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Inderal LA
Classes
Anti-arrhythmics, Class II
Non-Selective Beta-Blockers
Administration
Immediate-release tablets: Administer with food.
Sustained-release capsules (e.g., Inderal LA): Administer once daily. Do not crush or chew; swallow whole. If patients are switched from immediate-release tablets to sustained-release capsules, assure desired therapeutic effects are maintained. Substitution should not be simply considered 1:1 as lower plasma concentrations are achieved with the long-acting product. Further titration may be necessary.
Extended-release capsules (e.g., Innopran XL): Administer once daily at bedtime. Do not crush or chew; swallow whole. Take consistently either on an empty stomach or with food.
Generic Oral Solution (4 mg/mL or 8 mg/mL):
Administer with food.
Hemangeol Oral Solution (4.28 mg/mL; for infantile hemangioma):
Record the date on the box when the bottle is first opened.
Do not shake the bottle before use.
Administer during or right after a feeding. Do not administer the dose if the patient is not eating or vomiting.
Using an oral syringe, administer the medicine directly into the child's mouth, against the inside of the cheek. If this is not feasible, the solution may be diluted in a small quantity of milk or fruit juice and given immediately.
Keep the child in an upright position for a few minutes after giving the dose.
Monitor blood pressure and heart rate for 2 hours after the initial dose and after any significant dose increase.
Storage: Store the bottle in the box at room temperature and discard 2 months after opening.
Visually inspect parenteral products for particulate matter and discoloration prior to administration whenever solution and container permit.
IV bolus injection:
No dilution necessary. If dilution is necessary for accurate dose delivery, the drug may be diluted in 5% Dextrose Injection, 0.9% Sodium Chloride Injection, or Lactated Ringer's Injection.
Monitor ECG and central venous pressure during IV administration.[45870]
Adults: Administer at a rate not to exceed 1 mg/minute.
Children: Administer via slow IV push over 10 minutes; do not exceed a rate of 1 mg/minute.[45870]
Continuous IV infusion:
Dilute 15 mg in 500 mL 5% Dextrose Injection; may be concentrated to 15 mg propranolol in 250 mL 5% Dextrose Injection for fluid-restricted patients.
For adult patients, infuse at a rate of 2 to 3 mg/hour.
Adverse Reactions
AV block / Early / Incidence not known
bradycardia / Rapid / Incidence not known
heart failure / Delayed / Incidence not known
visual impairment / Early / Incidence not known
thrombosis / Delayed / Incidence not known
bronchospasm / Rapid / Incidence not known
coma / Early / Incidence not known
seizures / Delayed / Incidence not known
hyperkalemia / Delayed / Incidence not known
agranulocytosis / Delayed / Incidence not known
thrombotic thrombocytopenic purpura (TTP) / Delayed / Incidence not known
anaphylactoid reactions / Rapid / Incidence not known
erythema multiforme / Delayed / Incidence not known
laryngospasm / Rapid / Incidence not known
Stevens-Johnson syndrome / Delayed / Incidence not known
exfoliative dermatitis / Delayed / Incidence not known
toxic epidermal necrolysis / Delayed / Incidence not known
lupus-like symptoms / Delayed / Incidence not known
hypotension / Rapid / Incidence not known
hallucinations / Early / Incidence not known
memory impairment / Delayed / Incidence not known
confusion / Early / Incidence not known
depression / Delayed / Incidence not known
constipation / Delayed / Incidence not known
colitis / Delayed / Incidence not known
dyspnea / Early / Incidence not known
hypoglycemia / Early / Incidence not known
hyperglycemia / Delayed / Incidence not known
diabetes mellitus / Delayed / Incidence not known
hypertriglyceridemia / Delayed / Incidence not known
myopathy / Delayed / Incidence not known
elevated hepatic enzymes / Delayed / Incidence not known
impotence (erectile dysfunction) / Delayed / Incidence not known
penile fibrosis / Delayed / Incidence not known
psoriaform rash / Delayed / Incidence not known
psoriasis / Delayed / Incidence not known
sinus tachycardia / Rapid / Incidence not known
hypertension / Early / Incidence not known
palpitations / Early / Incidence not known
withdrawal / Early / Incidence not known
fatigue / Early / 5.0-7.0
dizziness / Early / 4.0-7.0
paresthesias / Delayed / Incidence not known
nightmares / Early / Incidence not known
emotional lability / Early / Incidence not known
agitation / Early / Incidence not known
irritability / Delayed / Incidence not known
insomnia / Early / Incidence not known
drowsiness / Early / Incidence not known
weakness / Early / Incidence not known
lethargy / Early / Incidence not known
vomiting / Early / Incidence not known
abdominal pain / Early / Incidence not known
anorexia / Delayed / Incidence not known
nausea / Early / Incidence not known
diarrhea / Early / Incidence not known
infection / Delayed / Incidence not known
cough / Delayed / Incidence not known
Peyronie's disease / Delayed / Incidence not known
alopecia / Delayed / Incidence not known
urticaria / Rapid / Incidence not known
pruritus / Rapid / Incidence not known
xerophthalmia / Early / Incidence not known
fever / Early / Incidence not known
pharyngitis / Delayed / Incidence not known
xerosis / Delayed / Incidence not known
diaphoresis / Early / Incidence not known
tremor / Early / Incidence not known
headache / Early / Incidence not known
Boxed Warning
Abrupt discontinuation of any chronically administered beta-adrenergic blocking agent, such as propranolol, can result in the exacerbation of angina and, in some cases, myocardial ischemia or myocardial infarction, ventricular arrhythmias, or severe hypertension, especially in patients with preexisting cardiac disease. If chronic, oral propranolol therapy is to be discontinued, gradually decrease the dosage over a minimum of 2 weeks. Downward titration of parenteral therapy may be advisable if the patient will discontinue propranolol treatment. Advise patients and caregivers against interruption or cessation of therapy without the advice of a physician. If exacerbation of angina occurs during discontinuation of therapy, it is advised to reinstitute propranolol therapy and take other measures appropriate for the management of unstable angina.
Common Brand Names
HEMANGEOL, Inderal, Inderal LA, Inderal XL, InnoPran XL
Dea Class
Rx
Description
Competitive, nonselective beta-blocker without intrinsic sympathomimetic activity
Used for many cardiac indications such as: angina, ventricular rate control, hypertension, PSVT, etc.
Also used for non-cardiac indications: migraine prophylaxis, tremor, infantile hemangioma
Dosage And Indications
Initially, 10 to 20 mg PO 2 to 4 times per day, then increase at 3 to 7 day intervals up to 160 to 320 mg/day, given in 2 to 4 divided doses. In geriatric patients, begin with conservative initial doses and titrate carefully; the elderly have unpredictable responses to beta-blockers.
80 mg PO once daily, then increase at 3 to 7 day intervals up to 160 to 320 mg PO once daily. In geriatric patients, begin with conservative initial doses and titrate carefully; the elderly have unpredictable responses to beta-blockers.
1 mg IV every 2 minutes as needed for up to 3 doses. The FDA-approved dosage is 1 to 3 mg IV every 2 minutes for 2 doses with further doses given after 4 hours or more. Reserve use for atrial fibrillation or flutter that is unresponsive to standard therapy or when more prolonged control is required. Guidelines recommend IV beta-blockers to slow the ventricular response to atrial fibrillation in the acute setting in the absence of pre-excitation and to slow rapid ventricular response with acute coronary syndrome and no heart failure, hemodynamic instability, or bronchospasm.
0.01 mg/kg/dose IV every 6 to 8 hours as needed. May titrate dosage gradually as needed for clinical effect. Max: 0.15 mg/kg/dose or 3 mg/dose, whichever is less.
0.01 mg/kg/dose IV every 6 to 8 hours as needed. May titrate dosage gradually as needed for clinical effect. Max: 0.15 mg/kg/dose or 1 mg/dose, whichever is less.
0.01 mg/kg/dose IV every 6 to 8 hours as needed. May titrate dosage gradually as needed for clinical effect. Max: 0.15 mg/kg/dose or 1 mg/dose, whichever is less.
10 to 40 mg PO 3 or 4 times daily. Guidelines recommend the use of beta blockers to control the ventricular rate for patients with paroxysmal, persistent, or permanent atrial fibrillation.
0.5 to 1 mg/kg/day PO divided every 6 to 8 hours, initially. Increase the dose by 1 mg/kg/day every 3 to 5 days as needed for clinical effect. Usual dose: 2 to 4 mg/kg/day. Max: 16 mg/kg/day or 60 mg/day, whichever is less. In older adolescents, 10 to 30 mg/dose PO every 6 to 8 hours may be given.
0.5 to 1 mg/kg/day PO divided every 6 to 8 hours, initially. Increase the dose by 1 mg/kg/day every 3 to 5 days as needed for clinical effect. Usual dose: 2 to 4 mg/kg/day. Max: 16 mg/kg/day or 60 mg/day, whichever is less.
1 mg IV every 2 minutes as needed for up to 3 doses. The FDA-approved dosage is 1 to 3 mg IV every 2 minutes for 2 doses with further doses given after 4 hours or more.
0.01 mg/kg/dose IV every 6 to 8 hours as needed. May titrate dosage gradually as needed for clinical effect. Max: 0.15 mg/kg/dose or 3 mg/dose, whichever is less.
0.01 mg/kg/dose IV every 6 to 8 hours as needed. May titrate dosage gradually as needed for clinical effect. Max: 0.15 mg/kg/dose or 1 mg/dose, whichever is less.
0.01 mg/kg/dose IV every 6 to 8 hours as needed. May titrate dosage gradually as needed for clinical effect. Max: 0.15 mg/kg/dose or 1 mg/dose, whichever is less.
10 mg PO 3 to 4 times daily, initially. Adjust dose as needed based on response. Max: 160 mg/day.
0.5 to 1 mg/kg/day PO divided every 6 to 8 hours, initially. Increase the dose by 1 mg/kg/day every 3 to 5 days as needed for clinical effect. Usual dose: 2 to 4 mg/kg/day. Max: 16 mg/kg/day or 60 mg/day, whichever is less. In older adolescents, 10 to 30 mg/dose PO every 6 to 8 hours may be given.
0.5 to 1 mg/kg/day PO divided every 6 to 8 hours, initially. Increase the dose by 1 mg/kg/day every 3 to 5 days as needed for clinical effect. Usual dose: 2 to 4 mg/kg/day. Max: 16 mg/kg/day or 60 mg/day, whichever is less.
60 mg PO once daily, initially. Adjust dose as needed based on response. Max: 160 mg/day.
NOTE: For ST-elevation myocardial infarction, oral beta-blocker therapy should be initiated in the first 24 hours for patients who do not have signs of cardiac failure, evidence of low output, increased risk for cardiogenic shock, or other contraindications for beta-blocker therapy.
Intravenous dosage Adults
0.1 mg/kg IV, administered in 3 equal divided doses at 2 to 3 minute intervals.
180 to 320 mg/day PO, given in 3 to 4 divided doses.
180 to 240 mg/day PO, given in 3 to 4 divided doses starting in the first 24 hours post-MI.
Initially, 40 mg PO twice daily, then increase at 3 to 7 day intervals up to 160 to 480 mg/day, given in 2 to 3 divided doses. Max: 640 mg/day. In geriatric patients, begin with conservative initial doses and titrate carefully; the elderly have unpredictable responses to beta-blockers.
Initially, 0.5 to 2 mg/kg/day PO in 2 to 4 divided doses. Titrate gradually every 3 to 7 days as needed for clinical effect; heart rate may be dose-limiting. Usual effective dosage is 1 to 6 mg/kg/day. Max: 8 mg/kg/day or 640 mg/day, whichever is less..
Initially, 0.25 mg/kg/dose PO every 6 to 8 hours. Titrate gradually as needed for clinical effect; heart rate may be dose-limiting. Max: 3.5 mg/kg/dose; others recommend a max of 5 mg/kg/day.
Initially, 80 mg PO once daily. Increase dosage at 3 to 7 day intervals up to 120 to 160 mg PO once daily. Max: 640 mg/day. In geriatric patients, begin with conservative initial doses and titrate carefully; the elderly have unpredictable responses to beta-blockers.
Initially, 80 mg PO once daily at bedtime (approximately 10 PM). If needed, increase dosage to 120 mg PO once daily at bedtime. Max: 120 mg/day. In geriatric patients, begin with conservative initial doses and titrate carefully; the elderly have unpredictable responses to beta-blockers.
Limited data suggest a continuous infusion of propranolol may be effective in post-surgical patients who cannot tolerate oral therapy. An infusion rate of 2 to 3 mg/hour achieved therapeutic propranolol serum levels within 3 hours. Continuous infusions were administered for up to 9 days.
0.01 mg/kg/dose slow IV push over 10 minutes, repeated every 6 to 8 hours as needed. Titrate gradually as needed for clinical effect; heart rate may be dose-limiting. Max: 0.15 mg/kg/dose.
20 to 40 mg PO 3 or 4 times daily. For geriatric patients, begin with low initial doses, followed by careful dosage titration; geriatric patients have unpredictable responses to beta-blockers.
80 to 160 mg PO once daily. For geriatric patients, begin with low initial doses, followed by careful dosage titration; geriatric patients have unpredictable responses to beta-blockers.
The usual dosage is 60 mg/day PO, given in divided doses for 3 days before surgery, in conjunction with an alpha-blocker. For the management of inoperable tumors, the usual dosage is 30 mg daily in divided doses as adjunctive therapy to alpha-adrenergic blockade. For geriatric patients, begin with low initial doses, followed by careful dosage titration; the elderly have unpredictable responses to beta-blockers.
0.6 to 3 mg/kg/day PO in 2 to 3 divided doses. Max: 120 mg/day. Pediatric patients receiving propranolol are possibly more likely than those receiving placebo to have at least a 50% reduction in headache frequency.[64586]
0.6 to 3 mg/kg/day PO in 2 to 3 divided doses. Max: 60 mg/day.[33312] [53692] [53693] [53694] [53695] [53696] Pediatric patients receiving propranolol are possibly more likely than those receiving placebo to have at least a 50% reduction in headache frequency.[64586]
80 mg/day PO in divided doses, initially. May increase the dose gradually as needed. Usual dose: 160 to 240 mg/day in divided doses. Discontinue if adequate results not achieved within 4 to 6 weeks. Guidelines classify propranolol as having established efficacy for migraine prophylaxis.[57981]
80 mg PO once daily, initially. May increase the dose gradually as needed. Usual dose: 160 to 240 mg/day. Discontinue if adequate results not achieved within 4 to 6 weeks. Guidelines classify propranolol as having established efficacy for migraine prophylaxis.[57981]
40 mg PO twice daily. Increase dose as needed to 120 to 320 mg/day PO given in 2 to 3 divided doses. In geriatric patients, begin with conservative initial doses and titrate carefully; geriatric patients have unpredictable responses to beta-blockers. Clinical practice guidelines consider propranolol effective for the treatment of essential tremor.
Limited data suggest 30 to 80 mg/day PO may be effective; the daily dose is divided into 3 or 4 doses for administration. A common starting dose is 10 mg PO 3 times daily. In a single-blind crossover comparison of propranolol and placebo in 10 patients with lithium-induced tremor, propranolol (30 to 80 mg/day PO) and placebo were administered during two 2-week periods, 1 week on propranolol and 1 on placebo in random order. In period 1, 8 patients reported a preference for propranolol over placebo and 5 patients in period 2 reported a preference for propranolol. Treatment with propranolol resulted in a reduction in the intensity of tremor from very troublesome or somewhat troublesome to noticeable but not troublesome or not present. No adverse reactions were reported with propranolol treatment. In a case report of 5 patients with lithium-induced tremor, treatment with propranolol 30 to 40 mg/day PO, in 3 or 4 divided doses, resulted in control of the tremor. Recurrence of the tremor was reported in 3 of the cases when propranolol therapy was discontinued. In geriatric patients, begin with conservative initial doses and titrate carefully; geriatric patients have unpredictable responses to beta-blockers.
Limited experience; dosage often not reported in the literature; efficacy rate of 50%, along with side effect profile may lead to pursuit of other treatment options. 0.5 to 1 mg/kg/day PO, given in 3 divided doses has been recommended by some experts as an initial dose. Titrate dosage gradually once weekly. Alternatively, 30 mg PO once daily, then increased to 30 mg PO twice daily has been effective in improving hand tremor. Many patients respond to a total daily dosage of 60 to 80 mg/day PO. Max: 4 mg/kg/day PO. Dosage may also be taken as needed 30 minutes prior to activities disrupted by essential tremor. Pharmacotherapy should be reserved for patients whose tremor is functionally or socially limiting. Once an optimal dosage is determined, patients may transition to an extended-release formulation of propranolol, to be given once daily. Many patients require larger doses after 1 year of therapy, due to drug tolerance and disease progression.
Limited experience; dosage often not reported in the literature; efficacy rate of 50%, along with side effect profile may lead to pursuit of other treatment options. 0.5 to 1 mg/kg/day PO, given in 3 divided doses has been recommended by some experts as an initial dose using immediate release dose forms. Titrate dosage gradually once weekly as necessary; many patients respond to a total daily dosage of 60 to 80 mg/day PO. Max: 4 mg/kg/day PO. Dosage may also be taken as needed 30 minutes prior to activities disrupted by essential tremor. Pharmacotherapy should be reserved for patients whose tremor is functionally or socially limiting; most do not require therapy until adolescence. Once an optimal dosage is determined, patients may transition to an extended-release formulation of propranolol, to be given once daily. Many patients require larger doses after 1 year of therapy, due to drug tolerance and disease progression.
To reduce the risk of hypoglycemia, administer propranolol immediately after or concurrently with a feeding. Avoid fasting; if inevitable, hold medication or support with a product such as Pedialyte or glucose-containing IV fluids. Vital signs and cardiorespiratory exam or ECG should be obtained at baseline. Obtain blood pressure and heart rate measurements at 1 and 2 hours after the initial dose and any significant dose increase (e.g., more than 0.5 mg/kg/day). Experts have recommended propranolol therapy continue until full involution of the lesion has occurred or the patient is at least 1 year of age; recurrences have been reported with early discontinuation. At the end of therapy, gradually taper propranolol over 2 to 4 weeks. If hemangiomas recur, treatment may reinitiated.
Oral dosage (FDA-approved dosage) Infants 5 weeks to 5 months at initiation
0.6 mg/kg/dose PO twice daily given at least 9 hours apart. After 1 week of treatment, increase dosage to 1.1 mg/kg/dose PO twice daily. After 2 weeks of treatment, increase dosage to 1.7 mg/kg/dose PO twice daily and maintain this dosage for 6 months. Readjust dosage periodically based on weight increases.
1 mg/kg/DAY PO initially, titrated to a target dose of 2 to 3 mg/kg/DAY, unless there are comorbidities (e.g., PHACE syndrome, progressive ulceration) or adverse reactions that require a lower dose. Administer in 2 to 3 divided doses; administer 3 times daily to minimize abrupt changes in blood pressure in high risk patients.[53721] [63864] [63885] Infantile hemangiomas often respond rapidly even to low doses of propranolol; dose escalation and optimal target dose should be based on individual patient response. Consensus guideline initiation protocols are based on corrected gestational age, social support status, and patient comorbidities affecting the cardiovascular or respiratory systems, and/or blood glucose maintenance. Inpatient initiation (neonates and infants younger than 8 weeks, inadequate social support, or comorbidities): 0.33 mg/kg/dose PO every 8 hours. If tolerated, increase dose to 0.66 mg/kg/dose PO every 8 hours and prepare for discharge. If the dose is not tolerated at any point in time, reduce the dosage and gradually increase to the target dose; it is recommended patients be discharged on a tolerated dose of at least 1 mg/kg/day. Outpatient initiation (infants older than 8 weeks and adequate social support): 0.33 mg/kg/dose PO given 3 times daily at least 6 hours apart. If tolerated for 3 to 7 days, increase dose to 0.5 mg/kg/dose PO given 3 times daily. If once again tolerated for 3 to 7 days, increase dose to 0.66 mg/kg/dose PO given 3 times daily. If the dose is not tolerated at any point in time, reduce the dosage and gradually increase to the target dose; consider a target dose of 1 mg/kg/day.[53721]
0.5 to 1 mg IV, followed in 1 to 2 hours by a switch to oral therapy. Per clinical practice guidelines, the intravenous dose can be reserved for high-risk patients and eliminated from the regimen in intermediate- and low-risk patients. In geriatric patients, use conservative dose; the elderly have unpredictable responses to beta-blockers.
40 to 80 mg PO every 6 to 8 hours; begin 1 to 2 hours after initial IV therapy. Per clinical practice guidelines, the intravenous dose can be reserved for high-risk patients and eliminated from the regimen in intermediate- and low-risk patients. In geriatric patients, begin with conservative initial doses and titrate carefully; the elderly have unpredictable responses to beta-blockers.
10 to 80 mg PO, given 1 hour prior to the anxiety-producing event. For geriatric patients, begin with low initial doses, followed by careful dosage titration; geriatric patients have unpredictable responses to beta-blockers.
10 to 40 mg PO every 6 to 8 hours.
2 mg/kg/day PO divided every 6 to 12 hours (Max: 40 mg/dose); occasionally higher doses are required. Flat doses of 20 to 40 mg PO every 6 to 8 hours have been used to treat older children with thyroid storm.
1 to 2 mg/kg/day PO divided doses every 6 to 12 hours; occasionally higher doses are required.[53710] [53711] [53712] [53713] [53714] [53785] [53786] [53787] [64934]
1 to 2 mg/kg/day PO divided doses every 6 to 12 hours; occasionally higher doses are required.
1 to 3 mg IV as a single dose.
10 to 40 mg PO every 6 to 8 hours.
60 to 80 mg PO every 4 hours.
1 to 2 mg IV every 15 minutes up to 10 mg.
Initially, 40 mg PO twice daily, then increase at 3 to 7 day intervals up to 160 to 480 mg/day PO to attain desired blood pressure response. For geriatric patients, begin with low initial doses, followed by careful dosage titration; geriatric patients have unpredictable responses to beta-blockers.
20 to 40 mg PO twice daily, initially. Increase the dose every 2 to 3 days until resting heart rate of 55 to 60 beats per minute with systolic blood pressure of 90 mmHg or more. Max: 320 mg/day in persons without ascites; 160 mg/day in persons with ascites. A non-selective beta-blocker, including propranolol, or endoscopic variceal ligation (EVL) is recommended to prevent first variceal hemorrhage (primary prophylaxis) in persons with medium/large esophageal varices or high-risk small esophageal varices, and the combination of propranolol plus EVL is recommended in the prevention of rebleeding (secondary prophylaxis).
Most of the literature describing positive outcomes in the treatment of chronic aggression with propranolol involved patients with co-existing organic brain disease or schizophrenia recalcitrant to other aggression modalities. For patients without preexisting cardiovascular disorders, some authors have suggested a beginning dose of 20 mg PO 3 times per day, increasing the total dose by 40 to 60 mg/day every 3 days. Mean dosages range from 160 to 320 mg/day. For geriatric patients, begin with low initial doses, followed by careful dosage titration; geriatric patients have unpredictable responses to beta-blockers.
1 mg/kg/day PO divided every 6 hours, initially. After 1 week, may titrate dose by 1 mg/kg/day every 24 hours as necessary. Average dose: 2.3 mg/kg/day (range: 0.8 to 5 mg/kg/day). Usual Max: 5 mg/kg/day. If the patient becomes refractory after initial control, may increase dose gradually to a maximum of 10 to 15 mg/kg/day; monitor heart size, heart rate, and cardiac contractility closely. Alternatively, 4 mg/kg/day PO divided every 6 hours has been used as an initial dose.
0.15 to 0.25 mg/kg/dose (Max: 1 mg/dose) IV; may repeat once. Alternatively, 0.01 to 0.02 mg/kg/dose IV has been used, reserving higher doses for refractory spells.
1 mg/kg/day PO, given in divided doses every 4 hours. Adjust dose as needed to achieve a target 20% reduction in heart rate from baseline to a maximum dose of 1.98 mg/kg/day. Median dose: 80 mg/day.
1 to 4 mg/kg/day PO, given in divided doses every 6 hours. Adjust dose as needed to decrease heart rate by 10% to 20% of the admission value or mean age-based population value. 4 mg/kg/day PO was the mean effective dose in an interim analysis of children (n = 90; mean age 7 +/- 5 years) with more than 30% total body surface area burns. Propranolol therapy began 96 hours postburn and continued for 1 year with few adverse effects. Propranolol therapy significantly reduced heart rate and resting energy expenditure, decreased truncal fat accumulation, prevented bone loss, and improved lean body mass accretion. Maximum dose not clearly defined; severely burned adult patients standardly receive 20 mg PO every 6 hours, with dosage titrated as needed.
Initially, 0.5 to 1 mg/kg/day PO, given in divided doses every 6 to 8 hours has been recommended for sympathetic inhibition. Titrate dosage gradually every 3 to 14 days to a target dose of 2 mg/kg/day PO (range: 1.5 to 3 mg/kg/day). Monitor heart rate and blood pressure.
10 to 40 mg PO every 6 hours.
60 to 160 mg PO every 12 hours.
1 to 3 mg IV every 5 minutes as needed up to a total of 5 mg.
†Indicates off-label use
Dosing Considerations
Since propranolol is primarily metabolized by the liver, initiate therapy at a reduced dosage for the specified indication; carefully titrate the dosage to attain the desired clinical goals.
Renal ImpairmentNo dosage adjustment needed.
Intermittent hemodialysis
No dosage adjustments are needed; propranolol is not significantly dialyzable.
Drug Interactions
Abiraterone: (Moderate) Monitor blood pressure and heart rate if coadministration of propranolol with abiraterone is necessary. Propranolol is a CYP2D6 substrate and abiraterone is a CYP2D6 inhibitor. Concomitant use may result in hypotension and bradycardia.
Acetaminophen; Aspirin, ASA; Caffeine: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Acetaminophen; Aspirin: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Acetaminophen; Aspirin; Diphenhydramine: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Adagrasib: (Moderate) Monitor for increased propranolol adverse reactions, including bradycardia and hypotension, during coadministration of adagrasib as concurrent use may increase propranolol exposure. Propranolol is a CYP2D6 substrate and adagrasib is moderate CYP2D6 inhibitor.
Adenosine: (Moderate) Use adenosine with caution in the presence of beta blockers due to the potential for additive or synergistic depressant effects on the sinoatrial and atrioventricular nodes.
Albuterol; Budesonide: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Aldesleukin, IL-2: (Moderate) Beta blockers may potentiate the hypotension seen with aldesleukin, IL 2.
Alemtuzumab: (Moderate) Alemtuzumab may cause hypotension. Careful monitoring of blood pressure and hypotensive symptoms is recommended especially in patients with ischemic heart disease and in patients on antihypertensive agents.
Alfentanil: (Moderate) Alfentanil may cause bradycardia. The risk of significant hypotension and/or bradycardia during therapy with alfentanil is increased in patients receiving beta-blockers.
Alfuzosin: (Moderate) The manufacturer warns that the combination of alfuzosin with antihypertensive agents has the potential to cause hypotension in some patients. Alfuzosin (2.5 mg, immediate-release) potentiated the hypotensive effects of atenolol (100 mg) in eight healthy young male volunteers. The Cmax and AUC of alfuzosin was increased by 28% and 21%, respectively. Alfuzosin increased the Cmax and AUC of atenolol by 26% and 14%, respectively. Significant reductions in mean blood pressure and in mean heart rate were reported with the combination.
Alogliptin; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Alpha-blockers: (Moderate) Orthostatic hypotension may be more likely if beta-blockers are coadministered with alpha-blockers.
Alpha-glucosidase Inhibitors: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Alprostadil: (Minor) The concomitant use of systemic alprostadil injection and antihypertensive agents, such as beta-clockers, may cause additive hypotension. Caution is advised with this combination. Systemic drug interactions with the urethral suppository (MUSE) or alprostadil intracavernous injection are unlikely in most patients because low or undetectable amounts of the drug are found in the peripheral venous circulation following administration. In those men with significant corpora cavernosa venous leakage, hypotension might be more likely. Use caution with in-clinic dosing for erectile dysfunction (ED) and monitor for the effects on blood pressure. In addition, the presence of medications in the circulation that attenuate erectile function may influence the response to alprostadil. However, in clinical trials with alprostadil intracavernous injection, anti-hypertensive agents had no apparent effect on the safety and efficacy of alprostadil.
Amifostine: (Major) Patients receiving beta-blockers should be closely monitored during amifostine infusions due to additive effects. Patients receiving amifostine at doses recommended for chemotherapy should have antihypertensive therapy interrupted 24 hours preceding administration of amifostine. If the antihypertensive cannot be stopped, patients should not receive amifostine.
Amiodarone: (Moderate) Concomitant administration of propranolol with amiodarone may cause additive electrophysiologic effects (slow sinus rate or worsen AV block), resulting in symptomatic bradycardia, sinus arrest, and atrioventricular block. This is particularly likely in patients with preexisting partial AV block or sinus node dysfunction. Because amiodarone is an inhibitor of CYP2D6, decreased clearance of propranolol, which is a CYP2D6 substrate, is also possible. Caution and close monitoring are recommended during coadministration; a dose reduction of one or both drugs may be needed based on response. It should be noted that post-hoc analysis of amiodarone therapy in patients after acute myocardial infarction in two clinical trials revealed that amiodarone in addition to a beta-blocker significantly lowered the incidence of cardiac and arrhythmic death or resuscitated cardiac arrest when compared with amiodarone or beta-blocker therapy alone.
Amlodipine: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
Amlodipine; Atorvastatin: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
Amlodipine; Benazepril: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
Amlodipine; Celecoxib: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
Amlodipine; Olmesartan: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
Amlodipine; Valsartan: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
Amlodipine; Valsartan; Hydrochlorothiazide, HCTZ: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
Amobarbital: (Moderate) Although concurrent use of amobarbital with antihypertensive agents may lead to hypotension, barbiturates, as a class, can enhance the hepatic metabolism of beta-blockers that are significantly metabolized by the liver. Beta-blockers that may be affected include betaxolol, labetalol, metoprolol, pindolol, propranolol, and timolol. Clinicians should closely monitor patients blood pressure during times of coadministration.
Antacids: (Moderate) Antacids may reduce the absorption of propranolol. The need to stagger doses of propranolol has not been established, but may be prudent. Monitor clinical response, and adjust propranolol dosage if needed to attain therapeutic goals.
Antithyroid agents: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.
Apalutamide: (Moderate) Monitor for decreased efficacy of propranolol if coadministration with apalutamide is necessary. Propranolol is a CYP2C19 substrate and apalutamide is a strong CYP2C19 inducer.
Apomorphine: (Moderate) Use of beta blockers and apomorphine together can increase the hypotensive effects of apomorphine. Monitor blood pressure regularly during use of this combination.
Apraclonidine: (Minor) Theoretically, additive blood pressure reductions could occur when apraclonidine is combined with antihypertensive agents.
Aripiprazole: (Minor) Aripiprazole may enhance the hypotensive effects of antihypertensive agents. It may be advisable to monitor blood pressure when these medications are coadministered.
Armodafinil: (Moderate) In vitro data indicate that armodafinil is an inhibitor of CYP2C19. In theory, dosage reductions may be required for drugs that are largely eliminated via CYP2C19 metabolism such as propranolol during coadministration with armodafinil.
Artemether; Lumefantrine: (Moderate) Lumefantrine is an inhibitor and propranolol is a substrate of the CYP2D6 isoenzyme; therefore, coadministration may lead to increased propranolol concentrations. Concomitant use warrants caution due to the potential for increased side effects.
Articaine; Epinephrine: (Moderate) Local anesthetics may cause additive hypotension in combination with antihypertensive agents. Thus, patients receiving antihypertensive agents may experience additive hypotensive effects.
Ascorbic Acid, Vitamin C: (Minor) Ascorbic acid may reduce the oral bioavailability of propranolol. Advise patients against taking large doses of ascorbic acid with doses of propranolol.
Asenapine: (Moderate) Secondary to alpha-blockade, asenapine can produce vasodilation that may result in additive effects during concurrent use of propranolol. The potential reduction in blood pressure can precipitate orthostatic hypotension and associated dizziness, tachycardia, and syncope. If concurrent use is necessary, patients should be counseled on measures to prevent orthostatic hypotension, such as sitting on the edge of the bed for several minutes prior to standing in the morning and rising slowly from a seated position. Close monitoring of blood pressure is recommended until the full effects of the combination therapy are known; the propranolol dosage may need to be adjusted.
Aspirin, ASA: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Aspirin, ASA; Butalbital; Caffeine: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Aspirin, ASA; Caffeine: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Aspirin, ASA; Caffeine; Orphenadrine: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Aspirin, ASA; Carisoprodol: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Aspirin, ASA; Carisoprodol; Codeine: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Aspirin, ASA; Citric Acid; Sodium Bicarbonate: (Major) Antacids may reduce the absorption of propranolol. The need to stagger doses of propranolol has not been established, but may be prudent. Monitor clinical response, and adjust propranolol dosage if needed to attain therapeutic goals. (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Aspirin, ASA; Dipyridamole: (Major) Beta-blockers should generally be withheld before dipyridamole-stress testing. Monitor the heart rate carefully following the dipyridamole injection. (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Aspirin, ASA; Omeprazole: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Aspirin, ASA; Oxycodone: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Atazanavir: (Moderate) Atazanavir can prolong the PR interval. Coadministration with other agents that prolong the PR interval, like beta blockers, may result in elevated risk of conduction disturbances and atrioventricular block.
Atazanavir; Cobicistat: (Moderate) Atazanavir can prolong the PR interval. Coadministration with other agents that prolong the PR interval, like beta blockers, may result in elevated risk of conduction disturbances and atrioventricular block. (Moderate) Coadministration of cobicistat (a CYP2D6 inhibitor) with beta-blockers metabolized by CYP2D6, such as propranolol, may result in elevated beta-blocker serum concentrations. If used concurrently, close clinical monitoring with appropriate beta-blocker dose reductions are advised.
Azelastine; Fluticasone: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Baclofen: (Moderate) Baclofen has been associated with hypotension. Concurrent use with baclofen and antihypertensive agents may result in additive hypotension. Dosage adjustments of the antihypertensive medication may be required.
Beclomethasone: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Berotralstat: (Moderate) Monitor for increased propranolol adverse reactions, including bradycardia and hypotension, during coadministration of berotralstat as concurrent use may increase propranolol exposure. Propranolol is a CYP2D6 substrate and berotralstat is moderate CYP2D6 inhibitor.
Beta-agonists: (Moderate) Beta-blockers will block the pulmonary effects of inhaled beta-agonists, and in some cases may exacerbate bronchospasm in patients with reactive airways. Beta-agonists can sometimes increase heart rate or have other cardiovascular effects, particularly when used in high doses or if hypokalemia is present. Use of a beta-1-selective (cardioselective) beta blocker is recommended whenever possible when this combination of drugs must be used together. Monitor the patient's lung and cardiovascular status closely. Beta-agonists and beta-blockers are pharmacologic opposites and will counteract each other to some extent when given concomitantly, especially when non-cardioselective beta blockers are used.
Betamethasone: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Bismuth Subsalicylate: (Moderate) Concurrent use of beta-blockers with bismuth subsalicylate and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Bismuth Subsalicylate; Metronidazole; Tetracycline: (Moderate) Concurrent use of beta-blockers with bismuth subsalicylate and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Bretylium: (Moderate) Bretylium and beta-blockers may have an additive effect when used concomitantly; monitor for hypotension or marked bradycardia, which may produce vertigo, syncope, or postural hypotension.
Brexpiprazole: (Moderate) Due to brexpiprazole's antagonism at alpha 1-adrenergic receptors, the drug may enhance the hypotensive effects of alpha-blockers and other antihypertensive agents.
Budesonide: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Budesonide; Formoterol: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Budesonide; Glycopyrrolate; Formoterol: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Bupivacaine Liposomal: (Major) Propranolol has been shown to significantly decrease the clearance of the amide local anesthetics (e.g., lidocaine, bupivacaine, and mepivacaine). Lidocaine and bupivacaine toxicity have been reported after coadministration with propranolol. The mechanism of the interaction between propranolol and lidocaine is thought to be due to propranolol-induced decreased hepatic blood flow causing decreased elimination of lidocaine. Local anesthetics may also cause additive hypotension in combination with antihypertensive agents. Use extreme caution with the concomitant use of bupivacaine and antihypertensive agents or rapid-onset vasodilators, such as nitrates. Peripheral vasodilation may occur after use of bupivacaine. Thus, patients receiving antihypertensive agents may experience additive hypotensive effects. Blood concentrations of local anesthetics achieved after therapeutic doses are associated with minimal change in peripheral vascular resistance. Higher blood concentrations of local anesthetics may occur due to inadvertent intravascular administration or repeated doses.
Bupivacaine: (Major) Propranolol has been shown to significantly decrease the clearance of the amide local anesthetics (e.g., lidocaine, bupivacaine, and mepivacaine). Lidocaine and bupivacaine toxicity have been reported after coadministration with propranolol. The mechanism of the interaction between propranolol and lidocaine is thought to be due to propranolol-induced decreased hepatic blood flow causing decreased elimination of lidocaine. Local anesthetics may also cause additive hypotension in combination with antihypertensive agents. Use extreme caution with the concomitant use of bupivacaine and antihypertensive agents or rapid-onset vasodilators, such as nitrates. Peripheral vasodilation may occur after use of bupivacaine. Thus, patients receiving antihypertensive agents may experience additive hypotensive effects. Blood concentrations of local anesthetics achieved after therapeutic doses are associated with minimal change in peripheral vascular resistance. Higher blood concentrations of local anesthetics may occur due to inadvertent intravascular administration or repeated doses.
Bupivacaine; Epinephrine: (Major) Propranolol has been shown to significantly decrease the clearance of the amide local anesthetics (e.g., lidocaine, bupivacaine, and mepivacaine). Lidocaine and bupivacaine toxicity have been reported after coadministration with propranolol. The mechanism of the interaction between propranolol and lidocaine is thought to be due to propranolol-induced decreased hepatic blood flow causing decreased elimination of lidocaine. Local anesthetics may also cause additive hypotension in combination with antihypertensive agents. Use extreme caution with the concomitant use of bupivacaine and antihypertensive agents or rapid-onset vasodilators, such as nitrates. Peripheral vasodilation may occur after use of bupivacaine. Thus, patients receiving antihypertensive agents may experience additive hypotensive effects. Blood concentrations of local anesthetics achieved after therapeutic doses are associated with minimal change in peripheral vascular resistance. Higher blood concentrations of local anesthetics may occur due to inadvertent intravascular administration or repeated doses.
Bupivacaine; Lidocaine: (Major) Drugs such as beta-blockers that decrease cardiac output reduce hepatic blood flow and thereby decrease lidocaine hepatic clearance. Also, opposing effects on conduction exist between lidocaine and beta-blockers while their effects to decrease automaticity may be additive. Propranolol has been shown to decrease lidocaine clearance and symptoms of lidocaine toxicity have been seen as a result of this interaction. This interaction is possible with other beta-blocking agents since most decrease hepatic blood flow. Monitoring of lidocaine concentrations is recommended during concomitant therapy with beta-blockers. (Major) Propranolol has been shown to significantly decrease the clearance of the amide local anesthetics (e.g., lidocaine, bupivacaine, and mepivacaine). Lidocaine and bupivacaine toxicity have been reported after coadministration with propranolol. The mechanism of the interaction between propranolol and lidocaine is thought to be due to propranolol-induced decreased hepatic blood flow causing decreased elimination of lidocaine. Local anesthetics may also cause additive hypotension in combination with antihypertensive agents. Use extreme caution with the concomitant use of bupivacaine and antihypertensive agents or rapid-onset vasodilators, such as nitrates. Peripheral vasodilation may occur after use of bupivacaine. Thus, patients receiving antihypertensive agents may experience additive hypotensive effects. Blood concentrations of local anesthetics achieved after therapeutic doses are associated with minimal change in peripheral vascular resistance. Higher blood concentrations of local anesthetics may occur due to inadvertent intravascular administration or repeated doses.
Bupivacaine; Meloxicam: (Major) Propranolol has been shown to significantly decrease the clearance of the amide local anesthetics (e.g., lidocaine, bupivacaine, and mepivacaine). Lidocaine and bupivacaine toxicity have been reported after coadministration with propranolol. The mechanism of the interaction between propranolol and lidocaine is thought to be due to propranolol-induced decreased hepatic blood flow causing decreased elimination of lidocaine. Local anesthetics may also cause additive hypotension in combination with antihypertensive agents. Use extreme caution with the concomitant use of bupivacaine and antihypertensive agents or rapid-onset vasodilators, such as nitrates. Peripheral vasodilation may occur after use of bupivacaine. Thus, patients receiving antihypertensive agents may experience additive hypotensive effects. Blood concentrations of local anesthetics achieved after therapeutic doses are associated with minimal change in peripheral vascular resistance. Higher blood concentrations of local anesthetics may occur due to inadvertent intravascular administration or repeated doses.
Bupropion: (Minor) Monitor for an increased incidence of propranolol-related adverse effects if bupropion and propranolol are used concomitantly. Coadministration of bupropion and propranolol may result in increased plasma concentrations of propranolol. Bupropion and hydroxybupropion, the major active metabolite, are inhibitors of CYP2D6 in vitro. Propranolol is a CYP2D6 substrate.
Bupropion; Naltrexone: (Minor) Monitor for an increased incidence of propranolol-related adverse effects if bupropion and propranolol are used concomitantly. Coadministration of bupropion and propranolol may result in increased plasma concentrations of propranolol. Bupropion and hydroxybupropion, the major active metabolite, are inhibitors of CYP2D6 in vitro. Propranolol is a CYP2D6 substrate.
Butalbital; Aspirin; Caffeine; Codeine: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Cabergoline: (Moderate) Cabergoline should be used cautiously with antihypertensive agents, including beta-blockers. Cabergoline has been associated with hypotension. Initial doses of cabergoline higher than 1 mg may produce orthostatic hypotension. It may be advisable to monitor blood pressure.
Calcium Carbonate: (Moderate) Antacids may reduce the absorption of propranolol. The need to stagger doses of propranolol has not been established, but may be prudent. Monitor clinical response, and adjust propranolol dosage if needed to attain therapeutic goals.
Calcium Carbonate; Famotidine; Magnesium Hydroxide: (Moderate) Antacids may reduce the absorption of propranolol. The need to stagger doses of propranolol has not been established, but may be prudent. Monitor clinical response, and adjust propranolol dosage if needed to attain therapeutic goals.
Calcium Carbonate; Magnesium Hydroxide: (Moderate) Antacids may reduce the absorption of propranolol. The need to stagger doses of propranolol has not been established, but may be prudent. Monitor clinical response, and adjust propranolol dosage if needed to attain therapeutic goals.
Calcium Carbonate; Magnesium Hydroxide; Simethicone: (Moderate) Antacids may reduce the absorption of propranolol. The need to stagger doses of propranolol has not been established, but may be prudent. Monitor clinical response, and adjust propranolol dosage if needed to attain therapeutic goals.
Calcium Carbonate; Simethicone: (Moderate) Antacids may reduce the absorption of propranolol. The need to stagger doses of propranolol has not been established, but may be prudent. Monitor clinical response, and adjust propranolol dosage if needed to attain therapeutic goals.
Calcium; Vitamin D: (Moderate) Antacids may reduce the absorption of propranolol. The need to stagger doses of propranolol has not been established, but may be prudent. Monitor clinical response, and adjust propranolol dosage if needed to attain therapeutic goals.
Canagliflozin; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Cannabidiol: (Moderate) Use caution when propranolol is administered with cannabidiol due to possible increased propranolol concentrations. Consider a dose reduction of propranolol as clinically appropriate, if adverse reactions occur when administered with cannabidiol. Propranolol is a CYP1A2 substrate and cannabidiol is a weak CYP1A2 inhibitor.
Capmatinib: (Moderate) Monitor for increased propranolol adverse reactions, including bradycardia and hypotension, during coadministration of capmatinib as concurrent use may increase propranolol exposure. Propranolol is a CYP1A2 substrate and capmatinib is moderate CYP1A2 inhibitor.
Carbidopa; Levodopa: (Moderate) Concomitant use of beta-blockers with levodopa can result in additive hypotensive effects.
Carbidopa; Levodopa; Entacapone: (Moderate) Concomitant use of beta-blockers with levodopa can result in additive hypotensive effects.
Cariprazine: (Moderate) Orthostatic vital signs should be monitored in patients who are at risk for hypotension, such as those receiving cariprazine in combination with antihypertensive agents. Atypical antipsychotics may cause orthostatic hypotension and syncope, most commonly during treatment initiation and dosage increases. Patients should be informed about measures to prevent orthostatic hypotension, such as sitting on the edge of the bed for several minutes prior to standing in the morning, or rising slowly from a seated position. Consider a cariprazine dose reduction if hypotension occurs.
Cenobamate: (Moderate) Monitor for increased propranolol adverse reactions, including bradycardia and hypotension, during coadministration of cenobamate as concurrent use may increase propranolol exposure. Propranolol is a CYP2C19 substrate and cenobamate is a moderate CYP2C19 inhibitor.
Ceritinib: (Major) Avoid concomitant use of ceritinib with propranolol if possible due to the risk of additive bradycardia. Both ceritinib and propranolol can cause bradycardia. An interruption of ceritinib therapy, dose reduction, or discontinuation of therapy may be necessary if bradycardia occurs.
Cevimeline: (Major) Cevimeline should be administered with caution to patients taking beta adrenergic antagonists, because of the possibility of conduction disturbances. Cevimeline can potentially alter cardiac conduction and/or heart rate. Patients with significant cardiovascular disease treated with beta-blockers may potentially be unable to compensate for transient changes in hemodynamics or rhythm induced by cevimeline. If use of these drugs together cannot be avoided, close monitoring of blood pressure, heart rate and cardiac function is advised.
Chloroprocaine: (Moderate) Local anesthetics may cause additive hypotension in combination with antihypertensive agents.
Chlorpromazine: (Moderate) Monitor for an increase in chlorpromazine and propranolol-related adverse effects during concomitant use. The concentrations of both medications may increase; concomitant use has been observed to increase propranolol concentrations by 70%,
Chlorthalidone; Clonidine: (Moderate) Monitor heart rate in patients receiving concomitant clonidine and agents known to affect sinus node function or AV nodal conduction (e.g., beta-blockers). Severe bradycardia resulting in hospitalization and pacemaker insertion has been reported during combination therapy with clonidine and other sympatholytic agents. Concomitant use of clonidine with beta-blockers can also cause additive hypotension. Beta-blockers should not be substituted for clonidine when modifications are made in a patient's antihypertensive regimen because beta-blocker administration during clonidine withdrawal can augment clonidine withdrawal, which may lead to a hypertensive crisis. If a beta-blocker is to be substituted for clonidine, clonidine should be gradually tapered and the beta-blocker should be gradually increased over several days to avoid the possibility of rebound hypertension; administration of beta-blockers during withdrawal of clonidine can precipitate severe increases in blood pressure as a result of unopposed alpha stimulation.
Cholestyramine: (Moderate) Absorption of propranolol may be reduced by concurrent administration with colestipol or cholestyramine. To minimize drug interactions, administer other drugs at least 1 hour before or at least 4 to 6 hours after the administration of cholestyramine.
Choline Salicylate; Magnesium Salicylate: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Ciclesonide: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Cimetidine: (Moderate) Monitor for increased propranolol adverse reactions, including bradycardia and hypotension, during coadministration of cimetidine as concurrent use may increase propranolol exposure. Propranolol is a CYP2D6 substrate and cimetidine is weak CYP2D6 inhibitor.
Cinacalcet: (Moderate) Monitor for increased propranolol adverse reactions, including bradycardia and hypotension, during coadministration of cinacalcet as concurrent use may increase propranolol exposure. Propranolol is a CYP2D6 substrate and cinacalcet is moderate CYP2D6 inhibitor.
Citalopram: (Minor) Citalopram mildly inhibits the hepatic CYP2D6 isoenzyme at therapeutic doses. This can result in increased concentrations of drugs metabolized via the same pathway, including propranolol. Increased serum levels of the beta-blockers could result in alterations in cardioselectivity or other clinical effects.
Clevidipine: (Moderate) Use clevidipine and propranolol with caution due to risk for additive negative effects on heart rate, AV conduction, and/or cardiac contractility.
Clobazam: (Moderate) A dosage reduction of CYP2D6 substrates, such as propranolol, may be necessary during co-administration of clobazam. Limited in vivo data suggest that clobazam is an inhibitor of CYP2D6. If propranolol is used in combination, it is advisable to monitor the patient for adverse reactions related to beta-blockers.
Clonidine: (Moderate) Monitor heart rate in patients receiving concomitant clonidine and agents known to affect sinus node function or AV nodal conduction (e.g., beta-blockers). Severe bradycardia resulting in hospitalization and pacemaker insertion has been reported during combination therapy with clonidine and other sympatholytic agents. Concomitant use of clonidine with beta-blockers can also cause additive hypotension. Beta-blockers should not be substituted for clonidine when modifications are made in a patient's antihypertensive regimen because beta-blocker administration during clonidine withdrawal can augment clonidine withdrawal, which may lead to a hypertensive crisis. If a beta-blocker is to be substituted for clonidine, clonidine should be gradually tapered and the beta-blocker should be gradually increased over several days to avoid the possibility of rebound hypertension; administration of beta-blockers during withdrawal of clonidine can precipitate severe increases in blood pressure as a result of unopposed alpha stimulation.
Clozapine: (Moderate) Clozapine used concomitantly with the antihypertensive agents can increase the risk and severity of hypotension by potentiating the effect of the antihypertensive drug.
Cobicistat: (Moderate) Coadministration of cobicistat (a CYP2D6 inhibitor) with beta-blockers metabolized by CYP2D6, such as propranolol, may result in elevated beta-blocker serum concentrations. If used concurrently, close clinical monitoring with appropriate beta-blocker dose reductions are advised.
Cocaine: (Major) Although beta-blockers are indicated to reduce cocaine-induced tachycardia, myocardial ischemia, and arrhythmias, concomitant use of cocaine and non-selective beta-adrenergic blocking agents, including ophthalmic preparations, can cause unopposed alpha-adrenergic activity, resulting in heart block, excessive bradycardia, or hypertension. In theory, the use of alpha-blocker and beta-blocker combinations or selective beta-blockers in low doses may not cause unopposed alpha stimulation in this situation. Labetalol, a beta-blocker with some alpha-blocking activity, has been used successfully to treat cocaine-induced hypertension. In addition, cocaine can reduce the therapeutic effects of beta-blockers.
Co-Enzyme Q10, Ubiquinone: (Moderate) Co-enzyme Q10, ubiquinone (CoQ10) may lower blood pressure. CoQ10 use in combination with antihypertensive agents may lead to additional reductions in blood pressure in some individuals. Patients who choose to take CoQ10 concurrently with antihypertensive medications should receive periodic blood pressure monitoring. Patients should be advised to inform their prescriber of their use of CoQ10.
Colestipol: (Moderate) Colestipol can bind with and possibly decrease the oral absorption of propranolol. To minimize drug interactions, administer other drugs at least 1 hour before or at least 4 to 6 hours after the administration of colestipol.
Corticosteroids: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Cortisone: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Crizotinib: (Major) Avoid coadministration of crizotinib with agents known to cause bradycardia, such as beta-blockers, to the extent possible due to the risk of additive bradycardia. If concomitant use is unavoidable, monitor heart rate and blood pressure regularly. An interruption of crizotinib therapy or dose adjustment may be necessary if bradycardia occurs.
Dacomitinib: (Moderate) Monitor for increased toxicity of propranolol if coadministered with dacomitinib. Coadministration may increase serum concentrations of propranolol. Propranolol is a CYP2D6 substrate; dacomitinib is a strong CYP2D6 inhibitor.
Dapagliflozin; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Darifenacin: (Moderate) Monitor for increased toxicity of propranolol if coadministered with darifenacin. Coadministration may increase serum concentrations of propranolol. Propranolol is a CYP2D6 substrate; darifenacin is a moderate CYP2D6 inhibitor.
Darunavir; Cobicistat: (Moderate) Coadministration of cobicistat (a CYP2D6 inhibitor) with beta-blockers metabolized by CYP2D6, such as propranolol, may result in elevated beta-blocker serum concentrations. If used concurrently, close clinical monitoring with appropriate beta-blocker dose reductions are advised.
Darunavir; Cobicistat; Emtricitabine; Tenofovir alafenamide: (Moderate) Coadministration of cobicistat (a CYP2D6 inhibitor) with beta-blockers metabolized by CYP2D6, such as propranolol, may result in elevated beta-blocker serum concentrations. If used concurrently, close clinical monitoring with appropriate beta-blocker dose reductions are advised.
Dasiglucagon: (Minor) A temporary increase in both blood pressure and pulse rate may occur following the administration of glucagon. Patients taking beta-blockers might be expected to have a greater increase in both pulse and blood pressure. Glucagon exerts positive inotropic and chronotropic effects and may, therefore, cause tachycardia and hypertension in some patients. The increase in blood pressure and pulse rate may require therapy in some patients with coronary artery disease.
Deflazacort: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Delavirdine: (Moderate) Propranolol is significantly metabolized by CYP2D6 isoenzymes and CYP2D6 inhibitors, such as delavirdine, could theoretically impair propranolol metabolism; the clinical significance of such interactions is unknown.
Desflurane: (Moderate) Concurrent use of beta-blockers with desflurane may result in exaggerated cardiovascular effects (e.g., hypotension and negative inotropic effects). Beta-blockers may be continued during general anesthesia as long as the patient is monitored for cardiac depressant and hypotensive effects. Withdrawal of a beta-blocker perioperatively may be detrimental to the patient's clinical status and is not recommended. Caution is advised if these drugs are administered together.
Desvenlafaxine: (Major) Dosage adjustments of some beta-blockers may be necessary during concurrent use of desvenlafaxine. Although clinical studies have shown that desvenlafaxine does not have a clinically relevant effect on CYP2D6 inhibition at doses of 100 mg/day, the manufacturer recommends that primary substrates of CYP2D6, such as propranolol, metoprolol, or nebivolol, be dosed at the original level when co-administered with desvenlafaxine 100 mg or lower or when desvenlafaxine is discontinued. The dose of these CYP2D6 substrates should be reduced by up to one-half if co-administered with desvenlafaxine 400 mg/day.
Dexamethasone: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Dexmedetomidine: (Moderate) Monitor blood pressure and heart rate during concomitant use of dexmedetomidine and beta-blockers due to the risk of additive bradycardia and hypotensive effects.
Dextromethorphan; Bupropion: (Minor) Monitor for an increased incidence of propranolol-related adverse effects if bupropion and propranolol are used concomitantly. Coadministration of bupropion and propranolol may result in increased plasma concentrations of propranolol. Bupropion and hydroxybupropion, the major active metabolite, are inhibitors of CYP2D6 in vitro. Propranolol is a CYP2D6 substrate.
Dextromethorphan; Quinidine: (Major) Patients receiving combined therapy with quinidine and propranolol should be monitored for potential hypotension, orthostasis, bradycardia and/or AV block and heart failure, Reduce the beta-blocker dosage if necessary. Quinidine may have additive effects (e.g., reduced heart rate, hypotension) on cardiovascular parameters when used together with beta-blockers, such as propranolol. Quinidine is a known inhibitor of CYP2D6, and may additionally impair the hepatic clearance of propanolol (CYP2D6 substrate); patients should be monitored for excess beta-blockade.
Diazoxide: (Moderate) Additive hypotensive effects can occur with the concomitant administration of diazoxide with other antihypertensive agent. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly. The manufacturer advises that IV diazoxide should not be administered to patients within 6 hours of receiving beta-blockers.
Digoxin: (Moderate) Monitor heart rate during concomitant digoxin and propranolol use due to increased risk for bradycardia. Both digoxin and propranolol slow atrioventricular conduction (AV) and decrease heart rate; additive effects on AV node conduction can result in bradycardia and advanced or complete heart block.
Dihydroergotamine: (Moderate) Monitor for an increase in the incidence and severity of vasospastic adverse reactions including cerebral and peripheral ischemia during concomitant use of ergotamine and propranolol. Propranolol may potentiate the vasoconstrictive action of ergotamine by blocking the vasodilating properties of epinephrine.
Diltiazem: (Major) Intravenous propranolol is contraindicated with intravenous diltiazem use in close proximity (within a few hours). Fatal cardiac arrests have occurred in patients receiving intravenous beta-blockers and intravenous calcium channel blockers. Use oral propranolol and oral diltiazem with caution due to risk for additive negative effects on heart rate, AV conduction, and/or cardiac contractility. If combination therapy is initiated or withdrawn in conjunction with propranolol, an adjustment in the propranolol dose may be warranted. Administration of diltiazem concomitantly with propranolol in 5 normal volunteers resulted in increased propranolol concentrations in all subjects, and bioavailability of propranolol was increased approximately 50%. In vitro, propranolol appears to be displaced from its binding sites by diltiazem.
Dipeptidyl Peptidase-4 Inhibitors: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Dipyridamole: (Major) Beta-blockers should generally be withheld before dipyridamole-stress testing. Monitor the heart rate carefully following the dipyridamole injection.
Disopyramide: (Major) Because the pharmacologic effects of propranolol include AV nodal conduction depression and negative inotropy, additive effects are possible when used in combination with disopyramide. Propranolol has occasionally been used with disopyramide; however, the manufacturer states that the concomitant use of disopyramide with propranolol should be reserved for patients with refractory life-threatening arrhythmias. Such use may produce serious negative inotropic effects, or may excessively prolong conduction. In healthy subjects, no significant drug interaction has been observed when propranolol is coadministered with disopyramide.
Donepezil: (Moderate) The increase in vagal tone induced by some cholinesterase inhibitors may produce bradycardia, hypotension, or syncope. The vagotonic effect of these drugs may be increased when given with other medications known to cause bradycardia such as beta-blockers. These interactions are pharmacodynamic in nature rather than pharmacokinetic.
Donepezil; Memantine: (Moderate) The increase in vagal tone induced by some cholinesterase inhibitors may produce bradycardia, hypotension, or syncope. The vagotonic effect of these drugs may be increased when given with other medications known to cause bradycardia such as beta-blockers. These interactions are pharmacodynamic in nature rather than pharmacokinetic.
Doxazosin: (Moderate) Orthostatic hypotension may be more likely if beta-blockers are coadministered with alpha-blockers.
Dronedarone: (Major) In dronedarone clinical trials, bradycardia was seen more frequently in patients also receiving beta blockers. If coadministration of dronedarone and a beta blocker is unavoidable, administer a low dose of the beta blocker initially and increase the dosage only after ECG verification of tolerability. Concomitant administration may decreased AV and sinus node conduction. Furthermore, dronedarone is an inhibitor of CYP2D6, and some beta blockers are substrates for CYP2D6 (e.g., metoprolol, propranolol, nebivolol, carvedilol). Coadministration of dronedarone with a single dose of propranolol and multiple doses of metoprolol increased propranolol and metoprolol exposure by 1.3- and 1.6-fold, respectively.
Dulaglutide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Duloxetine: (Moderate) Monitor blood pressure during concomitant duloxetine and propranolol use. Concomitant use increases the risk for hypotension, including orthostatic hypotension and syncope. Consider reducing the duloxetine dose or discontinuing duloxetine if symptomatic orthostatic hypotension, falls, or syncope occur during treatment.
Dutasteride; Tamsulosin: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Eletriptan: (Minor) Periodically monitor blood pressure in patients who regularly use eletriptan and are taking propranolol. Monitor for the rare patient who might experience an increase in dose-related side effects of eletriptan, such as nausea, dizziness, and drowsiness. No dosage adjustment appears to be needed for eletriptan. The Cmax and AUC of eletriptan were increased by 10 and 33%, respectively, in the presence of propranolol. No interactive increases in blood pressure were observed. The interaction should not be significant for most patients.
Eliglustat: (Moderate) Coadministration of propranolol and eliglustat may result in increased plasma concentrations of propranolol. Consider reducing the propranolol dosage and titrating to clinical effect. Propranolol is a CYP2D6 and P-glycoprotein (P-gp) substrate; eliglustat is a CYP2D6 and P-gp inhibitor.
Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Alafenamide: (Moderate) Coadministration of cobicistat (a CYP2D6 inhibitor) with beta-blockers metabolized by CYP2D6, such as propranolol, may result in elevated beta-blocker serum concentrations. If used concurrently, close clinical monitoring with appropriate beta-blocker dose reductions are advised.
Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Disoproxil Fumarate: (Moderate) Coadministration of cobicistat (a CYP2D6 inhibitor) with beta-blockers metabolized by CYP2D6, such as propranolol, may result in elevated beta-blocker serum concentrations. If used concurrently, close clinical monitoring with appropriate beta-blocker dose reductions are advised.
Empagliflozin; Linagliptin; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Empagliflozin; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Epoprostenol: (Moderate) Epoprostenol can have additive effects when administered with other antihypertensive agents, including beta-blockers. These effects can be used to therapeutic advantage, but dosage adjustments may be necessary.
Ergotamine: (Moderate) Monitor for an increase in the incidence and severity of vasospastic adverse reactions including cerebral and peripheral ischemia during concomitant use of ergotamine and propranolol. Propranolol may potentiate the vasoconstrictive action of ergotamine by blocking the vasodilating properties of epinephrine.
Ergotamine; Caffeine: (Moderate) Monitor for an increase in the incidence and severity of vasospastic adverse reactions including cerebral and peripheral ischemia during concomitant use of ergotamine and propranolol. Propranolol may potentiate the vasoconstrictive action of ergotamine by blocking the vasodilating properties of epinephrine.
Ertugliflozin; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate
Escitalopram: (Minor) Escitalopram modestly inhibits the hepatic CYP2D6 isoenzyme. This can result in increased concentrations of drugs metabolized via the same pathway, including propranolol. Increased serum levels of the beta-blockers could result in reductions in cardioselectivity.
Estradiol: (Minor) Estrogens can induce fluid retention and may increase blood pressure in some patients; patients who are receiving antihypertensive agents concurrently with hormonal contraceptives should be monitored for antihypertensive effectiveness.
Etomidate: (Major) General anesthetics can potentiate the antihypertensive effects of beta-blockers and can produce prolonged hypotension. Beta-blockers may be continued during general anesthesia as long as the patient is monitored for cardiac depressant and hypotensive effects.
Everolimus: (Moderate) Monitor for increased propranolol adverse reactions, including bradycardia and hypotension, during coadministration of everolimus as concurrent use may increase propranolol exposure. Propranolol is a CYP2D6 substrate and everolimus is a CYP2D6 inhibitor.
Exenatide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Ezetimibe; Simvastatin: (Minor) After administration of single doses of simvastatin and propranolol, there was a significant decrease in mean Cmax, with no change in AUC, of simvastatin. The clinical significance of this interaction is unknown. Monitor for potential reduced cholesterol-lowering efficacy when propranolol is coadministered with niacin; simvastatin.
Fedratinib: (Moderate) Monitor for increased propranolol adverse reactions including bradycardia and hypotension during coadministration of fedratinib. Propranolol exposure may increase. Fedratinib is a moderate CYP2D6 and CYP2C19 inhibitor and propranolol is a CYP2D6 and CYP2C19 substrate.
Fenofibric Acid: (Minor) At therapeutic concentrations, fenofibric acid is a weak inhibitor of CYP2C19. Concomitant use of fenofibric acid with CYP2C19 substrates, such as propranolol, has not been formally studied. Fenofibric acid may theoretically increase plasma concentrations of CYP2C19 substrates and could lead to toxicity for drugs that have a narrow therapeutic range. Monitor the therapeutic effect of propranolol during coadministration with fenofibric acid.
Fenoldopam: (Major) Avoid concomitant use of fenoldopam with beta-blockers due to the risk of hypotension. If used together, monitor blood pressure frequently. Beta-blockers may inhibit the sympathetic reflex response to fenoldopam.
Fingolimod: (Major) If possible, do not start fingolimod in a patient who is taking a drug that slows the heart rate or atrioventricular conduction such as beta-blockers. Use of these drugs during fingolimod initiation may be associated with severe bradycardia or heart block. Seek advice from the prescribing physician regarding the possibility to switch to drugs that do not slow the heart rate or atrioventricular conduction before initiating fingolimod. After the first fingolimod dose, overnight monitoring with continuous ECG in a medical facility is advised for patients who cannot stop taking drugs that slow the heart rate or atrioventricular conduction. Experience with fingolimod in patients receiving concurrent therapy with drugs that slow the heart rate or atrioventricular conduction is limited.
Fish Oil, Omega-3 Fatty Acids (Dietary Supplements): (Moderate) High doses of fish oil supplements may produce a blood pressure lowering effect It is possible that additive reductions in blood pressure may be seen when fish oils are used in a patient already taking antihypertensive agents.
Flecainide: (Moderate) Monitor heart rate during concomitant flecainide and propranolol use due to risk for additive negative inotropic effects.
Fludrocortisone: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Flunisolide: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Fluorescein: (Moderate) Patients on beta-blockers are at an increased risk of adverse reaction when administered fluorescein injection. It is thought that beta-blockers may worsen anaphylaxis severity by exacerbating bronchospasm or by increasing the release of anaphylaxis mediators; alternately, beta-blocker therapy may make the patient more pharmacodynamically resistance to epinephrine rescue treatment.
Fluoxetine: (Moderate) Monitor for increased propranolol adverse reactions, including bradycardia and hypotension, during coadministration of fluoxetine as concurrent use may increase propranolol exposure. Propranolol is a CYP2D6 substrate and fluoxetine is a moderate CYP2D6 inhibitor.
Fluticasone: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Fluticasone; Salmeterol: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Fluticasone; Umeclidinium; Vilanterol: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Fluticasone; Vilanterol: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Fluvoxamine: (Moderate) Fluvoxamine can also inhibit hepatic cytochrome P-450 isoenzymes and has been shown to interfere with propranolol clearance however clinical symptoms of excessive beta-blocker effects were not seen.
Food: (Major) Advise patients to avoid cannabis use during propranolol treatment due to decreased exposure of propranolol which may alter its efficacy. Cannabis use induces CYP1A2 and propranolol is a CYP1A2 substrate. The induction potential of cannabis is greatest with chronic inhalation. Other routes of administration or sporadic use may have less of an effect.
Formoterol; Mometasone: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Fosphenytoin: (Minor) Phenytoin has been shown to accelerate the hepatic metabolism of propranolol. Because fosphenytoin is metabolized to phenytoin, fosphenytoin will most likely also accelerate the hepatic metabolism of propranolol.
Gabapentin: (Minor) The combination of propranolol and gabapentin may induce dystonia via a pharmacodynamic interaction.
Galantamine: (Moderate) The increase in vagal tone induced by cholinesterase inhibitors, such as galantamine, may produce bradycardia or syncope. The vagotonic effect of galantamine may theoretically be increased when given with beta-blockers.
General anesthetics: (Major) General anesthetics can potentiate the antihypertensive effects of beta-blockers and can produce prolonged hypotension. Beta-blockers may be continued during general anesthesia as long as the patient is monitored for cardiac depressant and hypotensive effects.
Ginger, Zingiber officinale: (Minor) In vitro studies have demonstrated the positive inotropic effects of certain gingerol constituents of ginger; but it is unclear if whole ginger root exhibits these effects clinically in humans. It is theoretically possible that excessive doses of ginger could affect the action of inotropes; however, no clinical data are available.
Glipizide; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Glucagon: (Minor) A temporary increase in both blood pressure and pulse rate may occur following the administration of glucagon. Patients taking beta-blockers might be expected to have a greater increase in both pulse and blood pressure. Glucagon exerts positive inotropic and chronotropic effects and may, therefore, cause tachycardia and hypertension in some patients. The increase in blood pressure and pulse rate may require therapy in some patients with coronary artery disease.
Glyburide; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Guanfacine: (Moderate) Guanfacine can have additive effects when administered with other antihypertensive agents, including beta-blockers. These effects can be used to therapeutic advantage, but dosage adjustments may be necessary.
Haloperidol: (Moderate) Haloperidol should be used cautiously with propranolol due to the possibility of additive hypotension and increased concentrations of propranolol. Propranolol is significantly metabolized by CYP2D6 isoenzymes. A case report of 3 severe hypotension episodes (2 requiring cardiopulmonary resuscitation) has been reported in one 48 year old woman when propranolol and haloperidol have been coadministered. Additive hypotensive effects and haloperidol-mediated CYP2D6 inhibition may have contributed to this interaction.
Hydralazine; Isosorbide Dinitrate, ISDN: (Moderate) Nitroglycerin can cause hypotension. This action may be additive with other agents that can cause hypotension such as antihypertensive agents or other peripheral vasodilators. Patients should be monitored more closely for hypotension if nitroglycerin, including nitroglycerin rectal ointment, is used concurrently with any beta-blockers.
Hydrocortisone: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Icosapent ethyl: (Moderate) Beta-blockers may exacerbate hypertriglyceridemia and should be discontinued or changed to alternate therapy, if possible, prior to initiation of icosapent ethyl.
Iloperidone: (Moderate) Secondary to alpha-blockade, iloperidone can produce vasodilation that may result in additive effects during concurrent use with antihypertensive agents. The potential reduction in blood pressure can precipitate orthostatic hypotension and associated dizziness, tachycardia, and syncope. If concurrent use of iloperidone and antihypertensive agents is necessary, patients should be counseled on measures to prevent orthostatic hypotension, such as sitting on the edge of the bed for several minutes prior to standing in the morning and rising slowly from a seated position. Close monitoring of blood pressure is recommended until the full effects of the combination therapy are known.
Iloprost: (Moderate) Additive reductions in blood pressure may occur when inhaled iloprost is administered to patients receiving other antihypertensive agents.
Imatinib: (Moderate) Propranolol is significantly metabolized by CYP2D6 isoenzymes. CYP2D6 inhibitors, such as imatinib, could theoretically impair propranolol metabolism; the clinical significance of such interactions is unknown.
Incretin Mimetics: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Indocyanine Green: (Minor) In a study of 9 healthy adults given 0.5 mg/kg of indocyanine green, propranolol decreased clearance by 21%.
Insulin Degludec; Liraglutide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Insulin Glargine; Lixisenatide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Insulins: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Intravenous Lipid Emulsions: (Moderate) High doses of fish oil supplements may produce a blood pressure lowering effect It is possible that additive reductions in blood pressure may be seen when fish oils are used in a patient already taking antihypertensive agents.
Iobenguane I 131: (Major) Discontinue propranolol for at least 5 half-lives before the administration of the dosimetry dose or a therapeutic dose of iobenguane I-131. Do not restart propranolol until at least 7 days after each iobenguane I-131 dose. Drugs that reduce catecholamine uptake or deplete catecholamine stores, such as propranolol, may interfere with iobenguane I-131 uptake into cells and interfere with dosimetry calculations resulting in altered iobenguane I-131 efficacy.
Isocarboxazid: (Moderate) Additive hypotensive effects may be seen when monoamine oxidase inhibitors (MAOIs) are combined with antihypertensives. Careful monitoring of blood pressure is suggested during concurrent therapy of MAOIs with beta-blockers. Limited data suggest that bradycardia is worsened when MAOIs are administered to patients receiving beta-blockers. Although the sinus bradycardia observed was not severe, until more data are available, clinicians should use MAOIs cautiously in patients receiving beta-blockers. Patients should be instructed to rise slowly from a sitting position, and to report syncope or changes in blood pressure or heart rate to their health care provider.
Isoflurane: (Major) General anesthetics can potentiate the antihypertensive effects of beta-blockers and can produce prolonged hypotension. Beta-blockers may be continued during general anesthesia as long as the patient is monitored for cardiac depressant and hypotensive effects.
Isoniazid, INH; Pyrazinamide, PZA; Rifampin: (Moderate) Rifamycins are inducers of hepatic enzymes, and may alter the pharmacokinetics of beta-blockers including propranolol. Patients should be monitored for loss of propranolol effects if rifamycins are added.
Isoniazid, INH; Rifampin: (Moderate) Rifamycins are inducers of hepatic enzymes, and may alter the pharmacokinetics of beta-blockers including propranolol. Patients should be monitored for loss of propranolol effects if rifamycins are added.
Isosorbide Dinitrate, ISDN: (Moderate) Nitroglycerin can cause hypotension. This action may be additive with other agents that can cause hypotension such as antihypertensive agents or other peripheral vasodilators. Patients should be monitored more closely for hypotension if nitroglycerin, including nitroglycerin rectal ointment, is used concurrently with any beta-blockers.
Isosorbide Mononitrate: (Moderate) Nitroglycerin can cause hypotension. This action may be additive with other agents that can cause hypotension such as antihypertensive agents or other peripheral vasodilators. Patients should be monitored more closely for hypotension if nitroglycerin, including nitroglycerin rectal ointment, is used concurrently with any beta-blockers.
Isradipine: (Moderate) Although concomitant therapy with beta-blockers and isradipine is generally well tolerated and can even be beneficial in some cases, coadministration of these agents can induce excessive bradycardia or hypotension. Isradipine when used in combination with beta-blockers, especially in heart failure patients, can result in additive negative inotropic effects. Finally, angina has been reported when beta-adrenergic blocking agents are withdrawn abruptly when isradipine therapy is initiated. A gradual downward titration of the beta-adrenergic blocking agent dosage during initiation of isradipine therapy can minimize or eliminate this potential interaction. Patients should be monitored carefully, however, for excessive bradycardia, cardiac conduction abnormalities, or hypotension when these drugs are given together. In general, these reactions are more likely to occur with other non-dihydropyridine calcium channel blockers than with isradipine.
Ivabradine: (Moderate) Monitor heart rate if ivabradine is coadministered with other negative chronotropes like beta-blockers. Most patients receiving ivabradine will receive concomitant beta-blocker therapy. Coadministration of drugs that slow heart rate increases the risk for bradycardia.
Ketamine: (Major) General anesthetics can potentiate the antihypertensive effects of beta-blockers and can produce prolonged hypotension. Beta-blockers may be continued during general anesthesia as long as the patient is monitored for cardiac depressant and hypotensive effects.
Lacosamide: (Moderate) Use lacosamide with caution in patients taking concomitant medications that affect cardiac conduction, such as beta-blockers, because of the risk of AV block, bradycardia, or ventricular tachyarrhythmia. If use together is necessary, obtain an ECG prior to lacosamide initiation and after treatment has been titrated to steady-state. In addition, monitor patients receiving lacosamide via the intravenous route closely.
Lanreotide: (Moderate) Concomitant administration of bradycardia-inducing drugs (e.g., beta-adrenergic blockers) may have an additive effect on the reduction of heart rate associated with lanreotide. Adjust the beta-blocker dose if necessary.
Lasmiditan: (Moderate) Monitor heart rate if lasmiditan is coadministered with beta-blockers as concurrent use may increase the risk for bradycardia. Lasmiditan has been associated with lowering of heart rate. In a drug interaction study, addition of a single 200 mg dose of lasmiditan to a beta-blocker (propranolol) decreased heart rate by an additional 5 beats per minute.
Levamlodipine: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
Levodopa: (Moderate) Concomitant use of beta-blockers with levodopa can result in additive hypotensive effects.
Levothyroxine: (Minor) Because thyroid hormones cause cardiac stimulation including increased heart rate and increased contractility, the effects of beta-blockers may be reduced by thyroid hormones. The reduction of effects may be especially evident when a patient goes from a hypothyroid to a euthyroid state or when excessive amounts of thyroid hormone is given to the patient.
Levothyroxine; Liothyronine (Porcine): (Minor) Because thyroid hormones cause cardiac stimulation including increased heart rate and increased contractility, the effects of beta-blockers may be reduced by thyroid hormones. The reduction of effects may be especially evident when a patient goes from a hypothyroid to a euthyroid state or when excessive amounts of thyroid hormone is given to the patient.
Levothyroxine; Liothyronine (Synthetic): (Minor) Because thyroid hormones cause cardiac stimulation including increased heart rate and increased contractility, the effects of beta-blockers may be reduced by thyroid hormones. The reduction of effects may be especially evident when a patient goes from a hypothyroid to a euthyroid state or when excessive amounts of thyroid hormone is given to the patient.
Lidocaine: (Major) Drugs such as beta-blockers that decrease cardiac output reduce hepatic blood flow and thereby decrease lidocaine hepatic clearance. Also, opposing effects on conduction exist between lidocaine and beta-blockers while their effects to decrease automaticity may be additive. Propranolol has been shown to decrease lidocaine clearance and symptoms of lidocaine toxicity have been seen as a result of this interaction. This interaction is possible with other beta-blocking agents since most decrease hepatic blood flow. Monitoring of lidocaine concentrations is recommended during concomitant therapy with beta-blockers.
Lidocaine; Epinephrine: (Major) Drugs such as beta-blockers that decrease cardiac output reduce hepatic blood flow and thereby decrease lidocaine hepatic clearance. Also, opposing effects on conduction exist between lidocaine and beta-blockers while their effects to decrease automaticity may be additive. Propranolol has been shown to decrease lidocaine clearance and symptoms of lidocaine toxicity have been seen as a result of this interaction. This interaction is possible with other beta-blocking agents since most decrease hepatic blood flow. Monitoring of lidocaine concentrations is recommended during concomitant therapy with beta-blockers.
Lidocaine; Prilocaine: (Major) Drugs such as beta-blockers that decrease cardiac output reduce hepatic blood flow and thereby decrease lidocaine hepatic clearance. Also, opposing effects on conduction exist between lidocaine and beta-blockers while their effects to decrease automaticity may be additive. Propranolol has been shown to decrease lidocaine clearance and symptoms of lidocaine toxicity have been seen as a result of this interaction. This interaction is possible with other beta-blocking agents since most decrease hepatic blood flow. Monitoring of lidocaine concentrations is recommended during concomitant therapy with beta-blockers. (Moderate) Local anesthetics may cause additive hypotension in combination with antihypertensive agents.
Linagliptin; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Linezolid: (Moderate) Linezolid is an antibiotic that is also a reversible, non-selective MAO inhibitor. Bradycardia may be worsened when MAO-inhibitors are co-administered to patients receiving beta-blockers. Use linezolid cautiously in patients receiving beta-blockers.
Liothyronine: (Minor) Because thyroid hormones cause cardiac stimulation including increased heart rate and increased contractility, the effects of beta-blockers may be reduced by thyroid hormones. The reduction of effects may be especially evident when a patient goes from a hypothyroid to a euthyroid state or when excessive amounts of thyroid hormone is given to the patient.
Liraglutide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Lixisenatide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Lofexidine: (Major) Because both lofexidine and propranolol can cause hypotension and bradycardia, concurrent use should be avoided if possible. Patients being given lofexidine in an outpatient setting should be capable of and instructed on self-monitoring for hypotension, orthostasis, bradycardia, and associated symptoms. If clinically significant or symptomatic hypotension and/or bradycardia occur, the next dose of lofexidine should be reduced in amount, delayed, or skipped.
Lonafarnib: (Moderate) Monitor for increased propranolol adverse reactions, including bradycardia and hypotension, during coadministration of lonafarnib as concurrent use may increase propranolol exposure. Propranolol is a CYP2C19 substrate and lonafarnib is a moderate CYP2C19 inhibitor.
Lopinavir; Ritonavir: (Moderate) Concurrent administration of propranolol with ritonavir may result in elevated propranolol plasma concentrations. Cardiac and neurologic events have been reported when ritonavir is concurrently administered with beta-blockers. Propranolol is metabolized by the hepatic isoenzyme CYP2D6; ritonavir is an inhibitor of this enzyme. Caution and close monitoring are advised if these drugs are administered together. Decreased beta-blocker dosage may be needed.
Lumacaftor; Ivacaftor: (Minor) Concomitant use of propranolol and lumacaftor; ivacaftor may decrease the systemic exposure of propranolol; caution and monitoring of blood pressure and other therapeutic effects are advised if these drugs are used together. Propranolol is partially metabolized by CYP2C19; in vitro data suggest that lumacaftor may induce CYP2C19.
Lurasidone: (Moderate) Due to the antagonism of lurasidone at alpha-1 adrenergic receptors, the drug may enhance the hypotensive effects of alpha-blockers and other antihypertensive agents. If concurrent use of lurasidone and antihypertensive agents is necessary, patients should be counseled on measures to prevent orthostatic hypotension, such as sitting on the edge of the bed for several minutes prior to standing in the morning and rising slowly from a seated position. Close monitoring of blood pressure is recommended until the full effects of the combination therapy are known.
Magnesium Salicylate: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Mavacamten: (Moderate) Expect additive negative inotropic effects during concomitant use of mavacamten and beta-blockers. If concomitant therapy with beta-blockers is initiated, or if the dose is increased, monitor left ventricular ejection fraction closely until stable doses and clinical response have been achieved. Avoid concomitant use of mavacamten and a beta-blocker plus verapamil or diltiazem due to an increased risk of left ventricular systolic dysfunction and heart failure symptoms.
Mefloquine: (Major) Concurrent use of mefloquine and beta blockers can result in ECG abnormalities or cardiac arrest.
Meglitinides: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Mepivacaine: (Major) Propranolol has been shown to significantly decrease the clearance of the amide local anesthetics (e.g., lidocaine, bupivacaine, and mepivacaine). Lidocaine and bupivacaine toxicity have been reported after coadministration with propranolol. The mechanism of the interaction between propranolol and lidocaine is thought to be due to propranolol-induced decreased hepatic blood flow causing decreased elimination of lidocaine.
Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Metformin; Repaglinide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Metformin; Rosiglitazone: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Metformin; Saxagliptin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Metformin; Sitagliptin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Methacholine: (Moderate) Beta-blockers may impair reversal of methacholine-induced bronchoconstriction with an inhaled rapid-acting beta-agonist.
Methohexital: (Major) General anesthetics can potentiate the antihypertensive effects of beta-blockers and can produce prolonged hypotension.
Methylergonovine: (Moderate) Concurrent use of beta-blockers and ergot alkaloids should be approached with caution. Concomitant administration with beta-blockers may enhance the vasoconstrictive action of certain ergot alkaloids including dihydroergotamine, ergotamine, methylergonovine, and methysergide. The risk of peripheral ischemia, resulting in cold extremities or gangrene, has been reported to be increased when ergotamine or dihydroergotamine is coadministered with selected beta-blockers, including propranolol, a beta-blocker commonly used for migraine prophylaxis. However, the precise mechanism of these interactions remains elusive. Additionally, because of the potential to cause coronary vasospasm, these ergot alkaloids could antagonize the therapeutic effects of anti-anginal agents including beta-blockers; clinicians should keep in mind that ergot alkaloids are contraindicated for use in patients with coronary heart disease or hypertension.
Methylprednisolone: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Mexiletine: (Moderate) Mexiletine has been found to increase propranolol concentrations in patients receiving concomitant therapy. The significance of the elevated propranolol concentration is not known as beta-blockers have a wide therapeutic range. It may be prudent to monitor patients for adverse effects when mexiletine are combined with propranolol.
Milrinone: (Moderate) Concurrent administration of antihypertensive agents could lead to additive hypotension when administered with milrinone. Titrate milrinone dosage according to hemodynamic response.
Mirabegron: (Moderate) Mirabegron is a moderate CYP2D6 inhibitor. Exposure of drugs metabolized by CYP2D6 such as propranolol may be increased when co-administered with mirabegron. Propranolol is primarily metabolized by CYP2D6. Therefore, appropriate monitoring and dose adjustment may be necessary.
Modafinil: (Moderate) In vitro data indicate that modafinil is an inhibitor of CYP2C19. In theory, dosage reductions may be required for drugs that are largely eliminated via CYP2C19 metabolism such as propranolol during coadministration with modafinil.
Mometasone: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Nefazodone: (Minor) Although relatively infrequent, nefazodone may cause orthostatic hypotension in some patients; this effect may be additive with antihypertensive agents. Blood pressure monitoring and dosage adjustments of either drug may be necessary.
Nesiritide, BNP: (Major) The potential for hypotension may be increased when coadministering nesiritide with antihypertensive agents.
Neuromuscular blockers: (Moderate) Concomitant use of neuromuscular blockers and beta-blockers may prolong neuromuscular blockade.
Niacin, Niacinamide: (Moderate) Cutaneous vasodilation induced by niacin may become problematic if high-dose niacin is used concomitantly with other antihypertensive agents. This effect is of particular concern in the setting of acute myocardial infarction, unstable angina, or other acute hemodynamic compromise.
Niacin; Simvastatin: (Moderate) Cutaneous vasodilation induced by niacin may become problematic if high-dose niacin is used concomitantly with other antihypertensive agents. This effect is of particular concern in the setting of acute myocardial infarction, unstable angina, or other acute hemodynamic compromise. (Minor) After administration of single doses of simvastatin and propranolol, there was a significant decrease in mean Cmax, with no change in AUC, of simvastatin. The clinical significance of this interaction is unknown. Monitor for potential reduced cholesterol-lowering efficacy when propranolol is coadministered with niacin; simvastatin.
Nicardipine: (Moderate) Use propranolol and nicardipine with caution due to risk for additive negative effects on heart rate, AV conduction, and/or cardiac contractility. The mean Cmax and AUC of propranolol are increased by 80% and 47%, respectively, by coadministration of nicardipine.
Nifedipine: (Moderate) In general, concomitant therapy of nifedipine with beta-blockers is well tolerated and can even be beneficial in some cases (i.e., inhibition of nifedipine-induced reflex tachycardia by beta-blockade). Negative inotropic and/or chronotropic effects can be additive when these drugs are used in combination. Finally, angina has been reported when beta-adrenergic blocking agents are withdrawn abruptly and nifedipine therapy is initiated. A gradual downward titration of the beta-adrenergic blocking agent dosage during initiation of nifedipine therapy may minimize or eliminate this potential interaction. Hypotension and impaired cardiac performance can occur during coadministration of nifedipine with beta-blockers, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis. Monitor clinical response during coadministration; adjustment of nifedipine dosage may be needed during concurrent beta-blocker therapy.
Nimodipine: (Moderate) Nimodipine, a selective calcium-channel blocker, can enhance the antihypertensive effects of beta-blockers. Although often used together, concurrent use of calcium-channel blockers and beta-blockers may result in additive hypotensive, negative inotropic, and/or bradycardic effects in some patients.
Niraparib; Abiraterone: (Moderate) Monitor blood pressure and heart rate if coadministration of propranolol with abiraterone is necessary. Propranolol is a CYP2D6 substrate and abiraterone is a CYP2D6 inhibitor. Concomitant use may result in hypotension and bradycardia.
Nirmatrelvir; Ritonavir: (Moderate) Concurrent administration of propranolol with ritonavir may result in elevated propranolol plasma concentrations. Cardiac and neurologic events have been reported when ritonavir is concurrently administered with beta-blockers. Propranolol is metabolized by the hepatic isoenzyme CYP2D6; ritonavir is an inhibitor of this enzyme. Caution and close monitoring are advised if these drugs are administered together. Decreased beta-blocker dosage may be needed.
Nisoldipine: (Moderate) Concurrent use of nisoldipine with propranolol can be beneficial (i.e., inhibition of vasodilation-induced reflex tachycardia by beta-blockade); however, the additive negative inotropic and/or chronotropic effects can cause adverse effects, especially in patients with compromised ventricular function or conduction defects (e.g., sinus bradycardia or AV block). Pharmacokinetic interactions between nisoldipine and propranolol are variable and not significant. Propranolol attenuated the heart rate increase following the administration of immediate release nisoldipine.
Nitrates: (Moderate) Nitroglycerin can cause hypotension. This action may be additive with other agents that can cause hypotension such as antihypertensive agents or other peripheral vasodilators. Patients should be monitored more closely for hypotension if nitroglycerin, including nitroglycerin rectal ointment, is used concurrently with any beta-blockers.
Nitroglycerin: (Moderate) Nitroglycerin can cause hypotension. This action may be additive with other agents that can cause hypotension such as antihypertensive agents or other peripheral vasodilators. Patients should be monitored more closely for hypotension if nitroglycerin, including nitroglycerin rectal ointment, is used concurrently with any beta-blockers.
Nitroprusside: (Moderate) Additive hypotensive effects may occur when nitroprusside is used concomitantly with other antihypertensive agents. Dosages should be adjusted carefully, according to blood pressure.
Non-Ionic Contrast Media: (Moderate) Use caution when administering non-ionic contrast media to patients taking beta-blockers. Beta-blockers lower the threshold for and increase the severity of contrast reactions and reduce the responsiveness of treatment of hypersensitivity reactions with epinephrine.
Nonsteroidal antiinflammatory drugs: (Moderate) Monitor blood pressure during concomitant beta-blocker and nonsteroidal anti-inflammatory drug (NSAID) use. The antihypertensive effect of beta-blockers may be diminished by NSAIDs.
Octreotide: (Moderate) Monitor for bradycardia during concomitant use of beta-blockers and octreotide and adjust drug dosage based on response as appropriate. Both medications may cause bradycardia and concomitant use may increase bradycardia risk.
Olanzapine: (Moderate) Olanzapine may induce orthostatic hypotension and thus enhance the effects of antihypertensive agents.
Olanzapine; Fluoxetine: (Moderate) Monitor for increased propranolol adverse reactions, including bradycardia and hypotension, during coadministration of fluoxetine as concurrent use may increase propranolol exposure. Propranolol is a CYP2D6 substrate and fluoxetine is a moderate CYP2D6 inhibitor. (Moderate) Olanzapine may induce orthostatic hypotension and thus enhance the effects of antihypertensive agents.
Olanzapine; Samidorphan: (Moderate) Olanzapine may induce orthostatic hypotension and thus enhance the effects of antihypertensive agents.
Olmesartan; Amlodipine; Hydrochlorothiazide, HCTZ: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
Olopatadine; Mometasone: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Omeprazole; Amoxicillin; Rifabutin: (Moderate) Rifamycins are inducers of hepatic enzymes, and may alter the pharmacokinetics of beta-blockers including propranolol. Patients should be monitored for loss of propranolol effects if rifamycins are added.
Omeprazole; Sodium Bicarbonate: (Major) Antacids may reduce the absorption of propranolol. The need to stagger doses of propranolol has not been established, but may be prudent. Monitor clinical response, and adjust propranolol dosage if needed to attain therapeutic goals.
Oritavancin: (Moderate) Propranolol is metabolized by CYP2C19 and CYP2D6; oritavancin is a weak inhibitor of CYP2C19 and a weak CYP2D6 inducer. Coadministration may result in altered propranolol plasma concentrations. If these drugs are administered concurrently, blood pressure should be monitored closely.
Osilodrostat: (Moderate) Monitor for increased propranolol adverse reactions, including bradycardia and hypotension, during coadministration of osilodrostat as concurrent use may increase propranolol exposure. Propranolol is a CYP1A2 substrate and osilodrostat is a moderate CYP1A2 inhibitor.
Oxymetazoline: (Major) The vasoconstricting actions of oxymetazoline, an alpha adrenergic agonist, may reduce the antihypertensive effects produced by beta-blockers. If these drugs are used together, closely monitor for changes in blood pressure.
Ozanimod: (Moderate) Ozanimod may cause bradycardia and AV-conduction delays, which may be enhanced with the concomitant use of beta-blockers. If a calcium channel blocker that slows heart rate/cardiac conduction is also prescribed with ozanimod and a beta-blocker, a cardiologist should be consulted due to the likelyhood of additive effects.
Paliperidone: (Moderate) Paliperidone may cause orthostatic hypotension, thereby enhancing the hypotensive effects of antihypertensive agents. Orthostatic vital signs should be monitored in patients receiving paliperidone and beta-adrenergic blockers who are susceptible to hypotension.
Paroxetine: (Minor) Paroxetine impairs metabolism of the hepatic CYP2D6 isoenzyme pathway at therapeutic doses, resulting in substantial increases in concentrations of other drugs metabolized via the same pathway, including propranolol. Clinicians should use paroxetine cautiously with propranolol; downward dose adjustments of the beta-blocker may be required if paroxetine is initiated; alternatively an upward dose adjustment of the beta blocker may be needed if paroxetine is discontinued. Patients should be advised to report increased effects of these medications, including hypotension or increased dizziness to their health care professional.
Pasireotide: (Major) Pasireotide may cause a decrease in heart rate. Closely monitor patients who are also taking drugs associated with bradycardia such as beta-blockers. Dose adjustments of beta-blockers may be necessary.
Peginterferon Alfa-2b: (Moderate) Monitor for adverse effects associated with increased exposure to propranolol if peginterferon alfa-2b is coadministered. Peginterferon alfa-2b is a CYP2D6 inhibitor, while propranolol is a CYP2D6 substrate.
Pentoxifylline: (Moderate) Pentoxifylline has been used concurrently with antihypertensive drugs (beta blockers, diuretics) without observed problems. Small decreases in blood pressure have been observed in some patients treated with pentoxifylline; periodic systemic blood pressure monitoring is recommended for patients receiving concomitant antihypertensives. If indicated, dosage of the antihypertensive agents should be reduced.
Perindopril; Amlodipine: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
Perphenazine: (Moderate) Monitor for increased propranolol adverse reactions, including bradycardia and hypotension, during coadministration of perphenazine as concurrent use may increase propranolol exposure. Propranolol is a CYP2D6 substrate and perphenazine is weak CYP2D6 inhibitor.
Perphenazine; Amitriptyline: (Moderate) Monitor for increa sed propranolol adverse reactions, including bradycardia and hypotension, during coadministration of perphenazine as concurrent use may increase propranolol exposure. Propranolol is a CYP2D6 substrate and perphenazine is weak CYP2D6 inhibitor.
Phenelzine: (Moderate) Careful monitoring of blood pressure is suggested during concurrent therapy of MAOIs with beta-blockers. Additive hypotensive effects may be seen when phenelzine is combined with antihypertensives. Limited data suggest that bradycardia is worsened when MAOIs are administered to patients receiving beta-blockers. Although the sinus bradycardia observed was not severe, until more data are available, clinicians should use MAOIs cautiously in patients receiving beta-blockers. Patients should be instructed to rise slowly from a sitting position, and to report syncope or changes in blood pressure or heart rate to their health care provider.
Phenoxybenzamine: (Moderate) Orthostatic hypotension may be more likely if beta-blockers are coadministered with alpha-blockers.
Phentolamine: (Moderate) Orthostatic hypotension may be more likely if beta-blockers are coadministered with alpha-blockers.
Phenytoin: (Minor) Phenytoin is an inducer of hepatic enzymes, and has been shown to accelerate the hepatic metabolism of propranolol.
Pilocarpine: (Moderate) Systemically administered pilocarpine (e.g., when used for the treatment of xerostomia or xerophthalmia) should be administered with caution in patients taking beta-blockers because of the possibility of cardiac conduction disturbances. The risk of conduction disturbances with beta-blockers and ophthalmically administered pilocarpine is low.
Pioglitazone; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Ponesimod: (Moderate) Monitor for decreases in heart rate if concomitant use of ponesimod and beta-blockers is necessary. Consider a temporary interruption in beta-blocker therapy before initiating ponesimod in patients with a resting heart rate less than or equal to 55 bpm. Beta-blocker treatment can be initiated in patients receiving stable doses of ponesimod. Concomitant use of another beta-blocker with ponesimod resulted in a mean decrease in heart rate of 12.4 bpm after the first dose of ponesimod and 7.4 bpm after beginning maintenance ponesimod.
Pramlintide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Prazosin: (Moderate) Orthostatic hypotension may be more likely if beta-blockers are coadministered with alpha-blockers.
Prednisolone: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Prednisone: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Prilocaine: (Moderate) Local anesthetics may cause additive hypotension in combination with antihypertensive agents.
Prilocaine; Epinephrine: (Moderate) Local anesthetics may cause additive hypotension in combination with antihypertensive agents.
Primidone: (Moderate) Barbiturates can enhance the hepatic metabolism of beta-blockers that are significantly metabolized by the liver, such as propranolol. Clinicians should monitor patients for loss of beta-blockade.
Procainamide: (Major) High or toxic concentrations of procainamide may prolong AV nodal conduction time or induce AV block; these effects could be additive with the pharmacologic actions of beta-blockers, like propranolol. In general, patients receiving combined therapy with procainamide and beta-blockers should be monitored for potential bradycardia, AV block, and/or hypotension. Procainamide's elimination half-life was not significantly changed when administered concomitantly with propranolol.
Propafenone: (Major) Pharmacologically, beta-blockers, like propranolol, cause AV nodal conduction depression and additive effects are possible when used in combination with propafenone. When used together, AV block can occur. Additionally, propafenone, a CYP2D6 inhibitor, appears to inhibit the metabolism of propranolol. Coadministration of propafenone with propranolol increases the plasma concentrations and prolongs the elimination half-life of propranolol; these affects were associated with a 15% decrease in diastolic blood pressure. Patients should be monitored closely and a reduction in the dosage of propranolol may be indicated.
Propofol: (Major) General anesthetics can potentiate the antihypertensive effects of beta-blockers and can produce prolonged hypotension. Beta-blockers may be continued during general anesthesia as long as the patient is monitored for cardiac depressant and hypotensive effects.
Quinidine: (Major) Patients receiving combined therapy with quinidine and propranolol should be monitored for potential hypotension, orthostasis, bradycardia and/or AV block and heart failure, Reduce the beta-blocker dosage if necessary. Quinidine may have additive effects (e.g., reduced heart rate, hypotension) on cardiovascular parameters when used together with beta-blockers, such as propranolol. Quinidine is a known inhibitor of CYP2D6, and may additionally impair the hepatic clearance of propanolol (CYP2D6 substrate); patients should be monitored for excess beta-blockade.
Quinine: (Minor) Propranolol is significantly metabolized by CYP2D6 isoenzymes. CYP2D6 inhibitors, such as quinine, could theoretically impair propranolol metabolism; the clinical significance of such interactions is unknown.
Ranolazine: (Moderate) Propranolol is metabolized by CYP2D6 isoenzymes. CYP2D6 inhibitors, such as ranolazine, could theoretically impair propranolol metabolism. Lower doses of some CYP2D6 substrates than are usually prescribed may be needed during therapy with ranolazine; monitor therapeutic response during coadministration.
Rasagiline: (Moderate) Additive hypotensive effects may be seen when monoamine oxidase inhibitors (MAOIs) are combined with antihypertensives. Careful monitoring of blood pressure is suggested during concurrent therapy of MAOIs with beta-blockers. Limited data suggest that bradycardia is worsened when MAOIs are administered to patients receiving beta-blockers. Although the sinus bradycardia observed was not severe, until more data are available, clinicians should use MAOIs cautiously in patients receiving beta-blockers. Patients should be instructed to rise slowly from a sitting position, and to report syncope or changes in blood pressure or heart rate to their health care provider.
Remifentanil: (Moderate) The risk of significant hypotension and/or bradycardia during therapy with remifentanil may be increased in patients receiving beta-blockers or calcium-channel blockers due to additive hypotensive effects.
Rifabutin: (Moderate) Rifamycins are inducers of hepatic enzymes, and may alter the pharmacokinetics of beta-blockers including propranolol. Patients should be monitored for loss of propranolol effects if rifamycins are added.
Rifampin: (Moderate) Rifamycins are inducers of hepatic enzymes, and may alter the pharmacokinetics of beta-blockers including propranolol. Patients should be monitored for loss of propranolol effects if rifamycins are added.
Rifamycins: (Moderate) Rifamycins are inducers of hepatic enzymes, and may alter the pharmacokinetics of beta-blockers including propranolol. Patients should be monitored for loss of propranolol effects if rifamycins are added.
Rifapentine: (Moderate) Rifamycins are inducers of hepatic enzymes, and may alter the pharmacokinetics of beta-blockers including propranolol. Patients should be monitored for loss of propranolol effects if rifamycins are added.
Risperidone: (Moderate) Risperidone may induce orthostatic hypotension and thus enhance the hypotensive effects of propranolol. Lower initial doses or slower dose titration of risperidone may be necessary in patients receiving propranolol concomitantly.
Ritlecitinib: (Moderate) Monitor for increased propranolol adverse reactions, including bradycardia and hypotension, during coadministration of ritlecitinib as concurrent use may increase propranolol exposure. Propranolol is a CYP1A2 substrate and ritlecitinib is moderate CYP1A2 inhibitor.
Ritonavir: (Moderate) Concurrent administration of propranolol with ritonavir may result in elevated propranolol plasma concentrations. Cardiac and neurologic events have been reported when ritonavir is concurrently administered with beta-blockers. Propranolol is metabolized by the hepatic isoenzyme CYP2D6; ritonavir is an inhibitor of this enzyme. Caution and close monitoring are advised if these drugs are administered together. Decreased beta-blocker dosage may be needed.
Rivastigmine: (Moderate) The increase in vagal tone induced by some cholinesterase inhibitors may produce bradycardia, hypotension, or syncope. The vagotonic effect of these drugs may theoretically be increased when given with other medications known to cause bradycardia such as beta-blockers.
Rizatriptan: (Major) Recommendations for concomitant use of rizatriptan and propranolol vary by dosage form. Concomitant use of rizatriptan oral film and propranolol is contraindicated, and a dosage reduction may be necessary for rizatriptan oral tablets. Limit the rizatriptan dose to 5 mg/dose and 15 mg/24 hours for adults receiving rizatriptan tablets. Avoid use of rizatriptan tablets in pediatric patients weighing less than 40 kg and limit the rizatriptan dose to 5 mg/24 hours in pediatric patients weighing 40 kg or more. Rizatriptan oral film is contraindicated with propranolol because a dose adjustment is not possible. Coadministration has been observed to increase rizatriptan overall exposure by 70% without affecting concentrations of the active N-monodesmethyl metabolite.
Rolapitant: (Major) Use caution if propranolol and rolapitant are used concurrently, and monitor for propranolol-related adverse effects, including bradycardia. Propranolol is a CYP2D6 substrate that is individually dose-titrated, and rolapitant is a moderate CYP2D6 inhibitor; the inhibitory effect of rolapitant is expected to persist beyond 28 days for an unknown duration. Exposure to another CYP2D6 substrate, following a single dose of rolapitant increased about 3-fold on Days 8 and Day 22. The inhibition of CYP2D6 persisted on Day 28 with a 2.3-fold increase in the CYP2D6 substrate concentrations, the last time point measured.
Ropivacaine: (Moderate) Local anesthetics may cause additive hypotension in combination with antihypertensive agents.
Rucaparib: (Moderate) Monitor patients for hypotension and bradycardia if coadministration of propranolol with rucaparib is necessary. Propranolol is a CYP1A2 substrate and rucaparib is a moderate CYP1A2 inhibitor. Concomitant use of CYP1A2 inhibitors may increase exposure to propranolol.
Salsalate: (Moderate) Concurrent use of beta-blockers with salsalate and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
Semaglutide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Sevoflurane: (Major) General anesthetics can potentiate the antihypertensive effects of beta-blockers and can produce prolonged hypotension. Beta-blockers may be continued during general anesthesia as long as the patient is monitored for cardiac depressant and hypotensive effects.
SGLT2 Inhibitors: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Silodosin: (Moderate) During clinical trials with silodosin, the incidence of dizziness and orthostatic hypotension was higher in patients receiving concomitant antihypertensive treatment. Thus, caution is advisable when silodosin is administered with antihypertensive agents. In addition, increased concentrations of silodosin may occur if it is coadministered with carvedilol; exercise caution. Carvedilol is a P-glycoprotein (P-gp) inhibitor and silodosin is a P-gp substrate.
Simvastatin: (Minor) After administration of single doses of simvastatin and propranolol, there was a significant decrease in mean Cmax, with no change in AUC, of simvastatin. The clinical significance of this interaction is unknown. Monitor for potential reduced cholesterol-lowering efficacy when propranolol is coadministered with niacin; simvastatin.
Siponimod: (Moderate) Monitor for significant bradycardia with coadministration of siponimod and beta-blockers, as additive lowering effects on heart rate may occur; temporary interruption of beta-blocker treatment may be necessary prior to siponimod initiation. Beta-blocker treatment can be initiated in patients receiving stable doses of siponimod.
Sodium Bicarbonate: (Major) Antacids may reduce the absorption of propranolol. The need to stagger doses of propranolol has not been established, but may be prudent. Monitor clinical response, and adjust propranolol dosage if needed to attain therapeutic goals.
Sufentanil: (Moderate) The incidence and degree of bradycardia and hypotension during induction with sufentanil may be increased in patients receiving beta-blockers.
Sulfonylureas: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Sympathomimetics: (Moderate) Monitor hemodynamic parameters and for loss of efficacy during concomitant sympathomimetic agent and beta-blocker use; dosage adjustments may be necessary. Concomitant use may antagonize the cardiovascular effects of either drug.
Tamsulosin: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Tasimelteon: (Moderate) Advise patients to administer the beta-blocker in the morning if tasimelteon is used concomitantly. Nighttime administration of a beta-blocker may reduce the efficacy of tasimelteon by decreasing the production of melatonin via inhibition of beta1 receptors.
Telmisartan; Amlodipine: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
Terazosin: (Moderate) Orthostatic hypotension may be more likely if beta-blockers are coadministered with alpha-blockers.
Terbinafine: (Minor) Propranolol is significantly metabolized by CYP2D6 isoenzymes. CYP2D6 inhibitors, such as terbinafine, could theoretically impair propranolol metabolism.
Tetrabenazine: (Moderate) Tetrabenazine may induce orthostatic hypotension and thus enhance the hypotensive effects of antihypertensive agents. Lower initial doses or slower dose titration of tetrabenazine may be necessary in patients receiving antihypertensive agents concomitantly.
Tetracaine: (Moderate) Local anesthetics may cause additive hypotension in combination with antihypertensive agents. Use caution with the concomitant use of tetracaine and antihypertensive agents.
Thalidomide: (Moderate) Thalidomide and other agents that slow cardiac conduction such as beta-blockers should be used cautiously due to the potential for additive bradycardia.
Theophylline, Aminophylline: (Major) Propranolol may significantly decrease aminophylline clearance by inhibiting CYP1A2. In some patients, theophylline levels can increase up to 100%. On average, co-administration of theophylline with propranolol decreases theophylline oral clearance by 30% to 52%. If aminophylline is being initiated in a patient who is already taking a drug that inhibits its clearance, the dose required to achieve a therapeutic serum theophylline concentration will be smaller. Patients should be closely monitored for toxicity. Serum theophylline concentrations should be monitored. Because propranolol is non-selective, the beta-2 blocking activity may reduce the effectiveness of aminophylline and other treatments for asthma or COPD. Discontinuation of a concomitant drug that inhibits aminophylline clearance will result in decreased serum theophylline concentrations, unless the aminophylline dose is appropriately increased. (Major) Propranolol may significantly decrease theophylline clearance by inhibiting CYP1A2. In some patients, theophylline levels can increase up to 100%. On average, co-administration of theophylline with propranolol decreases theophylline oral clearance by 30% to 52%. If theophylline is being initiated in a patient who is already taking a drug that inhibits its clearance, the dose of theophylline required to achieve a therapeutic theophylline concentration will be smaller. Patients should be closely monitored for toxicity. Serum theophylline concentrations should be monitored. Because propranolol is non-selective, the beta-2 blocking activity may reduce the effectiveness of theophylline and other treatments for asthma or COPD. Discontinuation of a concomitant drug that inhibits theophylline clearance will result in decreased theophylline concentrations, unless the theophylline dose is appropriately increased.
Thiazolidinediones: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Thioridazine: (Contraindicated) Coadministration of thioridazine and propranolol is contraindicated due to the potential for increased thioridazine exposure. Increased plasma concentrations of thioridazine are expected to increase the prolongation of the QTc interval associated with thioridazine and may increase the risk of serious, potentially fatal, cardiac arrhythmias, such as torsade de pointes type arrhythmias. Propranolol has been observed to increase thioridazine exposure by 370%.
Thiothixene: (Moderate) Thiothixene should be used cautiously in patients receiving antihypertensive agents. Additive hypotensive effects are possible.
Thyroid hormones: (Minor) Because thyroid hormones cause cardiac stimulation including increased heart rate and increased contractility, the effects of beta-blockers may be reduced by thyroid hormones. The reduction of effects may be especially evident when a patient goes from a hypothyroid to a euthyroid state or when excessive amounts of thyroid hormone is given to the patient.
Tirzepatide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
Tizanidine: (Moderate) Concurrent use of tizanidine with antihypertensive agents can result in significant hypotension. Caution is advised when tizanidine is to be used in patients receiving concurrent antihypertensive therapy.
Tobacco: (Major) Advise patients to avoid smoking tobacco while taking propranolol. Smoking tobacco has been observed to decrease propranolol exposure by approximately 50% and may decrease efficacy.
Trandolapril; Verapamil: (Major) Intravenous propranolol is contraindicated with intravenous verapamil use in close proximity (within a few hours). Fatal cardiac arrests have occurred in patients receiving intravenous beta-blockers and intravenous calcium channel blockers. Use oral propranolol and oral verapamil with caution and close monitoring due to risk for additive negative effects on heart rate, AV conduction, and/or cardiac contractility. There have been reports of excess bradycardia and AV block, including complete heart block, when beta-blockers and verapamil have been used for the treatment of hypertension. A decrease in propranolol clearance has been observed when administered concomitantly with verapamil.
Tranylcypromine: (Major) Avoid concomitant use of beta-blockers and tranylcypromine due to the risk of additive hypotension and/or severe bradycardia. Potential for this interaction persists for up to 10 days after discontinuation of tranylcypromine (or 4 to 5 half-lives after discontinuation of the beta-blocker). If a medication-free interval is not feasible, initiate therapy at the lowest appropriate dose and monitor blood pressure and heart rate closely.
Trazodone: (Minor) Due to additive hypotensive effects, patients receiving antihypertensive agents concurrently with trazodone may have excessive hypotension. Decreased dosage of the antihypertensive agent may be required when given with trazodone.
Triamcinolone: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Trifluoperazine: (Moderate) Monitor for an increase in trifluoperazine and propranolol-related adverse effects during concomitant use. The concentrations of both medications may increase.
Vemurafenib: (Moderate) Propranolol is significantly metabolized by CYP2D6 and secondarily by the CYP1A2 isoenzymes. CYP2D6 and CYP1A2 inhibitors, such as vemurafenib, could theoretically impair propranolol metabolism. The clinical significance of such interactions is unknown.
Verapamil: (Major) Intravenous propranolol is contraindicated with intravenous verapamil use in close proximity (within a few hours). Fatal cardiac arrests have occurred in patients receiving intravenous beta-blockers and intravenous calcium channel blockers. Use oral propranolol and oral verapamil with caution and close monitoring due to risk for additive negative effects on heart rate, AV conduction, and/or cardiac contractility. There have been reports of excess bradycardia and AV block, including complete heart block, when beta-blockers and verapamil have been used for the treatment of hypertension. A decrease in propranolol clearance has been observed when administered concomitantly with verapamil.
Viloxazine: (Moderate) Monitor for increased propranolol adverse reactions, including bradycardia and hypotension, during coadministration of viloxazine as concurrent use may increase propranolol exposure. Propranolol is a CYP2D6 and CYP1A2 substrate and viloxazine is a strong 1A2 inhibitor and a weak CYP2D6 inhibitor.
Voriconazole: (Moderate) Voriconazole is metabolized by CYP3A4 and, theoretically, inhibitors of CYP3A4, such as propranolol, could lead to increased serum levels of voriconazole.
Warfarin: (Moderate) Propranolol has been shown to increase warfarin AUC, and concurrent increases in INR values have been reported. Patients should be monitored for changes in anticoagulation parameters during concurrent therapy with propranolol and warfarin.
Zileuton: (Moderate) Concomitant administration of zileuton and propranolol results in a significant increase in propranolol serum concentrations, AUC, and elimination half-life. Bradycardia is also potentiated by the drug combination. Clinicians should monitor vital signs carefully if zileuton is added to a regimen containing propranolol and adjust dosages as needed.
Ziprasidone: (Minor) Ziprasidone is a moderate antagonist of alpha-1 receptors and may cause orthostatic hypotension with or without tachycardia, dizziness, or syncope. Additive hypotensive effects are possible if ziprasidone is used concurrently with antihypertensive agents.
Zolmitriptan: (Minor) Periodically monitor blood pressure and for zolmitriptan-related side effects in patients who regularly use zolmitriptan and are taking propranolol. Rarely, a patient might experience an increase in dose-related common side effects of zolmitriptan, such as dizziness, nausea or drowsiness. No dosage adjustment of zolmitriptan appears to be needed. During pharmacokinetic studies, the Cmax and AUC of zolmitriptan increased 1.5-fold after 1 week of dosing with propranolol. Cmax and AUC of the active N-desmethyl metabolite of zolmitriptan were reduced by 30% and 15%, respectively. However, in clinical trials, the efficacy of zolmitriptan was not affected by the concurrent use of common migraine prophylactic drugs (e.g., propranolol). There were no interactive effects on blood pressure or pulse rate. The interaction should not be significant for most patients.
How Supplied
HEMANGEOL/Propranolol Hydrochloride Oral Sol: 1mL, 4.28mg, 5mL, 20mg, 40mg
Inderal LA/Inderal XL/InnoPran XL/Propranolol Hydrochloride Oral Cap ER: 60mg, 80mg, 120mg, 160mg
Inderal/Propranolol Hydrochloride Intravenous Inj Sol: 1mg, 1mL
Inderal/Propranolol Hydrochloride Oral Tab: 10mg, 20mg, 40mg, 60mg, 80mg
Maximum Dosage
160 mg/day PO for idiopathic hypertrophic subaortic stenosis (IHSS); 240 mg/day PO for migraine prophylaxis, myocardial infarction prophylaxis, or post-myocardial infarction; 320 mg/day PO for angina, paroxysmal supraventricular tachycardia (PSVT), or tremor; 640 mg/day PO for hypertension. NOTE: Assumes equivalent maximum daily dosage for immediate-release and extended-release products.
Geriatric160 mg/day PO for idiopathic hypertrophic subaortic stenosis (IHSS); 240 mg/day PO for migraine prophylaxis, myocardial infarction prophylaxis, or post-myocardial infarction; 320 mg/day PO for angina, paroxysmal supraventricular tachycardia (PSVT), or tremor; 640 mg/day PO for hypertension. NOTE: Assumes equivalent maximum daily dosage for immediate-release and extended-release products.
AdolescentsSafety and efficacy have not been established; the dose required is dependent on route of administration, indication, and often clinical response. For tachyarrhythmias, doses up to 60 mg/day PO (or 120 mg/day PO in older adolescents) or 0.25 mg/kg/dose IV (Max: 3 mg/dose) have been used. For hypertension, doses up to 8 mg/kg/day PO (Max: 640 mg/day) have been used. For migraine prophylaxis, doses up to 120 mg/day PO have been used. For essential tremor, doses up to 4 mg/kg/day PO have been used.
ChildrenChildren weighing more than 35 kg: Safety and efficacy have not been established; the dose required is dependent on route of administration, indication, and often clinical response. For tachyarrhythmias, doses up to 60 mg/day PO or 0.25 mg/kg/dose IV (Max: 3 mg/dose) have been used. For hypertension, doses up to 8 mg/kg/day PO (Max: 640 mg/day) have been used. For migraine prophylaxis, doses up to 120 mg/day PO have been used. For essential tremor, doses up to 4 mg/kg/day PO have been used. For tetralogy spells, doses up to 15 mg/kg/day PO have been used (doses more than 5 mg/kg/day PO require close monitoring).
Children weighing 35 kg or less: Safety and efficacy have not been established; the dose required is dependent on route of administration, indication, and often clinical response. For tachyarrhythmias, doses up to 60 mg/day PO or 0.25 mg/kg/dose IV (Max: 3 mg/dose) have been used. For hypertension, doses up to 8 mg/kg/day PO (Max: 640 mg/day) have been used. For migraine prophylaxis, doses up to 60 mg/day PO have been used. For essential tremor, doses up to 4 mg/kg/day PO have been used. For tetralogy spells, doses up to 15 mg/kg/day PO have been used (doses more than 5 mg/kg/day PO require close monitoring).
3.4 mg/kg/day PO for infantile hemangiomas. Safety and efficacy for other indications have not been established; the dose required is dependent on route of administration, indication, and often clinical response. For tachyarrhythmias, doses up to 16 mg/kg/day PO (Max: 60 mg/day) or 0.15 mg/kg/dose IV (Max: 1 mg/dose) have been used. For hypertension, doses up to 3.5 mg/kg/dose PO have been used. For tetralogy spells, doses up to 15 mg/kg/day PO have been used (doses more than 5 mg/kg/day PO require close monitoring).
NeonatesSafety and efficacy have not been established; the dose required is dependent on route of administration, indication, and often clinical response. For tachyarrhythmias, doses up to 16 mg/kg/day PO (Max: 60 mg/day) or 0.15 mg/kg/dose IV (Max: 1 mg/dose) have been used. For hypertension, doses up to 3.5 mg/kg/dose PO or 0.15 mg/kg/dose IV have been used.
Mechanism Of Action
Mechanism of Action: Like other beta-adrenergic antagonists, propranolol competes with adrenergic neurotransmitters (e.g., catecholamines) for binding at sympathetic receptor sites. Similar to atenolol and metoprolol, propranolol blocks sympathetic stimulation mediated by beta1-adrenergic receptors in the heart and vascular smooth muscle. Pharmacodynamic consequences of beta1-receptor blockade include a decrease in both resting and exercise heart rate and cardiac output, and a decrease in both systolic and diastolic blood pressure. Propranolol may reduce reflex orthostatic hypotension. The fall in cardiac output induced by beta1 effects is often countered by a moderate reflex increase in peripheral vascular resistance that can be magnified by beta2 blockade (unmasked alpha stimulation). As a result, nonselective beta-blocking agents can produce a more modest decrease in (diastolic) blood pressure compared with selective beta1-antagonists. In addition, propranolol also can competitively block beta2-adrenergic responses in the bronchial muscles, potentially inducing bronchospasm.Actions that make propranolol useful in treating hypertension include a negative chronotropic effect that decreases heart rate at rest and after exercise; a negative inotropic effect that decreases cardiac output; reduction of sympathetic outflow from the CNS; and suppression of renin release from the kidneys. Thus, propranolol, like other beta-blockers, affects blood pressure via multiple mechanisms. In general, beta-blockers without intrinsic sympathomimetic activity (ISA) exert detrimental effects on LVH and the lipid profile, and cause sexual dysfunction.Actions that make propranolol useful in treating hypertension also apply to managing chronic stable angina. The reduction in myocardial oxygen demand induced by propranolol results in decreases in the frequency of anginal attacks and requirements of nitrate, and increases exercise tolerance. Other postulated anti-anginal actions include an increase in oxygen delivery to tissues, due to propranolol-induced lowering of hemoglobin's affinity for oxygen, and a reduction of platelet aggregation, postulated to be related to interference with calcium ion flux.Propranolol has been used to treat portal hypertension and to prevent bleeding of esophageal varices. Nonselective beta-blockers decrease portal venous pressure, decrease blood flow in the superior portosystemic collateral circulation, and decrease blood flow in the splanchnic region. Beta-blockade decreases cardiac output reducing hepatic arterial and portal venous perfusion. Activation of unopposed alpha-receptors lead to splanchnic vasoconstriction, thus decreasing portal perfusion.Propranolol is used to treat hypertension and the subsequent decline of renal function in patients with scleroderma renal crisis (SRC). SRC is associated with elevated peripheral renin concentrations. Propranolol blocks beta-receptors located on the surface of the juxtaglomerular cells which decreases the release of renin. In turn, this affects the renin-angiotensin-aldosterone system reducing blood pressure.Numerous mechanisms may contribute to the efficacy of propranolol in preventing migraine headaches. Beta-blockade can prevent arterial dilation, inhibit renin secretion, and can interfere with catecholamine-induced lipolysis. A decrease in lipolysis decreases arachidonic acid synthesis and, subsequent, prostaglandin production. Inhibition of platelet aggregation is due to this decrease in prostaglandins and blockade of catecholamine-induced platelet adhesion. Other actions include increased oxygen delivery to tissues and prevention of coagulation during epinephrine release.Propranolol has two roles in the treatment of thyrotoxicosis; these actions are determined by the different isomers of propranolol. L-propranolol causes beta-blockade and can ameliorate the symptoms associated with thytotoxicosis such as tremor, palpitations, anxiety, and heat intolerance. D-propranolol blocks the conversion of T4 to T3, but the therapeutic effect of this action is minimal.Propranolol has been used in the management of hereditary or familial essential tremor. Beta-blockade controls the involuntary, rhythmic and oscillatory movements of essential tremor. Tremor amplitude is reduced, but not the frequency of tremor. The mechanism of action is unclear, but the antitremor effect may be mediated by blockade of peripheral beta2 receptor mechanisms.Propranolol can dampen the peripheral physiologic symptoms of anxiety. Beta-blockade can attenuate somatic symptoms of anxiety such as palpitations and tremor, but it is less effective in controlling psychologic components, such as intense fear. These effects are thought to be due to improvement in somatic symptoms secondary to beta-blockade, although the mechanism of action is unclear.
Pharmacokinetics
Propranolol is administered orally or intravenously. Propranolol is highly lipophilic and is widely distributed throughout the body. It readily crosses the blood-brain barrier and the placenta, and is distributed into breast milk. Propranolol is about 90% bound to plasma proteins, the R(+)-enantiomer primarily binds albumin while the S(-)-enantiomer is primarily bound to alpha-1 acid glycoprotein. The volume of distribution is about 4 L/kg. In normal subjects receiving oral doses of racemic propranolol, S(-)-enantiomer concentrations exceeded those of the R(+)-enantiomer by 40-90% as a result of stereoselective hepatic metabolism.
Propranolol is extensively metabolized upon first pass through the liver, and the extent of metabolism is dependent on liver blood flow. The drug also binds to and saturates nonspecific hepatic binding sites before the drug reaches the systemic circulation. An equipotent, pharmacologically active metabolite, 4-hydroxypropranolol, is produced with the initiation of oral therapy, but it is eliminated faster than the parent drug. With chronic or IV therapy, this metabolite is produced to a lesser degree. Overall, at least eight metabolites of propranolol have been identified. Important differences may exist among ethnic groups in the ability to metabolize propranolol, which can affect the overall efficacy of the drug in some instances. Excretion of propranolol occurs renally, primarily as metabolites, with only 1—4% of a dose excreted fecally as unchanged drug. Clearance of the pharmacologically active S(-)-propranolol is lower than R(+)-propranolol after intravenous and oral doses. The elimination half-life of propranolol ranges from 2—6 hours, with chronic administration yielding longer half-lives, possibly due to saturation of liver binding sites and/or systemic clearance.
Affected cytochrome P450 enzymes:
Cytochrome P450 enzymes involved in the metabolism of propranolol include 2D6, 1A2, and 2C19. Propranolol is also a substrate for the efflux transporter PGP. The aromatic hydroxylation of propranolol to form the active metabolite, 4-hydroxypropranolol, is mediated by CYP2D6. 4-hydroxypropranolol is a substrate and weak inhibitor of CYP2D6. In healthy subjects, no difference in clearance or half-life of propranolol was observed between extensive and poor CYP2D6 metabolizers. In extensive metabolizers, a significant increase in 4-hydroxypropranolol clearance and a significant decrease in the clearance of naphthyloxyactic acid, an inactive metabolite, was noted.
After oral administration of immediate-release propranolol, the dose is almost completely absorbed, however, due to high first pass metabolism, bioavailability is only about 25%. Peak concentrations of immediate release tablets and long acting capsules are achieved in 1-4 hours and about 6 hours, respectively. Food can increase the bioavailability of the immediate release formulation by approximately 50% but does not affect the time to peak concentration. The effect of food on the bioavailability of the sustained-release formulation has not been investigated.
Intravenous RouteThe distribution half-life of intervenously administered propranolol is 5 to 10 minutes. Pharmacodynamic effects are seen immediately and maintained for 2—4 hours.
Pregnancy And Lactation
Prolonged experience with propranolol in pregnancy, based on published interventional and observational studies, has not identified a drug-associated risk of major birth defects, miscarriage, or other adverse maternal outcomes. Propranolol crosses the placenta. Bradycardia, hypoglycemia, and respiratory depression have been observed with exposure to beta-blockers in utero near the time of obstetric delivery. Monitor neonates with in utero exposure to propranolol closely at birth and manage accordingly. There are inconsistent reports of intrauterine growth restriction associated with propranolol; hypertension also increases fetal risk for intrauterine growth restriction.