Version July 2025
Dosage guidance:
Dosing: 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. Oral IR (usually dosed 2 to 4 times daily), ER (usually dosed once daily), and IV injection formulations are available. 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 (Ref).
Angina, chronic stable (alternative agent):
Note: For vasospastic angina, beta-blockers are not recommended; calcium channel blockers and nitrates are preferred. For nonvasospastic angina, titrate beta-blocker to relieve angina or equivalent symptoms (Ref).
Oral: Initial: 80 mg/day in 1 to 4 divided doses based on chosen formulation (may choose an IR or ER formulation); increase dose as tolerated to desired effect; usual dosage range: 80 to 320 mg/day in 1 to 4 divided doses based on chosen formulation. Also see “Note: Dosage Forms” above.
Atrial fibrillation/flutter, rate control:
Note: For unstable patients, electrical cardioversion is preferred (Ref).
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 (Ref).
Maintenance of ventricular rate control:
Immediate release: Oral: Initial: 10 mg 3 to 4 times daily; increase dose gradually as tolerated to achieve ventricular rate control up to 40 mg 3 to 4 times daily (Ref).
Extended release: Oral: 60 mg once daily; increase dose gradually as tolerated to achieve ventricular rate control up to 160 mg once daily (Ref).
Burns, moderate to severe (hypermetabolism modulation) (adjunctive agent) (off-label use):
Immediate release: Oral: Initial: 10 to 20 mg 3 to 4 times daily; titrate as tolerated to a heart rate decrease of 15% to 20% from baseline. Generally, start within the first ~7 days following injury, after the patient is hemodynamically stable; usual total daily dosage range: 0.5 to 2 mg/kg/day in 3 to 6 equally divided doses (Ref).
Essential tremor:
Note: For patients with inadequate response, may add or switch to another agent (Ref).
Oral : Initial: 40 to 80 mg/day in 1 to 4 divided doses based on chosen formulation (may choose an IR or ER formulation). Gradually increase dose (eg, intervals of ≥7 days) as needed based on response and tolerability. Usual dosage range: 60 to 360 mg/day in 1 to 4 divided doses based on chosen formulation (Ref). Also see "Dosage Guidance" above.
Situational exacerbations:
Oral: Immediate release: 10 to 20 mg once as needed, administered 1 hour prior to anticipated exacerbating situation (Ref).
Hypertension (alternative agent):
Note: Not recommended in the absence of specific comorbidities (eg, ischemic heart disease, essential tremor, migraine) (Ref).
Oral: Initial: 80 mg/day in 1 to 4 divided doses based on chosen formulation (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 in 1 to 4 divided doses based on chosen formulation (Ref). Also see "Note: Dosage Forms" above.
Migraine, prevention:
Note: An adequate trial for assessment of effect is considered to be at least 2 to 3 months at a therapeutic dose (Ref).
Oral: Initial: 40 to 80 mg/day in 1 to 4 divided doses based on chosen formulation (may choose an IR or ER formulation); increase dose gradually based on response and tolerability to usual effective dosage range of 40 to 240 mg/day in 1 to 4 divided doses based on chosen formulation (Ref). Also see "Note: Dosage Forms" above.
Myocardial infarction, early treatment and secondary prevention (alternative agent):
Note: An oral beta-blocker is recommended within the first 24 hours for most patients. Patients who did not receive a beta-blocker within 24 hours of myocardial infarction should be reevaluated for secondary prevention at a later date (Ref).
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. The optimal duration of therapy is unknown; reassess need for long-term beta-blocker use (>1 year) if no other primary indication exists (eg, angina, arrhythmia, or hypertension) (Ref).
Performance anxiety disorder (off-label use):
Note: Advise patient to take a trial dose of propranolol in advance of the anxiety-provoking situation to assess for efficacy and tolerability (Ref).
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 (Ref).
Pheochromocytoma (adjunctive agent):
Note: An alpha-1 blocker must be started several days before propranolol (Ref).
Immediate release: Oral: Initial: 20 mg 3 times daily; begin 3 to 4 days after initiation of an alpha-1 blocker and adjust to goal heart rate up to 120 mg/day in 3 divided doses (Ref).
Postural orthostatic tachycardia syndrome (off-label use):
Immediate release: Oral: Initial: 10 mg twice daily; may increase based on response and tolerability to a maximum of 20 mg twice daily (Ref).
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 (Ref).
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 (Ref).
Thyroid storm (off-label use):
Note: For control of adrenergic symptoms until thyroid storm has resolved (Ref). Avoid use in patients with decompensated low-output heart failure (systolic dysfunction) (Ref).
Immediate release: Oral: Initial: 60 to 80 mg every 4 to 6 hours adjusted based on heart rate and blood pressure (Ref).
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 (Ref).
Thyrotoxicosis (alternative agent) (off-label use):
Note: For control of cardiovascular effects until euthyroidism established.
Oral: Initial: 30 to 160 mg/day in 1 to 4 divided doses based on chosen formulation (may choose an IR or ER formulation) adjusted for heart rate and blood pressure (Ref). Also see “Note: Dosage Forms” above.
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 (Ref).
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) (Ref).
Maximal daily dose:
No ascites: 320 mg/day (Ref).
Ascites: 160 mg/day (Ref).
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). Propranolol may be preferred over other beta-blockers in this setting (Ref). A beta-blocker may also be used to reduce shocks in patients with an implantable cardioverter defibrillator (Ref).
IV: 1 to 3 mg every 5 minutes up to a total of 5 mg in combination with an IV antiarrhythmic (Ref).
Immediate release: Oral: 40 mg every 6 hours in combination with an IV antiarrhythmic (Ref).
Prevention of ventricular tachycardia:
Immediate release: Oral: Initial: 10 to 40 mg every 6 hours; adjust dose as needed based on response and tolerability (Ref).
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 (Ref). Some experts recommend initiating 10 mg every 8 to 12 hours; then titrate based on response and tolerability to the lowest effective dose that alleviates symptoms; maximum dose: 320 mg/day (Ref).
Extended release: Oral: Initial: 80 mg once daily; then titrate based on response and tolerability to the lowest effective dose that alleviates symptoms; maximum dose: 320 mg/day (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
Altered kidney function: No dosage adjustment necessary for any degree of kidney dysfunction (Ref); use with caution, particularly in patients with more advanced kidney impairment, as decreased hepatic extraction has been reported and patients may be more prone to adverse effects when initiating therapy (Ref).
Hemodialysis, intermittent (thrice weekly): Not significantly dialyzed (Ref): No supplemental dose or dosage adjustment necessary (Ref); use with caution.
Peritoneal dialysis: Unlikely to be significantly dialyzed (large Vd): No dosage adjustment necessary (Ref); use with caution.
CRRT: No dosage adjustment necessary (Ref).
PIRRT (eg, sustained, low-efficiency diafiltration): No dosage adjustment necessary (Ref).
There are no dosage adjustments provided in the manufacturer’s labeling. However, hepatic impairment increases systemic exposure to propranolol. Use with caution.
IV: Use caution; initiate at lower end of the dosing range.
Oral: Refer to adult dosing; consider lower initial doses and titrate to response.
(For additional information see "Propranolol: Pediatric drug information")
Dosage guidance:
Safety: Oral liquid solutions are available in multiple concentrations (generic oral solution: 4 mg/mL [20 mg/5 mL] and 8 mg/mL [40 mg/5 mL]; Hemangeol: 4.28 mg/mL); precautions should be taken to verify and avoid confusion between the different concentrations; dose should be clearly presented as "mg."
Dosing: Dosage should be individualized based on patient response.
Cyclic vomiting syndrome, prophylaxis: Limited data available:
Note: Prophylaxis is recommended for patients experiencing frequent symptoms (eg, monthly) or severe symptoms (eg, requiring hospitalization, lasting >2 days, resulting in significant school/work absences) (Ref).
Children and Adolescents: Oral: Immediate-release formulations: 0.25 to 1 mg/kg/day in 2 to 3 divided doses (Ref). Maximum daily dose: 80 mg/day (Ref).
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 (Ref).
Hemangioma, infantile; proliferating:
In-person evaluation:
Hemangeol: Infants ≥5 weeks and ≥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 increase dose to 1.1 mg/kg/dose twice daily for 1 week, and then increase to a maintenance dose of 1.7 mg/kg/dose twice daily for 6 months; doses should be separated by at least 9 hours; readjust dose for patient growth. May repeat course if hemangiomas recur.
Immediate-release formulations: Limited data available: Infants and Children <5 years: Oral: Initial: 1 mg/kg/day in 2 or 3 divided doses, increase by 1 mg/kg/day at weekly intervals to maintenance dose; usual daily maintenance dose: 1 to 3 mg/kg/day in 2 or 3 divided doses; 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 (Ref).
Telemedicine evaluation: Hemangeol, immediate-release formulations: Limited data available: Infants >5 weeks: Oral: Initial: 0.5 mg/kg/day in 2 divided doses; may increase by 0.5 mg/kg/day every 3 to 4 days as tolerated to a target dose of 2 to 3 mg/kg/day in 2 divided doses (Ref).
Hypertension, chronic (alternate agent): Note: Beta-blockers are not recommended as initial antihypertensive agents in children (Ref).
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 daily dose: 4 mg/kg/day up to 640 mg/day; sustained-release formulation may be dosed once daily (Ref). Others have suggested a higher maximum daily dose of 16 mg/kg/day up to 640 mg/day (Ref).
Migraine, prophylaxis: Limited data available; efficacy results variable; optimal dose not established:
Oral: Immediate-release formulations:
Weight-directed dosing: Children ≥3 years and Adolescents: Oral: 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 recommended; maximum daily dose: 120 mg/day (Ref).
Fixed dose: Children ≥7 years and Adolescents: Oral: Initial: 10 mg daily; increase at weekly intervals in 10 mg increments; reported dose range: 10 to 40 mg three times daily; maximum dose: 120 mg/day (Ref).
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 (Ref).
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 (Ref).
Tetralogy spells: Limited data available:
Oral: Immediate-release formulations: Infants and Children: 0.5 to 1 mg/kg/dose every 6 hours (Ref). 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 (Ref).
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 (Ref); 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 (Ref).
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 (Ref); usual frequency in adolescents and adults is every 4 to 6 hours (Ref).
Adolescents:
Oral: Immediate-release formulations: 20 to 40 mg every 4 to 6 hours (Ref); titrate based on blood pressure and heart rate; doses as high as 60 to 80 mg every 4 hours have been recommended (Ref).
IV: 0.5 to 1 mg slow IV push over 10 minutes, then may repeat dose with 1 to 3 mg slow IV push over 10 to 15 minutes every several hours with continuous cardiac monitoring until heart rate controlled or oral therapy initiated (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Immediate-release formulations: Not dialyzable. There are no dosage adjustments provided in the manufacturer's labeling; however, renal impairment increases systemic exposure to propranolol. Use with caution.
Immediate-release formulations: There are no dosage adjustments provided in the manufacturer's labeling; however, propranolol is extensively metabolized by the liver; hepatic impairment increases systemic exposure to propranolol. Use with caution.
Beta-blockers may cause first-degree atrioventricular (AV) block, second-degree atrioventricular block, or complete atrioventricular block (Ref). At maintenance dosing, second- or third-degree AV block are less likely (Ref). Beta-blocking agents with intrinsic sympathomimetic activity (eg, pindolol) may cause fewer AV conduction abnormalities than those without intrinsic sympathomimetic activity (eg, propranolol) due to their partial agonist effects (Ref). In most cases (up to 72%), AV block associated with a beta-blocker will resolve upon discontinuation; however, there are reported cases of recurrent AV block and nearly 50% of patients with more severe AV block may require a permanent pacemaker (Ref).
Mechanism: Dose-related; related to the pharmacologic action. Blockade of cardiac beta-1 adrenergic receptors results in slowed conduction and prolongation in the refractory period of the AV node. Slowing of AV conduction can lead to AV block (Ref).
Onset: Varied; one study included patients who were on beta-blocker for more than one month (Ref); however, other studies noted prolongation of the PR interval or AV nodal refractory period occurring anywhere from one dose to several days following treatment initiation (Ref).
Risk factors:
• Impaired AV node conduction or sinus node dysfunction (Ref)
• Acute myocardial infarction (MI) (especially inferior and posterior MI) or heart failure (Ref)
• Concurrent use of other agents that impair AV nodal conduction (eg, nondihydropyridine calcium channel blockers, digoxin, ivabradine, select antiarrhythmic agents) (Ref)
• Older patients (Ref)
Nonselective beta-blockers (eg, propranolol) have a higher risk of bronchospasm compared to cardioselective beta-blockers (Ref) and may lead to drug discontinuation in patients with chronic obstructive pulmonary disease (COPD) or asthma (Ref). Concurrent use of inhaled bronchodilators and/or corticosteroids are protective against beta-blocker-induced bronchospasm in patients with COPD or asthma (Ref). Bronchospasm is reversible upon discontinuation (Ref).
Mechanism: Dose-related; related to pharmacologic action. Beta-blocking agents can lead to airway smooth muscle constriction by antagonism of beta-2 receptors (Ref).
Onset: Varied; reports after one dose (Ref). In another study with carvedilol-induced bronchospasm, the onset appeared to be slightly longer (Ref).
Risk factors:
• Patients with asthma who possess 1 or 2 copies of arginine-16 beta-2 receptor polymorphism (Ref)
• Acute use (Ref)
Beta-blockers may cause reversible CNS effects such as fatigue, insomnia, vivid dreams, memory impairment, and sexual disorder (Ref). Sexual disorders may occur; however, patients who require beta-blocker therapy have risk factors for erectile dysfunction (eg, coronary artery disease, heart failure) (Ref). In addition, there may be a psychosomatic component (Ref). Lipophilic beta-blockers (such as propranolol, which is highly lipophilic) penetrate the blood-brain barrier to a greater extent than hydrophilic beta-blockers, possibly leading to a greater incidence of CNS effects; however, other studies have refuted this theory (Ref). CNS effects generally resolve with dose reduction or discontinuation (Ref).
Mechanism: Dose-related; exact mechanism is not fully understood. Proposed mechanisms include presence of beta receptors in the brain, affinity and in some instances, inhibition of beta-blocking agents towards serotonin (5-HT) receptors in the brain (affecting mood and sleep), and beta-blocker-induced decreases in central sympathetic output (Ref). Beta-1 blockade may also impact sleep by blocking sympathetic signaling to the pineal gland, resulting in suppression of nighttime levels of melatonin (Ref). Beta-blockers may cause erectile dysfunction through decreased sympathetic nervous system output and subsequent decreases in luteinizing hormone secretion and testosterone stimulation (Ref).
Onset: Intermediate; CNS effects often occur within the first few weeks of treatment (Ref).
Risk factors:
• Higher starting doses (Ref)
• Older patients (Ref)
Beta-blockers may worsen, prolong, or cause hypoglycemia (Ref). Additionally, beta-blockers may mask symptoms of hypoglycemia (tremor, irritability, palpitations), making diaphoresis the only symptom unaffected by beta-blockers (Ref). It is unclear if non-selective or selective beta blockers are more likely to cause hypoglycemia as data are conflicting (Ref).
Mechanism: Dose-related; related to the pharmacologic action. Beta-blockers inhibit hepatic gluconeogenesis and glycogenolysis (Ref). Beta-blockers also reduce activation of the sympathetic nervous system, therefore masking hypoglycemic symptoms that are catecholamine-mediated (Ref).
Onset: Varied; blood glucose recovery was significantly reduced following one dose or one day of therapy (Ref). In another study, episodes of severe hypoglycemia were reported over the course of 4 years (Ref).
Risk factors:
• Diabetes mellitus, especially insulin-dependent diabetes and type 2 diabetes (Ref)
• Patients who are fasting (ie, surgery, not eating regularly, vomiting)
• Patients who are hospitalized and not requiring basal insulin (Ref)
Beta-blocker therapy should not be withdrawn abruptly, but gradually tapered to avoid acute tachycardia, hypertension, and/or ischemia in patients with underlying cardiovascular disease (Ref). Beta-blocker withdrawal (propranolol withdrawal syndrome), characterized by the development of severe exacerbation of angina pectoris, ventricular arrhythmias, and acute myocardial infarction (MI) has been reported following abrupt withdrawal of beta-blocker therapy (Ref). Some studies have found an increase in propensity-adjusted mortality and cardiovascular events; however, one study did not find changes in infarct size and left ventricular function when beta-blocker was abruptly withdrawn in patients with MI (Ref).
Mechanism: Dose-dependent; related to the pharmacologic action. Beta blockade causes upregulation of beta-receptors, enhanced receptor sensitivity, and decreased sympathetic nervous system response. Abrupt withdrawal leads to a transient sympathetic hyper-response (Ref). Another proposed mechanism involves increased platelet aggregability to epinephrine and thrombin (Ref).
Onset: Rapid/varied and transient; increases in heart rate and blood pressure appear 24 hours after abrupt withdrawal, peak after 48 hours, and subside after 7 days (Ref). Anginal symptoms reported to begin 12 to 24 hours after discontinuation (Ref). Development of adverse reactions also reported to occur 1 to 21 days after withdrawal (Ref).
Risk factors:
• Abrupt withdrawal in chronic users (Ref)
• Past medical history of coronary artery disease (including chronic stable angina) (Ref)
• Past medical history of hypertension (Ref)
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
>10%:
Nervous system: Sleep disorder (infants: 16% to 18%)
Respiratory: Bronchiolitis (infants), bronchitis (infants: 8% to 13%)
1% to 10%:
Cardiovascular: Cold extremity (infants: 7% to 8%)
Gastrointestinal: Abdominal pain (infants: 4%), constipation (1% to 3%), decreased appetite (infants: 3% to 4%), diarrhea (infants: 5% to 6%)
Nervous system: Agitation (infants: 5% to 9%), dizziness (4% to 7%), drowsiness (infants: 5%), fatigue (5% to 7%), irritability (infants: 6%), nightmares (infants: 6%)
<1%: Dermatologic: Alopecia, urticaria
Postmarketing:
Cardiovascular: Acute myocardial infarction (with drug withdrawal) (Ref), arterial insufficiency, arterial mesenteric thrombosis (Ref), bradycardia (Ref), complete atrioventricular block (Ref), exacerbation of angina pectoris (with drug withdrawal) (Ref), first-degree atrioventricular block (Ref), heart failure (Ref), hypertension (with drug withdrawal) (Ref), hypotension (Ref), peripheral arterial disease (exacerbation), Raynaud disease (Ref), second-degree atrioventricular block (including infants and patients with an underlying conduction disorder) (Ref), tachycardia (with drug withdrawal) (Ref)
Dermatologic: Dermal ulcer, dermatitis (Ref), erythema multiforme, exfoliative dermatitis, psoriasiform eruption (Ref), purpuric rash, Stevens-Johnson syndrome (Ref), toxic epidermal necrolysis
Endocrine & metabolic: Hypoglycemia (higher risk in infants) (Ref), increased serum potassium (Ref), weight gain (Ref)
Gastrointestinal: Abdominal cramps, epigastric discomfort (Ref), increased appetite (Ref), ischemic colitis, nausea (Ref), sore throat, vomiting
Genitourinary: Peyronie disease (Ref), sexual disorder (Ref)
Hematologic & oncologic: Agranulocytosis (Ref), immune thrombocytopenia, nonthrombocytopenic purpura (Ref)
Hepatic: Increased serum alkaline phosphatase (Ref), increased serum transaminases (Ref)
Hypersensitivity: Anaphylaxis (Ref), nonimmune anaphylaxis (Ref)
Nervous system: Asthenia (Ref), depression (Ref), emotional lability, generalized ache or pain, hallucination (Ref), insomnia (Ref), lassitude, memory impairment, tingling of extremities (hands), vivid dream (Ref), withdrawal syndrome (Ref)
Neuromuscular & skeletal: Laryngospasm, lupus-like syndrome (Ref), myopathy, myotonia, systemic lupus erythematosus
Ophthalmic: Dry eye syndrome, oculomucocutaneous syndrome (involving the skin) (Ref), visual disturbance (Ref)
Respiratory: Bronchospasm (Ref), dyspnea (Ref), pharyngitis, respiratory distress (Ref)
Miscellaneous: Fever (Ref)
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; BP <50/30 mm Hg; pheochromocytoma; history of bronchospasm.
Canadian labeling: Additional contraindications (not in US labeling): Bronchospasm; right ventricular failure secondary to pulmonary hypertension; allergic rhinitis during pollen season; patients prone to hypoglycemia; hypotension (BP parameters not specified in labeling); metabolic acidosis; vasospastic angina (also referred to as Prinzmetal angina or variant angina); severe peripheral arterial circulatory disturbance; untreated pheochromocytoma; hereditary problems of galactose intolerance, glucose-galactose malabsorption, or congenital lactase deficiency (lactose-containing products only).
Hemangiol (additional contraindications): Infants weighing <2.5 kg; breastfed infants if mother is treated with medicines contraindicated with propranolol; heart rate <100 bpm or BP <65/45 mm Hg (<3 months of age), heart rate <90 bpm or BP <70/50 mm Hg (3 to <6 months of age), heart rate <80 bpm or BP <80/55 mm Hg (6 to 12 months of age).
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:
• 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 advanced renal impairment during initiation of therapy, as decreased hepatic extraction may result in elevated propranolol concentrations and increase the risk of side effects (Lowenthal 1974).
• 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 alpha-1 adrenergic receptor blocking activity should be avoided in patients with vasospastic angina since unopposed alpha-1 adrenergic receptors mediate coronary vasoconstriction and can worsen anginal symptoms (Mayer 1998).
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. Administer during or after a feeding to minimize the risk for hypoglycemia. 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.
• Smokers: Cigarette smoking may decrease plasma levels of propranolol by increasing metabolism. Patients should be advised to avoid smoking.
Other warnings/precautions:
• Major surgery: Chronic beta-blocker therapy should not be routinely withdrawn prior to major surgery.
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 corn starch, fd&c blue #1 (brilliant blue)]
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 (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
Yes
Capsule ER 24 Hour Therapy Pack (Inderal LA Oral)
60 mg (per each): $77.00
80 mg (per each): $89.95
120 mg (per each): $99.06
160 mg (per each): $103.41
Capsule ER 24 Hour Therapy Pack (Inderal XL Oral)
80 mg (per each): $88.82
120 mg (per each): $88.82
Capsule ER 24 Hour Therapy Pack (InnoPran XL Oral)
80 mg (per each): $88.82
120 mg (per each): $88.82
Capsule ER 24 Hour Therapy Pack (Propranolol HCl ER Oral)
60 mg (per each): $2.06
80 mg (per each): $2.41
120 mg (per each): $2.98
160 mg (per each): $3.90
Solution (Hemangeol Oral)
4.28 mg/mL (per mL): $6.25
Solution (Propranolol HCl Intravenous)
1 mg/mL (per mL): $9.60 - $13.78
Solution (Propranolol HCl Oral)
20 mg/5 mL (per mL): $0.84
40 mg/5 mL (per mL): $0.19
Tablets (Propranolol HCl Oral)
10 mg (per each): $0.41
20 mg (per each): $0.51 - $0.61
40 mg (per each): $0.72
60 mg (per each): $1.22 - $1.74
80 mg (per each): $0.90 - $0.97
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Capsule Extended Release 24 Hour, Oral, as hydrochloride:
Inderal LA: 60 mg [DSC], 80 mg [DSC], 120 mg [DSC], 160 mg [DSC] [contains fd&c blue #1 (brilliant blue)]
Generic: 60 mg, 80 mg, 120 mg, 160 mg
Solution, Intravenous, as hydrochloride:
Generic: 1 mg/mL (1 mL)
Solution, Oral, as hydrochloride:
Generic: 4.28 mg/mL (120 mL)
Tablet, Oral:
Generic: 120 mg [DSC]
Tablet, Oral, as hydrochloride:
Generic: 10 mg, 20 mg, 40 mg, 80 mg
Prescriptions for Hemangeol may be obtained via the Hemangeol Patient Access program. Visit http://www.hemangeol.com/hcp/hemangeol-direct/ or call 855-618-4950 for ordering information.
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.
Bariatric surgery: Capsule, extended release: Some institutions may have specific protocols that conflict with these recommendations; refer to institutional protocols as appropriate. ER capsules should be swallowed whole. Do not crush or chew. IR tablet, oral solution, and injectable formulations are available. If safety and efficacy can be effectively monitored, no change in formulation or administration is required after bariatric surgery; however, selection of IR formulations or alternative therapy should be strongly considered for cardiovascular and other high-risk labeled and off-label indications for propranolol.
Oral:
Immediate-release tablets: Take on an empty stomach.
Extended-release capsules: Administer consistently either with food or on an empty stomach; do not chew or crush sustained- or extended-release capsules; swallow whole.
Oral solution: Note: Oral liquid solutions are available in multiple concentrations (generic oral solution: 4 mg/mL [20 mg/5 mL] and 8 mg/mL [40 mg/5 mL]; Hemangeol: 4.28 mg/mL; precautions should be taken to verify and avoid confusion between the different concentrations; dose should be clearly presented as mg.
Hemangeol oral solution: Infants: Administer Hemangeol directly into the child's mouth using the supplied oral dosing syringe; if needed, dose may be diluted with a small quantity of milk or fruit juice and administered in a baby's bottle. Administer during or after a feeding to minimize the risk for hypoglycemia; skip the dose if the patient is not eating or is vomiting. Administer doses at least 9 hours apart. Do not shake bottle before use.
Parenteral: Note: IV dose is much smaller than oral dose. When administered acutely for cardiac treatment, monitor ECG and blood pressure; consult individual institutional policies and procedures.
Neonates, Infants, Children, and Adolescents: Administer by slow IV injection/infusion over 10 to 15 minutes (Ref).
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]).
Hypertrophic cardiomyopathy with left ventricular outflow tract obstruction: Symptomatic treatment of hypertrophic cardiomyopathy with left ventricular outflow tract obstruction.
Migraine, prevention: 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.
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.
Akathisia, antipsychotic-induced; Burns, moderate to severe (hypermetabolism modulation) (adjunctive agent); Performance anxiety disorder; Postural orthostatic tachycardia syndrome; Thyroid storm; Thyrotoxicosis; Tremor, lithium-induced, moderate to severe; Variceal hemorrhage prophylaxis
Propranolol may be confused with prasugrel, Pravachol, Propulsid.
Inderal may be confused with Adderall, Enduron, Imdur, Imuran, Inderide, Isordil, Toradol.
The Institute for Safe Medication Practices (ISMP) includes this medication among its list of drug classes (adrenergic antagonist, IV) which have a heightened risk of causing significant patient harm when used in error (High-Alert Medications in Acute Care Settings).
Propranolol is identified in the Screening Tool of Older Person's Prescriptions (STOPP) criteria as a potentially inappropriate medication in older adults (≥65 years of age). Some disease states of concern include diabetes mellitus, bradycardia, heart block, and severe aortic stenosis. Use is not recommended as monotherapy for the treatment of uncomplicated hypertension (O’Mahony 2023).
Significant differences exist between oral and IV dosing. Use caution when converting from one route of administration to another.
Deralin [Australia, Israel] may be confused with Deptran brand name for doxepin [Australia].
Inderal [Canada and multiple international markets], Inderal LA [US], and Inderal XL [US] may be confused with Indiaral brand name for loperamide [France] or Indamol brand name for indapamide [Italy].
Substrate of CYP1A2 (Major), CYP2C19 (Minor), CYP2D6 (Major), CYP3A4 (Minor); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential; Inhibits CYP1A2 (Weak);
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Acetylcholinesterase Inhibitors: May increase bradycardic effects of Beta-Blockers. Risk C: Monitor
Ajmaline: May increase serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Risk C: Monitor
Alcohol (Ethyl): May decrease serum concentration of Propranolol. Alcohol (Ethyl) may increase serum concentration of Propranolol. Risk C: Monitor
Alfuzosin: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Alpha2-Agonists: Beta-Blockers may increase rebound hypertensive effects of Alpha2-Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. Alpha2-Agonists may increase AV-blocking effects of Beta-Blockers. Sinus node dysfunction may also be enhanced. 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. Risk D: Consider Therapy Modification
Amifostine: Blood Pressure Lowering Agents may increase hypotensive effects of Amifostine. Management: When used at chemotherapy doses, hold blood pressure lowering medications for 24 hours before amifostine administration. If blood pressure lowering therapy cannot be held, do not administer amifostine. Use caution with radiotherapy doses of amifostine. Risk D: Consider Therapy Modification
Amiodarone: May increase bradycardic effects of Beta-Blockers. Possibly to the point of cardiac arrest. Amiodarone may increase serum concentration of Beta-Blockers. Risk C: Monitor
Amphetamines: May decrease antihypertensive effects of Antihypertensive Agents. Risk C: Monitor
Antidiabetic Agents: Beta-Blockers (Nonselective) may increase hypoglycemic effects of Antidiabetic Agents. Beta-Blockers (Nonselective) may increase adverse/toxic effects of Antidiabetic Agents. Specifically, beta-blockers may mask the hypoglycemic symptoms of antidiabetic agents. Risk C: Monitor
Antipsychotic Agents (Phenothiazines): May increase hypotensive effects of Beta-Blockers. Beta-Blockers may decrease metabolism of Antipsychotic Agents (Phenothiazines). Antipsychotic Agents (Phenothiazines) may decrease metabolism of Beta-Blockers. Risk C: Monitor
Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may increase hypotensive effects of Antipsychotic Agents (Second Generation [Atypical]). Risk C: Monitor
Arginine: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Artemether and Lumefantrine: May increase serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Risk C: Monitor
Barbiturates: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Benperidol: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Beta2-Agonists: Beta-Blockers (Nonselective) may decrease bronchodilatory effects of Beta2-Agonists. Risk X: Avoid
Bile Acid Sequestrants: May decrease serum concentration of Propranolol. Risk C: Monitor
Bradycardia-Causing Agents: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Brigatinib: May decrease antihypertensive effects of Antihypertensive Agents. Brigatinib may increase bradycardic effects of Antihypertensive Agents. Risk C: Monitor
Brimonidine (Topical): May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Broccoli: May decrease serum concentration of CYP1A2 Substrates (High risk with Inducers). Risk C: Monitor
Bromperidol: May decrease hypotensive effects of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may increase hypotensive effects of Bromperidol. Risk X: Avoid
BUPivacaine: Propranolol may increase serum concentration of BUPivacaine. Risk C: Monitor
Cafedrine: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may decrease therapeutic effects of Cafedrine. Risk C: Monitor
Cannabis: Beta-Blockers may increase adverse/toxic effects of Cannabis. Specifically, the risk of hypoglycemia may be increased. Risk C: Monitor
Cannabis: May decrease serum concentration of CYP1A2 Substrates (High risk with Inducers). Risk C: Monitor
Ceritinib: Bradycardia-Causing Agents may increase bradycardic effects 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. Risk D: Consider Therapy Modification
Certoparin: May increase serum concentration of Propranolol. Risk C: Monitor
Charcoal, Activated: May decrease therapeutic effects of Propranolol. Risk C: Monitor
Cholinergic Agonists: Beta-Blockers may increase adverse/toxic effects of Cholinergic Agonists. Of particular concern are the potential for cardiac conduction abnormalities and bronchoconstriction. Risk C: Monitor
Cimetidine: May increase serum concentration of Propranolol. Risk C: Monitor
CloZAPine: CYP1A2 Inhibitors (Weak) may increase serum concentration of CloZAPine. Risk C: Monitor
CYP1A2 Inducers (Moderate): May decrease serum concentration of Propranolol. Risk C: Monitor
CYP1A2 Inhibitors (Moderate): May increase serum concentration of Propranolol. Risk C: Monitor
CYP1A2 Inhibitors (Strong): May increase 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. Risk D: Consider Therapy Modification
CYP2D6 Inhibitors (Moderate): May increase serum concentration of Propranolol. Risk C: Monitor
CYP2D6 Inhibitors (Strong): May increase serum concentration of Propranolol. Risk C: Monitor
Dexmethylphenidate: May decrease therapeutic effects of Antihypertensive Agents. Risk C: Monitor
Diazoxide Choline: May increase serum concentration of CYP1A2 Substrates (High risk with Inhibitors). Risk X: Avoid
Diazoxide: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Dipyridamole: May increase bradycardic effects of Beta-Blockers. Risk C: Monitor
Disopyramide: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may increase negative inotropic effects of Disopyramide. Risk C: Monitor
DOBUTamine: Beta-Blockers may decrease therapeutic effects of DOBUTamine. Risk C: Monitor
Doxofylline: Propranolol may increase serum concentration of Doxofylline. Risk C: Monitor
Dronedarone: May increase bradycardic effects of Beta-Blockers. Dronedarone may increase 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. Increase monitoring for clinical response and adverse effects. Risk D: Consider Therapy Modification
DULoxetine: Blood Pressure Lowering Agents may increase hypotensive effects of DULoxetine. Risk C: Monitor
EPHEDrine (Systemic): Beta-Blockers may decrease therapeutic effects of EPHEDrine (Systemic). Risk C: Monitor
EPINEPHrine (Nasal): Beta-Blockers (Nonselective) may increase hypertensive effects of EPINEPHrine (Nasal). Risk C: Monitor
EPINEPHrine (Oral Inhalation): Beta-Blockers (Nonselective) may increase hypertensive effects of EPINEPHrine (Oral Inhalation). Risk C: Monitor
EPINEPHrine (Systemic): Beta-Blockers (Nonselective) may increase hypertensive effects of EPINEPHrine (Systemic). Risk C: Monitor
Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates): Beta-Blockers may increase vasoconstricting effects of Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates). Risk C: Monitor
Etilefrine: Beta-Blockers may decrease therapeutic effects of Etilefrine. Etilefrine may increase bradycardic effects of Beta-Blockers. Risk C: Monitor
Etofylline: Beta-Blockers may decrease therapeutic effects of Etofylline. Risk X: Avoid
Etrasimod: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Fexinidazole: Bradycardia-Causing Agents may increase arrhythmogenic effects of Fexinidazole. Risk X: Avoid
Fezolinetant: CYP1A2 Inhibitors (Weak) may increase serum concentration of Fezolinetant. Risk X: Avoid
Fingolimod: Bradycardia-Causing Agents may increase bradycardic effects of Fingolimod. Management: Consult with the prescriber of any bradycardia-causing agent to see if the agent could be switched to an agent that does not cause bradycardia prior to initiating fingolimod. If combined, perform continuous ECG monitoring after the first fingolimod dose. Risk D: Consider Therapy Modification
Flunarizine: May increase therapeutic effects of Antihypertensive Agents. Risk C: Monitor
Grass Pollen Allergen Extract (5 Grass Extract): Beta-Blockers may increase adverse/toxic effects 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. Management: Consider alternatives to either grass pollen allergen extract (5 grass extract) or beta-blockers in patients with indications for both agents. Canadian product labeling specifically lists this combination as contraindicated. Risk D: Consider Therapy Modification
Guggul: May decrease serum concentration of Propranolol. Risk C: Monitor
Herbal Products with Blood Pressure Increasing Effects: May decrease antihypertensive effects of Antihypertensive Agents. Risk C: Monitor
Herbal Products with Blood Pressure Lowering Effects: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Hypotension-Associated Agents: Blood Pressure Lowering Agents may increase hypotensive effects of Hypotension-Associated Agents. Risk C: Monitor
Iloperidone: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Indoramin: May increase hypotensive effects of Antihypertensive Agents. Risk C: Monitor
Insulin: Beta-Blockers (Nonselective) may increase hypoglycemic effects of Insulin. Beta-Blockers (Nonselective) may decrease therapeutic effects of Insulin. Risk C: Monitor
Isocarboxazid: May increase antihypertensive effects of Antihypertensive Agents. Risk X: Avoid
Isoproterenol: Beta-Blockers may decrease therapeutic effects of Isoproterenol. Risk C: Monitor
Ivabradine: Bradycardia-Causing Agents may increase bradycardic effects of Ivabradine. Risk C: Monitor
Lacidipine: May increase hypotensive effects of Propranolol. Lacidipine may increase serum concentration of Propranolol. Propranolol may decrease serum concentration of Lacidipine. Risk C: Monitor
Lacosamide: Bradycardia-Causing Agents may increase AV-blocking effects of Lacosamide. Risk C: Monitor
Landiolol: Bradycardia-Causing Agents may increase bradycardic effects of Landiolol. Risk X: Avoid
Lasmiditan: May increase bradycardic effects of Propranolol. Lasmiditan may decrease therapeutic effects of Propranolol. Specifically, blood pressure may increase during coadministration. Risk C: Monitor
Levodopa-Foslevodopa: Blood Pressure Lowering Agents may increase hypotensive effects of Levodopa-Foslevodopa. Risk C: Monitor
Lidocaine (Systemic): Propranolol may increase serum concentration of Lidocaine (Systemic). Risk C: Monitor
Liraglutide: May decrease therapeutic effects of Propranolol. Specifically, the heart rate lowering effect of propranolol may be diminished. Propranolol may increase hypoglycemic effects of Liraglutide. Propranolol may decrease therapeutic effects of Liraglutide. Risk C: Monitor
Loop Diuretics: May increase hypotensive effects of Antihypertensive Agents. Risk C: Monitor
Lormetazepam: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Mavacamten: Beta-Blockers may increase adverse/toxic effects of Mavacamten. Specifically, negative inotropic effects may be increased. Risk C: Monitor
Mavorixafor: May increase serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Risk X: Avoid
Mepivacaine: Propranolol may increase serum concentration of Mepivacaine. Risk C: Monitor
Metergoline: May decrease antihypertensive effects of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may increase orthostatic hypotensive effects of Metergoline. Risk C: Monitor
Methacholine: Beta-Blockers may increase adverse/toxic effects of Methacholine. Risk C: Monitor
Methylphenidate: May decrease antihypertensive effects of Antihypertensive Agents. Risk C: Monitor
Midodrine: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Mivacurium: Beta-Blockers may increase therapeutic effects of Mivacurium. Risk C: Monitor
Molsidomine: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Naftopidil: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Nicergoline: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Nicorandil: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
NIFEdipine (Topical): May increase adverse/toxic effects of Beta-Blockers. Risk C: Monitor
NIFEdipine: May increase hypotensive effects of Beta-Blockers. NIFEdipine may increase negative inotropic effects of Beta-Blockers. Risk C: Monitor
Nitrendipine: May increase therapeutic effects of Beta-Blockers. Risk C: Monitor
Nitroprusside: Blood Pressure Lowering Agents may increase hypotensive effects of Nitroprusside. Risk C: Monitor
Nonsteroidal Anti-Inflammatory Agents (Topical): May decrease therapeutic effects of Beta-Blockers. Risk C: Monitor
Nonsteroidal Anti-Inflammatory Agents: May decrease antihypertensive effects of Beta-Blockers. Risk C: Monitor
Obinutuzumab: May increase hypotensive effects 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. Risk D: Consider Therapy Modification
Opipramol: Beta-Blockers may increase serum concentration of Opipramol. Opipramol may increase serum concentration of Beta-Blockers. Risk C: Monitor
Ozanimod: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Peginterferon Alfa-2b: May decrease serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Peginterferon Alfa-2b may increase serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Risk C: Monitor
Pentoxifylline: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Perazine: May increase hypotensive effects of Antihypertensive Agents. Risk C: Monitor
Pholcodine: Blood Pressure Lowering Agents may increase hypotensive effects of Pholcodine. Risk C: Monitor
Phosphodiesterase 5 Inhibitors: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Ponesimod: Bradycardia-Causing Agents may increase bradycardic effects of Ponesimod. Management: Avoid coadministration of ponesimod with drugs that may cause bradycardia when possible. If combined, monitor heart rate closely and consider obtaining a cardiology consult. Do not initiate ponesimod in patients on beta-blockers if HR is less than 55 bpm. Risk D: Consider Therapy Modification
Prazosin: Antihypertensive Agents may increase hypotensive effects of Prazosin. Risk C: Monitor
Primaquine: May increase serum concentration of CYP1A2 Substrates (High risk with Inhibitors). Risk C: Monitor
Propafenone: May increase serum concentration of Propranolol. Propranolol may increase serum concentration of Propafenone. Risk C: Monitor
Prostacyclin Analogues: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Quinagolide: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
QuiNIDine: May increase serum concentration of Propranolol. Risk C: Monitor
Reserpine: May increase hypotensive effects of Beta-Blockers. Reserpine may increase bradycardic effects of Beta-Blockers. Risk C: Monitor
RifAMPin: May decrease serum concentration of Propranolol. Risk C: Monitor
Rifapentine: May decrease serum concentration of Propranolol. Risk C: Monitor
Rivastigmine: May increase bradycardic effects of Beta-Blockers. Risk X: Avoid
Rizatriptan: Propranolol may increase serum concentration of Rizatriptan. Management: Adults: limit rizatriptan to 5 mg (max 3 doses/24 hrs). Pediatrics: if weight 40 kg or more, limit rizatriptan to single 5 mg dose/24 hrs; do not combine if weight less than 40 kg. Rizatriptan oral film and meloxicam-rizatriptan combo are contraindicated. Risk D: Consider Therapy Modification
Silodosin: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Siponimod: Bradycardia-Causing Agents may increase bradycardic effects of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. If combined, consider obtaining a cardiology consult regarding patient monitoring. Risk D: Consider Therapy Modification
Succinylcholine: Beta-Blockers may increase neuromuscular-blocking effects of Succinylcholine. Risk C: Monitor
Sulfonylureas: Beta-Blockers (Nonselective) may increase hypoglycemic effects of Sulfonylureas. Beta-Blockers (Nonselective) may decrease therapeutic effects of Sulfonylureas. Risk C: Monitor
Tasimelteon: Beta-Blockers may decrease therapeutic effects of Tasimelteon. Management: Consider avoiding nighttime administration of beta-blockers during tasimelteon therapy due to the potential for reduced tasimelteon efficacy. Risk D: Consider Therapy Modification
Terazosin: Antihypertensive Agents may increase hypotensive effects of Terazosin. Risk C: Monitor
Theodrenaline: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may decrease therapeutic effects of Theodrenaline. Risk C: Monitor
Theophylline Derivatives: Beta-Blockers (Nonselective) may decrease bronchodilatory effects of Theophylline Derivatives. Risk C: Monitor
Theophylline Derivatives: CYP1A2 Inhibitors (Weak) may increase serum concentration of Theophylline Derivatives. Risk C: Monitor
Thioridazine: Propranolol may increase serum concentration of Thioridazine. Thioridazine may increase serum concentration of Propranolol. Risk X: Avoid
TiZANidine: CYP1A2 Inhibitors (Weak) may increase serum concentration of TiZANidine. Management: Avoid the use of tizanidine with weak CYP1A2 inhibitors when possible. If combined, monitor closely for increased tizanidine toxicities (eg, hypotension, bradycardia, drowsiness). Tizanidine dose reduction or discontinuation may be necessary. Risk D: Consider Therapy Modification
Tobacco (Smoked): May decrease serum concentration of Propranolol. Risk C: Monitor
Urapidil: Antihypertensive Agents may increase hypotensive effects of Urapidil. Risk C: Monitor
White Birch Allergen Extract: Beta-Blockers may increase adverse/toxic effects of White Birch Allergen Extract. Specifically, beta-blockers may reduce the effectiveness of beta-agonists that may be required to treat systemic reactions to white birch allergen extract. Risk X: Avoid
Zileuton: May increase serum concentration of Propranolol. Risk C: Monitor
Ethanol: Ethanol may increase or decrease plasma levels of propranolol. Reports are variable and have shown both enhanced as well as inhibited hepatic metabolism (of propranolol). Management: Caution advised with consumption of ethanol and monitor for heart rate and/or blood pressure changes.
Food: Propranolol serum levels may be increased if taken with food. Protein-rich foods may increase bioavailability; a change in diet from high carbohydrate/low protein to low carbohydrate/high protein may result in increased oral clearance. Management: Tablets (immediate release) should be taken on an empty stomach. Capsules (extended release) may be taken with or without food, but be consistent with regard to food.
Medications considered acceptable for the treatment of chronic hypertension during pregnancy may generally be used in patients trying to conceive. Propranolol is generally not a preferred agent for use in pregnant patients (ACC/AHA [Whelton 2018]; ACOG 2019); however, use may be considered (SOGC [Magee 2022]).
Propranolol is approved for prevention of migraines. In general, preventive treatment for migraine in patients trying to become pregnant should be avoided. Options for patients planning a pregnancy should be considered as part of a shared decision-making process. Nonpharmacologic interventions should be considered initially. When needed, preventive treatment should be individualized considering the available safety data and needs of the patient should pregnancy occur. A gradual discontinuation of preventive medications is generally preferred when the decision is made to stop treatment prior to conception (ACOG 2022; AHS [Ailani 2021]).
Erectile dysfunction and male impotence are noted in product labeling following use of propranolol. As a class, outcomes from available studies evaluating beta-blockers and sexual dysfunction are inconsistent, and the negative effects on erectile function and libido are considered controversial. A clear relationship between use of beta-blockers and erectile dysfunction has not been established. Hypertension itself is associated with erectile dysfunction. Patients on a beta-blocker presenting with sexual dysfunction should be evaluated for underlying disease (Farmakis 2021; Levine 2012; Semet 2017; Terentes-Printzios 2022; Viigimaa 2020).
Propranolol crosses the placenta.
Exposure to beta-blockers during the third trimester of pregnancy may increase the risk for bradycardia, hypoglycemia, hypotension, and respiratory depression in the neonate. Newborns should be monitored and managed accordingly. If maternal use of a beta-blocker is needed, monitor fetal growth during pregnancy; monitor the newborn 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 the 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 2019).
The pharmacokinetics of propranolol are not significantly changed by pregnancy (Livingstone 1983; O'Hare 1984; Rubin 1987; Smith 1983).
Patients with preexisting hypertension may continue their medication during pregnancy unless contraindications exist (ESC [Regitz-Zagrosek 2018]). When treatment of hypertension is initiated during pregnancy, agents other than propranolol may be preferred (ACOG 2019; ESC [Cífková 2020]; ESC [Regitz-Zagrosek 2018]); however, use may be considered (SOGC [Magee 2022]).
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 (ATA [Alexander 2017]).
In general, preventive treatment for migraine should be avoided during pregnancy. Options for pregnant patients should be considered as part of a shared decision-making process. Nonpharmacologic interventions should be considered initially. When needed, preventive treatment should be individualized considering the available safety data, the potential for adverse maternal and fetal events, and needs of the patient (ACOG 2022; AHS [Ailani 2021]). If preventive therapy is needed, beta-blockers may be considered (ACOG 2022). Based on available data, propranolol may be used if prophylaxis of migraine is needed in pregnant patients; 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 (CHS [Pringsheim 2012]).
Propranolol and its inactive metabolites are present in breast milk (Smith 1983).
Data related to the presence of propranolol in breast milk are available from 3 lactating patients 1-week postpartum receiving propranolol for hypertension. Breast milk was sampled ~3, 4, 6, and 8 hours after the maternal dose. The first 2 patients received propranolol 1.2 mg/kg/day and the third received propranolol 2.6 mg/kg/day. The highest propranolol milk concentration was 74.9 ng/mL observed in the first patient ~3 hours after the dose. The lowest propranolol milk concentration was 13.5 ng/mL in the second patient, observed ~8 hours after the dose. The overall half-life of propranolol in breast milk was 6.5 ± 3.4 hours. In comparison, the overall half-life in the maternal plasma was 2.6 ± 1.2 hours (Smith 1983). Peak milk concentrations are reported to occur between 2 to 3 hours after an oral dose (Bauer 1979).
Bradycardia was reported in an infant exposed to propranolol via breast milk (Soussan 2014).
In general, preventive treatment for migraine in lactating patients should be avoided. When needed, therapy should be individualized considering the available safety data and needs of the patient (AHS [Ailani 2021]). Based on available data, propranolol may be used if prophylaxis of migraine is needed in lactating patients (CHS [Pringsheim 2012]).
When used for hypertension, propranolol is compatible for use in patients who are breastfeeding (ACOG 2019; ESC [Cífková 2020]).
In general, propranolol may be compatible with breastfeeding when used at usual doses. Breastfeeding infants should be monitored for bradycardia, cyanosis, and hypoglycemia (WHO 2002).
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.
Acute cardiac treatment: ECG, heart rate, and blood pressure.
Hypertension: Blood pressure, heart rate.
Mental alertness; signs and symptoms of bronchospasm in patients with existing bronchospastic disease; serum glucose (in patients with diabetes).
Proliferating infantile hemangioma (Hemangeol): Monitor heart rate and blood pressure for 2 hours after initiation or dose increases.
Blood pressure goal: May vary depending on clinical conditions, different clinical practice guidelines, and expert opinion. Refer to "Clinical Practice Guidelines" for specific treatment goals.
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.
Onset of action: Beta-blockade: Oral: 1 to 2 hours; IV: ≤5 minutes; Peak effect: Hypertension: A few days to several weeks.
Duration: Immediate release: 6 to 12 hours; Extended-release formulations: ~24 to 27 hours.
Absorption: Oral: Rapid and complete.
Distribution: Vd: 4 L/kg (adults); crosses the blood-brain barrier.
Protein binding: Newborns: 68%; Adults: ~90% (S-isomer primarily to alpha-1 acid glycoprotein; R-isomer primarily to albumin).
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.
Bioavailability: ~25% reaches systemic circulation due to high first-pass metabolism; oral bioavailability may be increased in children with Down syndrome; protein-rich foods increase bioavailability by ~50%.
Half-life elimination:
Neonates: GA 23 to 26 weeks: 13.8 ± 3.9 hours, GA 27 to 34 weeks: 15.7 ± 5.1 hours, GA 35 to 42 weeks: 15.5 ± 0.7 hours (Filippi 2013); 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.
Time to peak: Immediate release: Neonates: 2.6 ± 0.9 hours (Filippi 2013); Infants: ≤2 hours (Hemangeol); Adults: 1 to 4 hours; Extended-release capsule (Inderal XL, InnoPran XL): Adults: 12 to 14 hours; Long-acting capsule (Inderal LA): Adults: 6 hours.
Excretion: Metabolites are excreted primarily in urine (96% to 99%); <1% excreted in urine as unchanged drug.
