|Betachron E-R® Capsule; Inderal®;
Antiarrhythmic Agent, Class II; Beta Blocker, Nonselective
Management of hypertension, angina pectoris, pheochromocytoma, essential
tremor, tetralogy of Fallot cyanotic spells, and arrhythmias (such as atrial
fibrillation and flutter, A-V nodal re-entrant tachycardias, and
catecholamine-induced arrhythmias); prevention of myocardial infarction,
migraine headache; symptomatic treatment of hypertrophic subaortic stenosis
C (per manufacturer); D (in 2nd and 3rd trimesters, per expert
Clinical effects on the fetus: Crosses the placenta. IUGR, hypoglycemia,
bradycardia, respiratory depression, hyperbilirubinemia, polycythemia,
polydactyly reported. IUGR probably related to maternal hypertension. Preterm
labor has been reported. Available evidence suggests safe use during pregnancy
and breast-feeding. Monitor breast-fed infant for symptoms of beta-blockade.
Breast-feeding/lactation: Crosses into breast milk. American Academy of
Pediatrics considers compatible with breast-feeding.
Hypersensitivity to propranolol or any component; sinus bradycardia; sinus
node dysfunction; heart block greater than first degree (except in patients with
a functioning artificial pacemaker); cardiogenic shock; uncompensated cardiac
failure unless the heart failure is due to a tachyarrhythmia; bronchospastic
disease; pregnancy (2nd and 3rd trimesters)
Administer cautiously in compensated heart failure and monitor for a
worsening of the condition (efficacy of propranolol in CHF has not been
demonstrated). Avoid abrupt discontinuation in patients with a history of CAD;
slowly wean while monitoring for signs and symptoms of ischemia. Use caution in
patient with PVD. Use caution with concurrent use of beta-blockers and either
verapamil or diltiazem; bradycardia or heart block can occur. Avoid concurrent
I.V. use of both agents. Use cautiously in diabetics because it can mask
prominent hypoglycemic symptoms. Can mask signs of thyrotoxicosis. Can cause
fetal harm when administered in pregnancy. Use cautiously in hepatic dysfunction
(dosage adjustment required). Use care with anesthetic agents which decrease
Cardiovascular: Bradycardia, congestive heart failure, reduced peripheral
circulation, thrombocytopenia, purpura, chest pain, hypotension, impaired
myocardial contractility, worsening of A-V conduction disturbance, cardiogenic
Central nervous system: Mental depression, lightheadedness, amnesia,
emotional lability, confusion, hallucinations, dizziness, insomnia, fatigue,
vivid dreams, lethargy, cold extremities, vertigo, syncope, cognitive
dysfunction, psychosis, hallucinations, hypersomnolence
Dermatologic: Rash, alopecia, exfoliative dermatitis, psoriasiform eruptions,
eczematous eruptions, hyperkeratosis, nail changes, pruritus, urticaria,
ulcerative lichenoid, contact dermatitis
Endocrine & metabolic: Hypoglycemia, hyperglycemia, lipid abnormal,
Gastrointestinal: Diarrhea, nausea, vomiting, stomach discomfort,
Genitourinary: Impotence, proteinuria (rare), oliguria (rare), interstitial
Hematologic: Agranulocytosis, thrombocytopenia
Neuromuscular & skeletal: Weakness, carpal tunnel syndrome (rare),
paresthesias, myotonus, polyarthritis arthropathy
Respiratory: Wheezing, pharyngitis, bronchospasm, pulmonary edema
Ocular: Hyperemia of the conjunctiva, decreased tear production, decreased
visual acuity, mydriasis
Symptoms of intoxication include cardiac disturbances, CNS toxicity,
bronchospasm, hypoglycemia and hyperkalemia. The most common cardiac symptoms
include hypotension and bradycardia; atrioventricular block, intraventricular
conduction disturbances, cardiogenic shock, and asystole may occur with severe
overdose, especially with membrane-depressant drugs (eg, propranolol); CNS
effects include convulsions, coma, and respiratory arrest is commonly seen with
propranolol and other membrane-depressant and lipid-soluble drugs.
Treatment includes symptomatic treatment of seizures, hypotension,
hyperkalemia and hypoglycemia; bradycardia and hypotension resistant to
atropine, isoproterenol or pacing may respond to glucagon; wide QRS defects
caused by the membrane-depressant poisoning may respond to hypertonic sodium
bicarbonate; repeat-dose charcoal, hemoperfusion, or hemodialysis may be helpful
in removal of only those beta-blockers with a small Vd, long
half-life or low intrinsic clearance (acebutolol, atenolol, nadolol, sotalol)
CYP1A2, 2C18, 2C19, and 2D6 enzyme substrate
Alpha-blockers (prazosin, terazosin): Concurrent use of beta-blockers may
increase risk of orthostasis.
Antipyrine's clearance is reduced by 30% to 40%.
Cimetidine increases the plasma concentration of propranolol and its
pharmacodynamic effects may be increased.
Clonidine: Hypertensive crisis after or during withdrawal of either agent.
Drugs which slow AV conduction (digoxin): Effects may be additive with
Epinephrine (including local anesthetics with epinephrine): Propranolol may
Flecainide: Pharmacological activity of both agents may be increased when
Fluoxetine may inhibit the metabolism of propranolol, resulting in cardiac
Glucagon: Propranolol may blunt hyperglycemic action.
Haloperidol: Hypotensive effects may be potentiated.
Hydralazine: The bioavailability propranolol (rapid release) and hydralazine
may be enhanced with concurrent dosing.
Insulin: Propranolol inhibits recovery and may cause hypertension and
bradycardia following insulin-induced hypoglycemia. Also masks the tachycardia
that usually accompanies insulin-induced hypoglycemia.
NSAIDs (ibuprofen, indomethacin, naproxen, piroxicam) may reduce the
antihypertensive effects of beta-blockers.
Salicylates may reduce the antihypertensive effects of beta-blockers.
Sulfonylureas: Beta-blockers may alter response to hypoglycemic agents.
Verapamil or diltiazem may have synergistic or additive pharmacological
effects when taken concurrently with beta-blockers; avoid concurrent I.V. use of
Compatible in saline, incompatible with
HCO3-; protect injection from light; solutions have
maximum stability at pH of 3 and decompose rapidly in alkaline pH; propranolol
is stable for 24 hours at room temperature in D5W or
Nonselective beta-adrenergic blocker (class II antiarrhythmic); competitively
blocks response to beta1- and beta2-adrenergic stimulation
which results in decreases in heart rate, myocardial contractility, blood
pressure, and myocardial oxygen demand
Onset of beta-blockade: Oral: Within 1-2 hours
Duration: ~6 hours
Distribution: Vd: 3.9 L/kg in adults; crosses the placenta; small
amounts appear in breast milk
Protein binding: Newborns: 68%; Adults: 93%
Metabolism: Extensive first-pass effect; metabolized in the liver to active
and inactive compounds
Bioavailability: 30% to 40%; oral bioavailability may be increased in Down
Half-life: Neonates and Infants: Possible increased half-life; Children:
3.9-6.4 hours; Adults: 4-6 hours
Elimination: Primarily in urine (96% to 99%)
Children: Initial: 0.5-1 mg/kg/day in divided doses every 6-8 hours; titrate
dosage upward every 3-7 days; usual dose: 2-4 mg/kg/day; higher doses may be
needed; do not exceed 16 mg/kg/day or 60 mg/day
Adults: 10-30 mg/dose every 6-8 hours
Elderly: Initial: 10 mg twice daily; increase dosage every 3-7 days; usual
dosage range: 10-320 mg given in 2 divided doses
Children: 0.01-0.1 mg/kg slow IVP over 10 minutes; maximum dose: 1 mg
Adults: 1 mg/dose slow IVP; repeat every 5 minutes up to a total of 5 mg
Children: Initial: 0.5-1 mg/kg/day in divided doses every 6-12 hours;
increase gradually every 3-7 days; maximum: 2 mg/kg/24 hours
Adults: Initial: 40 mg twice daily; increase dosage every 3-7 days; usual
dose: less than or equal to 320 mg divided in 2-3 doses/day; maximum daily dose:
Migraine headache prophylaxis: Oral:
Children: 0.6-1.5 mg/kg/day or
less than or equal to 35 kg: 10-20 mg 3 times/day
>35 kg: 20-40 mg 3 times/day
Adults: Initial: 80 mg/day divided every 6-8 hours; increase by 20-40 mg/dose
every 3-4 weeks to a maximum of 160-240 mg/day given in divided doses every 6-8
hours; if satisfactory response not achieved within 6 weeks of starting therapy,
drug should be withdrawn gradually over several weeks
Tetralogy spells: Children:
Oral: 1-2 mg/kg/day every 6 hours as needed, may increase by 1 mg/kg/day to a
maximum of 5 mg/kg/day, or if refractory may increase slowly to a maximum of
I.V.: 0.15-0.25 mg/kg/dose slow IVP; may repeat in 15 minutes
Adolescents and Adults: Oral: 10-40 mg/dose every 6 hours
Adults: I.V.: 1-3 mg/dose slow IVP as a single dose
Angina: 80-320 mg/day in doses divided 2-4 times/day
Pheochromocytoma: 30-60 mg/day in divided doses
Myocardial infarction prophylaxis: 180-240 mg/day in 3-4 divided doses
Hypertrophic subaortic stenosis: 20-40 mg 3-4 times/day
Essential tremor: 40 mg twice daily initially; maintenance doses: usually
Dosing adjustment in renal impairment:
Clcr 31-40 mL/minute: Administer every 24-36 hours or administer
50% of normal dose.
Clcr 10-30 mL/minute: Administer every 24-48 hours or administer
50% of normal dose.
Clcr <10 mL/minute: Administer every 40-60 hours or administer
25% of normal dose.
Hemodialysis: Not dialyzable (0% to 5%); supplemental dose is not necessary.
Peritoneal dialysis: Supplemental dose is not necessary.
Dosing adjustment/comments in hepatic disease: Marked slowing of
heart rate may occur in cirrhosis with conventional doses. Low initial dose and
regular heart rate monitoring.
Avoid natural licorice (causes sodium and water retention and increases
potassium loss); protein-rich foods may increase bioavailability; a change in
diet from high carbohydrate/low protein to low carbohydrate/high protein may
result in increased oral clearance
Blood pressure, EKG, heart rate, CNS and cardiac effects
Therapeutic: 50-100 ng/mL (SI: 190-390 nmol/L) at end of dose
Hypertension: Beta-blocker therapy in the treatment of hypertension has been
associated with improved cardiovascular outcomes. This class of drug is
beneficial for elderly patients with hypertension. A recent UKPDS study showed
that beta-blocker therapy (atenolol) was as effective as an ACE inhibitor in
reducing cardiovascular events and that the benefits of therapy were related
more to the degree of antihypertensive efficacy rather than the class of drug
Myocardial infarction: Beta-blockers, in general without intrinsic
sympathomimetic activity (ISA), have been shown to decrease morbidity and
mortality when initiated in the acute treatment of myocardial infarction and
continued long-term. In this setting, therapy should be avoided in patients with
hypotension, cardiogenic shock, or heart block.
Surgery: Atenolol has also been shown to improve cardiovascular outcomes when
used in the perioperative period in patients with underlying cardiovascular
disease who are undergoing noncardiac surgery. Bisoprolol in high-risk patients
undergoing vascular surgery reduced the perioperative incidence of death from
cardiac causes and nonfatal myocardial infarction.
Atrial fibrillation: Beta-blocker therapy provides effective rate control in
patients with atrial fibrillation.
Angina: Beta-blockers are effective in the treatment of angina as monotherapy
or when combined with nitrates and/or calcium channel blockers. In patients with
severe intractable angina requiring negative cardiac chronotropic medications,
pacemaker placement has been carried out to maintain heart rate in the setting
of large doses of beta-blockers and/or calcium channel blockers. Beta-blockers
are ineffective in the treatment of pure vasospastic (Prinzmetal) angina.
Withdrawal: Beta-blocker therapy should not be withdrawn abruptly, but
gradually tapered to avoid acute tachycardia and hypertension.
Heart failure: There is emerging evidence that beta-blocker therapy, without
intrinsic sympathomimetic activity (ISA), should be initiated in select patients
with stable congestive heart failure (NYHA Class II-III). To date,
carvedilol, sustained release metoprolol, and bisoprolol have demonstrated a
beneficial effect on morbidity and mortality. It is important that beta-blocker
therapy be instituted initially at very low doses with gradual and very careful
|Mental Health: Effects
on Mental Status|
Fatigue and malaise are common and often mistaken for depression; may also
cause dizziness, confusion, insomnia, or hallucinations
Effects on Psychiatric
Low-dose propranolol is considered by many to be the drug of choice for
akathisia; concurrent use with psychotropic drugs may produce additive
hypotensive effects; monitor blood pressure
|Dental Health: Local
Use with caution; epinephrine has interacted with nonselective beta-blockers
to result in initial hypertensive episode followed by
Effects on Dental Treatment|
Noncardioselective beta-blockers (ie, propranolol, nadolol) enhance the
pressor response to epinephrine, resulting in hypertension and bradycardia. Many
nonsteroidal anti-inflammatory drugs such as ibuprofen and indomethacin can
reduce the hypotensive effect of beta-blockers after 3 or more weeks of therapy
with the NSAID. Short-term NSAID use (ie, 3 days) requires no special
precautions in patients taking beta-blockers.
Take exactly as directed; do not increase, decrease, or discontinue without
consulting prescriber. Take at the same time each day. Tablets may be crushed
and taken with liquids. Do not alter dietary intake of protein or carbohydrates
without consulting prescriber. You may experience orthostatic hypotension,
dizziness, drowsiness, or blurred vision (use caution when driving, climbing
stairs, or changing position - rising from sitting or lying to standing - or
engaging in tasks requiring alertness until response to drug is known); nausea,
vomiting, or stomach discomfort (small frequent meals, frequent mouth care,
chewing gum, or sucking lozenges may help); decreased sexual ability
(reversible). If diabetic, monitor serum glucose closely. Report unusual
swelling of extremities, difficulty breathing, unresolved cough, or unusual
weight gain, cold extremities, persistent diarrhea, confusion, hallucinations,
headache, nervousness, lack of improvement, or worsening of condition.
Pregnancy/breast-feeding precautions: Inform prescriber if you are or intend
to be pregnant. Consult prescriber if breast-feeding.
Patient's therapeutic response may be evaluated by looking at blood pressure,
apical and radial pulses, fluid I & O, daily weight, respirations, and
circulation in extremities before and during therapy
Capsule, as hydrochloride, sustained action: 60 mg, 80 mg, 120 mg, 160 mg
Injection, as hydrochloride: 1 mg/mL (1 mL)
Solution, oral, as hydrochloride (strawberry-mint flavor): 4 mg/mL (5 mL, 500
mL); 8 mg/mL (5 mL, 500 mL)
Solution, oral, concentrate, as hydrochloride: 80 mg/mL (30 mL)
Tablet, as hydrochloride: 10 mg, 20 mg, 40 mg, 60 mg, 80 mg
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"High-Dose Propranolol Therapy in the Management of Supraventricular Tachycardia,"
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