Maximum reduction in exercise tachycardia occurs within 5 minutes of an intravenous dose. For both orally and intravenously administered drug, the duration of action is dose related and also bears a linear relationship to the logarithm of plasma TENORMIN concentration.
The effect on exercise tachycardia of a single 10 mg intravenous dose is largely dissipated by 12 hours, whereas beta-blocking activity of single oral doses of 50 mg and mg is still evident beyond 24 hours following administration.
However, as has been shown for all beta-blocking agents, the antihypertensive effect does not appear to be related to plasma level. In normal subjects, the beta1 selectivity of TENORMIN has been shown by its reduced ability to reverse the beta2-mediated vasodilating effect of isoproterenol as compared to equivalent beta-blocking doses of propranolol. In asthmatic patients, a dose of TENORMIN producing a greater effect on resting heart rate than propranolol resulted in much less increase in airway resistance.
In a placebo controlled comparison of approximately equipotent oral doses of several beta blockers , TENORMIN produced a significantly smaller decrease of FEV1 than nonselective beta blockers such as propranolol and, unlike those agents, did not inhibit bronchodilation in response to isoproterenol. Conduction in the AV node is also prolonged. TENORMIN is devoid of membrane stabilizing activity, and increasing the dose well beyond that producing beta blockade does not further depress myocardial contractility.
In controlled clinical trials, TENORMIN, given as a single daily oral dose, was an effective antihypertensive agent providing hour reduction of blood pressure. TENORMIN has been studied in combination with thiazide type diuretics, and the blood pressure effects of the combination are approximately additive. TENORMIN is also compatible with methyldopa, hydralazine, and prazosin, each combination resulting in a larger fall in blood pressure than with the single agents. The mechanisms of the antihypertensive effects of beta-blocking agents have not been established.
Several possible mechanisms have been proposed and include: By blocking the positive chronotropic and inotropic effects of catecholamines and by decreasing blood pressure, atenolol generally reduces the oxygen requirements of the heart at any given level of effort, making it useful for many patients in the long-term management of angina pectoris.
On the other hand, atenolol can increase oxygen requirements by increasing left ventricular fiber length and end diastolic pressure, particularly in patients with heart failure.
Thirty-eight percent of each group were treated within 4 hours of onset of pain. The mean time from onset of pain to entry was 5. The groups were similar in demographic and medical history characteristics and in electrocardiographic evidence of myocardial infarction, bundle branch block, and first degree atrioventricular block at entry. During the treatment period days , the vascular mortality rates were 3. Patients with coronary artery disease, who are being treated with atenolol, should be advised against abrupt discontinuation of therapy.
Severe exacerbation of angina and the occurrence of myocardial infarction and ventricular arrhythmias have been reported in angina patients following the abrupt discontinuation of therapy with beta blockers. The last two complications may occur with or without preceding exacerbation of the angina pectoris.
As with other beta blockers, when discontinuation of atenolol is planned, the patients should be carefully observed and advised 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. Concomitant Use of Calcium Channel Blockers Bradycardia and heart block can occur and the left ventricular end diastolic pressure can rise when beta blockers are administered with verapamil or diltiazem.
Because of its relative beta1 selectivity, however, atenolol may be used with caution in patients with bronchospastic disease who do not respond to, or cannot tolerate, other antihypertensive treatment. Since beta1 selectivity is not absolute, the lowest possible dose of atenolol should be used with therapy initiated at 50 mg and a beta2- stimulating agent bronchodilator should be made available.
If dosage must be increased, dividing the dose should be considered in order to achieve lower peak blood levels. Major Surgery Chronically administered beta-blocking therapy should not be routinely withdrawn prior to major surgery; however the impaired ability of the heart to respond to reflex adrenergic stimuli may augment the risks of general anesthesia and surgical procedures.
Diabetes and Hypoglycemia Atenolol should be used with caution in diabetic patients if a beta-blocking agent is required. Beta blockers may mask tachycardia occurring with hypoglycemia, but other manifestations such as dizziness and sweating may not be significantly affected. At recommended doses atenolol does not potentiate insulin-induced hypoglycemia and, unlike nonselective beta blockers, does not delay recovery of blood glucose to normal levels.
Thyrotoxicosis Beta-adrenergic blockade may mask certain clinical signs e. Untreated Pheochromocytoma Atenolol should not be given to patients with untreated pheochromocytoma. Pregnancy and Fetal Injury Atenolol can cause fetal harm when administered to a pregnant woman. Atenolol crosses the placental barrier and appears in cord blood.
Administration of atenolol, starting in the second trimester of pregnancy, has been associated with the birth of infants that are small for gestational age.
The half-life is markedly longer in the elderly compared to younger subjects. The reduction in atenolol clearance follows the general trend that the elimination of renally excreted drugs is decreased with increasing age. Lowering blood pressure lowers the risk of fatal and non-fatal cardiovascular events, primarily strokes and myocardial infarctions. These benefits have been seen in controlled trials of antihypertensive drugs from a wide variety of pharmacologic classes including atenolol.
Control of high blood pressure should be part of comprehensive cardiovascular risk management, including, as appropriate, lipid control, diabetes management, antithrombotic therapy, smoking cessation, exercise, and limited sodium intake.
Many patients will require more than 1 drug to achieve blood pressure goals. Numerous antihypertensive drugs, from a variety of pharmacologic classes and with different mechanisms of action, have been shown in randomized controlled trials to reduce cardiovascular morbidity and mortality, and it can be concluded that it is blood pressure reduction, and not some other pharmacologic property of the drugs, that is largely responsible for those benefits.
The largest and most consistent cardiovascular outcome benefit has been a reduction in the risk of stroke, but reductions in myocardial infarction and cardiovascular mortality also have been seen regularly. Elevated systolic or diastolic pressure causes increased cardiovascular risk, and the absolute risk increase per mmHg is greater at higher blood pressures, so that even modest reductions of severe hypertension can provide substantial benefit.
Relative risk reduction from blood pressure reduction is similar across populations with varying absolute risk, so the absolute benefit is greater in patients who are at higher risk independent of their hypertension for example, patients with diabetes or hyperlipidemia , and such patients would be expected to benefit from more aggressive treatment to a lower blood pressure goal.
Some antihypertensive drugs have smaller blood pressure effects as monotherapy in black patients, and many antihypertensive drugs have additional approved indications and effects e. These considerations may guide selection of therapy. Atenolol Tablets USP may be administered with other antihypertensive agents. Angina Pectoris Due to Coronary Atherosclerosis: Atenolol is indicated for the long-term management of patients with angina pectoris.
Atenolol is indicated in the management of hemodynamically stable patients with definite or suspected acute myocardial infarction to reduce cardiovascular mortality. Treatment can be initiated as soon as the patient's clinical condition allows. In general, there is no basis for treating patients like those who were excluded from the ISIS-1 trial blood pressure less than mm Hg systolic, heart rate less than 50 bpm or have other reasons to avoid beta-blockade. As noted above, some subgroups e. Atenolol is contraindicated in those patients with a history of hypersensitivity to the atenolol or any of the drug product's components Warnings Cardiac Failure Sympathetic stimulation is necessary in supporting circulatory function in congestive heart failure, and beta-blockade carries the potential hazard of further depressing myocardial contractility and precipitating more severe failure.
In patients with acute myocardial infarction, cardiac failure which is not promptly and effectively controlled by 80 mg of intravenous furosemide or equivalent therapy is a contraindication to beta-blocker treatment. In Patients Without a History of Cardiac Failure Continued depression of the myocardium with beta-blocking agents over a period of time can, in some cases, lead to cardiac failure.
At the first sign or symptom of impending cardiac failure, patients should be treated appropriately according to currently recommended guidelines, and the response observed closely. Anaesthetic agents causing myocardial depression such as cyclopropane and trichlorethylene, lidocaine, procainamide and beta-adrenoceptor stimulants such as noradrenaline norepinephrine are best avoided. Not recommended association with monoamineoxidase inhibitors except MAO-B inhibitors Not recommended association with Baclofen: Causes an increased antihypertensive activity.
Not recommended association with contrast media, iodinated: Atenolol may impede the compensatory cardiovascular reactions associated with hypotension or shock induced by iodinated contrast products. Combination with atenolol may result in additive depressant effects on conduction and negative inotropic effects, especially in patients with underlying sinus node dysfunction or atrioventricular node dysfunction.
May reduce the bioavailability of atenolol. Therefore the physician should watch for evidence of altered atenolol response especially when large doses of ampicillin are administered concomitantly Peripheral muscle relaxants e.
Pregnancy Atenolol crosses the placental barrier and appears in the cord blood. No studies have been performed on the use of Atenolol in the first trimester and the possibility of foetal injury cannot be excluded.
Atenolol has been used under close supervision for the treatment of hypertension in the third trimester. Administration of Atenolol to pregnant women in the management of mild to moderate hypertension has been associated with intra-uterine growth retardation. If you stop taking it suddenly: If you suddenly stop taking atenolol for high blood pressure, chest pain, or after a heart attack, you raise your risk of heart attack.
Not taking atenolol every day, skipping days, or taking doses at different times of day also come with risks. Your blood pressure might fluctuate too often.
That might increase your risk for a heart attack. If you miss a dose: If you miss a dose, just take the next dose as planned. How to tell if the drug is working: You can tell that atenolol is working if it lowers your blood pressure. Keep these considerations in mind if your doctor prescribes atenolol for you. General You can cut or crush the tablet.
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