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Propranolol 60 mg er capital investments babaei investment abstract

Propranolol 60 mg er capital investments

The manufacturers of propranolol hydrochloride injection state that a reduction in the dosage of propranolol hydrochloride may be necessary in geriatric patients. For the management of hypertension in adults, the initial oral dosage of propranolol hydrochloride, administered either alone or in combination with a diuretic, is 40 mg twice daily as conventional tablets or oral solution or 80 mg once daily as extended-release capsules.

The usual effective oral dosage is mg daily as conventional tablets or oral solution or mg once daily as extended-release capsules; some manufacturers state that some patients may require dosages up to mg daily. However, the manufacturer of Innopran XL states that dosage of the extended-release capsules may be increased, if needed, up to mg once daily, since dosages exceeding mg once daily did not provide additional hypotensive effects. Some experts recommend a dosage of mg daily given in 2 divided doses as conventional tablets or oral solution or mg once daily as extended-release capsules.

The rationale for such reduced dosages is that it usually is preferable to add another antihypertensive agent to the regimen than to continue increasing propranolol hydrochloride dosage since the patient may not tolerate such continued increases. The full hypotensive effect of the drug usually is evident within weeks, but the timing is variable. While twice-daily dosing using the conventional tablets or oral solution is usually effective, some patients may require larger doses or 3 divided doses daily to maintain effective blood pressure control throughout the day.

Target dosages of antihypertensive agents generally can be achieved within weeks, but it may take up to several months. When combination therapy is required, the manufacturers recommend that commercially available preparations containing propranolol hydrochloride in fixed combination with a thiazide diuretic should not be used initially.

Dosage should first be adjusted by administering each drug separately. If it is determined that the optimum maintenance dosage corresponds to the ratio in the commercial combination preparation, the fixed combination may be used.

Therapy with propranolol hydrochloride in fixed combination with hydrochlorothiazide is administered twice daily for a total daily dosage of up to mg of propranolol hydrochloride and 50 mg of hydrochlorothiazide; use of this combination formulation is not appropriate for propranolol hydrochloride dosages exceeding mg daily since it would provide an excessive dosage of the thiazide component.

When necessary, another antihypertensive agent may be added gradually using half of the usual initial dosage to avoid an excessive decrease in blood pressure. Careful monitoring of blood pressure during initial titration or subsequent upward adjustment in dosage of propranolol hydrochloride is recommended. The goal of hypertension management and prevention is to achieve and maintain optimal control of blood pressure; specific target levels of blood pressure should be individualized based on consideration of multiple factors, including patient age and comorbidities, and the currently available evidence from clinical studies.

For the management of angina pectoris, the initial oral dosage of propranolol hydrochloride extended-release capsules is 80 mg daily; dosage is gradually increased as needed to control symptoms, usually at 3- to 7-day intervals. Although optimum response usually occurs at a dosage of mg daily, there is a wide variation in individual requirements. When using conventional tablets or oral solutions, the usual dosage of propranolol hydrochloride is mg daily given in divided doses.

The value and safety of dosages greater than mg daily have not been established, but some clinicians have stated that dosage may be increased further if there is only a partial response to usual dosage. During chronic therapy, the patient should be periodically reevaluated to determine the need for dosage alteration or continued therapy.

When propranolol hydrochloride is to be discontinued, dosage should be reduced slowly over a period of at least a few weeks about 2. The usual adult oral dosage of propranolol hydrochloride for the treatment of arrhythmias is mg 3 or 4 times daily as conventional tablets or oral solution. For arrhythmias in adults which are life-threatening or occur during anesthesia, the manufacturer states that mg may be administered IV under careful monitoring e.

If necessary, a second IV dose may be administered after 2 minutes. Additional IV doses may be administered at intervals of no less than 4 hours until the desired response is obtained. For the acute treatment of supraventricular tachycardia SVT e. The usual oral maintenance dosage for ongoing treatment of SVT is mg daily in divided doses or single doses with long-acting preparations.

To slow ventricular response in adults with acute atrial fibrillation, experts recommend an initial IV propranolol hydrochloride dose of 1 mg administered over 1 minute; additional doses may be given at 2-minute intervals up to a total of 3 doses. The usual oral maintenance dosage for ongoing treatment of atrial fibrillation is mg daily in divided doses. Hypertrophic subaortic stenosis in adults is usually treated with mg of propranolol hydrochloride orally 3 or 4 times daily as conventional tablets or oral solution or mg once daily as extended-release capsules.

For prophylaxis of migraine in adults, the initial oral dosage of propranolol hydrochloride is 80 mg daily, given in divided doses as the conventional tablets or oral solution or once daily as the extended-release capsules. Dosage may be increased gradually to achieve optimum migraine prophylaxis. The usual effective dosage is mg daily. If an adequate response is not obtained within weeks after reaching the maximum dose, propranolol therapy should be discontinued; it may be advisable to withdraw the drug gradually over several weeks.

When used for secondary prevention after the acute phase of myocardial infarction MI , the recommended oral dosage of propranolol hydrochloride is mg daily in divided doses as conventional tablets or oral solution. In the study demonstrating mortality benefit with propranolol, the drug was initiated days following infarction. Although the drug was given in 3 or 4 divided doses daily in clinical studies, there are considerable clinical, pharmacologic, and pharmacokinetic data suggesting that a twice-daily dosing regimen would also be adequate.

Safety and efficacy of propranolol hydrochloride dosages exceeding mg daily for the prevention of cardiac mortality have not been established; however, higher dosages may be required for the treatment of coexisting conditions such as angina or hypertension. The initial oral dosage of propranolol hydrochloride for the management of essential tremor in adults is 40 mg twice daily as conventional tablets.

Response to the drug is variable and dosage must be individualized; optimum suppression of tremor usually is achieved with a dosage of mg daily administered in 3 divided doses daily when conventional tablets are used. In adjusting propranolol hydrochloride dosage, it should be remembered that complete suppression of essential tremor rarely is achieved. Some evidence suggests that dosages exceeding mg daily do not provide substantial added benefit but are associated with an increased risk of adverse effects.

Although currently not recommended by the manufacturer, usual dosages administered once daily each morning as extended-release capsules appear to be at least as effective as equivalent dosages administered in divided doses daily as conventional tablets. Some patients may benefit from intermittent rather than chronic therapy; single to mg doses as conventional tablets have been administered hours before planned activity or anticipated stress associated with tremor.

Propranolol has not been as extensively or systematically studied in children as in adults, but specific dosing information has been reasonably studied. Weight-adjusted dosage of propranolol hydrochloride in children only serves as an approximation for initial therapy, and dosage must be adjusted according to the therapeutic response of the patient. Dosage should be calculated on a weight basis rather than a body surface area basis since the latter method may result in excessive plasma concentrations of the drug.

Dosage should be titrated according to blood pressure response and patient tolerance. Oral propranolol hydrochloride therapy has been initiated at 1. The manufacturers of propranolol hydrochloride injection state that a reduction in the dosage of propranolol hydrochloride may be necessary in patients with hepatic impairment. Adverse reactions are more frequent and may be more severe after IV administration than after oral administration.

In one large study of hospitalized patients receiving propranolol, reactions were most common in azotemic patients and in those older than 60 years of age. The incidence of adverse reactions to oral propranolol was unrelated to the dose, and adverse reactions usually occurred soon after the initiation of therapy.

The most common adverse cardiovascular effect of propranolol is bradycardia, especially in patients with digitalis intoxication. Bradycardia is occasionally severe and may be accompanied by hypotension, syncope, shock, or angina pectoris. Severe bradycardia should be treated with IM or IV administration of atropine sulfate. See Drug Interactions: Sympathomimetic Agents.

In patients with Wolff-Parkinson-White syndrome, propranolol has produced severe bradycardia requiring a demand pacemaker. In patients with heart failure, sympathetic stimulation is vital for the support of circulatory function. A decrease in exercise tolerance may be experienced by patients with left ventricular dysfunction.

In patients without a prior history of heart failure, prolonged depression of the myocardium by propranolol has resulted in heart failure in rare instances. Intensification of AV block, AV dissociation, AV conduction delays, complete heart block, or cardiac arrest may occur, especially in patients with preexisting partial heart block caused by a cardiac glycoside or other factors. Ventricular fibrillation has been reported in a patient with hypertrophic subaortic stenosis.

After sudden cessation of propranolol therapy in some patients treated for angina, increased frequency, duration, and severity of angina episodes have occurred, often within 24 hours. These episodes are unstable and are not relieved by nitroglycerin. Acute and sometimes fatal myocardial infarction and sudden death have also occurred after abrupt withdrawal of propranolol therapy in some patients treated for angina. In hypertensive patients, sudden cessation of propranolol has produced a syndrome similar to florid thyrotoxicosis, characterized by tenseness, anxiety, tachycardia, and excessive perspiration; these symptoms occurred within one week of cessation of the drug and were relieved by reinstituting propranolol therapy.

During surgery, some patients who have been receiving propranolol may experience severe, protracted hypotension and, occasionally, difficulty in restarting and maintaining heart beat. Severe hypertension has been reported in a few patients with schizophrenic disorder who received only propranolol orally in rapidly increasing doses; the hypertension responded to treatment with IV phentolamine followed by oral phenoxybenzamine.

Fluid retention, pulmonary edema, and peripheral arterial insufficiency, usually of the Raynaud's type, may occur in patients receiving propranolol. When the drug is used alone, dietary sodium restriction may be necessary. Intermittent claudication has occurred in patients with previously asymptomatic peripheral arterial disease who received propranolol, although one study which used the drug for the treatment of intermittent claudication did not note any deterioration of occlusive peripheral arterial disease.

A number of adverse CNS effects which are usually reversible after withdrawal of the drug have been reported. Adverse CNS effects usually occur after long-term treatment with high doses of propranolol and range from lightheadedness, giddiness, ataxia, dizziness, irritability, sleepiness, hearing loss, and visual disturbances to vivid dreams, hallucinations, and confusion.

Insomnia, lassitude, weakness, fatigue, and mental depression progressing to catatonia have been reported. Dosages exceeding mg daily, when administered in divided doses exceeding 80 mg each, may be associated with an increased incidence of fatigue, lethargy, and vivid dreams. Organic brain syndrome, characterized by disorientation to time and place, short-term memory loss, emotional lability, slightly clouded sensorium, and decreased performance on neuropsychometric tests, has been reported rarely.

Paresthesia of the hands, peripheral neuropathy, and precipitation of myotonia have been reported. Impotence has been reported rarely. Ptosis has been reported in 2 patients. Two patients receiving propranolol for hypertrophic obstructive cardiomyopathy developed migraine; in one patient this was associated with sensory disturbances and teichopsia. Adverse GI effects such as nausea, vomiting, diarrhea, epigastric distress, abdominal cramping, constipation, and flatulence may occur in patients receiving propranolol and occasionally necessitate reduction of dosage or withdrawal of the drug.

Mesenteric arterial thrombosis and ischemic colitis have also occurred. Rarely, rashes have been reported during propranolol usage. Rashes are most commonly erythematous maculopapular or acneiform , dry, scaly, pruritic, psoriasiform lesions which occur on the trunk, extremities, and scalp. Hyperkeratosis of the scalp, palms, and soles of the feet have been reported during treatment with propranolol; nail changes such as thickening, pitting, and discoloration have occurred.

At least one case of exfoliative dermatitis has been reported. Dermatologic reactions disappear after the drug is withdrawn. Other allergic manifestations reported during propranolol therapy include fever accompanied by aching and sore throat, rhinitis, dry mouth, laryngospasm, respiratory distress, and pharyngitis. A lupus-like syndrome characterized by fever, pruritus, severe myalgia, and positive lupus erythematosus cell tests has been reported in at least one patient receiving propranolol.

Reversible alopecia, which recurred following readministration of the drug, has been reported. In this study, the number of new cases of diabetes per person-years was Acute increases in blood pressure have occurred after insulin-induced hypoglycemia in patients receiving propranolol. Propranolol may cause elevated BUN in patients with severe heart disease, elevated serum creatinine, aminotransferase, alkaline phosphatase, or lactic dehydrogenase concentrations.

In hypertensive patients, propranolol may cause small increases in serum potassium concentration. Peyronie's disease and dry eyes have been reported rarely. Generalized hyperemia of the conjunctivae with decreased tear production and a prickling sensation of the eyes has been reported in a patient receiving the drug.

Eye dryness and pain occurred in one patient receiving propranolol. Discoloration of the tongue and bad taste were reported in two patients receiving the drug. When propranolol is used as a fixed-combination preparation that includes hydrochlorothiazide, the cautions, precautions, and contraindications associated with thiazide diuretics must be considered in addition to those associated with propranolol. Patients receiving propranolol therapy should be instructed to consult their physician at the first sign or symptom of impending cardiac failure and should be adequately treated e.

Abrupt withdrawal of propranolol may exacerbate angina symptoms or precipitate myocardial infarction in patients with coronary artery disease. Abrupt withdrawal of the drug in patients treated for hypertension has also been associated with adverse effects. See Cautions: Cardiovascular Effects.

Therefore, patients receiving propranolol especially those with ischemic heart disease should be warned not to interrupt or discontinue therapy without consulting their clinician. When discontinuance of propranolol therapy is planned, particularly in patients with ischemic heart disease, dosage of the drug should be gradually reduced over a period of at least a few weeks about 2. When propranolol therapy is discontinued, patients should be carefully monitored and their activity restricted.

If exacerbation of angina occurs after propranolol therapy is interrupted, treatment with the drug should generally be reinstituted and appropriate measures taken for the management of unstable angina pectoris. Because coronary artery disease is common and may be unrecognized, the manufacturers caution that it may be prudent not to discontinue propranolol therapy abruptly, even in patients receiving the drug for conditions other than angina.

If propranolol therapy is discontinued prior to major surgery, oral therapy with the drug may be restarted as soon after surgery as possible; patients who are unable to take oral drugs after surgery may be treated with IV propranolol if necessary. Caution should be used when administering propranolol to patients with sinus node dysfunction, since the drug can cause marked depression of SA node automaticity.

Propranolol should be used with extreme caution for the management of arrhythmias occurring during anesthesia with myocardial depressant anesthetics e. Signs of hyperthyroidism may be masked by propranolol, and patients with thyrotoxicosis who receive the drug should be monitored closely. In addition, the drug may alter thyroid function test results, increasing thyroxine T 4 and reverse triiodothyronine rT 3 and decreasing triiodothyronine T 3 determinations.

It is recommended that propranolol be used with caution in patients with diabetes mellitus especially those with labile diabetes or those prone to hypoglycemia since the drug also may block the signs and symptoms of hypoglycemia e. In addition, the drug occasionally causes hypoglycemia, even in nondiabetic patients, presumably by interfering with catecholamine-induced glycogenolysis. Propranolol may also inhibit the insulin-releasing mechanism of the pancreas and has been implicated in hyperglycemic reactions.

Propranolol-induced alterations in glucose tolerance appear to occur only rarely. See Cautions: Endocrine Effects. Some sources state that hypertensive patients who are prone to hypoglycemia should not receive propranolol because the drug may cause a sharp rise in blood pressure.

Propranolol should be used with caution in patients with a history of nonallergic bronchospasm e. Bronchospasm may be treated with IV administration of aminophylline; isoproterenol may also be administered. IV administration of atropine has been suggested if the patient fails to respond to the above or if bradycardia is present.

Withdrawal of propranolol may lead to an increase in intraocular pressure. Propranolol should be used with caution in patients with renal or hepatic impairment. Laboratory parameters should be monitored in patients receiving prolonged therapy with the drug. These patients may be unresponsive to usual doses of epinephrine or may develop a paradoxical response to epinephrine when it is used to treat anaphylactic reactions. Propranolol is contraindicated in patients with Raynaud's syndrome, bronchial asthma, sinus bradycardia and heart block greater than first degree, and overt and decompensated heart failure unless the failure is secondary to a tachyarrhythmia treatable with propranolol.

The drug is not indicated in the management of hypertensive emergencies. Although the manufacturers state that propranolol is contraindicated in patients with cardiogenic shock, results of some studies indicate that the drug may have a beneficial effect in patients with myocardial infarction with or without cardiogenic shock.

See Uses: Acute Myocardial Infarction. Because propranolol has produced a myasthenic condition characterized by ptosis, weakness of limbs, and double vision in 2 patients, the drug may be contraindicated in patients with myasthenia gravis. In addition, since propranolol appears to impair metabolism of thioridazine which may result in increased plasma concentrations of thioridazine that may be associated with prolongation of the QT interval, the manufacturer of thioridazine states that concomitant use of thioridazine and propranolol is contraindicated.

Although safety and efficacy of propranolol have not been as extensively or systematically studied in children as in adults, current information from the medical literature allows fair estimates, and specific dosing information has been reasonably studied. Cardiovascular diseases that are common to adults and children generally are as responsive to propranolol therapy in children as in adults, and adverse reactions also are similar.

One manufacturer states that the possibility that oral bioavailability of propranolol hydrochloride may be increased in children with Down's syndrome should be considered. Safety and efficacy of propranolol hydrochloride extended-release capsules, oral solution, and injection have not been established in children. Clinical studies of propranolol tablets, injections, and extended-release capsules did not include sufficient numbers of patients 65 years of age and older to determine whether geriatric patients respond differently than younger patients.

If propranolol is used in geriatric patients, dosage of the drug should be selected with caution, usually initiating therapy at the low end of the dosage range since decreased hepatic, renal, or cardiac function and concomitant disease or other drug therapy are more common in this age group than in younger patients.

Decreased propranolol clearance and a prolonged elimination half-life have been reported in geriatric patients receiving propranolol hydrochloride injection, and the manufacturers recommend that dosage reduction be considered in these patients. In long-term studies in animals, no evidence of propranolol-related tumorigenic effects was observed.

There are no adequate and well-controlled studies to date using propranolol in pregnant women. Safe use of propranolol during pregnancy has not been established. Low birthweight infants with respiratory distress and hypoglycemia have been born to women who received propranolol throughout pregnancy. Bradycardia, hypoglycemia, and respiratory depression also have been reported in neonates whose mothers received propranolol at parturition; adequate facilities for monitoring such infants at birth should be available.

The manufacturers state that the drug should be used during pregnancy only when the possible benefits outweigh the potential risks to the fetus. Reproduction studies in animals using propranolol have not revealed evidence of impaired fertility. Since propranolol is distributed into milk, the drug should be used with caution in nursing women. Because metabolism of propranolol is mediated by cytochrome P CYP isoenzymes 2D6, 1A2, and 2C19, drugs that induce or inhibit these isoenzymes may alter the metabolism of propranolol, which may result in clinically important drug interactions.

Inhibitors or substrates of the isoenzymes 2D6 e. Drugs that induce cytochrome P activity e. Phenothiazines and propranolol may have additive hypotensive activity, especially when phenothiazines are administered in large doses. Chlorpromazine has been shown to reduce the clearance of propranolol and increase plasma propranolol concentrations. Increased plasma concentrations of chlorpromazine also have been reported in patients receiving the drug concomitantly with propranolol.

Hypotension and cardiac arrest have occurred during concomitant therapy with propranolol and haloperidol. Because such increased concentrations of thioridazine may enhance thioridazine-induced prolongation of the QT c interval, and increase the risk of serious, potentially fatal cardiac arrhythmias e. Complete heart block has been reported in a patient receiving fluoxetine concomitantly with propranolol.

Decreased metabolism and increased plasma concentrations of diazepam and its metabolites have been reported in patients receiving the drug concomitantly with propranolol; propranolol does not appear to alter pharmacokinetics of other benzodiazepines e.

Diazepam does not alter pharmacokinetics of propranolol. The effects of propranolol also can be reversed by administration of dobutamine. In addition, propranolol may reduce sensitivity to dobutamine stress echocardiography in patients undergoing evaluation for myocardial ischemia. In patients receiving propranolol, epinephrine should be administered with caution since a decrease in pulse rate with first- and second-degree heart block may occur.

Antimuscarinic agents, such as atropine, may counteract the bradycardia caused by propranolol by reestablishing the balance between sympathetic and parasympathetic actions on the heart. Tricyclic antidepressants e. When propranolol and a catecholamine-depleting drug e. Excessive reduction of resting sympathetic nervous system activity, which may lead to hypotension, severe bradycardia, vertigo, syncope, or orthostatic hypotension, has been reported in patients receiving both drugs concurrently.

Concomitant use of reserpine and propranolol also may potentiate depression. Increased concentrations of zolmitriptan and rizatriptan have been reported in patients receiving concomitant propranolol therapy. When propranolol is administered with diuretics or other antihypertensive drugs, the hypotensive effect of propranolol may be increased.

This effect is usually used to therapeutic advantage, but careful adjustment of dosage is necessary when these drugs are used concomitantly. See Drug Interactions: Catecholamine-depleting Drugs. Increased bronchial hyperreactivity has been reported in patients receiving ACE inhibitors concomitantly with propranolol. When propranolol is administered with antiarrhythmic drugs such as lidocaine, phenytoin, procainamide, quinidine, or verapamil , cardiac effects may be additive or antagonistic and toxic effects may be additive.

Slowing or complete suppression of SA node activity with development of slow ventricular rates e. Severe bradycardia, asystole, heart failure, and cardiovascular collapse have been reported in patients receiving propranolol concomitantly with disopyramide or verapamil. In addition, bradycardia, hypotension, high-degree heart block, and heart failure have been reported in patients with cardiac disease receiving concomitant therapy with propranolol and diltiazem.

In patients currently receiving a cardiac glycoside, concomitant propranolol therapy may reduce the positive inotropic effect of the glycoside. Increased propafenone exposure has been reported in patients receiving the drug concomitantly with propranolol. Verapamil does not appear to affect pharmacokinetics of propranolol and propranolol does not affect pharmacokinetics of verapamil or norverapamil.

Increased propranolol concentrations have been reported in patients receiving concomitant therapy with nisoldipine or nicardipine with propranolol; increased concentrations of nifedipine may occur in patients receiving the drug concomitantly with propranolol. Reduced lidocaine metabolism and clearance resulting in lidocaine toxicity have been reported in patients receiving the drug concomitantly with propranolol.

Decreased propranolol plasma concentrations have been reported in patients receiving the drug concomitantly with cholestyramine or colestipol. Decreased plasma concentrations of lovastatin and pravastatin have been reported in patients receiving the drugs concomitantly with propranolol; however, the pharmacodynamics of the antilipemics were not altered. Increases in warfarin bioavailability and prothrombin time have been reported in patients receiving warfarin concomitantly with propranolol.

Prothrombin time should be monitored in patients receiving warfarin concomitantly with propranolol. High doses of propranolol may potentiate the effects of neuromuscular blocking agents such as tubocurarine chloride, possibly because of propranolol's interference with ionic permeability of the postjunctional membrane. Propranolol should be administered with caution to patients who are receiving neuromuscular blocking agents or who are recovering from their effects.

Signs of hypoglycemia e. One case of severe peripheral vasoconstriction with pain and cyanosis has been reported in a patient who received propranolol orally and high doses of ergotamine in a rectal suppository concurrently for the treatment of migraine; however, several patients have received these drugs concomitantly without adverse effects. Caution should be used during simultaneous administration of propranolol and high doses of ergot alkaloids because of the possibility of additive peripheral vasoconstriction.

Cimetidine can substantially reduce the clearance of propranolol apparently by inhibiting the hepatic metabolism of propranolol , which results in increased propranolol concentrations. Concomitant oral administration of an aluminum hydroxide antacid with propranolol may reduce the GI absorption of propranolol. In a study in healthy adults, oral administration of 30 mL of an aluminum hydroxide 1. Ventricular fibrillation has been reported in a patient with hypertrophic subaortic stenosis.

After sudden cessation of propranolol therapy in some patients treated for angina, increased frequency, duration, and severity of angina episodes have occurred, often within 24 hours. These episodes are unstable and are not relieved by nitroglycerin. Acute and sometimes fatal myocardial infarction and sudden death have also occurred after abrupt withdrawal of propranolol therapy in some patients treated for angina. In hypertensive patients, sudden cessation of propranolol has produced a syndrome similar to florid thyrotoxicosis, characterized by tenseness, anxiety, tachycardia, and excessive perspiration; these symptoms occurred within one week of cessation of the drug and were relieved by reinstituting propranolol therapy.

During surgery, some patients who have been receiving propranolol may experience severe, protracted hypotension and, occasionally, difficulty in restarting and maintaining heart beat. Severe hypertension has been reported in a few patients with schizophrenic disorder who received only propranolol orally in rapidly increasing doses; the hypertension responded to treatment with IV phentolamine followed by oral phenoxybenzamine.

Fluid retention, pulmonary edema, and peripheral arterial insufficiency, usually of the Raynaud's type, may occur in patients receiving propranolol. When the drug is used alone, dietary sodium restriction may be necessary. Intermittent claudication has occurred in patients with previously asymptomatic peripheral arterial disease who received propranolol, although one study which used the drug for the treatment of intermittent claudication did not note any deterioration of occlusive peripheral arterial disease.

A number of adverse CNS effects which are usually reversible after withdrawal of the drug have been reported. Adverse CNS effects usually occur after long-term treatment with high doses of propranolol and range from lightheadedness, giddiness, ataxia, dizziness, irritability, sleepiness, hearing loss, and visual disturbances to vivid dreams, hallucinations, and confusion.

Insomnia, lassitude, weakness, fatigue, and mental depression progressing to catatonia have been reported. Dosages exceeding mg daily, when administered in divided doses exceeding 80 mg each, may be associated with an increased incidence of fatigue, lethargy, and vivid dreams. Organic brain syndrome, characterized by disorientation to time and place, short-term memory loss, emotional lability, slightly clouded sensorium, and decreased performance on neuropsychometric tests, has been reported rarely.

Paresthesia of the hands, peripheral neuropathy, and precipitation of myotonia have been reported. Impotence has been reported rarely. Ptosis has been reported in 2 patients. Two patients receiving propranolol for hypertrophic obstructive cardiomyopathy developed migraine; in one patient this was associated with sensory disturbances and teichopsia. Adverse GI effects such as nausea, vomiting, diarrhea, epigastric distress, abdominal cramping, constipation, and flatulence may occur in patients receiving propranolol and occasionally necessitate reduction of dosage or withdrawal of the drug.

Mesenteric arterial thrombosis and ischemic colitis have also occurred. Rarely, rashes have been reported during propranolol usage. Rashes are most commonly erythematous maculopapular or acneiform , dry, scaly, pruritic, psoriasiform lesions which occur on the trunk, extremities, and scalp.

Hyperkeratosis of the scalp, palms, and soles of the feet have been reported during treatment with propranolol; nail changes such as thickening, pitting, and discoloration have occurred. At least one case of exfoliative dermatitis has been reported.

Dermatologic reactions disappear after the drug is withdrawn. Other allergic manifestations reported during propranolol therapy include fever accompanied by aching and sore throat, rhinitis, dry mouth, laryngospasm, respiratory distress, and pharyngitis. A lupus-like syndrome characterized by fever, pruritus, severe myalgia, and positive lupus erythematosus cell tests has been reported in at least one patient receiving propranolol.

Reversible alopecia, which recurred following readministration of the drug, has been reported. In this study, the number of new cases of diabetes per person-years was Acute increases in blood pressure have occurred after insulin-induced hypoglycemia in patients receiving propranolol.

Propranolol may cause elevated BUN in patients with severe heart disease, elevated serum creatinine, aminotransferase, alkaline phosphatase, or lactic dehydrogenase concentrations. In hypertensive patients, propranolol may cause small increases in serum potassium concentration. Peyronie's disease and dry eyes have been reported rarely.

Generalized hyperemia of the conjunctivae with decreased tear production and a prickling sensation of the eyes has been reported in a patient receiving the drug. Eye dryness and pain occurred in one patient receiving propranolol. Discoloration of the tongue and bad taste were reported in two patients receiving the drug. When propranolol is used as a fixed-combination preparation that includes hydrochlorothiazide, the cautions, precautions, and contraindications associated with thiazide diuretics must be considered in addition to those associated with propranolol.

Patients receiving propranolol therapy should be instructed to consult their physician at the first sign or symptom of impending cardiac failure and should be adequately treated e. Abrupt withdrawal of propranolol may exacerbate angina symptoms or precipitate myocardial infarction in patients with coronary artery disease. Abrupt withdrawal of the drug in patients treated for hypertension has also been associated with adverse effects.

See Cautions: Cardiovascular Effects. Therefore, patients receiving propranolol especially those with ischemic heart disease should be warned not to interrupt or discontinue therapy without consulting their clinician. When discontinuance of propranolol therapy is planned, particularly in patients with ischemic heart disease, dosage of the drug should be gradually reduced over a period of at least a few weeks about 2.

When propranolol therapy is discontinued, patients should be carefully monitored and their activity restricted. If exacerbation of angina occurs after propranolol therapy is interrupted, treatment with the drug should generally be reinstituted and appropriate measures taken for the management of unstable angina pectoris.

Because coronary artery disease is common and may be unrecognized, the manufacturers caution that it may be prudent not to discontinue propranolol therapy abruptly, even in patients receiving the drug for conditions other than angina. If propranolol therapy is discontinued prior to major surgery, oral therapy with the drug may be restarted as soon after surgery as possible; patients who are unable to take oral drugs after surgery may be treated with IV propranolol if necessary.

Caution should be used when administering propranolol to patients with sinus node dysfunction, since the drug can cause marked depression of SA node automaticity. Propranolol should be used with extreme caution for the management of arrhythmias occurring during anesthesia with myocardial depressant anesthetics e. Signs of hyperthyroidism may be masked by propranolol, and patients with thyrotoxicosis who receive the drug should be monitored closely.

In addition, the drug may alter thyroid function test results, increasing thyroxine T 4 and reverse triiodothyronine rT 3 and decreasing triiodothyronine T 3 determinations. It is recommended that propranolol be used with caution in patients with diabetes mellitus especially those with labile diabetes or those prone to hypoglycemia since the drug also may block the signs and symptoms of hypoglycemia e. In addition, the drug occasionally causes hypoglycemia, even in nondiabetic patients, presumably by interfering with catecholamine-induced glycogenolysis.

Propranolol may also inhibit the insulin-releasing mechanism of the pancreas and has been implicated in hyperglycemic reactions. Propranolol-induced alterations in glucose tolerance appear to occur only rarely. See Cautions: Endocrine Effects. Some sources state that hypertensive patients who are prone to hypoglycemia should not receive propranolol because the drug may cause a sharp rise in blood pressure.

Propranolol should be used with caution in patients with a history of nonallergic bronchospasm e. Bronchospasm may be treated with IV administration of aminophylline; isoproterenol may also be administered. IV administration of atropine has been suggested if the patient fails to respond to the above or if bradycardia is present.

Withdrawal of propranolol may lead to an increase in intraocular pressure. Propranolol should be used with caution in patients with renal or hepatic impairment. Laboratory parameters should be monitored in patients receiving prolonged therapy with the drug. These patients may be unresponsive to usual doses of epinephrine or may develop a paradoxical response to epinephrine when it is used to treat anaphylactic reactions.

Propranolol is contraindicated in patients with Raynaud's syndrome, bronchial asthma, sinus bradycardia and heart block greater than first degree, and overt and decompensated heart failure unless the failure is secondary to a tachyarrhythmia treatable with propranolol.

The drug is not indicated in the management of hypertensive emergencies. Although the manufacturers state that propranolol is contraindicated in patients with cardiogenic shock, results of some studies indicate that the drug may have a beneficial effect in patients with myocardial infarction with or without cardiogenic shock.

See Uses: Acute Myocardial Infarction. Because propranolol has produced a myasthenic condition characterized by ptosis, weakness of limbs, and double vision in 2 patients, the drug may be contraindicated in patients with myasthenia gravis. In addition, since propranolol appears to impair metabolism of thioridazine which may result in increased plasma concentrations of thioridazine that may be associated with prolongation of the QT interval, the manufacturer of thioridazine states that concomitant use of thioridazine and propranolol is contraindicated.

Although safety and efficacy of propranolol have not been as extensively or systematically studied in children as in adults, current information from the medical literature allows fair estimates, and specific dosing information has been reasonably studied. Cardiovascular diseases that are common to adults and children generally are as responsive to propranolol therapy in children as in adults, and adverse reactions also are similar.

One manufacturer states that the possibility that oral bioavailability of propranolol hydrochloride may be increased in children with Down's syndrome should be considered. Safety and efficacy of propranolol hydrochloride extended-release capsules, oral solution, and injection have not been established in children. Clinical studies of propranolol tablets, injections, and extended-release capsules did not include sufficient numbers of patients 65 years of age and older to determine whether geriatric patients respond differently than younger patients.

If propranolol is used in geriatric patients, dosage of the drug should be selected with caution, usually initiating therapy at the low end of the dosage range since decreased hepatic, renal, or cardiac function and concomitant disease or other drug therapy are more common in this age group than in younger patients. Decreased propranolol clearance and a prolonged elimination half-life have been reported in geriatric patients receiving propranolol hydrochloride injection, and the manufacturers recommend that dosage reduction be considered in these patients.

In long-term studies in animals, no evidence of propranolol-related tumorigenic effects was observed. There are no adequate and well-controlled studies to date using propranolol in pregnant women. Safe use of propranolol during pregnancy has not been established. Low birthweight infants with respiratory distress and hypoglycemia have been born to women who received propranolol throughout pregnancy. Bradycardia, hypoglycemia, and respiratory depression also have been reported in neonates whose mothers received propranolol at parturition; adequate facilities for monitoring such infants at birth should be available.

The manufacturers state that the drug should be used during pregnancy only when the possible benefits outweigh the potential risks to the fetus. Reproduction studies in animals using propranolol have not revealed evidence of impaired fertility. Since propranolol is distributed into milk, the drug should be used with caution in nursing women.

Because metabolism of propranolol is mediated by cytochrome P CYP isoenzymes 2D6, 1A2, and 2C19, drugs that induce or inhibit these isoenzymes may alter the metabolism of propranolol, which may result in clinically important drug interactions. Inhibitors or substrates of the isoenzymes 2D6 e. Drugs that induce cytochrome P activity e. Phenothiazines and propranolol may have additive hypotensive activity, especially when phenothiazines are administered in large doses.

Chlorpromazine has been shown to reduce the clearance of propranolol and increase plasma propranolol concentrations. Increased plasma concentrations of chlorpromazine also have been reported in patients receiving the drug concomitantly with propranolol. Hypotension and cardiac arrest have occurred during concomitant therapy with propranolol and haloperidol. Because such increased concentrations of thioridazine may enhance thioridazine-induced prolongation of the QT c interval, and increase the risk of serious, potentially fatal cardiac arrhythmias e.

Complete heart block has been reported in a patient receiving fluoxetine concomitantly with propranolol. Decreased metabolism and increased plasma concentrations of diazepam and its metabolites have been reported in patients receiving the drug concomitantly with propranolol; propranolol does not appear to alter pharmacokinetics of other benzodiazepines e.

Diazepam does not alter pharmacokinetics of propranolol. The effects of propranolol also can be reversed by administration of dobutamine. In addition, propranolol may reduce sensitivity to dobutamine stress echocardiography in patients undergoing evaluation for myocardial ischemia. In patients receiving propranolol, epinephrine should be administered with caution since a decrease in pulse rate with first- and second-degree heart block may occur.

Antimuscarinic agents, such as atropine, may counteract the bradycardia caused by propranolol by reestablishing the balance between sympathetic and parasympathetic actions on the heart. Tricyclic antidepressants e. When propranolol and a catecholamine-depleting drug e.

Excessive reduction of resting sympathetic nervous system activity, which may lead to hypotension, severe bradycardia, vertigo, syncope, or orthostatic hypotension, has been reported in patients receiving both drugs concurrently. Concomitant use of reserpine and propranolol also may potentiate depression. Increased concentrations of zolmitriptan and rizatriptan have been reported in patients receiving concomitant propranolol therapy.

When propranolol is administered with diuretics or other antihypertensive drugs, the hypotensive effect of propranolol may be increased. This effect is usually used to therapeutic advantage, but careful adjustment of dosage is necessary when these drugs are used concomitantly.

See Drug Interactions: Catecholamine-depleting Drugs. Increased bronchial hyperreactivity has been reported in patients receiving ACE inhibitors concomitantly with propranolol. When propranolol is administered with antiarrhythmic drugs such as lidocaine, phenytoin, procainamide, quinidine, or verapamil , cardiac effects may be additive or antagonistic and toxic effects may be additive.

Slowing or complete suppression of SA node activity with development of slow ventricular rates e. Severe bradycardia, asystole, heart failure, and cardiovascular collapse have been reported in patients receiving propranolol concomitantly with disopyramide or verapamil. In addition, bradycardia, hypotension, high-degree heart block, and heart failure have been reported in patients with cardiac disease receiving concomitant therapy with propranolol and diltiazem. In patients currently receiving a cardiac glycoside, concomitant propranolol therapy may reduce the positive inotropic effect of the glycoside.

Increased propafenone exposure has been reported in patients receiving the drug concomitantly with propranolol. Verapamil does not appear to affect pharmacokinetics of propranolol and propranolol does not affect pharmacokinetics of verapamil or norverapamil. Increased propranolol concentrations have been reported in patients receiving concomitant therapy with nisoldipine or nicardipine with propranolol; increased concentrations of nifedipine may occur in patients receiving the drug concomitantly with propranolol.

Reduced lidocaine metabolism and clearance resulting in lidocaine toxicity have been reported in patients receiving the drug concomitantly with propranolol. Decreased propranolol plasma concentrations have been reported in patients receiving the drug concomitantly with cholestyramine or colestipol. Decreased plasma concentrations of lovastatin and pravastatin have been reported in patients receiving the drugs concomitantly with propranolol; however, the pharmacodynamics of the antilipemics were not altered.

Increases in warfarin bioavailability and prothrombin time have been reported in patients receiving warfarin concomitantly with propranolol. Prothrombin time should be monitored in patients receiving warfarin concomitantly with propranolol. High doses of propranolol may potentiate the effects of neuromuscular blocking agents such as tubocurarine chloride, possibly because of propranolol's interference with ionic permeability of the postjunctional membrane.

Propranolol should be administered with caution to patients who are receiving neuromuscular blocking agents or who are recovering from their effects. Signs of hypoglycemia e. One case of severe peripheral vasoconstriction with pain and cyanosis has been reported in a patient who received propranolol orally and high doses of ergotamine in a rectal suppository concurrently for the treatment of migraine; however, several patients have received these drugs concomitantly without adverse effects.

Caution should be used during simultaneous administration of propranolol and high doses of ergot alkaloids because of the possibility of additive peripheral vasoconstriction. Cimetidine can substantially reduce the clearance of propranolol apparently by inhibiting the hepatic metabolism of propranolol , which results in increased propranolol concentrations. Concomitant oral administration of an aluminum hydroxide antacid with propranolol may reduce the GI absorption of propranolol.

In a study in healthy adults, oral administration of 30 mL of an aluminum hydroxide 1. The mechanism of this potential interaction has not been elucidated, but propranolol adsorption to or complexation with aluminum hydroxide does not appear to be involved.

In another study in healthy adults, however, concomitant oral administration of 30 mL of an aluminum hydroxide suspension with a single, mg dose of propranolol hydrochloride did not substantially affect bioavailability of propranolol.

The need to avoid concomitant use or stagger dosing of an aluminum hydroxide antacid and propranolol has not been fully elucidated, but increasing propranolol dosage may be considered if an interaction is suspected. Propranolol may antagonize the hypotensive and positive inotropic effects of levodopa.

This interaction is not well documented; however, the possibility of its occurrence should be kept in mind. Propranolol decreases the clearance of theophylline in a dose-dependent manner by inhibiting hepatic microsomal metabolism principally demethylation. In addition, propranolol can antagonize theophylline-induced bronchodilation. Propranolol is almost completely absorbed from the GI tract; however, plasma concentrations attained are quite variable among individuals.

There is no difference in the rate of absorption of the 2 isomers of propranolol. Propranolol appears in the plasma within 30 minutes, and peak plasma concentrations are reached about minutes after oral administration of the conventional tablets. The time when peak plasma concentrations are reached may be delayed, but concentrations are not necessarily lowered, when the drug is administered with food.

One manufacturer states that oral bioavailability of the drug may be increased in children with Down's syndrome; higher than expected plasma propranolol concentrations have been observed in such children. Bioavailability of a single mg oral dose of propranolol hydrochloride as a conventional tablet or oral solution reportedly is equivalent in adults.

Propranolol hydrochloride is slowly absorbed following administration of the drug as extended-release capsules, and peak blood concentrations are reached about 6 hours after administration. The lower AUC is probably caused by the slower rate of absorption of the drug from the extended-release capsules with resultant greater hepatic metabolism. After administration of a single dose of propranolol as the extended-release capsules, blood concentrations are fairly constant for about 12 hours and then decline exponentially during the following 12 hours.

Plasma propranolol concentrations attained after IV administration of the drug are relatively consistent among individuals. After administration of a 0. Following IV administration of propranolol, the onset of action is almost immediate. Animal studies indicate that propranolol is rapidly absorbed after IM administration. After absorption from the GI tract, propranolol is bound by the liver through nonspecific tissue binding.

There are large individual differences in hepatic extraction, probably because of differences in hepatic blood flow. Following oral administration, the drug does not reach the general circulation until hepatic binding sites are saturated. Once saturation occurs, hepatic binding no longer affects the passage of the drug into the blood. The amount of drug that reaches the circulation after oral administration also depends on the amount of drug metabolized on the first pass through the liver.

Propranolol decreases its own rate of metabolism by decreasing hepatic blood flow. Studies indicate that hepatic extraction and possibly metabolism of propranolol are reduced following oral administration of the drug in patients with chronic renal disease, resulting in higher peak plasma concentrations of the drug after the first dose than are attained in patients with normal renal function.

There are several possible metabolic explanations for the discrepancies between plasma concentrations and therapeutic effect. See Pharmacokinetics: Elimination. Individual differences in sympathetic tone may also contribute to interpatient differences in response. Propranolol is widely distributed into body tissues including lungs, liver, kidneys, and heart.

Propranolol readily crosses the blood-brain barrier and the placenta. The drug is distributed into milk. The apparent volume of distribution of propranolol at steady-state varies widely in proportion to the fraction of unbound drug in whole blood. Both free and protein-bound propranolol are metabolized. Increased plasma protein binding of the drug increases its metabolism and decreases its volume of distribution, resulting in a shorter terminal half-life.

The reported elimination half-life varies considerably among different studies. After IV administration of 10 mg of propranolol hydrochloride at a rate of 1. When usual therapeutic doses of propranolol are administered chronically, the half-life ranges from 3. Single-dose studies generally have shown a shorter half-life of hours. This difference in half-life between chronic and single-dose studies may be the result of initial removal of the drug into a large extravascular space especially hepatic binding sites and also a saturation of systemic clearance including drug metabolizing enzymes and excretion.

The half-life of propranolol may decrease with decreasing renal function; however, there is insufficient evidence to indicate that any alteration in maintenance dosage is necessary in patients with impaired renal function. During initial oral therapy but not during IV or chronic oral therapy , an active metabolite, 4-hydroxypropranolol, is formed.

This metabolite is eliminated more rapidly than propranolol and is virtually absent from the plasma 6 hours after oral administration of the drug. Individual variations in ability to hydroxylate propranolol to the active metabolite may also exist.

Propranolol is almost completely metabolized in the liver and at least 8 metabolites have been identified in urine. In patients with severely impaired renal function, a compensatory increase in fecal excretion of propranolol occurs. Reduced propranolol plasma clearance and increased peak plasma concentrations have been reported in patients with chronic renal failure compared with healthy individuals and patients receiving dialysis. Chronic renal failure may be associated with reduced drug metabolism secondary to downregulation of hepatic cytochrome P CYP enzyme system activity.

Propranolol is apparently not substantially removed by hemodialysis. Decreased propranolol clearance and prolonged elimination half-life have been reported in geriatric patients compared with younger patients. In addition, reduced clearance, increased volume of distribution, decreased protein binding, and considerable variation in elimination half-life of propranolol have been reported in patients with chronic liver disease compared with individuals with normal liver function.

Increased propranolol exposure and decreased clearance also have been reported in obese individuals compared with nonobese individuals. Order Your Prescriptions Place your order online or over the phone with a licensed pharmacy staff member.

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