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Ubrogepant. Management: Use an initial ubrogepant dose of 50 mg and second dose (at least 2 hours later if needed) of 50 mg when used with a P-gp inhibitor. Consider therapy modification

Venetoclax: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Venetoclax. Management: Reduce the venetoclax dose by at least 50% in patients requiring concomitant treatment with P-glycoprotein (P-gp) inhibitors. Resume the previous venetoclax dose 2 to 3 days after discontinuation of a P-gp inhibitor. Consider therapy modification

VinCRIStine (Liposomal): P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of VinCRIStine (Liposomal). Avoid combination

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. Avoid combination

Yohimbine: May diminish the antihypertensive effect of Antihypertensive Agents. Monitor therapy

Test Interactions

May lead to false-positive aldosterone/renin ratio (ARR) (Funder 2016).

Adverse Reactions

The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.

>10%:

Cardiovascular: Hypotension (≤20%), orthostatic hypotension (≤20%)

Central nervous system: Dizziness (2% to 32%), fatigue (24%)

Endocrine & metabolic: Weight gain (10% to 12%), hyperglycemia (5% to 12%)

Gastrointestinal: Diarrhea (1% to 12%)

Neuromuscular & skeletal: Asthenia (11%)

1% to 10%:

Cardiovascular: Bradycardia (≤10%), syncope (≤8%), peripheral edema (1% to 7%), angina pectoris (6%), edema (5% to 6%), atrioventricular block (>1% to ≤3%), cerebrovascular accident (>1% to ≤3%), exacerbation of angina pectoris (>1% to ≤3%), hypertension (>1% to ≤3%), lower extremity edema (>1% to ≤3%), palpitations (>1% to ≤3%), peripheral vascular disease (>1% to ≤3%), peripheral ischemia (≤1%), tachycardia (≤1%)

Central nervous system: Headache (5% to 8%), depression (>1% to ≤3%), drowsiness (>1% to ≤3%), hypoesthesia (>1% to ≤3%), hypotonia (>1% to ≤3%), malaise (>1% to ≤3%), vertigo (>1% to ≤3%), paresthesia (1% to ≤3%), insomnia (1% to 2%), abnormality in thinking (≤1%), emotional lability (≤1%), exacerbation of depression (≤1%), lack of concentration (≤1%), nervousness (≤1%), nightmares (≤1%), sleep disorder (≤1%)

Dermatologic: Diaphoresis (≤1%), erythematous rash (≤1%), maculopapular rash (≤1%), pruritus (≤1%), psoriasiform eruption (≤1%), skin photosensitivity (≤1%)

Endocrine & metabolic: Increased nonprotein nitrogen (6%), dependent edema (4%), hypercholesterolemia (4%), albuminuria (>1% to ≤3%), diabetes mellitus (>1% to ≤3%), glycosuria (>1% to ≤3%), gout (>1% to ≤3%), hyperkalemia (>1% to ≤3%), hyperuricemia (>1% to ≤3%), hypervolemia (>1% to ≤3%), hypoglycemia (>1% to ≤3%), hyponatremia (>1% to ≤3%), hypovolemia (>1% to ≤3%), impotence (>1% to ≤3%), increased gamma-glutamyl transferase (>1% to ≤3%), weight loss (>1% to ≤3%), decreased libido (≤1%), hypertriglyceridemia (≤1%), hypokalemia (≤1%)

Gastrointestinal: Nausea (2% to 9%), vomiting (6%), melena (>1% to ≤3%), periodontitis (>1% to ≤3%), gastrointestinal pain (1% to ≤3%), xerostomia (≤1%)

Genitourinary: Hematuria (>1% to ≤3%), urinary frequency (≤1%)

Hematologic & oncologic: Hypoprothrombinemia (>1% to ≤3%), nonthrombocytopenic purpura (>1% to ≤3%), thrombocytopenia (1% to ≤3%), leukopenia (≤1%)

Hepatic: Increased serum alanine aminotransferase (>1% to ≤3%), increased serum alkaline phosphatase (>1% to ≤3%), increased serum aspartate aminotransferase (>1% to ≤3%), hyperbilirubinemia (≤1%), increased liver enzymes (≤1%)

Hypersensitivity: Hypersensitivity reaction (>1% to ≤3%)

Neuromuscular & skeletal: Arthralgia (6%), arthritis (>1% to ≤3%), muscle cramps (>1% to ≤3%), hypokinesia (≤1%)

Ophthalmic: Visual disturbance (5%), blurred vision (>1% to ≤3%)

Otic: Tinnitus (≤1%)

Renal: Increased blood urea nitrogen (≤6%), increased serum creatinine (>1% to ≤3%), renal insufficiency (>1% to ≤3%)

Respiratory: Increased cough (5%), nasopharyngitis (4%), rales (4%), dyspnea (>3%), flu-like symptoms (>1% to ≤3%), nasal congestion (1%), paranasal sinus congestion (1%), asthma (≤1%)

Miscellaneous: Fever (>1% to ≤3%)

Frequency not defined:

Hematologic & oncologic: Anemia

Respiratory: Pulmonary edema

<1%, postmarketing, and/or case reports: Abnormal lymphocytes, alopecia, anaphylactoid shock, anaphylaxis, angioedema, aplastic anemia, amnesia, auditory impairment, bronchospasm, bundle branch block, cerebrovascular disease, complete atrioventricular block, decreased HDL cholesterol, erythema multiforme, exfoliative dermatitis, gastrointestinal hemorrhage, interstitial pneumonitis, ischemic heart disease, migraine, neuralgia, pancytopenia, paresis, respiratory alkalosis, seizure, Stevens-Johnson syndrome, toxic epidermal necrolysis, urinary incontinence

Warnings/Precautions

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.

• Bradycardia: May occur; reduce dosage if heart rate drops to <55 beats/minute.

• Floppy iris syndrome: Intraoperative floppy iris syndrome has been observed in cataract surgery patients who were on or were previously treated with alpha1-blockers; there appears to be no benefit in discontinuing alpha-blocker therapy prior to surgery. Instruct patients to inform ophthalmologist of carvedilol use when considering eye surgery.

• Hypotension/syncope: Symptomatic hypotension with or without syncope may occur with carvedilol (usually within the first 30 days of therapy); close monitoring of patient is required especially with initial dosing and dosing increases; blood pressure must be lowered at a rate appropriate for the patient's clinical condition. Initiation with a low dose, gradual up-titration, and administration with food may help to decrease the occurrence of hypotension or syncope. Advise patients to avoid driving or other hazardous tasks during initiation of therapy due to the risk of syncope.

Disease-related concerns:

• Angina: Use with caution in patients suspected of having vasospastic angina.

• Bronchospastic disease: In general, patients with bronchospastic disease should not receive beta-blockers; if used at all, should be used cautiously with close monitoring.

• Diabetes: Use with caution in patients with diabetes mellitus; may potentiate hypoglycemia and/or mask signs and symptoms (eg, sweating, anxiety, tachycardia). In patients with heart failure and diabetes, use of carvedilol may worsen hyperglycemia; may require adjustment of antidiabetic agents.

• Heart failure (HF): Heart failure patients may experience a worsening of renal function (rare); risk factors include ischemic heart disease, diffuse vascular disease, underlying renal dysfunction, and/or systolic BP <100 mm Hg. Initiate cautiously, titrate gradually, and monitor for possible deterioration in patient status (eg, symptoms of HF). Worsening heart failure or fluid retention may occur during upward titration; dose reduction or temporary discontinuation may be necessary. Adjustment of other medications (ACE inhibitors and/or diuretics) may also be required.

• Hepatic impairment: Use with caution in patients with mild to moderate hepatic impairment; use is contraindicated in patients with severe hepatic impairment.

• Myasthenia gravis: Use with caution in patients with myasthenia gravis.

• Peripheral vascular disease (PVD): May precipitate or aggravate symptoms of arterial insufficiency in patients with PVD; use with caution and monitor for progression of arterial obstruction.

• Pheochromocytoma (untreated): Use with caution; adequate alpha-blockade should be initiated prior to use of any beta-blocker.

• Psoriasis: Beta-blocker use has been associated with induction or exacerbation of psoriasis, but cause and effect have not been firmly established.

• 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:

• Elderly: Bradycardia may be observed more frequently in elderly patients (>65 years of age); dosage reductions may be necessary.

Dosage form specific issues:

• Polysorbate 80: Some dosage forms may contain polysorbate 80 (also known as Tweens). Hypersensitivity reactions, usually a delayed reaction, have been reported following exposure to pharmaceutical products containing polysorbate 80 in certain individuals (Isaksson 2002; Lucente 2000; Shelley 1995). Thrombocytopenia, ascites, pulmonary deterioration, and renal and hepatic failure have been reported in premature neonates after receiving parenteral products containing polysorbate 80 (Alade 1986; CDC 1984). See manufacturer's labeling.

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 and prompt resumption of beta-blocker therapy may be indicated with worsening of angina or acute coronary insufficiency.

• Major surgery: Chronic beta-blocker therapy should not be routinely withdrawn prior to major surgery.

Monitoring Parameters

Heart rate, blood pressure (base need for dosage increase on trough blood pressure measurements and for tolerance on standing systolic pressure 1 hour after dosing); renal studies, BUN, liver function; blood glucose in diabetics; in patients with increased risk for developing renal dysfunction, monitor during dosage titration.

Hypertension: The 2017 Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults (ACC/AHA [Whelton 2018]):

Confirmed hypertension and known CVD or 10-year ASCVD risk ≥10%: Target blood pressure <130/80 mm Hg is recommended.

Confirmed hypertension without markers of increased ASCVD risk: Target blood pressure <130/80 mm Hg may be reasonable.

Pregnancy Considerations

Exposure to beta-blockers during pregnancy may increase the risk for adverse events in the neonate. 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]).

Chronic maternal hypertension is also associated with adverse events in the fetus/infant. Chronic maternal hypertension may increase the risk of birth defects, low birth weight, premature delivery, stillbirth, and neonatal death. Actual fetal/neonatal risks may be related to duration and severity of maternal hypertension. Untreated chronic hypertension may also increase the risks of adverse maternal outcomes, including gestational diabetes, preeclampsia, delivery complications, stroke, and myocardial infarction (ACOG 203 2019).

When treatment of chronic hypertension in pregnancy is indicated, agents other than carvedilol are preferred (ACOG 203 2019; ESC [Regitz-Zagrosek 2018]; Magee 2014). Females with preexisting hypertension may continue their medication during pregnancy unless contraindications exist (ESC [Regitz-Zagrosek 2018]). Carvedilol may be considered for use in pregnant patients with heart failure (ESC [Regitz-Zagrosek 2018]).

Patient Education

What is this drug used for?

• It is used to treat heart failure (weak heart).

• It is used to treat high blood pressure.

• It is used to help heart function after a heart attack.

• It may be given to you for other reasons. Talk with the doctor.

All drugs may cause side effects. However, many people have no side effects or only have minor side effects. Call your doctor or get medical help if any of these side effects or any other side effects bother you or do not go away:

• Fatigue

• Loss of strength and energy

• Diarrhea

• Headache

• Nausea

• Vomiting

• Weight gain

• Joint pain

• Contact lens discomfort

WARNING/CAUTION: Even though it may be rare, some people may have very bad and sometimes deadly side effects when taking a drug. Tell your doctor or get medical help right away if you have any of the following signs or symptoms that may be related to a very bad side effect:

• High blood sugar like confusion, fatigue, increased thirst, increased hunger, passing a lot of urine, flushing, fast breathing, or breath that smells like fruit

• Low blood sugar like dizziness, headache, fatigue, feeling weak, shaking, fast heartbeat, confusion, increased hunger, or sweating

• Heart problems like cough or shortness of breath that is new or worse, swelling of the ankles or legs, abnormal heartbeat, weight gain of more than five pounds in 24 hours, dizziness, or passing out

• Severe dizziness

• Passing out

• Unable to pass urine

• Change in amount of urine passed

• Chest pain

• Slow heartbeat

• Burning or numbness feeling

• Cold in the arms or legs

• Vision changes

• Signs of an allergic reaction, like rash; hives; itching; red, swollen, blistered, or peeling skin with or without fever; wheezing; tightness in the chest or throat; trouble breathing, swallowing, or talking; unusual hoarseness; or swelling of the mouth, face, lips, tongue, or throat.

Note: This is not a comprehensive list of all side effects. Talk to your doctor if you have questions.

Consumer Information Use and Disclaimer: This information should not be used to decide whether or not to take this medicine or any other medicine. Only the healthcare provider has the knowledge and training to decide which medicines are right for a specific patient. This information does not endorse any medicine as safe, effective, or approved for treating any patient or health condition. This is only a limited summary of general information about the medicine's uses from the patient education leaflet and is not intended to be comprehensive. This limited summary does NOT include all information available about the possible uses, directions, warnings, precautions, interactions, adverse effects, or risks that may apply to this medicine. This information is not intended to provide medical advice, diagnosis or treatment and does not replace information you receive from the healthcare provider. For a more detailed summary of information about the risks and benefits of using this medicine, please speak with your healthcare provider and review the entire patient education leaflet.

Further information

Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.