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Propranolol

Generic name: propranolol systemic

Brand names: Inderal, Inderal LA, InnoPran XL, Hemangeol, Inderal XL

Boxed Warning

Cardiac ischemia after abrupt discontinuation (Inderal LA, Inderal XL, Innopran XL):

Following abrupt discontinuation of therapy with beta-blockers, exacerbations of angina pectoris and myocardial infarction (MI) have occurred.

When discontinuing long-term administration of propranolol, particularly in patients with ischemic heart disease, gradually reduce the dose over a period of 1 to 2 weeks and monitor the patient. If angina markedly worsens or acute coronary insufficiency develops, promptly resume therapy, at least temporarily, and take other measures appropriate for the management of unstable angina. Warn patients against interruption or discontinuation of therapy without health care provider's advice.

Because coronary artery disease is common and may be unrecognized, avoid abrupt discontinuation of propranolol therapy, even in patients treated only for hypertension.

Dosage Forms

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Capsule Extended Release 24 Hour, Oral, as hydrochloride:

Inderal LA: 60 mg, 80 mg, 120 mg, 160 mg [contains brilliant blue fcf (fd&c blue #1)]

Inderal XL: 80 mg, 120 mg

InnoPran XL: 80 mg, 120 mg

Generic: 60 mg, 80 mg, 120 mg, 160 mg

Solution, Intravenous, as hydrochloride:

Generic: 1 mg/mL (1 mL)

Solution, Oral, as hydrochloride:

Hemangeol: 4.28 mg/mL (120 mL) [alcohol free, paraben free, sugar free; contains saccharin sodium]

Generic: 20 mg/5 mL (500 mL); 40 mg/5 mL (500 mL)

Tablet, Oral, as hydrochloride:

Generic: 10 mg, 20 mg, 40 mg, 60 mg, 80 mg

Pharmacology

Mechanism of Action

Nonselective beta-adrenergic blocker (class II antiarrhythmic); competitively blocks response to beta1- and beta2-adrenergic stimulation which results in decreases in heart rate, myocardial contractility, blood pressure, and myocardial oxygen demand. Nonselective beta-adrenergic blockers (propranolol, nadolol) reduce portal pressure by producing splanchnic vasoconstriction (beta2 effect) thereby reducing portal blood flow.

Pharmacokinetics/Pharmacodynamics

Absorption

Oral: Rapid and complete

Distribution

Vd: 4 L/kg in adults; crosses the blood-brain barrier

Metabolism

Extensive first-pass effect, hepatically metabolized to active and inactive compounds; the 3 main metabolic pathways include: Aromatic hydroxylation (primarily 4-hydroxylation), N-dealkylation followed by further side-chain oxidation and direct glucuronidation; the 4 primary metabolites include: Propranolol glucuronide, naphthyloxylactic acid, and sulfate and glucuronic acid conjugates of 4-hydroxy propranolol; Note: Aromatic hydroxylation is catalyzed primarily by isoenzyme CYP2D6; side chain oxidation is mainly via CYP1A2, but also CYP2D6; 4-hydroxypropranolol possesses beta-adrenergic receptor blocking activity and is a weak inhibitor of CYP2D6.

Excretion

Metabolites are excreted primarily in urine (96% to 99%); <1% excreted in urine as unchanged drug

Onset of Action

Beta-blockade: Oral: 1 to 2 hours; IV: ≤5 minutes; Peak effect: Hypertension: A few days to several weeks.

Time to Peak

Immediate release: Adults: 1 to 4 hours; Infants: ≤2 hours (Hemangeol); Extended release capsule (Inderal XL, InnoPran XL): 12 to 14 hours; Long acting capsule (Inderal LA): 6 hours

Duration of Action

Immediate release: 6 to 12 hours; Extended-release formulations: ~24 to 27 hours

Half-Life Elimination

Neonates: Possible increased half-life; Infants (35 to 150 days of age): Median 3.5 hours; Children: 3.9 to 6.4 hours; Adults: Immediate release formulation: 3 to 6 hours; Extended-release formulations: 8 to 10 hours

Protein Binding

Newborns: 68%; Adults: ~90% (S-isomer primarily to alpha-1 acid glycoprotein; R-isomer primarily to albumin)

Use: Labeled Indications

Angina, chronic stable: To decrease angina frequency and increase exercise tolerance in patients with angina pectoris.

Cardiac arrhythmias: Control of supraventricular arrhythmias (eg, atrial fibrillation and flutter, atrioventricular nodal reentrant tachycardia) and ventricular tachycardias (eg, catecholamine-induced arrhythmias, digoxin toxicity).

Essential tremor: Management of familial or hereditary essential tremor.

Hypertension: Management of hypertension. Note: Beta-blockers are not recommended as first-line therapy (ACC/AHA [Whelton 2018]).

Migraine headache prophylaxis: Prophylaxis of common migraine headache.

Myocardial infarction, early treatment and secondary prevention: To reduce cardiovascular mortality in patients who have survived the acute phase of myocardial infarction and are clinically stable.

Obstructive hypertrophic cardiomyopathy: Symptomatic treatment of obstructive hypertrophic cardiomyopathy (formerly known as hypertrophic subaortic stenosis).

Pheochromocytoma: As an adjunct to alpha-adrenergic blockade to control blood pressure and reduce symptoms of catecholamine-secreting tumors.

Proliferating infantile hemangioma (Hemangeol): Treatment of proliferating infantile hemangioma requiring systemic therapy.

Use: Off Label

Akathisia, antipsychotic-inducedcyes

Data from a limited number of patients in 5 randomized, double-blind, controlled studies support the use of propranolol in antipsychotic-induced akathisia Adler 1986, Adler 1993, Kramer 1988, Kramer 1989, Poyurovsky 2006.

Based on the American Psychiatric Association and World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for the treatment of schizophrenia, propranolol is an effective and recommended agent in the management of antipsychotic-induced akathisia; however, the WFSBP notes that good evidence-based data to support this use are lacking.

Performance anxiety disorderc

Data from a limited number of patients studied in 2 double-blind trials suggest that propranolol may be beneficial for the treatment of performance anxiety Brantigan 1982, Hartley 1983.

Thyroid stormcyes

Clinical experience suggests the utility of IV propranolol in the management of thyroid storm Braverman 2013.

Based on the American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis, beta-blockers, including propranolol, as part of a multimodality approach, are effective and recommended for the treatment of thyroid storm.

Thyrotoxicosisyes

Based on the American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis, beta-blockers, including propranolol, are effective and recommended in the treatment of symptomatic thyrotoxicosis. Beta-blockers should also be considered in asymptomatic patients who are at increased risk of complications due to worsening hyperthyroidism.

Tremor, lithium-induced, moderate to severec

Data from a limited number of patients studied suggest that propranolol may be beneficial for the treatment of lithium-induced tremor Gelenberg 1995, Kirk 1973, Lapierre 1976.

Variceal hemorrhage prophylaxisayes

Data from meta-analyses of randomized controlled trials support the use of propranolol for prophylaxis of variceal hemorrhage, reducing risk of recurrent bleeding and mortality Cheng 2003, Poynard 1991.

Based on the

Contraindications

Hypersensitivity to propranolol, beta-blockers, or any component of the formulation; uncompensated heart failure (unless the failure is due to tachyarrhythmias being treated with propranolol); cardiogenic shock; severe sinus bradycardia; sick sinus syndrome; or heart block greater than first-degree (except in patients with a functioning artificial pacemaker); bronchial asthma

Hemangeol (additional contraindications): Premature infants with corrected age <5 weeks; infants weighing <2 kg; heart rate <80 bpm; blood pressure <50/30 mm Hg; pheochromocytoma; history of bronchospasm

Documentation of allergenic cross-reactivity for beta-blockers is limited. However, because of similarities in chemical structure and/or pharmacologic actions, the possibility of cross-sensitivity cannot be ruled out with certainty.

Canadian labeling: Additional contraindications (not in US labeling): Cor pulmonale; allergic rhinitis during pollen season; patients prone to hypoglycemia; hypotension (blood pressure parameters not specified in labeling); metabolic acidosis; vasospastic angina (also referred to as Prinzmetal angina or variant angina); severe peripheral arterial circulatory disturbance

Hemangiol (additional contraindications): Infants weighing <2.5 kg; breastfed infants if mother is treated with medicines contraindicated with propranolol; heart rate <100 bpm or blood pressure <65/45 mm Hg (<3 months of age), heart rate <90 bpm or blood pressure <70/50 mm Hg (3 to <6 months of age), heart rate <80 bpm or blood pressure <80/55 mm Hg (6 to 12 months of age)

Dosage and Administration

Dosing: Adult

Note: Dosing recommendations are expressed as the total daily dose unless stated otherwise. The total daily oral dose is given in 1 to 4 divided doses per day, depending on the type of preparation. Available preparations include: oral immediate release (usually dosed 2 to 4 times daily), extended release (usually dosed once daily), and IV injection. If tolerability is a concern, immediate release may be preferred initially; after establishing appropriate maintenance dose, may convert to once-daily extended release using same total daily dose.

Akathisia, antipsychotic-induced (off-label use):

Immediate release: Oral: Initial: 10 mg twice daily; if needed, adjust dose based on response and tolerability (eg, at intervals of ≥1 week) up to 120 mg/day (Adler 1986; Adler 1993; APA [Lehman 2004]; Kramer 1989; Marder 2019; WFSBP [Hasan 2013]).

Angina, chronic stable (alternative agent):

Note: For vasospastic angina, beta-blockers are not recommended; other agents (eg, calcium channel blockers, nitrates) are preferred. For nonvasospastic angina, guidelines recommend titrating dose to a resting heart rate of 55 to 60 beats per minute (ACCF/AHA [Fihn 2012]), while other experts recommend targeting 60 to 70 beats per minute (Kannam 2019). Some experts prefer a cardioselective beta-blocker (Kannam 2019).

Oral: Initial: 80 mg/day (may choose an IR or ER formulation); increase dose as tolerated to desired effect; usual dosage range: 80 to 320 mg/day.

Atrial fibrillation/flutter:

Acute ventricular rate control (alternative agent):

IV: 1 mg over 1 minute; repeat as needed every 2 minutes up to a maximum of 3 doses (AHA/ACC/HRS [January 2014]; Ganz 2019).

Maintenance of ventricular rate control:

Immediate release: Oral: Usual dosage range: 30 to 160 mg/day in 3 to 4 divided doses (AHA/ACC/HRS [January 2014]).

Essential tremor:

Note: May be used as monotherapy or in combination with primidone (AAN [Zesiewicz 2005]).

Oral: Initial: 60 to 80 mg/day (may choose an IR or ER formulation); increase dose as needed based on response and tolerability; usual dosage range: 60 to 320 mg/day (AAN [Zesiewicz 2005]; AAN [Zesiewicz 2011]; Deuschl 2011).

Hypertension (alternative agent):

Note: Not recommended in the absence of specific comorbidities (eg, ischemic heart disease, essential tremor, migraine) (ACC/AHA [Whelton 2018]).

Oral: Initial: 80 mg/day (may choose an IR or ER formulation); titrate at ≥1-week intervals as needed based on patient response; usual dosage range: 80 to 160 mg/day (ACC/AHA [Whelton 2018]). Some experts favor using an ER formulation unless there is concern for tolerability, in which case the IR formulation may be appropriate (Mann 2019).

Migraine headache, prophylaxis:

Oral: Initial: 40 to 80 mg/day (may choose an IR or ER formulation); increase dose gradually based on response and tolerability to usual effective dosage range of 40 to 160 mg/day (Linde 2004; Pringsheim 2010; Smith 2019). Some patients may benefit from titration to a maximum of 240 mg/day (manufacturer's labeling). The maximum tolerated dose should be maintained for ≥3 months before deeming treatment failure. Some experts recommend beginning the IR formulation at 20 mg twice daily with up-titration as needed (Smith 2019).

Myocardial infarction, early treatment and secondary prevention (alternative agent):

Note: An oral beta-blocker is recommended within the first 24 hours for most patients (ACCF/AHA [O'Gara 2013]). Some experts prefer a cardioselective beta-blocker. Patients who did not receive a beta-blocker within 24 hours of myocardial infarction should be reevaluated for secondary prevention at a later date. The optimal duration of therapy is unknown; some experts treat for a minimum of 3 years and continue longer for patients with high-risk features at initial presentation (Rosenson 2019).

Immediate release: Oral: Initial: 60 to 120 mg/day in 2 to 3 divided doses; titrate dose based on heart rate and blood pressure as tolerated up to 240 mg/day (BHAT 1982; Hansteen 1982).

Performance anxiety disorder (off-label use):

Immediate release: Oral: 10 or 20 mg administered 30 to 60 minutes prior to anxiety-provoking situation; if initial dose is not sufficiently effective, may increase by 10 to 20 mg prior to next anxiety-provoking situation up to a maximum of 60 mg (Hartley 1983; Stein 2019).

Pheochromocytoma (adjunctive agent):

Note: An alpha-1 blocker must be started several days before propranolol (ES [Lenders 2014]).

Immediate release: Oral: Initial: 10 mg every 6 hours (Young 2019) or 20 mg 3 times daily (ES [Lenders 2014]); begin 3 to 4 days after initiation of an alpha-1 blocker and adjust to goal heart rate up to 120 mg/day in divided doses (ES [Lenders 2014]).

Supraventricular tachycardia (eg, atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, focal atrial tachycardia):

Acute treatment (alternative agent) (off-label dose):

IV: Initial: 1 mg over 1 minute; repeat as needed every 2 minutes up to 3 doses.

Note: Initiate cautiously in patients with heart failure. Avoid in patients with decompensated heart failure; electrical cardioversion preferred (ACC/AHA/HRS [Page 2016]).

Maintenance therapy (off-label use):

Immediate release: Oral: Initial: 30 to 60 mg/day in 2 or 3 divided doses titrated to effect; maximum recommended dose: 160 mg/day (ACC/AHA/HRS [Page 2016]).

Thyroid storm (off-label use):

Immediate release: Oral: Initial: 60 to 80 mg every 4 to 6 hours adjusted for heart rate and blood pressure (ATA [Ross 2016]; Ross 2019).

IV: 0.5 to 1 mg administered over 10 minutes while under continuous cardiac monitoring; a repeat dose of 1 to 3 mg over 10 to 15 minutes may be given every few hours as needed until oral therapy can be initiated and takes effect (Braverman 2013; Ross 2019).

Thyrotoxicosis (alternative agent) (off-label use):

Note: For control of cardiovascular effects until euthyroidism established.

Oral: Initial: 30 to 160 mg/day (may choose an IR or ER formulation) adjusted for heart rate and blood pressure (ATA [Ross 2016]).

Tremor, lithium-induced, moderate to severe (off-label use):

Immediate release: Oral: Initial: 10 mg 3 to 4 times daily; if needed, titrate dose based on response and tolerability up to 80 mg/day (Gelenberg 1995; Kirk 1973; Lapierre 1976).

Variceal hemorrhage prophylaxis (off-label use):

Immediate release: Oral: Initial: 10 to 20 mg twice daily; titrate according to resting heart rate (target 55 to 60 beats per minute), while maintaining blood pressure (eg, systolic blood pressure ≥90 mm Hg) (AASLD [Garcia-Tsao 2017]; Bañares 2002; Sanyal 2019a; Sanyal 2019b).

Maximal daily dose:

No ascites: 320 mg/day (AASLD [Garcia-Tsao 2017]).

Ascites: 160 mg/day (AASLD [Garcia-Tsao 2017]).

Ventricular arrhythmias:

Ventricular tachycardia, hemodynamically stable:

Acute ventricular tachycardia (incessant ventricular tachycardia or electrical storm) (adjunctive agent):

Note: Beta-blockers are generally administered in addition to an IV antiarrhythmic drug (eg, amiodarone), and some experts prefer propranolol over other beta-blockers in this setting (Chatzidou 2018; Passman 2019). A beta-blocker may also be used to reduce shocks in patients with an implantable cardioverter defibrillator (AHA/ACC/HRS [Al-Khatib 2018]).

IV: 1 to 3 mg every 5 minutes up to a total of 5 mg in combination with an IV antiarrhythmic (AHA/ACC/HRS [Al-Khatib 2018]).

Immediate release: Oral: 40 mg every 6 hours in combination with an IV antiarrhythmic (Chatzidou 2018); additional IV doses may be given for breakthrough ventricular arrhythmias (Passman 2019).

Prevention of ventricular tachycardia:

Immediate release: Oral: Initial: 10 to 40 mg every 6 hours; adjust dose as needed based on response and tolerability (AHA/ACC/HRS [Al-Khatib 2018]; Chatzidou 2018; Nademanee 2000).

Nonsustained ventricular tachycardia or ventricular premature beats, symptomatic:

Immediate release: Oral: Initial: 10 to 40 mg every 6 hours; adjust dose as needed based on patient response and tolerability (AHA/ACC/HRS [Al-Khatib 2018]).

Dosing: Geriatric

IV: Use caution; initiate at lower end of the dosing range.

Oral:

Hypertension: Consider lower initial doses and titrate to response (Aronow 2011).

Cardiac arrhythmias, maintenance or prevention: Immediate release: Oral: Initial: 10 mg twice daily; increase dosage every 3 to 7 days; usual dose range: 10 to 320 mg/day given in divided doses.

Refer to adult dosing for additional uses.

Dosing: Pediatric

Note: Dosage should be individualized based on patient response.

Essential tremor: Limited data available: Children and Adolescents: Oral: Immediate release formulations: Initial: 0.5 to 1 mg/kg/day in 3 divided doses; maximum daily dose: 4 mg/kg/day (Ferrara 2009)

Hemangioma, infantile; proliferating:

Manufacturer's labeling (Hemangeol): Infants ≥5 weeks weighing at least 2 kg: Note: Therapy should be initiated at age 5 weeks to 5 months: Oral: Initial dose: 0.6 mg/kg/dose twice daily for 1 week then beginning with week 2, increase dose to 1.1 mg/kg/dose twice daily and then for week 3 begin maintenance dose of 1.7 mg/kg/dose twice daily; doses should be separated by at least 9 hours; continue maintenance dose for 6 months; readjust dose for patient growth. May repeat course if hemangiomas recur.

Alternate dosing: Infants and Children <5 years: Oral: Immediate release formulations: Initial: 1 mg/kg/day in 2 or 3 divided doses, titrate by 1 mg/kg/day at weekly intervals to maintenance dose; usual daily maintenance dose: 2 to 3 mg/kg/day (Hogeling 2011; Léauté-Labrèze 2015). Optimal duration not defined; duration ranged from 3 to 12 months; discontinuation of therapy may be gradually tapered over 1 to 3 weeks to prevent rebound sinus tachycardia (Darrow 2015).

Hypertension: Note: Beta-blockers are not recommended as initial antihypertensive agents in children (AAP [Flynn 2017). Children and Adolescents ≤17 years: Immediate release formulations: Oral: Initial: 1 to 2 mg/kg/day divided in 2 to 3 doses/day; titrate dose to effect; maximum dose: 4 mg/kg/day up to 640 mg/day; sustained release formulation may be dosed once daily (NHBPEP 2004; NHLBI 2012). Others have suggested a higher maximum daily dose of 16 mg/kg/day up to 640 mg/day (Flynn 2006; Kavay 2010).

Migraine headache; prophylaxis: Limited data available; efficacy results variable; optimal dose not established: Oral: Immediate release formulations:

Weight-directed dosing: Children ≥3 years and Adolescents: Reported range: 0.5 to 3 mg/kg/day in 2 to 3 divided doses; some trials initiated therapy at the low end of the range and titrated upward to response; doses as low as 0.5 to 1 mg/kg/day may be effective; doses up to 4 mg/kg/day have been used; maximum daily dose: 120 mg/day (AAN [Lewis 2004]; Ashrafi 2005; Bonfert 2013; Eidlitz-Markus 2012; El-Chammas 2013; Lanteri-Minet 2014)

Fixed dose: Children ≥7 years and Adolescents: Initial: 10 mg daily; increase at weekly intervals in 10 mg increments; usual dose range: 10 to 20 mg 3 times daily (Kliegman 2016); doses as high as 120 mg daily have been used (AAN [Lewis 2004])

Tachyarrhythmias: Limited data available: Infants, Children, and Adolescents:

Oral: Immediate release formulations: Initial: 0.5 to 1 mg/kg/day in divided doses every 6 to 8 hours; titrate dosage upward every 3 to 5 days; usual daily dose: 2 to 4 mg/kg/day; higher doses may be needed; maximum daily dose: 16 mg/kg/day or 60 mg/day (Kliegman 2016; Park 2014)

IV: 0.01 to 0.15 mg/kg/dose slow IV over 10 minutes; may repeat every 6 to 8 hours as needed; maximum dose is age-dependent: Infants: 1 mg/dose; children and adolescents: 3 mg/dose (Kliegman 2016; Park 2014)

Tetralogy spells:

Oral: Palliative therapy: Infants and Children: 0.5 to 1 mg/kg/dose every 6 hours (Kliegman 2016). Others have used the following: Initial: 0.25 mg/kg/dose every 6 hours (1 mg/kg/day); if ineffective within first week of therapy, may increase by 1 mg/kg/day every 24 hours to maximum of 5 mg/kg/day; if patient becomes refractory may increase slowly to a maximum of 10 to 15 mg/kg/day but must carefully monitor heart rate, heart size, and cardiac contractility; average dose: 2.3 mg/kg/day; range: 0.8 to 5 mg/kg/day (Garson 1981).

IV: Infants and Children: 0.15 to 0.25 mg/kg/dose infused over 10 minutes; maximum initial dose: 1 mg; may repeat dose once (AAP [Hegenbarth 2008]); alternatively, initiate lower doses of 0.015 to 0.02 mg/kg/dose and titrate to effect, up to 0.1 to 0.2 mg/kg/dose (Anderson 2009)

Thyrotoxicosis: Limited data available:

Infants and Children: Oral: Immediate release formulations: 0.5 to 2 mg/kg/day divided every 8 hours; maximum dose: 40 mg/dose (Kliegman 2016)

Adolescents: Oral: Immediate release formulations: 10 to 40 mg every 6 to 8 hours (ATA [Ross 2016])

Thyroid Storm: Limited data available:

Infants and Children: Oral: Immediate release formulations: 1 to 4 mg/kg/day in divided doses, titrate based on blood pressure and heart rate (Cameron 2012; Fuhrman 2011); usual frequency in adolescents and adults is every 4 to 6 hours (ATA [Ross 2016]; Kleigman 2016)

Adolescents:

Oral: Immediate release formulations: 20 to 40 mg every 4 to 6 hours (Kliegman 2016); titrate based on blood pressure and heart rate; doses as high as 60 to 80 mg every 4 hours have been recommended (ATA [Ross 2016])

IV: 0.5 to 1 mg slow IV push over 10 minutes (Braverman 2013; Kliegman 2016). Dosing interval in adolescents is not defined; in adults, doses may be repeated every several hours with continuous cardiac monitoring; when transitioning to oral therapy, IV therapy may need to be continued until the effects of oral therapy are achieved (Braverman 2013)

Administration

IV: IV dose is much smaller than oral dose. When administered acutely for cardiac treatment, monitor ECG and blood pressure. May administer by rapid infusion (IV push) at a rate of 1 mg/minute or by slow infusion over ~30 minutes. Necessary monitoring for surgical patients who are unable to take oral beta-blockers (prolonged ileus) has not been defined. Some institutions require monitoring of baseline and postinfusion heart rate and blood pressure when a patient's response to beta-blockade has not been characterized (ie, the patient's initial dose or following a change in dose). Consult individual institutional policies and procedures.

Oral: Tablets (immediate release) should be taken on an empty stomach; capsules (extended release) may be taken with or without food, but should always be taken consistently (with food or on an empty stomach). Do not crush long-acting oral forms.

Dietary Considerations

Tablets (immediate release) should be taken on an empty stomach; capsules (extended release) may be taken with or without food, but should always be taken consistently (with food or on an empty stomach). Hemangeol should be administered during or right after a feeding to reduce the risk of hypoglycemia; skip dose if child is not eating or is vomiting.

Storage

Injection: Store at 20°C to 25°C (68°F to 77°F); protect from freezing or excessive heat. Once diluted, propranolol is stable for 24 hours at room temperature in D5W or NS. Protect from light. Solution has a maximum stability at pH of 3 and decomposes rapidly in alkaline pH.

Capsule, tablet, oral solution: Store at controlled room temperature; protect from freezing or excessive heat. Protect from light and moisture. Dispense Hemangeol in original container; discard 2 months after first opening.

Propranolol Images

Drug Interactions

Abiraterone Acetate: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Management: Avoid concurrent use of abiraterone with CYP2D6 substrates that have a narrow therapeutic index whenever possible. When concurrent use is not avoidable, monitor patients closely for signs/symptoms of toxicity. Consider therapy modification

Acetylcholinesterase Inhibitors: May enhance the bradycardic effect of Beta-Blockers. Monitor therapy

Ajmaline: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Alcohol (Ethyl): May decrease the serum concentration of Propranolol. Alcohol (Ethyl) may increase the serum concentration of Propranolol. Monitor therapy

Alfuzosin: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Alpha1-Blockers: Beta-Blockers may enhance the orthostatic hypotensive effect of Alpha1-Blockers. The risk associated with ophthalmic products is probably less than systemic products. Monitor therapy

Alpha2-Agonists: May enhance the AV-blocking effect of Beta-Blockers. Sinus node dysfunction may also be enhanced. Beta-Blockers may enhance the rebound hypertensive effect of Alpha2-Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. Management: Closely monitor heart rate during treatment with a beta blocker and clonidine. Withdraw beta blockers several days before clonidine withdrawal when possible, and monitor blood pressure closely. Recommendations for other alpha2-agonists are unavailable. Exceptions: Apraclonidine. Consider therapy modification

Amifostine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Amifostine. Management: When amifostine is used at chemotherapy doses, blood pressure lowering medications should be withheld for 24 hours prior to amifostine administration. If blood pressure lowering therapy cannot be withheld, amifostine should not be administered. Consider therapy modification

Aminoquinolines (Antimalarial): May decrease the metabolism of Beta-Blockers. Monitor therapy

Amiodarone: May enhance the bradycardic effect of Beta-Blockers. Possibly to the point of cardiac arrest. Amiodarone may increase the serum concentration of Beta-Blockers. Monitor therapy

Amphetamines: May diminish the antihypertensive effect of Antihypertensive Agents. Monitor therapy

Antipsychotic Agents (Phenothiazines): May enhance the hypotensive effect of Beta-Blockers. Beta-Blockers may decrease the metabolism of Antipsychotic Agents (Phenothiazines). Antipsychotic Agents (Phenothiazines) may decrease the metabolism of Beta-Blockers. Monitor therapy

Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may enhance the hypotensive effect of Antipsychotic Agents (Second Generation [Atypical]). Monitor therapy

Asunaprevir: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Consider therapy modification

Barbiturates: May decrease the serum concentration of Beta-Blockers. Monitor therapy

Barbiturates: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Benperidol: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Beta2-Agonists: Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Beta2-Agonists. Avoid combination

Bile Acid Sequestrants: May decrease the serum concentration of Propranolol. Monitor therapy

Bradycardia-Causing Agents: May enhance the bradycardic effect of other Bradycardia-Causing Agents. Monitor therapy

Brigatinib: May diminish the antihypertensive effect of Antihypertensive Agents. Brigatinib may enhance the bradycardic effect of Antihypertensive Agents. Monitor therapy

Brimonidine (Topical): May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Broccoli: May decrease the serum concentration of CYP1A2 Substrates (High risk with Inducers). Monitor therapy

Bromperidol: Blood Pressure Lowering Agents may enhance the hypotensive effect of Bromperidol. Bromperidol may diminish the hypotensive effect of Blood Pressure Lowering Agents. Avoid combination

Bupivacaine: Beta-Blockers may increase the serum concentration of Bupivacaine. Monitor therapy

Calcium Channel Blockers (Nondihydropyridine): May enhance the hypotensive effect of Beta-Blockers. Bradycardia and signs of heart failure have also been reported. Calcium Channel Blockers (Nondihydropyridine) may increase the serum concentration of Beta-Blockers. Exceptions: Bepridil. Monitor therapy

Cannabis: May decrease the serum concentration of CYP1A2 Substrates (High risk with Inducers). Monitor therapy

Cardiac Glycosides: Beta-Blockers may enhance the bradycardic effect of Cardiac Glycosides. Monitor therapy

Ceritinib: Bradycardia-Causing Agents may enhance the bradycardic effect of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Exceptions are discussed in separate monographs. Consider therapy modification

Cholinergic Agonists: Beta-Blockers may enhance the adverse/toxic effect of Cholinergic Agonists. Of particular concern are the potential for cardiac conduction abnormalities and bronchoconstriction. Monitor therapy

CloBAZam: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

CloZAPine: CYP1A2 Inhibitors (Weak) may increase the serum concentration of CloZAPine. Management: Drugs listed as exceptions to this monograph are discussed in further detail in separate drug interaction monographs. Monitor therapy

Cobicistat: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

CYP1A2 Inducers (Moderate): May decrease the serum concentration of Propranolol. Monitor therapy

CYP1A2 Inhibitors (Moderate): May increase the serum concentration of Propranolol. Monitor therapy

CYP1A2 Inhibitors (Strong): May increase the serum concentration of Propranolol. Management: Use a lower initial propranolol dose and be more cautious during propranolol dose titration when combined with strong CYP1A2 inhibitors. Consider therapy modification

CYP2D6 Inhibitors (Moderate): May decrease the metabolism of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

CYP2D6 Inhibitors (Strong): May decrease the metabolism of CYP2D6 Substrates (High risk with Inhibitors). Consider therapy modification

Dacomitinib: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Management: Avoid concurrent use of dacomitinib with CYP2D6 subtrates that have a narrow therapeutic index. Consider therapy modification

Darunavir: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Dexmethylphenidate: May diminish the therapeutic effect of Antihypertensive Agents. Monitor therapy

Diazoxide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Dipyridamole: May enhance the bradycardic effect of Beta-Blockers. Monitor therapy

Disopyramide: May enhance the bradycardic effect of Beta-Blockers. Beta-Blockers may enhance the negative inotropic effect of Disopyramide. Monitor therapy

Doxofylline: Propranolol may increase the serum concentration of Doxofylline. Monitor therapy

Dronedarone: May enhance the bradycardic effect of Beta-Blockers. Dronedarone may increase the serum concentration of Beta-Blockers. This likely applies only to those agents that are metabolized by CYP2D6. Management: Use lower initial beta-blocker doses; adequate tolerance of the combination, based on ECG findings, should be confirmed prior to any increase in beta-blocker dose. Consider therapy modification

DULoxetine: Blood Pressure Lowering Agents may enhance the hypotensive effect of DULoxetine. Monitor therapy

EPINEPHrine (Nasal): Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Nasal). Monitor therapy

EPINEPHrine (Oral Inhalation): Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Oral Inhalation). Monitor therapy

Epinephrine (Racemic): Beta-Blockers (Nonselective) may enhance the hypertensive effect of Epinephrine (Racemic). Monitor therapy

EPINEPHrine (Systemic): Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Systemic). Monitor therapy

Ergot Derivatives: Beta-Blockers may enhance the vasoconstricting effect of Ergot Derivatives. Exceptions: Nicergoline. Consider therapy modification

Fexinidazole [INT]: Bradycardia-Causing Agents may enhance the arrhythmogenic effect of Fexinidazole [INT]. Avoid combination

Fingolimod: Beta-Blockers may enhance the bradycardic effect of Fingolimod. Management: Avoid the concomitant use of fingolimod and beta-blockers if possible. If coadministration is necessary, patients should have overnight continuous ECG monitoring conducted after the first dose of fingolimod. Monitor patients for bradycardia. Consider therapy modification

Floctafenine: May enhance the adverse/toxic effect of Beta-Blockers. Avoid combination

Grass Pollen Allergen Extract (5 Grass Extract): Beta-Blockers may enhance the adverse/toxic effect of Grass Pollen Allergen Extract (5 Grass Extract). More specifically, Beta-Blockers may inhibit the ability to effectively treat severe allergic reactions to Grass Pollen Allergen Extract (5 Grass Extract) with epinephrine. Some other effects of epinephrine may be unaffected or even enhanced (e.g., vasoconstriction) during treatment with Beta-Blockers. Consider therapy modification

Herbs (Hypertensive Properties): May diminish the antihypertensive effect of Antihypertensive Agents. Monitor therapy

Herbs (Hypotensive Properties): May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Hypotension-Associated Agents: Blood Pressure Lowering Agents may enhance the hypotensive effect of Hypotension-Associated Agents. Monitor therapy

Imatinib: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Insulins: Beta-Blockers may enhance the hypoglycemic effect of Insulins. Monitor therapy

Ivabradine: Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. Monitor therapy

Lacidipine: May enhance the hypotensive effect of Propranolol. Lacidipine may increase the serum concentration of Propranolol. Propranolol may decrease the serum concentration of Lacidipine. Monitor therapy

Lacosamide: Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. Monitor therapy

Levodopa-Containing Products: Blood Pressure Lowering Agents may enhance the hypotensive effect of Levodopa-Containing Products. Monitor therapy

Lidocaine (Systemic): Beta-Blockers may increase the serum concentration of Lidocaine (Systemic). Monitor therapy

Lidocaine (Topical): Beta-Blockers may increase the serum concentration of Lidocaine (Topical). Monitor therapy

Lormetazepam: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Lumefantrine: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Mepivacaine: Beta-Blockers may increase the serum concentration of Mepivacaine. Monitor therapy

Methacholine: Beta-Blockers may enhance the adverse/toxic effect of Methacholine. Monitor therapy

Methoxyflurane: May enhance the hypotensive effect of Beta-Blockers. Monitor therapy

Methylphenidate: May diminish the antihypertensive effect of Antihypertensive Agents. Monitor therapy

Midodrine: May enhance the bradycardic effect of Bradycardia-Causing Agents. Monitor therapy

Molsidomine: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Naftopidil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Nicergoline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Nicorandil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

NIFEdipine: May enhance the hypotensive effect of Beta-Blockers. NIFEdipine may enhance the negative inotropic effect of Beta-Blockers. Monitor therapy

Nitroprusside: Blood Pressure Lowering Agents may enhance the hypotensive effect of Nitroprusside. Monitor therapy

Nonsteroidal Anti-Inflammatory Agents: May diminish the antihypertensive effect of Beta-Blockers. Monitor therapy

Obinutuzumab: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Management: Consider temporarily withholding blood pressure lowering medications beginning 12 hours prior to obinutuzumab infusion and continuing until 1 hour after the end of the infusion. Consider therapy modification

Opioids (Anilidopiperidine): May enhance the bradycardic effect of Beta-Blockers. Opioids (Anilidopiperidine) may enhance the hypotensive effect of Beta-Blockers. Monitor therapy

Panobinostat: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Peginterferon Alfa-2b: May decrease the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Peginterferon Alfa-2b may increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Pentoxifylline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Perhexiline: CYP2D6 Substrates (High risk with Inhibitors) may increase the serum concentration of Perhexiline. Perhexiline may increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Pholcodine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Pholcodine. Monitor therapy

Phosphodiesterase 5 Inhibitors: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Propafenone: May increase the serum concentration of Propranolol. Monitor therapy

Prostacyclin Analogues: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Quinagolide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

QuiNIDine: May increase the serum concentration of Propranolol. Monitor therapy

QuiNINE: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Regorafenib: May enhance the bradycardic effect of Beta-Blockers. Monitor therapy

Reserpine: May enhance the hypotensive effect of Beta-Blockers. Monitor therapy

Rifamycin Derivatives: May decrease the serum concentration of Beta-Blockers. Exceptions: Rifabutin. Monitor therapy

Rivastigmine: May enhance the bradycardic effect of Beta-Blockers. Avoid combination

Rizatriptan: Propranolol may increase the serum concentration of Rizatriptan. Management: Rizatriptan adult dose should be reduced to 5 mg in patients who are also being treated with propranolol. Consider therapy modification

Ruxolitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Management: Ruxolitinib Canadian product labeling recommends avoiding use with bradycardia-causing agents to the extent possible. Monitor therapy

Selective Serotonin Reuptake Inhibitors: May increase the serum concentration of Beta-Blockers. Exceptions: Citalopram; Escitalopram; FluvoxaMINE. Monitor therapy

Siponimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. Consider therapy modification

Sulfonylureas: Beta-Blockers may enhance the hypoglycemic effect of Sulfonylureas. Cardioselective beta-blockers (eg, acebutolol, atenolol, metoprolol, and penbutolol) may be safer than nonselective beta-blockers. All beta-blockers appear to mask tachycardia as an initial symptom of hypoglycemia. Ophthalmic beta-blockers are probably associated with lower risk than systemic agents. Monitor therapy

Terlipressin: May enhance the bradycardic effect of Bradycardia-Causing Agents. Monitor therapy

Theophylline Derivatives: Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Theophylline Derivatives. Monitor therapy

Theophylline Derivatives: CYP1A2 Inhibitors (Weak) may increase the serum concentration of Theophylline Derivatives. Exceptions: Dyphylline. Monitor therapy

TiZANidine: CYP1A2 Inhibitors (Weak) may increase the serum concentration of TiZANidine. Management: Avoid these combinations when possible. If combined use is necessary, initiate tizanidine at an adult dose of 2 mg and increase in 2 to 4 mg increments based on patient response. Monitor for increased effects of tizanidine, including adverse reactions. Consider therapy modification

Tobacco (Smoked): May decrease the serum concentration of Propranolol. Monitor therapy

Tofacitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Monitor therapy

Yohimbine: May diminish the antihypertensive effect of Antihypertensive Agents. Monitor therapy

Zileuton: May increase the serum concentration of Propranolol. Monitor therapy

ZOLMitriptan: Propranolol may increase the serum concentration of ZOLMitriptan. Monitor therapy

Test Interactions

May lead to false-positive aldosterone/renin ratio (ARR) (Funder 2016)

Adverse Reactions

Frequency not always defined.

Cardiovascular: Cold extremities (infants: 7% to 8%), angina pectoris, atrioventricular conduction disturbance, bradycardia, cardiac failure, cardiogenic shock, hypotension, ineffective myocardial contractions, syncope

Central nervous system: Sleep disorder (infants: 16% to 18%), agitation (infants: 5% to 9%), fatigue (5% to 7%), dizziness (4% to 7%), nightmares (infants: 2% to 6%), irritability (infants: 1% to 6%), drowsiness (infants: 1% to 5%), amnesia, carpal tunnel syndrome (rare), catatonia, cognitive dysfunction, confusion, hypersomnia, lethargy, paresthesia, psychosis, vertigo

Dermatologic: Changes in nails, contact dermatitis, dermal ulcer, eczematous rash, erosive lichen planus, hyperkeratosis, pruritus, skin rash

Endocrine & metabolic: Hyperglycemia, hyperkalemia, hyperlipidemia, hypoglycemia

Gastrointestinal: Diarrhea (infants: 5% to 6%), abdominal pain (infants: ≤4%), decreased appetite (infants: 3% to 4%), constipation (1% to 3%), anorexia, stomach discomfort

Genitourinary: Oliguria (rare), proteinuria (rare)

Hematologic & oncologic: Immune thrombocytopenia, thrombocytopenia

Hepatic: Increased serum alkaline phosphatase, increased serum transaminases

Neuromuscular & skeletal: Arthropathy, oculomucocutaneous syndrome, polyarthritis

Ophthalmic: Conjunctival hyperemia, decreased visual acuity, mydriasis

Renal: Increased blood urea nitrogen, interstitial nephritis (rare)

Respiratory: Bronchitis (infants: 8% to 13%; associated with cough, fever, diarrhea, and vomiting), bronchiolitis (infants; associated with cough, fever, diarrhea, and vomiting), bronchospasm, dyspnea, pulmonary edema, wheezing

Miscellaneous: Ulcer

<1%, postmarketing, and/or case reports: Abdominal cramps, agranulocytosis, alopecia, altered mental status, arterial insufficiency, arterial mesenteric thrombosis, decreased heart rate (infants), decreased serum glucose (infants), depression, emotional lability, epigastric distress, erythema multiforme, erythematous rash, exfoliative dermatitis, fever combined with generalized ache, sore throat, laryngospasm, and respiratory distress), hallucination, hypersensitivity reaction (including anaphylaxis, anaphylactoid reaction), impotence, insomnia, ischemic colitis, lassitude, lupus-like syndrome, myotonia, myopathy, nausea, nonthrombocytopenic purpura, peripheral arterial disease (exacerbation), Peyronie's disease, pharyngitis, psoriasiform eruption, purpura, Raynaud's phenomenon, second degree atrioventricular block (infants; in a patient with an underlying conduction disorder), Stevens-Johnson syndrome, systemic lupus erythematosus, temporary amnesia, tingling of extremities (hands), toxic epidermal necrolysis, urticaria, visual disturbance, vivid dream, vomiting, weakness, xerophthalmia

Warnings/Precautions

Concerns related to adverse events:

  • Anaphylactic reactions: Use caution with history of severe anaphylaxis to allergens; patients taking beta-blockers may become more sensitive to repeated challenges. Treatment of anaphylaxis (eg, epinephrine) in patients taking beta-blockers may be ineffective or promote undesirable effects.

Disease-related concerns:

  • Bronchospastic disease: In general, patients with bronchospastic disease should not receive beta-blockers; if used at all, should be used cautiously with close monitoring.
  • Conduction abnormality: Consider pre-existing conditions such as sick sinus syndrome before initiating.
  • Diabetes: Use with caution in patients with diabetes mellitus; may potentiate hypoglycemia and/or mask signs and symptoms.
  • Heart failure: Use with caution in patients with compensated heart failure and monitor for a worsening of the condition (efficacy of propranolol in heart failure has not been demonstrated).
  • Hepatic impairment: Use with caution in patients with hepatic impairment; dosage adjustment may be required.
  • Myasthenia gravis: Use with caution in patients with myasthenia gravis.
  • Peripheral vascular disease and Raynaud disease: Can precipitate or aggravate symptoms of arterial insufficiency in patients with peripheral vascular disease and Raynaud disease. Use with caution and monitor for progression of arterial obstruction.
  • Pheochromocytoma (untreated): Adequate alpha-blockade is required prior to use of any beta-blocker.
  • Psoriasis: Beta-blocker use has been associated with induction or exacerbation of psoriasis, but cause and effect have not been firmly established.
  • Renal impairment: Use with caution in patients with renal impairment; may have increased side effects.
  • Thyroid disease: May mask signs of hyperthyroidism (eg, tachycardia). If thyrotoxicosis is suspected, carefully manage and monitor; abrupt withdrawal may exacerbate symptoms of hyperthyroidism or precipitate thyroid storm. Alterations in thyroid function tests may be observed.
  • Vasospastic angina: Beta-blockers without alpha1-adrenergic receptor blocking activity should be avoided in patients with vasospastic angina since unopposed alpha1-adrenergic receptors mediate coronary vasoconstriction and can worsen anginal symptoms (Mayer 1998).

Concurrent drug therapy issues:

  • Drug-drug interactions: Potentially significant interactions may exist, requiring dose or frequency adjustment, additional monitoring, and/or selection of alternative therapy. Consult drug interactions database for more detailed information.

Special populations:

  • Infants and children: Considerations when treating infantile hemangioma:

- Cardiovascular concerns: Bradycardia and/or hypotension may occur or be worsened; monitor heart rate and blood pressure after propranolol initiation or increase in dose; discontinue treatment if severe (<80 bpm) or symptomatic bradycardia or hypotension (systolic blood pressure <50 mm Hg) occurs. Infants with large facial infantile hemangioma should be investigated for potential arteriopathy associated with PHACE syndrome prior to propranolol therapy; decreases in blood pressure caused by propranolol may increase risk of stroke in PHACE syndrome patients with cerebrovascular anomalies.

- Hypoglycemia: May potentiate hypoglycemia and/or mask signs and symptoms. Withhold the dose in infants or children who are not feeding regularly or who are vomiting; discontinue therapy and seek immediate treatment if hypoglycemia occurs.

- Respiratory concerns: May cause bronchospasm. Interrupt therapy in infants or children with lower respiratory tract infection associated with dyspnea or wheezing.

  • Elderly: Bradycardia may be observed more frequently in elderly patients (>65 years of age); dosage reductions may be necessary.
  • Smokers: Cigarette smoking may decrease plasma levels of propranolol by increasing metabolism. Patients should be advised to avoid smoking.

Other warnings/precautions:

  • Abrupt withdrawal: [US Boxed Warning]: Beta-blocker therapy should not be withdrawn abruptly (particularly in patients with coronary artery disease), but gradually tapered to avoid acute tachycardia, hypertension, and/or ischemia. Severe exacerbation of angina, ventricular arrhythmias, and myocardial infarction have been reported following abrupt withdrawal of beta-blocker therapy. Temporary but prompt resumption of beta-blocker therapy may be indicated with worsening of angina or acute coronary insufficiency.
  • Major surgery: Chronic beta-blocker therapy should not be routinely withdrawn prior to major surgery.

Monitoring Parameters

Acute cardiac treatment: Monitor ECG, heart rate, and blood pressure with IV administration; heart rate and blood pressure with oral administration.

Consult individual institutional policies and procedures.

Hypertension: Blood pressure, heart rate, serum glucose regularly (in patients with diabetes).

The 2017 Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults (ACC/AHA [Whelton 2018]):

Confirmed hypertension and known CVD or 10-year ASCVD risk ≥10%: Target blood pressure <130/80 mm Hg is recommended.

Confirmed hypertension without markers of increased ASCVD risk: Target blood pressure <130/80 mm Hg may be reasonable.

Proliferating infantile hemangioma (Hemangeol): Monitor heart rate and blood pressure for 2 hours after initiation or dose increases.

Pregnancy

Pregnancy Considerations

Propranolol crosses the placenta.

According to the manufacturer, congenital abnormalities have been reported following maternal use of propranolol. Exposure to propranolol during pregnancy may also increase the risk for other adverse events in the neonate. If maternal use of a beta-blocker is needed, fetal growth should be monitored during pregnancy and the newborn should be monitored for 48 hours after delivery for bradycardia, hypoglycemia, and respiratory depression (ESC [Regitz-Zagrosek 2018]).

Chronic maternal hypertension is also associated with adverse events in the fetus/infant. Chronic maternal hypertension may increase the risk of birth defects, low birth weight, premature delivery, stillbirth, and neonatal death. Actual fetal/neonatal risks may be related to duration and severity of maternal hypertension. Untreated chronic hypertension may also increase the risks of adverse maternal outcomes, including gestational diabetes, preeclampsia, delivery complications, stroke, and myocardial infarction (ACOG 203 2019).

The pharmacokinetics of propranolol are not significantly changed by pregnancy (Livingstone 1983; O'Hare 1984; Rubin 1987; Smith 1983).

When treatment of chronic hypertension in pregnancy is indicated, agents other than propranolol are preferred (ACOG 203 2019; ESC [Regitz-Zagrosek 2018]); however, use of propranolol may be considered (Magee 2014). Females with preexisting hypertension may continue their medication during pregnancy unless contraindications exist (ESC [Regitz-Zagrosek 2018]).

Propranolol may be used for the treatment of maternal ventricular arrhythmias, atrial fibrillation/atrial flutter, or supraventricular tachycardia during pregnancy; consult current guidelines for specific recommendations (ACC/AHA/HRS [Page 2016]; ESC [Regitz-Zagrosek 2018]).

Propranolol is recommended for use in controlling hypermetabolic symptoms of thyrotoxicosis in pregnancy (Alexander 2017).

Propranolol may be used if prophylaxis of migraine is needed in pregnant women; it should be discontinued 2 to 3 days prior to delivery to decrease the risk of adverse events to the fetus/neonate and potential reductions in uterine contraction (Pringsheim 2012).

Patient Education

What is this drug used for?

  • It is used to treat high blood pressure.
  • It is used to treat chest pain or pressure.
  • It is used to help certain heart problems.
  • It is used to prevent migraine headaches.
  • It is used to treat tremor (essential).
  • It is used after a heart attack to help prevent future heart attacks and lengthen life.
  • It is used to treat pheochromocytoma.
  • It is used to treat certain types of abnormal heartbeats.
  • It may be given to you for other reasons. Talk with the doctor.

Frequently reported side effects of this drug

  • Constipation
  • Abdominal pain
  • Abdominal cramps
  • Diarrhea
  • Fatigue
  • Loss of strength and energy
  • Nausea
  • Vomiting
  • Nightmares
  • Trouble sleeping

Other side effects of this drug: Talk with your doctor right away if you have any of these signs of:

  • Severe dizziness
  • Passing out
  • Chest pain
  • Confusion
  • Sensing things that seem real but are not
  • Trouble with memory
  • Mood changes
  • Depression
  • Burning or numbness feeling
  • Vision changes
  • Shortness of breath
  • Excessive weight gain
  • Swelling of arms or legs
  • Bruising
  • Bleeding
  • Chills
  • Sore throat
  • Slow heartbeat
  • Abnormal heartbeat
  • Sensation of cold
  • Sexual dysfunction
  • Low blood sugar like dizziness, headache, fatigue, feeling weak, shaking, fast heartbeat, confusion, increased hunger, or sweating
  • Lupus like rash on the cheeks or other body parts, sunburn easy, muscle or joint pain, chest pain or shortness of breath, or swelling in the arms or legs
  • Stevens-Johnson syndrome/toxic epidermal necrolysis like red, swollen, blistered, or peeling skin (with or without fever); red or irritated eyes; or sores in mouth, throat, nose, or eyes
  • Signs of a significant reaction like wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat.

Note: This is not a comprehensive list of all side effects. Talk to your doctor if you have questions.

Consumer Information Use and Disclaimer: This information should not be used to decide whether or not to take this medicine or any other medicine. Only the healthcare provider has the knowledge and training to decide which medicines are right for a specific patient. This information does not endorse any medicine as safe, effective, or approved for treating any patient or health condition. This is only a brief summary of general information about this medicine. It does NOT include all information about the possible uses, directions, warnings, precautions, interactions, adverse effects, or risks that may apply to this medicine. This information is not specific medical advice and does not replace information you receive from the healthcare provider. You must talk with the healthcare provider for complete information about the risks and benefits of using this medicine.

Source: Wolters Kluwer Health. Last updated January 23, 2020.