The easiest way to lookup drug information, identify pills, check interactions and set up your own personal medication records. Available for Android and iOS devices. Subscribe to Drugs. This material is provided for educational purposes only and is not intended for medical advice, diagnosis or treatment. We comply with the HONcode standard for trustworthy health information - verify here. Skip to Content. Propranolol hydrochloride tablets are indicated for the prophylaxis of common migraine headache.
The efficacy of propranolol in the treatment of a migraine attack that has started has not been established, and propranolol is not indicated for such use.
DailyMed - PROPRANOLOL HYDROCHLORIDE tablet
Propranolol hydrochloride tablets are 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 hydrochloride tablets cause a reduction in the tremor amplitude, but not in the tremor frequency.
Propranolol hydrochloride tablets are not indicated for the treatment of tremor associated with Parkinsonism.
Propranolol hydrochloride tablets improve NYHA functional class in symptomatic patients with hypertrophic subaortic stenosis. Propranolol hydrochloride tablets are indicated as an adjunct to alpha-adrenergic blockade to control blood pressure and reduce symptoms of catecholamine-secreting tumors.
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Propranolol is contraindicated in 1 cardiogenic shock; 2 sinus bradycardia and greater than first degree block; 3 bronchial asthma; and 4 in patients with known hypersensitivity to propranolol hydrochloride. There have been reports of exacerbation of angina and, in some cases, myocardial infarction, following abrupt discontinuance of propranolol therapy.
If propranolol therapy is interrupted and exacerbation of angina occurs, it usually is advisable to reinstitute propranolol therapy and take other measures appropriate for the management of angina pectoris. Since coronary artery disease may be unrecognized, it may be prudent to follow the above advice in patients considered at risk of having occult atherosclerotic heart disease who are given propranolol for other indications.
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. 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.
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. 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. 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. 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. 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. Propranolol should be used with caution in patients with impaired hepatic or renal function. Propranolol hydrochloride tablets are not indicated for the treatment of hypertensive emergencies.
Beta-adrenergic receptor blockade can cause reduction of intraocular pressure.
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Patients should be told that propranolol hydrochloride tablets may interfere with the glaucoma screening test. Withdrawal may lead to a return of increased intraocular pressure. While taking beta blockers, patients with a history of severe anaphylactic reaction to a variety of allergens may be more reactive to repeated challenge, either accidental, diagnostic, or therapeutic. Such patients may be unresponsive to the usual doses of epinephrine used to treat allergic reaction. In patients with hypertension, use of propranolol has been associated with elevated levels of serum potassium, serum transaminases and alkaline phosphatase.
In severe heart failure, the use of propranolol has been associated with increases in Blood Urea Nitrogen.
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Caution should be exercised when propranolol hydrochloride tablets are administered with drugs that have an effect on CYP2D6, 1A2, or 2C19 metabolic pathways. Propafenone has negative inotropic and beta-blocking properties that can be additive to those of propranolol. Quinidine increases the concentration of propranolol and produces greater degrees of clinical beta-blockade and may cause postural hypotension. The clearance of lidocaine is reduced with administration of propranolol. Lidocaine toxicity has been reported following coadministration with propranolol.
Caution should be exercised when administering propranolol hydrochloride tablets with drugs that slow A-V nodal conduction, e. Both digitalis glycosides and beta-blockers slow atrioventricular conduction and decrease heart rate. Concomitant use can increase the risk of bradycardia. Both agents may depress myocardial contractility or atrioventricular conduction.
There have been reports of significant bradycardia, heart failure, and cardiovascular collapse with concurrent use of verapamil and beta-blockers. Co-administration of propranolol and diltiazem in patients with cardiac disease has been associated with bradycardia, hypotension, high-degree heart block, and heart failure.
When combined with beta-blockers, ACE inhibitors can cause hypotension, particularly in the setting of acute myocardial infarction. The antihypertensive effects of clonidine may be antagonized by beta-blockers. Propranolol hydrochloride tablets should be administered cautiously to patients withdrawing from clonidine. Prazosin has been associated with prolongation of first dose hypotension in the presence of beta-blockers. Postural hypotension has been reported in patients taking both beta-blockers and terazosin or doxazosin. Patients receiving catecholamine-depleting drugs, such as reserpine, should be closely observed for excessive reduction of resting sympathetic nervous activity, which may result in hypotension, marked bradycardia, vertigo, syncopal attacks, or orthostatic hypotension.
Patients on long-term therapy with propranolol may experience uncontrolled hypertension if administered epinephrine as a consequence of unopposed alpha-receptor stimulation.
Propranolol is a competitive inhibitor of beta-receptor agonists, and its effects can be reversed by administration of such agents, e. Also, propranolol may reduce sensitivity to dobutamine stress echocardiography in patients undergoing evaluation for myocardial ischemia. Nonsteroidal anti-inflammatory drugs NSAIDS have been reported to blunt the antihypertensive effect of beta-adrenoreceptor blocking agents.
Administration of indomethacin with propranolol may reduce the efficacy of propranolol in reducing blood pressure and heart rate. The hypotensive effects of MAO inhibitors or tricyclic antidepressants may be exacerbated when administered with beta-blockers by interfering with the beta blocking activity of propranolol.
Methoxyflurane and trichloroethylene may depress myocardial contractility when administered with propranolol. Propranolol when administered with warfarin increases the concentration of warfarin.
Prothrombin time, therefore, should be monitored. Hypotension and cardiac arrest have been reported with the concomitant use of propranolol and haloperidol. Thyroxine may result in a lower than expected T 3 concentration when used concomitantly with propranolol. Alcohol, when used concomitantly with propranolol, may increase plasma levels of propranolol. On a body surface area basis, this dose in the mouse and rat is, respectively, about equal to and about twice the maximum recommended human oral daily dose MRHD of mg propranolol hydrochloride.