has started has not been established, and propranolol is not indicated for such use. essential tremor propranolol hydrochloride is indicated in the management of familial or hereditary essential tremor. familial or essential tremor consists of involuntary, rhythmic, oscillatory movements, usually limited to the upper limbs. it is absent at rest, but occurs when the limb is held in a fixed posture or position against gravity and during active movement. propranolol causes a reduction in the tremor amplitude, but not in the tremor frequency. propranolol hydrochloride is not indicated for the treatment of tremor associated with parkinsonism. hypertrophic subaortic stenosis propranolol hydrochloride improves nyha functional class in symptomatic patients with hypertrophic subaortic stenosis. pheochromocytoma propranolol hydrochloride is indicated as an adjunct to alpha-adrenergic blockade to control blood pressure and reduce symptoms of catecholamine-secreting tumors.

n of propranolol (see adverse reactions ). cutaneous reactions, including stevens-johnson syndrome, toxic epidermal necrolysis, exfoliative dermatitis, erythema multiforme, and urticaria, have been reported with use of propranolol (see adverse reactions ). cardiac failure sympathetic stimulation may be a vital component supporting circulatory function in patients with congestive heart failure, and its inhibition by beta-blockade may precipitate more severe failure. although beta-blockers should be avoided in overt congestive heart failure, some have been shown to be highly beneficial when used with close follow-up in patients with a history of failure who are well compensated and are receiving additional therapies, including diuretics as needed. beta-adrenergic blocking agents do not abolish the inotropic action of digitalis on heart muscle. in patients without a history of heart failure , continued use of beta-blockers can, in some cases, lead to cardiac failure. nonallergic bronchospasm (e.g., chronic bronchitis, emphysema) in general, patients with bronchospastic lung disease should not receive beta-blockers. propranolol should be administered with caution in this setting since it may provoke a bronchial asthmatic attack by blocking bronchodilation produced by endogenous and exogenous catecholamine stimulation of beta-receptors. major surgery chronically administered beta-blocking therapy should not be routinely withdrawn prior to major surgery, however the impaired ability of the heart to respond to reflex adrenergic stimuli may augment the risks of general anesthesia and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 beta-adrenergic blockade may prevent the appearance of certain premonitory signs and symptoms (pulse rate and pressure changes) of acute hypoglycemia, especially in labile insulin-dependent diabetics. in these patients, it may be more difficult to adjust the dosage of insulin. propranolol therapy, particularly when given to infants and children, diabetic or not, has been associated with hypoglycemia, especially during fasting as in preparation for surgery. hypoglycemia has been reported in patients taking propranolol after prolonged physical exertion and in patients with renal insufficiency. thyrotoxicosis beta-adrenergic blockade may mask certain clinical signs of hyperthyroidism. therefore, abrupt withdrawal of propranolol may be followed by an exacerbation of symptoms of hyperthyroidism, including thyroid storm. propranolol may change thyroid-function tests, increasing t 4 and reverse t 3 and decreasing t 3 . wolff-parkinson-white syndrome beta-adrenergic blockade in patients with wolf-parkinson-white syndrome and tachycardia has been associated with severe bradycardia requiring treatment with a pacemaker. in one case, this result was reported after an initial dose of 5 mg propranolol. pheochromocytoma blocking only the peripheral dilator (beta) action of epinephrine with propranolol leaves its constrictor (alpha) action unopposed. in the event of hemorrhage or shock, there is a disadvantage in having both beta and alpha blockade since the combination prevents the increase in heart rate and peripheral vasoconstriction needed to maintain blood pressure.

the day. if control is not adequate, a larger dose, or 3-times-daily therapy may achieve better control. angina pectoris total daily doses of 80 mg to 320 mg propranolol, when administered orally, twice a day, three times a day, or four times a day, have been shown to increase exercise tolerance and to reduce ischemic changes in the ecg. if treatment is to be discontinued, reduce dosage gradually over a period of several weeks. (see warnings .) atrial fibrillation the recommended dose is 10 mg to 30 mg propranolol three or four times daily before meals and at bedtime. myocardial infarction in the beta-blocker heart attack trial (bhat), the initial dose was 40 mg t.i.d., with titration after 1 month to 60 mg to 80 mg t.i.d. as tolerated. the recommended daily dosage is 180 mg to 240 mg propranolol per day in divided doses. although a t.i.d. regimen was used in the bhat and a q.i.d. regimen in the norwegian multicenter trial, there is a reasonable basis for the use of either a t.i.d. or b.i.d. regimen (see pharmacodynamics and clinical effects ). the effectiveness and safety of daily dosages greater than 240 mg for prevention of cardiac mortality have not been established. however, higher dosages may be needed to effectively treat co-existing diseases such as angina or hypertension (see above). migraine the initial dose is 80 mg propranolol daily in divided doses. the usual effective dose range is 160 mg to 240 mg per day. the dosage may be increased gradually to achieve optimum migraine prophylaxis. if a satisfactory response is not obtained within four to six weeks after reaching the maximum dose, propranolol therapy should be discontinued. it may be advisable to withdraw the drug gradually over a period of several weeks. essential tremor the initial dosage is 40 mg propranolol twice daily. optimum reduction of essential tremor is usually achieved with a dose of 120 mg per day. occasionally, it may be necessary to administer 240 mg to 320 mg per day. hypertrophic subaortic stenosis the usual dosage is 20 mg to 40 mg propranolol three or four times daily before meals and at bedtime. pheochromocytoma the usual dosage is 60 mg propranolol daily in divided doses for three days prior to surgery as adjunctive therapy to alpha-adrenergic blockade. for the management of inoperable tumors, the usual dosage is 30 mg daily in divided doses as adjunctive therapy to alpha-adrenergic blockade.

hylactoid reactions, pharyngitis and agranulocytosis; erythematous rash, fever combined with aching and sore throat; laryngospasm, and respiratory distress. respiratory: bronchospasm. hematologic: agranulocytosis, nonthrombocytopenic purpura, thrombocytopenic purpura. autoimmune: systemic lupus erythematosus (sle). skin and mucous membranes: stevens-johnson syndrome, toxic epidermal necrolysis, dry eyes, exfoliative dermatitis, erythema multiforme, urticaria, alopecia, sle-like reactions, and psoriasiform rashes. oculomucocutaneous syndrome involving the skin, serous membranes and conjunctivae reported for a beta-blocker (practolol) have not been associated with propranolol. genitourinary: male impotence; peyronie’s disease.

rom vasomotor centers in the brain. although total peripheral resistance may increase initially, it readjusts to or below the pretreatment level with chronic use of propranolol. effects of propranolol on plasma volume appear to be minor and somewhat variable. in angina pectoris, propranolol generally reduces the oxygen requirement of the heart at any given level of effort by blocking the catecholamine-induced increases in the heart rate, systolic blood pressure, and the velocity and extent of myocardial contraction. propranolol may increase oxygen requirements by increasing left ventricular fiber length, end diastolic pressure, and systolic ejection period. the net physiologic effect of beta-adrenergic blockade is usually advantageous and is manifested during exercise by delayed onset of pain and increased work capacity. propranolol exerts its antiarrhythmic effects in concentrations associated with beta-adrenergic blockade, and this appears to be its principal antiarrhythmic mechanism of action. in dosages greater than required for beta-blockade, propranolol also exerts a quinidine-like or anesthetic-like membrane action, which affects the cardiac action potential. the significance of the membrane action in the treatment of arrhythmias is uncertain. the mechanism of the antimigraine effect of propranolol has not been established. beta-adrenergic receptors have been demonstrated in the pial vessels of the brain. the specific mechanism of propranolol’s antitremor effects has not been established, but beta-2 (noncardiac) receptors may be involved. a central effect is also possible. clinical studies have demonstrated that propranolol is of benefit in exaggerated physiological and essential (familial) tremor.