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Atenolol

Medically reviewed on Sep 10, 2018

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

Acute MI: Management of hemodynamically stable patients with definite or suspected acute MI to reduce cardiovascular mortality.

Guideline recommendations: According to the American College of Cardiology Foundation/American Heart Association (ACC/AHA) guidelines for the management of ST-elevation myocardial infarction (STEMI) and the ACC/AHA guidelines for the management of non-ST-elevation ACS (NSTE-ACS), oral beta-blockers 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. However, recommendations do not specify any particular beta-blocking agent for optimal treatment of NSTE-ACS. Thus, clinicians must use practical experience to determine proper therapy in managing patients (ACC/AHA [Amsterdam 2014]; ACC/AHA [O'Gara 2013]).

Angina pectoris caused by coronary atherosclerosis: 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 2017]).

Off Label Uses

Atrial fibrillation (rate control)

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

Pediatric hypertension

Guidelines for the management of pediatric hypertension generally recommend the same drug classes that are indicated for management of adult hypertension. Particular consideration should be given to medications for which published pediatric experience is available, including appropriate dosing ranges. Similar to adults, prescribers should assess for concomitant disease states that would present a compelling indication for use of a particular drug. As a beta-blocker, atenolol would be a preferred agent for children with concomitant hypertension and migraine headaches. Other patient-specific factors, such as the potential for a patient to become pregnant while on therapy, can narrow selection. Atenolol is among the therapeutic options for pediatric hypertension identified by the National High Blood Pressure Education Program, based on published case series in children (NHBPEP 2004).

Supraventricular tachycardia (AV nodal reentrant tachycardia [AVNRT], AV reentrant tachycardia [AVRT], atrial flutter, focal atrial tachycardia [AT])

Based on the American College of Cardiology/American Heart Association/Heart Rhythm Society 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 (AVNRT, AVRT, focal AT) 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) in hemodynamically stable patients with atrial flutter.

Thyrotoxicosis

Based on the 2016 American Thyroid Association guidelines for 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 [Ross 2016].

Ventricular arrhythmias

In patients with arrhythmogenic right ventricular cardiomyopathy (ARVC), data from observational studies suggest that atenolol may be beneficial at reducing ventricular arrhythmias [Marcus 2009]. The American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) guideline for management of patients with ventricular arrhythmias and prevention of sudden cardiac death recommends beta-blocker therapy in patients with ARVC and history of ventricular arrhythmia and suggests that beta-blockers may be considered in patients without a history of ventricular arrhythmia.

In patients with congenital long QT syndrome, data from observational studies suggest that beta-blockers may be beneficial at reducing the risk of cardiac events, including ventricular arrhythmias, especially in patients with long QT syndrome type 1 or type 2 [Chockalingam 2012], [Goldenberg 2010], [Moss 2000], [Sauer 2007]. Atenolol, nadolol, and propranolol may be preferred choices for patients with long QT syndrome based on the currently available data and American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) guideline for management of patients with ventricular arrhythmias and prevention of sudden cardiac death [ACC/AHA/HRS [Al-Khatib 2017]].

Based on the American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) guideline for 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.

Additional Off-Label Uses

Acute ethanol withdrawal (in combination with a benzodiazepine)

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 pectoris: Oral: Initial: 50 mg once daily; may increase to 100 mg once daily. Some patients may require 200 mg once daily.

Atrial fibrillation (rate control) (off-label use): Usual maintenance dose: 25 to 100 mg once daily (AHA/ACC/HRS [January 2014])

Hypertension (alternative agent): Oral: Initial: 50 mg once daily; titrate as needed based on patient response every 1 to 2 weeks up to 100 mg once daily. Doses >100 mg are unlikely to produce any further benefit.

MI (ST elevation MI or NSTE-ACS): Oral: Initial: 50 to 100 mg in 1 or 2 divided doses with titration to desired effect. In general, oral beta-blockers should be initiated within the first 24 hours post myocardial infarction and continued indefinitely for most patients (ISIS-1 1986; ACC/AHA [Amsterdam 2014]; ACCF/AHA [O'Gara 2013]).

Supraventricular tachycardia (off-label use): Oral: Initial: 25 to 50 mg daily; maximum maintenance dose: 100 mg/day (ACC/AHA/HRS [Page 2015])

Thyrotoxicosis (off-label use): Oral: 25 to 100 mg once or twice daily (Ross 2016)

Ventricular arrhythmias (off-label use): Oral: 25 to 100 mg/day (AHA/ACC/HRS [Al-Khatib 2017]; Krittatphong 2002)

Dosing: Geriatric

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

Dosing: Pediatric

Hypertension: Oral: Children and Adolescents: Initial: 0.5 to 1 mg/kg/dose either once daily or divided in doses twice daily; titrate dose to effect; usual range: 0.5 to 1.5 mg/kg/day; maximum dose: 2 mg/kg/day up to 100 mg/day (NHBPEP 2004; NLHBI 2011).

Dosing: Renal Impairment

CrCl >35 mL/minute/1.73 m2: No dosage adjustment necessary.

CrCl 15 to 35 mL/minute/1.73 m2: Maximum dose: 50 mg daily

CrCl <15 mL/minute/1.73 m2: Maximum dose: 25 mg daily

Hemodialysis: Moderately dialyzable (20% to 50%) via hemodialysis; administer dose postdialysis or administer 25 to 50 mg supplemental dose.

Peritoneal dialysis: Elimination is not enhanced; supplemental dose is not necessary.

Dosing: Hepatic Impairment

There are no dosage adjustments provided in the manufacturer’s labeling; however, atenolol undergoes minimal hepatic metabolism.

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. 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

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

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

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. Exceptions: Bepridil. 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. 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

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. Exceptions: Nicergoline. Consider therapy modification

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. 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: 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

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. Avoid combination

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

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

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

Opioids (Anilidopiperidine): May enhance the bradycardic effect of Beta-Blockers. Opioids (Anilidopiperidine) may enhance the hypotensive effect of Beta-Blockers. 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

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

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

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

1% to 10%:

Cardiovascular: Bradycardia (persistent), cardiac failure, chest pain, cold extremities, complete atrioventricular block, edema, hypotension, Raynaud's phenomenon, second degree atrioventricular block

Central nervous system: Confusion, decreased mental acuity, depression, dizziness, fatigue, headache, insomnia, lethargy, nightmares

Gastrointestinal: Constipation, diarrhea, nausea

Genitourinary: Impotence

<1% (Limited to important or life-threatening): Alopecia, dyspnea (especially with large doses), hallucination, increased liver enzymes, lupus-like syndrome, Peyronie's disease, positive ANA titer, psoriasiform eruption, psychosis, thrombocytopenia, wheezing

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.

• Prinzmetal variant 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).

• 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.

Concurrent drug therapy issues:

• Drug-drug interactions: Potentially significant interactions may exist, requiring dose or frequency adjustment, additional monitoring, and/or selection of alternative therapy. Consult drug interactions database for more detailed information.

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 2017]):

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. Adequate facilities for monitoring infants at birth is generally recommended. The maternal pharmacokinetic parameters of atenolol during the second and third trimesters are within the ranges reported in nonpregnant patients (Hebert 2005).

Untreated chronic maternal hypertension and preeclampsia are associated with adverse events in the fetus, infant, and mother (ACOG 2015; Magee 2014). Although beta-blockers may be used when treatment of hypertension in pregnancy is indicated, agents other than atenolol are preferred (ACOG 2013; Magee 2014; Regitz-Zagrosek 2011).

Patient Education

• 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 loss of strength and energy. Have patient report immediately to prescriber severe dizziness, passing out, sensation of cold, depression, shortness of breath, excessive weight gain, swelling of arm or leg, or bradycardia (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.

Further information

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

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