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Atenolol

Medically reviewed by Drugs.com. Last updated on Jul 19, 2020.

Pronunciation

(a TEN oh lole)

Index Terms

  • Atenolol+SyrSpend SF PH4

Dosage Forms

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

Tablet, Oral:

Tenormin: 25 mg, 50 mg, 100 mg

Generic: 25 mg, 50 mg, 100 mg

Brand Names: U.S.

  • Tenormin

Pharmacologic Category

  • Antianginal Agent
  • Antihypertensive
  • Beta-Blocker, Beta-1 Selective

Pharmacology

Competitively blocks response to beta-adrenergic stimulation, selectively blocks beta1-receptors with little or no effect on beta2-receptors except at high doses

Absorption

Oral: Rapid, incomplete (~50%)

Distribution

Low lipophilicity; does not cross blood-brain barrier

Metabolism

Limited hepatic

Excretion

Feces (50%); urine (40% as unchanged drug)

Onset of Action

Oral: ≤1 hour; Peak effect: Oral: 2 to 4 hours

Time to Peak

Plasma: Oral: 2 to 4 hours

Duration of Action

Normal renal function: Beta-blocking effect: 12 to 24 hours; Antihypertensive effect: Oral: 24 hours

Half-Life Elimination

Beta:

Newborns (<24 hours of age) born to mothers receiving atenolol: Mean: 16 hours; up to 35 hours (Rubin 1983)

Children and Adolescents 5 to 16 years of age: Mean: 4.6 hours; range: 3.5 to 7 hours; Patients >10 years of age may have longer half-life (>5 hours) compared to children 5 to 10 years of age (<5 hours) (Buck 1989)

Adults: Normal renal function: 6 to 7 hours, prolonged with renal impairment; End-stage renal disease (ESRD): 15 to 35 hours

Protein Binding

6% to 16%

Special Populations: Renal Function Impairment

Elimination is closely related to GFR. Significant accumulation occurs when CrCl falls below 35 mL/minute/1.73 m2.

Special Populations: Elderly

Total clearance is about 50% lower than in younger subjects. Half-life is markedly longer in elderly patients.

Use: Labeled Indications

Angina: Long-term management of patients with angina pectoris.

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

Myocardial infarction, early treatment and secondary prevention: Management of hemodynamically stable patients with definite or suspected acute myocardial infarction to reduce cardiovascular mortality.

Off Label Uses

Atrial fibrillation/flutter, maintenance of ventricular rate control

Based on the 2014 American Heart Association (AHA)/American College of Cardiology (ACC)/Heart Rhythm Society (HRS) guideline for the management of patients with atrial fibrillation, the use of beta-blockers, including atenolol, is effective and recommended for ventricular rate control in patients with paroxysmal, persistent, or permanent atrial fibrillation [AHA/ACC/HRS [January 2014]].

Marfan syndrome with aortic aneurysm

Based on the American College of Cardiology Foundation/AHA/American Association for Thoracic Surgery 2010 guidelines for the diagnosis and management of patients with thoracic aortic disease, a beta-blocker is recommended for patients with Marfan syndrome to slow aortic dilatation unless there are contraindications [ACCF/AHA/AATS [Hiratzka 2010]].

Migraine prophylaxis

Data from a small, prospective, open-label study suggest that atenolol is effective at reducing the frequency of migraine episodes [Edvardsson 2013].

Based on the American Academy of Neurology and the American Headache Society evidence-based guideline on pharmacologic treatment for episodic migraine prevention in adults, atenolol may be effective for migraine prevention [AAN [Silberstein 2012]].

Supraventricular tachycardia (atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, focal atrial tachycardia, multifactorial atrial tachycardia), maintenance of ventricular rate control

Based on the ACC/AHA/HRS guidelines for the management of patients with supraventricular arrhythmias, the use of an oral beta-blocker, including atenolol, is an effective and recommended treatment option for the ongoing management of a variety of symptomatic supraventricular tachycardias (atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, focal atrial tachycardia) without pre-excitation in patients who are not candidates for, or prefer not to undergo, catheter ablation. Oral beta-blockers, including atenolol, may also be useful for the ongoing management (acute rate control) of hemodynamically stable patients with atrial flutter [ACC/AHA/HRS [Page 2016]].

Thyrotoxicosis

Based on the 2016 American Thyroid Association guidelines for the diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis, beta-blockers, including atenolol, are effective and recommended in the treatment of symptomatic thyrotoxicosis. Beta-blockers should also be considered in asymptomatic patients who are at increased risk of complications due to worsening hyperthyroidism [ATA [Ross 2016]].

Ventricular arrhythmias or ventricular premature beats (symptomatic), prevention

Based on the AHA/ACC/HRS guideline for the management of patients with ventricular arrhythmias and prevention of sudden cardiac death, beta-blockers are effective for control of ventricular arrhythmias and ventricular premature beats [AHA/ACC/HRS [Al-Khatib 2017]].

Contraindications

Hypersensitivity to atenolol or any component of the formulation; sinus bradycardia; heart block greater than first-degree (except in patients with a functioning artificial pacemaker); cardiogenic shock; uncompensated cardiac failure

Documentation of allergenic cross-reactivity for beta-blockers 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): Bradycardia (regardless of origin); cor pulmonale; hypotension; severe peripheral arterial disorders; anesthesia with agents that produce myocardial depression; Pheochromocytoma (in the absence of alpha-blockade); metabolic acidosis

Dosing: Adult

Angina:

Note: For vasospastic angina, beta-blockers are not recommended; calcium channel blockers and 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 2020).

Oral: Initial: 50 mg once daily; may increase dose at weekly intervals based on frequency and severity of anginal symptoms and tolerability; usual dosage range: 50 to 100 mg once daily.

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

Oral: Initial: 25 mg once daily; increase dose gradually as needed to achieve ventricular rate control; usual dosage range: 25 to 100 mg once daily (AHA/ACC/HRS [January 2014]).

Hypertension (alternative agent):

Note: Recommended only in patients with specific comorbidities (eg, myocardial infarction [MI], arrhythmia) (ACC/AHA [Whelton 2018]).

Oral: Initial: 25 mg once or twice daily; titrate at ≥1 week intervals as needed based on response and tolerability up to 100 mg/day in 1 or 2 divided doses (ACC/AHA [Whelton 2018]; manufacturer's labeling); some experts do not recommend doses >50 mg/day to control hypertension because adverse effects may be greater without additional antihypertensive benefit (Mann 2020).

Marfan syndrome with aortic aneurysm (off-label use):

Note: Data for specific dosing are limited but a beta-blocker is recommended, if tolerated, to slow aortic dilatation (ACCF/AHA/AATS [Hiratzka 2010]).

Oral: Some experts generally begin with 0.5 mg/kg/day administered once daily and titrated to maintain heart rate <100 beats per minute after submaximal exercise (eg, running up and down 2 flights of stairs); doses should be rounded to the nearest 25 mg increment; usual dosage range: 25 to 100 mg/day; maximum dose: 200 mg/day (Wright 2020).

Migraine prophylaxis (off-label use) (alternative agent):

Oral: Initial: 25 mg once daily; titrate gradually (eg, every 1 to 2 weeks) based on response and tolerability up to 100 mg once daily; maintain for at least 3 months before considering treatment failure (AAN/AHS [Silberstein 2012]; Edvardsson 2013; Ha 2019; Silberstein 2015; Smith 2020).

Myocardial infarction, early treatment and secondary prevention:

Note: An oral beta-blocker is recommended within the first 24 hours for most patients (ACCF/AHA [O'Gara 2013]). Patients who did not receive a beta-blocker within 24 hours of MI should be reevaluated for secondary prevention at a later date (Rosenson 2020).

Oral: Initial: 25 to 50 mg twice daily; some experts suggest a starting dose of 12.5 mg once daily when there is concern for adverse effects; titrate as tolerated based on heart rate and BP up to a usual maximum dose of 100 mg/day administered in 1 or 2 divided doses (ISIS-1 1986; Rosenson 2020; Simons 2020; manufacturer's labeling). Note: Optimal duration of therapy is unknown; some experts treat for a minimum of 3 years and continue longer for patients with high-risk features at initial presentation (ACC/AHA [Amsterdam 2014]; ACCF/AHA [O'Gara 2013]; Rosenson 2020; Simons 2020).

Supraventricular tachycardia (eg, atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, focal atrial tachycardia, multifactorial atrial tachycardia), maintenance of ventricular rate control (off-label use):

Oral: Initial: 25 to 50 mg once daily; titrate based on response and tolerability; maximum recommended dose: 100 mg once daily (ACC/AHA/HRS [Page 2016]).

Thyrotoxicosis (off-label use):

Note: For control of adrenergic symptoms until euthyroidism is established (ATA [Ross 2016]).

Oral: Initial: 25 to 50 mg once daily; titrate as needed to control symptoms (eg, tachycardia, palpitations, tremulousness) up to a maximum of 200 mg/day in 2 divided doses. Doses ≥50 mg/day can be administered in 2 divided doses if adrenergic symptoms become noticeable toward the end of the dosing interval with once daily dosing (ATA [Ross 2016]; Ross 2020).

Ventricular arrhythmia or ventricular premature beats (symptomatic), prevention (off-label use):

Oral: Initial: 25 mg once daily; titrate dose as needed based on response and tolerability up to a maximum dose of 200 mg/day in 1 or 2 divided doses; usual dosage range: 25 to 100 mg/day (AHA/ACC/HRS [Al-Khatib 2017]; Krittayaphong 2002; Manolis 2020).

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. In the management of hypertension, consider lower initial doses and titrate to response (Aronow 2011).

Dosing: Pediatric

Note: Dosage should be individualized based on patient response.

Arrhythmias: Limited data available: Infants, Children, and Adolescents: Oral:

Long QT syndrome: Usual range: 0.5 to 1 mg/kg/day either once daily or in divided doses every 12 hours (Kliegman, 2011). In a retrospective trial (n=57; mean age: 9 ± 6 years) that titrated atenolol to achieve a maximum heart rate less than 150 bpm (Holter monitor and exercise treadmill), higher doses were reported; mean effective dose: 1.4 ± 0.5 mg/kg/day in 2 divided doses (Moltedo, 2011)

Supraventricular tachycardia: Usual range: 0.3 to 1 mg/kg/day either once daily or in divided doses every 12 hours (Kliegman, 2011, Mehta, 1996; Trippel, 1989). In two separate trials, titration of the dose to >1.4 mg/kg/day did not show additional treatment successes and potentially increased the risk of adverse effects (Mehta, 1996; Trippel, 1989).

Hemangioma, infantile: Limited data available: Infants and Children <2 years: Oral: 1 mg/kg/dose once daily for 6 months; dosing based on a randomized, controlled noninferiority trial compared to propranolol (n=23 total, atenolol treatment group: n=13); atenolol was found to be as effective as propranolol; no significant adverse effects were reported in either group (Abarzua-Araya, 2014)

Hypertension: Children and Adolescents: Oral: Initial: 0.5 to 1 mg/kg/day either once daily or divided in doses twice daily; titrate dose to effect; usual range: 0.5 to 1.5 mg/kg/day; maximum daily dose: 2 mg/kg/day not to exceed 100 mg/day (NHBPEP, 2004; NLHBI, 2011)

Thyrotoxicosis: Limited data available: Children and Adolescents: Oral: 1 to 2 mg/kg once daily; may increase to twice daily if needed; maximum dose: 100 mg/dose (Bahn 2011; Kliegman 2011)

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

Extemporaneously Prepared

2 mg/mL Oral Suspension (ASHP Standard Concentration) (ASHP 2017)

A 2 mg/mL oral suspension may be made with tablets. Crush four 50 mg tablets in a mortar and reduce to a fine powder. Add a small amount of glycerin and mix to a uniform paste. Mix while adding Ora-Sweet SF 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 90 days at room temperature.

Nahata MC and Pai VB. Pediatric Drug Formulations. 6th ed. Cincinnati, OH: Harvey Whitney Books Co; 2014.Patel D, Doshi DH, Desai A. Short-term stability of atenolol in oral liquid formulations. Int J Pharm Compd. 1997;1(6):437-439.23989440

Administration

Oral: May be administered without regard to meals.

Storage

Store at 20°C to 25°C (68°F to 77°F).

Drug Interactions

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

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

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

Ampicillin: May decrease the bioavailability of Atenolol. Monitor therapy

Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may enhance the hypotensive effect of Antipsychotic Agents (Second Generation [Atypical]). Monitor therapy

Bacampicillin: May decrease the bioavailability of Atenolol. 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 (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

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

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

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

EPINEPHrine (Nasal): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of EPINEPHrine (Nasal). Monitor therapy

EPINEPHrine (Oral Inhalation): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of EPINEPHrine (Oral Inhalation). Monitor therapy

Epinephrine (Racemic): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of Epinephrine (Racemic). Monitor therapy

EPINEPHrine (Systemic): Beta-Blockers (Beta1 Selective) 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

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

Glycopyrrolate (Systemic): May increase the serum concentration of Atenolol. 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

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

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

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

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

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

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

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

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

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

Terlipressin: May enhance the bradycardic effect of Bradycardia-Causing 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

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

Increased glucose; decreased HDL; 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. Incidence rates are from studies in hypertensive patients unless otherwise noted.

>10%:

Cardiovascular: Hypotension (acute myocardial infarction: 25%), cardiac failure (acute myocardial infarction: 19%), bradycardia (acute myocardial infarction: 18%; 3%), ventricular tachycardia (acute myocardial infarction: 16%), cold extremities (12%), supraventricular tachycardia (acute myocardial infarction: 12%)

Central nervous system: Fatigue (≤26%), dizziness (1% to 13%), depression (≤12%)

1% to 10%:

Cardiovascular: Bundle branch block (acute myocardial infarction: 7%), atrial fibrillation (acute myocardial infarction: 5%), heart block (acute myocardial infarction: 5%), atrial flutter (acute myocardial infarction: 2%), orthostatic hypotension (2%), pulmonary embolism (acute myocardial infarction: 1%)

Central nervous system: Abnormal dreams (3%), lethargy (1% to 3%), vertigo (2%), drowsiness (≤2%)

Gastrointestinal: Nausea (3% to 4%), diarrhea (2% to 3%)

Neuromuscular & skeletal: Limb pain (3%)

Respiratory: Bronchospasm (acute myocardial infarction: 1%)

<1%, postmarketing, and/or case reports: Antibody development, cardiogenic shock, exacerbation of psoriasis, hallucination, headache, impotence, increased liver enzymes, increased serum bilirubin, lupus-like syndrome, nonthrombocytopenic purpura, Peyronie disease, psoriasiform eruption, psychosis, Raynaud disease, renal failure syndrome, sick sinus syndrome, thrombocytopenia, transient alopecia, visual disturbance, xerostomia

ALERT: U.S. Boxed Warning

Cessation of therapy:

Advise patients with coronary artery disease who are being treated with atenolol against abrupt discontinuation of therapy. Severe exacerbation of angina and the occurrence of myocardial infarction (MI) and ventricular arrhythmias have been reported in patients with angina following the abrupt discontinuation of therapy with beta-blockers. The last 2 complications may occur with or without preceding exacerbation of the angina pectoris. As with other beta-blockers, when discontinuation of atenolol is planned, observe the patient carefully and advise the patient to limit physical activity to a minimum. If the angina worsens or acute coronary insufficiency develops, it is recommended that atenolol be promptly reinstituted, at least temporarily. Because coronary artery disease is common and may be unrecognized, it may be prudent not to discontinue atenolol therapy abruptly, even in patients treated only for hypertension.

Warnings/Precautions

Concerns related to adverse events:

• 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.

Disease-related concerns:

• Bronchospastic disease: In general, patients with bronchospastic disease should not receive beta-blockers; however, atenolol, with B1 selectivity, has been used cautiously with close monitoring.

• Conduction abnormality: Consider preexisting conditions such as sick sinus syndrome before initiating.

• 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 (efficacy of atenolol in HF has not been demonstrated).

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

• Peripheral vascular disease (PVD) and Raynaud disease: May precipitate or aggravate symptoms of arterial insufficiency in patients with PVD and Raynaud 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.

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

• Renal impairment: Use with caution in patients with renal impairment; dosage adjustment required.

• Thyroid disease: May mask signs of hyperthyroidism (eg, tachycardia). If hyperthyroidism is suspected, carefully manage and monitor; abrupt withdrawal may precipitate thyroid storm. Alterations in thyroid function tests may be observed.

• Vasospastic angina: Beta-blockers without alpha1-adrenergic receptor blocking activity should be avoided in patients with Prinzmetal variant angina since unopposed alpha1-adrenergic receptors mediate coronary vasoconstriction and can worsen anginal symptoms (Mayer 1998).

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: [US Boxed Warning]: 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.

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

Monitoring Parameters

Acute cardiac treatment: Monitor ECG and blood pressure.

Hypertension: Blood pressure, heart rate, serum glucose regularly (in patients with diabetes)

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 Risk Factor

D

Pregnancy Considerations

Atenolol crosses the placenta and is found in cord blood.

Maternal use of atenolol may cause harm to the fetus. Adverse events, such as bradycardia, hypoglycemia and reduced birth weight, have been observed following in utero exposure to atenolol. 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).

The maternal pharmacokinetic parameters of atenolol during the second and third trimesters are within the ranges reported in nonpregnant patients (Hebert 2005). When treatment of chronic hypertension in pregnancy is indicated, atenolol is not recommended due to adverse fetal/neonatal events (ACOG 203 2019; ESC [Regitz-Zagrosek 2018]; Magee 2014). If atenolol is used in women with preexisting hypertension, it should be discontinued as soon as pregnancy is diagnosed (Magee 2014). Atenolol is also not recommended for the treatment of atrial fibrillation or supraventricular tachycardia during pregnancy; consult current guidelines for specific recommendations (ESC [Regitz-Zagrosek 2018]).

Patient Education

What is this drug used for?

• It is used to treat high blood pressure.

• It is used to treat a type of long-term chest pain (stable angina) in some people.

• It is used after a heart attack to lower the chance of death.

• 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:

• Loss of strength and energy

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:

• Chest pain

• Severe dizziness

• Passing out

• Sensation of cold

• Depression

• Shortness of breath

• Excessive weight gain

• Swelling of arm or leg

• Slow heartbeat

• 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.

Frequently Asked Questions