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.
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 2021).
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.
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
Altered kidney function (Kirch 1981; McAinsh 1980):
CrCl >30 mL/minute: No dosage adjustment necessary.
CrCl 10 to 30 mL/minute: Maximum dose: 50 mg daily.
CrCl <10 mL/minute: Maximum dose: 25 mg daily.
Hemodialysis, intermittent (thrice weekly): Moderately dialyzable (20% to 50%) (Campese 1985; Flouvat 1980; Tieu 2018):
Daily dosing: 25 to 50 mg daily; when scheduled dose falls on a dialysis day, administer post dialysis (Golightly 2013).
Three times weekly (post dialysis) dosing: Initial: 25 to 50 mg 3 times weekly administered post dialysis on dialysis days; titrate based on patient response to a maximum of 100 mg 3 times weekly administered post dialysis on dialysis days (Agarwal 2014; Kirch 1981).
Peritoneal dialysis: Not significantly dialyzed (Salahudeen 1984): Maximum: 25 mg daily (Golightly 2013).
There are no dosage adjustments provided in the manufacturer’s labeling; however, atenolol undergoes minimal hepatic metabolism.
(For additional information see "Atenolol: Pediatric drug information")
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.
Altered kidney function: Infants, Children, and Adolescents: Oral:
GFR >50 mL/minute/1.73 m2: No dosage adjustment necessary (Aronoff 2007).
GFR 30 to 50 mL/minute/1.73 m2: Maximum dose: 1 mg/kg/dose every 24 hours; maximum adult daily dose: 50 mg/day (Aronoff 2007).
GFR 10 to <30 mL/minute/1.73 m2: Maximum dose: 1 mg/kg/dose every 48 hours (Aronoff 2007); based on adult information, maximum dose should not exceed 50 mg/dose (Kirch 1981).
GFR <10 mL/minute/1.73 m2: Maximum dose: 1 mg/kg/dose every 48 hours (Aronoff 2007); based on adult information, maximum dose should not exceed 25 mg/dose (Kirch 1981).
Intermittent hemodialysis: Infants, Children, and Adolescents: Oral: Moderately dialyzable (20% to 50%) (Tieu 2018): Maximum dose: 1 mg/kg/dose every 48 hours; give after hemodialysis (Aronoff 2007). Note: Usual adult dose is 25 to 50 mg/day (Golightly 2013).
Peritoneal dialysis: Infants, Children, and Adolescents: Oral: Not significantly dialyzed (Salahudeen 1984): Maximum dose: 1 mg/kg/dose every 48 hours (Aronoff 2007); based on adult information, maximum dose should not exceed 25 mg/dose (Golightly 2013).
There are no dosage adjustments provided in the manufacturer's labeling; however, atenolol undergoes minimal hepatic metabolism.
Refer to adult dosing. In the management of hypertension, consider lower initial doses and titrate to response (Aronow 2011).
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
Yes
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral:
Tenormin: 50 mg, 100 mg [contains corn starch]
Generic: 25 mg, 50 mg, 100 mg
Oral: May be administered without regard to meals.
Oral: May be administered without regard to food
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.
Atrial fibrillation/flutter, maintenance of ventricular rate control; Marfan syndrome with aortic aneurysm; Migraine prophylaxis; Supraventricular tachycardia (atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, focal atrial tachycardia, multifactorial atrial tachycardia), maintenance of ventricular rate control; Thyrotoxicosis; Ventricular arrhythmias or ventricular premature beats (symptomatic), prevention
Atenolol may be confused with albuterol, Altenol, timolol, Tylenol
Tenormin may be confused with Imuran, Norpramin, thiamine, Trovan
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
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
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.
None known.
Acetylcholinesterase Inhibitors: May enhance the bradycardic effect of Beta-Blockers. Risk C: Monitor therapy
Alfuzosin: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: 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. Risk C: 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. Risk D: 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. Risk D: 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. Risk C: Monitor therapy
Amphetamines: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy
Ampicillin: May decrease the bioavailability of Atenolol. Risk C: Monitor therapy
Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may enhance the hypotensive effect of Antipsychotic Agents (Second Generation [Atypical]). Risk C: Monitor therapy
Bacampicillin: May decrease the bioavailability of Atenolol. Risk C: Monitor therapy
Barbiturates: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Benperidol: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: 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. Risk C: Monitor therapy
Bradycardia-Causing Agents: May enhance the bradycardic effect of other Bradycardia-Causing Agents. Risk C: Monitor therapy
Brigatinib: May diminish the antihypertensive effect of Antihypertensive Agents. Brigatinib may enhance the bradycardic effect of Antihypertensive Agents. Risk C: Monitor therapy
Brimonidine (Topical): May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Bromperidol: May diminish the hypotensive effect of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may enhance the hypotensive effect of Bromperidol. Risk X: Avoid combination
Bupivacaine: Beta-Blockers may increase the serum concentration of Bupivacaine. Risk C: 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. Risk D: 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. Risk C: Monitor therapy
Dexmethylphenidate: May diminish the therapeutic effect of Antihypertensive Agents. Risk C: Monitor therapy
Diazoxide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Dipyridamole: May enhance the bradycardic effect of Beta-Blockers. Risk C: Monitor therapy
Disopyramide: May enhance the bradycardic effect of Beta-Blockers. Beta-Blockers may enhance the negative inotropic effect of Disopyramide. Risk C: Monitor therapy
DOBUTamine: Beta-Blockers may diminish the therapeutic effect of DOBUTamine. Risk C: 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. Risk D: Consider therapy modification
DULoxetine: Blood Pressure Lowering Agents may enhance the hypotensive effect of DULoxetine. Risk C: Monitor therapy
EPHEDrine (Systemic): Beta-Blockers may diminish the therapeutic effect of EPHEDrine (Systemic). Risk C: Monitor therapy
EPINEPHrine (Nasal): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of EPINEPHrine (Nasal). Risk C: Monitor therapy
EPINEPHrine (Oral Inhalation): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of EPINEPHrine (Oral Inhalation). Risk C: Monitor therapy
Epinephrine (Racemic): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of Epinephrine (Racemic). Risk C: Monitor therapy
EPINEPHrine (Systemic): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of EPINEPHrine (Systemic). Risk C: Monitor therapy
Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates): Beta-Blockers may enhance the vasoconstricting effect of Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates). Risk C: Monitor therapy
Etofylline: Beta-Blockers may diminish the therapeutic effect of Etofylline. Risk X: Avoid combination
Fexinidazole: Bradycardia-Causing Agents may enhance the arrhythmogenic effect of Fexinidazole. Risk X: Avoid combination
Fingolimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Fingolimod. Management: Consult with the prescriber of any bradycardia-causing agent to see if the agent could be switched to an agent that does not cause bradycardia prior to initiating fingolimod. If combined, perform continuous ECG monitoring after the first fingolimod dose. Risk D: Consider therapy modification
Glycopyrrolate (Systemic): May increase the serum concentration of Atenolol. Risk C: 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. Risk D: Consider therapy modification
Herbal Products with Blood Pressure Increasing Effects: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy
Herbal Products with Blood Pressure Lowering Effects: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Hypotension-Associated Agents: Blood Pressure Lowering Agents may enhance the hypotensive effect of Hypotension-Associated Agents. Risk C: Monitor therapy
Insulins: Beta-Blockers may enhance the hypoglycemic effect of Insulins. Risk C: Monitor therapy
Ivabradine: Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. Risk C: Monitor therapy
Lacosamide: Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. Risk C: Monitor therapy
Levodopa-Containing Products: Blood Pressure Lowering Agents may enhance the hypotensive effect of Levodopa-Containing Products. Risk C: Monitor therapy
Lidocaine (Systemic): Beta-Blockers may increase the serum concentration of Lidocaine (Systemic). Risk C: Monitor therapy
Lormetazepam: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Mepivacaine: Beta-Blockers may increase the serum concentration of Mepivacaine. Risk C: Monitor therapy
Methacholine: Beta-Blockers may enhance the adverse/toxic effect of Methacholine. Risk C: Monitor therapy
Methoxyflurane: May enhance the hypotensive effect of Beta-Blockers. Risk C: Monitor therapy
Methylphenidate: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy
Midodrine: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Molsidomine: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Naftopidil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Nicergoline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Nicorandil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
NIFEdipine: May enhance the hypotensive effect of Beta-Blockers. NIFEdipine may enhance the negative inotropic effect of Beta-Blockers. Risk C: Monitor therapy
Nitroprusside: Blood Pressure Lowering Agents may enhance the hypotensive effect of Nitroprusside. Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents: May diminish the antihypertensive effect of Beta-Blockers. Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents (Topical): May diminish the therapeutic effect of Beta-Blockers. Risk C: 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. Risk D: Consider therapy modification
Ozanimod: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Pentoxifylline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Pholcodine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Pholcodine. Risk C: Monitor therapy
Phosphodiesterase 5 Inhibitors: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Ponesimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Ponesimod. Management: Avoid coadministration of ponesimod with drugs that may cause bradycardia when possible. If combined, monitor heart rate closely and consider obtaining a cardiology consult. Do not initiate ponesimod in patients on beta-blockers if HR is less than 55 bpm. Risk D: Consider therapy modification
Prostacyclin Analogues: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Quinagolide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Reserpine: May enhance the hypotensive effect of Beta-Blockers. Risk C: Monitor therapy
Rivastigmine: May enhance the bradycardic effect of Beta-Blockers. Risk X: Avoid combination
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. Risk D: Consider therapy modification
Succinylcholine: Beta-Blockers may enhance the neuromuscular-blocking effect of Succinylcholine. Risk C: 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. Risk C: Monitor therapy
Tasimelteon: Beta-Blockers may diminish the therapeutic effect of Tasimelteon. Management: Consider avoiding nighttime administration of beta-blockers during tasimelteon therapy due to the potential for reduced tasimelteon efficacy. Risk D: Consider therapy modification
Terlipressin: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: 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. Risk C: Monitor therapy
Tofacitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: 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. Risk X: Avoid combination
Atenolol serum concentrations may be decreased if taken with food. Management: Administer without regard to meals.
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]).
Atenolol is present in breast milk.
Bradycardia has been observed in some breastfeeding infants and neonates may also be at risk for hypoglycemia. Adverse events may be more likely in premature infants or infants with impaired renal function.
Atenolol can be detected in the plasma of breastfeeding infants not previously exposed during pregnancy (Lwin 2018). Per the manufacturer, the milk/plasma ratio of atenolol is 1.5 to 6.8; however, larger ranges have been reported and ratios have been shown to vary within the same patient (Holt 1982; Lwin 2018). Beta-blockers with higher M/P ratios, such as atenolol, should be avoided while breastfeeding (Beardmore 2002). The relative infant dose (RID) of atenolol has also been calculated by authors of various studies, providing a large variability in ranges (~3% to ~35%) which may also reflect postpartum age and maternal dose (Atkinson 1988; Eyal 2010; Lwin 2018). In general, breastfeeding is considered acceptable when the RID of a medication is <10%; when the RID is >25% breastfeeding should generally be avoided (Anderson 2016; Ito 2000).
The manufacturer recommends that caution be exercised when administering atenolol to breastfeeding women. Use of a beta-blocker other than atenolol may be preferred in a breastfeeding female (Anderson 2017; Ito 2000).
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.
Competitively blocks response to beta-adrenergic stimulation, selectively blocks beta1-receptors with little or no effect on beta2-receptors except at high doses
Onset of action: Beta-blocking effect: Onset: Oral: ≤1 hour; Peak effect: Oral: 2 to 4 hours
Duration: Normal renal function: Beta-blocking effect: 12 to 24 hours; Antihypertensive effect: Oral: 24 hours
Absorption: Oral: Rapid, incomplete (~50%)
Distribution: Low lipophilicity; does not cross blood-brain barrier
Protein binding: 6% to 16%
Metabolism: Limited hepatic
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
Time to peak, plasma: Oral: 2 to 4 hours
Excretion: Feces (50%); urine (40% as unchanged drug)
Renal function impairment: Elimination is closely related to glomerular filtration rate. Significant accumulation occurs when CrCl falls below 35 mL/minute per 1.73 m2.
Geriatric: Total clearance is about 50% lower than in younger subjects. Half-life is markedly longer in elderly patients.
Tablets (Atenolol Oral)
25 mg (per each): $0.24 - $0.82
50 mg (per each): $0.83 - $0.89
100 mg (per each): $1.22 - $1.49
Tablets (Tenormin Oral)
25 mg (per each): $16.03
50 mg (per each): $16.03
100 mg (per each): $16.03
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