Yes

Beta Blocker, Beta₁ Selective

Treatment of hypertension, alone or in combination with other agents; management of angina pectoris, postmyocardial infarction patients

D

Clinical effects on the fetus: Crosses the placenta; persistent beta-blockade, bradycardia, IUGR; IUGR probably related to maternal hypertension. Available evidence suggests safe use during pregnancy and breast-feeding. Monitor breast-fed infant for symptoms of beta-blockade.

Breast-feeding/lactation: Crosses into breast milk. American Academy of Pediatrics considers compatible with breast-feeding.

Clinical effects on the infant: Symptoms have been reported of beta-blockade including cyanosis, hypothermia, bradycardia.

Hypersensitivity to atenolol or any component; sinus bradycardia; sinus node dysfunction; heart block greater than first-degree (except in patients with a functioning artificial pacemaker); cardiogenic shock; uncompensated cardiac failure; pulmonary edema; pregnancy

Administer cautiously in compensated heart failure and monitor for a worsening of the condition (efficacy of atenolol in heart failure has not been established). Avoid abrupt discontinuation in patients with a history of CAD; slowly wean while monitoring for signs and symptoms of ischemia. Use caution with concurrent use of beta-blockers and either verapamil or diltiazem; bradycardia or heart block can occur. Avoid concurrent I.V. use of both agents. Beta-blockers should be avoided in patients with bronchospastic disease and peripheral vascular disease (may aggravate arterial insufficiency). Atenolol, with B1 selectivity, has been used cautiously in bronchospastic disease with close monitoring. Use cautiously in diabetics - may mask hypoglycemic symptoms. May mask signs of thyrotoxicosis. May cause fetal harm when administered in pregnancy. Use cautiously in the renally impaired (dosage adjustment required). Use care with anesthetic agents which decrease myocardial function. Caution in myasthenia gravis.

1% to 10%:

Cardiovascular: Persistent bradycardia, hypotension, chest pain, edema, heart failure, second- or third-degree A-V block, Raynaud's phenomenon

Central nervous system: Dizziness, fatigue, insomnia, lethargy, confusion, mental impairment, depression, headache, nightmares

Gastrointestinal: Constipation, diarrhea, nausea

Genitourinary: Impotence

Miscellaneous: Cold extremities

<1% (Limited to important or life-threatening symptoms): Dyspnea (especially with large doses), wheezing

Symptoms of intoxication include cardiac disturbances, CNS toxicity, bronchospasm, hypoglycemia and hyperkalemia. The most common cardiac symptoms include hypotension and bradycardia; atrioventricular block, intraventricular conduction disturbances, cardiogenic shock, and asystole may occur with severe overdose, especially with membrane-depressant drugs (eg, propranolol); CNS effects include convulsions, coma, and respiratory arrest (commonly seen with propranolol and other membrane-depressant and lipid-soluble drugs).

Treatment includes symptomatic treatment of seizures, hypotension, hyperkalemia, and hypoglycemia; bradycardia and hypotension resistant to atropine, isoproterenol, or pacing may respond to glucagon; wide QRS defects caused by the membrane-depressant poisoning may respond to hypertonic sodium bicarbonate; repeat-dose charcoal, hemoperfusion, or hemodialysis may be helpful in removal of only those beta-blockers with a small V_d, long half-life, or low intrinsic clearance (acebutolol, atenolol, nadolol, sotalol)

Alpha-blockers (prazosin, terazosin): Concurrent use of beta-blockers may increase risk of orthostasis.

Ampicillin, in single doses of 1 gram, decrease atenolol's pharmacologic actions.

Antacids (magnesium-aluminum, calcium antacids or salts) may reduce the bioavailability of atenolol.

Clonidine: Hypertensive crisis after or during withdrawal of either agent.

Drugs which slow AV conduction (digoxin): Effects may be additive with beta-blockers.

Glucagon: Atenolol may blunt the hyperglycemic action of glucagon.

Insulin and oral hypoglycemics: Atenolol masks the tachycardia that usually accompanies hypoglycemia.

NSAIDs (ibuprofen, indomethacin, naproxen, piroxicam) may reduce the antihypertensive effects of beta-blockers.

Salicylates may reduce the antihypertensive effects of beta-blockers.

Sulfonylureas: Beta-blockers may alter response to hypoglycemic agents.

Verapamil or diltiazem may have synergistic or additive pharmacological effects when taken concurrently with beta-blockers.

Protect from light

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

Peak concentrations in 1-2 hours with oral; more rapid with I.V.

Duration: 12-24 hours in normal renal function

Absorption: Incomplete from GI tract

Distribution: Low lipophilicity; does not cross the blood-brain barrier

Protein binding: Low at 3% to 15%

Metabolism: Partial hepatic

Half-life, beta:

Neonates: Mean: 16 hours, up to 35 hours

Children: 4.6 hours; children >10 years of age may have longer half-life (>5 hours) compared to children 5-10 years of age (<5 hours)

Adults:

Normal renal function: 6-9 hours, longer in those with renal impairment

End-stage renal disease: 15-35 hours

Time to peak: Oral: Within 2-4 hours

Elimination: 40% excreted as unchanged drug in urine, 50% in feces

Oral:

Children: 0.8-1 mg/kg/dose given daily; range of 0.8-1.5 mg/kg/day; maximum dose: 2 mg/kg/day

Adults:

Hypertension: 50 mg once daily, may increase to 100 mg/day. Doses >100 mg are unlikely to produce any further benefit.

Angina pectoris: 50 mg once daily, may increase to 100 mg/day. Some patients may require 200 mg/day.

Postmyocardial infarction: Follow I.V. dose with 100 mg/day or 50 mg twice daily for 6-9 days postmyocardial infarction.

I.V.: Postmyocardial infarction: Early treatment: 5 mg slow I.V. over 5 minutes; may repeat in 10 minutes. If both doses are tolerated, may start oral atenolol 50 mg every 12 hours or 100 mg/day for 6-9 days postmyocardial infarction.

Dosing interval for oral atenolol in renal impairment:

Cl_cr 15-35 mL/minute: Administer 50 mg/day maximum.

Cl_cr <15 mL/minute: Administer 50 mg every other day maximum.

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

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

May be administered without regard to meals

Monitor blood pressure, apical and radial pulses, fluid I & O, daily weight, respirations, and circulation in extremities before and during therapy

glucose; HDL

Hypertension: Beta-blocker therapy in the treatment of hypertension has been associated with improved cardiovascular outcomes. This class of drug is beneficial for elderly patients with hypertension. A recent UKPDS study showed that beta-blocker therapy (atenolol) was as effective as an ACE inhibitor in reducing cardiovascular events and that the benefits of therapy were related more to the degree of antihypertensive efficacy rather than the class of drug used.

Myocardial infarction: Beta-blockers, in general without intrinsic sympathomimetic activity (ISA), have been shown to decrease morbidity and mortality when initiated in the acute treatment of myocardial infarction and continued long-term. In this setting, therapy should be avoided in patients with hypotension, cardiogenic shock, or heart block.

Surgery: Atenolol has also been shown to improve cardiovascular outcomes when used in the perioperative period in patients with underlying cardiovascular disease who are undergoing noncardiac surgery. Bisoprolol in high-risk patients undergoing vascular surgery reduced the perioperative incidence of death from cardiac causes and nonfatal myocardial infarction.

Atrial fibrillation: Beta-blocker therapy provides effective rate control in patients with atrial fibrillation.

Angina: Beta-blockers are effective in the treatment of angina as monotherapy or when combined with nitrates and/or calcium channel blockers. In patients with severe intractable angina requiring negative cardiac chronotropic medications, pacemaker placement has been carried out to maintain heart rate in the setting of large doses of beta-blockers and/or calcium channel blockers. Beta-blockers are ineffective in the treatment of pure vasospastic (Prinzmetal) angina.

Withdrawal: Beta-blocker therapy should not be withdrawn abruptly, but gradually tapered to avoid acute tachycardia and hypertension.

Heart failure: There is emerging evidence that beta-blocker therapy, without intrinsic sympathomimetic activity (ISA), should be initiated in select patients with stable congestive heart failure (NYHA Class II-III). To date, carvedilol, sustained release metoprolol, and bisoprolol have demonstrated a beneficial effect on morbidity and mortality. It is important that beta-blocker therapy be instituted initially at very low doses with gradual and very careful titration.

May cause fatigue, insomnia, and confusion which can clinically look like depression

Concurrent use with other psychotropics may produce an additive hypotensive response (especially low potency antipsychotics and TCAs)

No information available to require special precautions

Noncardioselective beta-blockers (ie, propranolol, nadolol) enhance the pressor response to epinephrine, resulting in hypertension and bradycardia. This has not been reported for atenolol, a cardioselective beta-blocker. Therefore, local anesthetic with vasoconstrictor can be safely used in patients medicated with atenolol. Many nonsteroidal anti-inflammatory drugs such as ibuprofen and indomethacin can reduce the hypotensive effect of beta-blockers after 3 or more weeks of therapy with the NSAID. Short-term NSAID use (ie, 3 days) requires no special precautions in patients taking beta-blockers.

Take exactly as directed. Do not increase, decrease, or adjust dosage without consulting prescriber. Take pulse daily, prior to medication and follow prescriber's instruction about holding medication. Do not take with antacids. Do not use alcohol or OTC medications (eg, cold remedies) without consulting prescriber. If diabetic, monitor serum sugars closely (may alter glucose tolerance or mask signs of hypoglycemia). May cause fatigue, dizziness, or postural hypotension; use caution when changing position from lying or sitting to standing, when driving, or when climbing stairs until response to medication is known. May cause alteration in sexual performance (reversible). Report unresolved swelling of extremities, difficulty breathing or new cough, unresolved fatigue, unusual weight gain, unresolved constipation, or unusual muscle weakness. Pregnancy/breast-feeding precautions: Use appropriate contraceptive measures; do not get pregnant while taking this drug. Consult prescriber if breast-feeding.

Modify dosage in patients with renal insufficiency; administer by slow I.V. injection at a rate not to exceed 1 mg/minute; the injection can be administered undiluted or diluted with a compatible I.V. solution

Monitor blood pressure, heart rate, fluid I & O, daily weight, respiratory rate

Injection: 0.5 mg/mL (10 mL)

Tablet: 25 mg, 50 mg, 100 mg

A 2 mg/mL atenolol oral liquid compounded from tablets and a commercially available oral diluent was found to be stable for up to 40 days when stored at 5°C or 25°C

Buck ML, Wiest D, Gillette PC, et al, "Pharmacokinetics and Pharmacodynamics of Atenolol in Children," Clin Pharmacol Ther, 1989, 46(6):629-33.

Case CL, Trippel DL, and Gillette PC, "New Antiarrhythmic Agents in Pediatrics," Pediatr Clin North Am, 1989, 36(5):1293-320.

De Lima LG, Kharasch ED, and Butler S, "Successful Pharmacologic Treatment of Massive Atenolol Overdose: Sequential Hemodynamics and Plasma Atenolol Concentrations," Anesthesiology, 1995, 83(1):204-7.

Foster CA and Aston SJ, "Propranolol-Epinephrine Interaction: A Potential Disaster," Plast Reconstr Surg, 1983, 72(1):74-8.

Lewis RV and McDevitt DG, "Adverse Reactions and Interactions With Beta-Adrenoceptor Blocking Drugs," Med Toxicol Adverse Drug Exp, 1986, 1(5):343-61.

Schallreuter KU, "Beta-Adrenergic Blocking Drugs May Exacerbate Vitiligo," Br J Dermatol, 1995, 132(1):168-9.

Shanahan FL and Counihan TB, "Atenolol Self-Poisoning," Br Med J, 1978, 2(6139):773.

Stoschitzky K, Kahr S, Donnerer J, et al, "Stereoselective Increase of Plasma Concentrations of the Enantiomers of Propranolol and Atenolol During Exercise," Clin Pharmacol Ther, 1995, 57(5):543-51.

Trippel DL and Gillette PC, "Atenolol in Children With Supraventricular Tachycardia," Am J Cardiol, 1989, 64(3):233-6.

Trippel DL and Gillette PC, "Atenolol in Children With Ventricular Arrhythmias," Am Heart J, 1990, 119(6):1312-6.

Wong DG, Spence JD, Lamki L, et al, "Effect of Nonsteroidal Anti-inflammatory Drugs on Control of Hypertension of Beta-Blockers and Diuretics," Lancet, 1986, 1(8488):997-1001.

Wynn RL, "Dental Nonsteroidal Anti-inflammatory Drugs and Prostaglandin-Based Drug Interactions-Part Two," Gen Dent, 1992, 40(2):104, 106, 108.

Wynn RL, "Epinephrine Interactions With Beta-Blockers," Gen Dent, 1994, 42(1):16, 18.

Yusuf SW and Mishra RM, "Hepatic Dysfunction Associated With Atenolol," Lancet, 1995, 346(8968):192.