Beta Blocker, Beta1 Selective
Treatment of hypertension, alone or in combination with other agents
C (per manufacturer); D (in 2nd and 3rd trimesters, based on expert
Hypersensitivity to bisoprolol or any component; sinus bradycardia; heart
block greater than first-degree (except in patients with a functioning
artificial pacemaker); cardiogenic shock; uncompensated cardiac failure;
pulmonary edema; pregnancy (2nd and 3rd trimesters)
Administer cautiously in compensated heart failure and monitor for a
worsening of the condition. Avoid abrupt discontinuation in patients with a
history of CAD; slowly wean while monitoring for signs and symptoms of ischemia.
Use caution in patients with PVD (can aggravate arterial insufficiency). Use
caution with concurrent use of beta-blockers and either verapamil or diltiazem;
bradycardia or heart block can occur. In general, beta-blockers should be
avoided in patients with bronchospastic disease. Bisoprolol, with B1
selectivity, should be used cautiously in bronchospastic disease with close
monitoring. Use cautiously in diabetics because it can mask prominent
hypoglycemic symptoms. Can mask signs of thyrotoxicosis. Can cause fetal harm
when administered in pregnancy. Dosage adjustment is required in patients with
significant hepatic or renal dysfunction. Use care with anesthetic agents which
decrease myocardial function.
Central nervous system: Drowsiness, insomnia
Endocrine & metabolic: Decreased sexual ability
1% to 10%:
Cardiovascular: Bradycardia, palpitations, edema, congestive heart failure,
reduced peripheral circulation
Central nervous system: Mental depression
Gastrointestinal: Diarrhea or constipation, nausea, vomiting, stomach
Ocular: Mild ocular stinging and discomfort, tearing, photophobia, decreased
corneal sensitivity, keratitis
Miscellaneous: Cold extremities
<1% (Limited to important or life-threatening symptoms): Chest pain,
arrhythmias, orthostatic hypotension, nervousness, headache, depression,
hallucinations, confusion (especially in the elderly), psoriasiform eruption,
itching, thrombocytopenia, leukopenia, shortness of breath
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 (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)
CYP2D6 enzyme substrate
Clonidine: Hypertensive crisis after or during withdrawal of either agent.
Drugs which slow AV conduction (digoxin): Effects may be additive with
Glucagon: Bisoprolol may blunt the hyperglycemic action of glucagon.
Insulin: Bisoprolol may mask tachycardia from 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.
Selective inhibitor of beta1-adrenergic receptors; competitively
blocks beta1-receptors, with little or no effect on
beta2-receptors at doses <10 mg
Onset of effect: 1-2 hours
Absorption: Rapid and almost complete from GI tract
Distribution: Distributed widely to body tissues; highest concentrations in
heart, liver, lungs, and saliva; crosses the blood-brain barrier; distributes
into breast milk
Protein binding: 26% to 33%
Metabolism: Significant first-pass metabolism; extensively metabolized in the
Half-life: 9-12 hours
Time to peak: 1.7-3 hours
Elimination: In urine (3% to 10% as unchanged drug); <2% excreted in feces
Elderly: Initial dose: 2.5 mg/day; may be increased by 2.5-5 mg/day; maximum
recommended dose: 20 mg/day
Dosing adjustment in renal/hepatic impairment: Clcr <40
mL/minute: Initial: 2.5 mg/day; increase cautiously.
Hemodialysis: Not dialyzable
May be administered without regard to meals
Blood pressure, EKG, neurologic status
cholesterol (S), glucose;
triglycerides, uric acid;
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
titration. In the CIBIS-II trial, bisoprolol (beta-1 selective beta-blocker)
improved morbidity and mortality in patients with moderate heart failure (NYHA
|Mental Health: Effects
on Mental Status|
Fatigue is common; may cause insomnia, confusion, and
Effects on Psychiatric
Barbiturates may decrease the effects of beta-blockers
|Dental Health: Local
No information available to require special precautions
Effects on Dental Treatment|
Noncardioselective beta-blockers (ie, propranolol, nadolol) enhance the
pressor response to epinephrine, resulting in hypertension and bradycardia. This
has not been reported for bisoprolol, a cardioselective beta-blocker. Therefore
local anesthetic with vasoconstrictor can be safely used in patients medicated
with bisoprolol. 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 adjust dosage without
consulting prescriber. Do not take with antacids and do not use alcohol or OTC
medications (eg, cold remedies) without consulting prescriber. If diabetic,
monitor serum sugars closely (may alter glucose tolerance or mask signs of
hypoglycemia). May cause fatigue, dizziness, or postural hypotension; use
caution when changing position from lying or sitting to standing, or when
driving or climbing stairs until response to medication is known. May cause
alteration in sexual performance (reversible). Report palpitations, unresolved
swelling of extremities, difficulty breathing or new cough, unresolved fatigue,
unusual weight gain, unresolved constipation, or unusual muscle weakness.
Pregnancy/breast-feeding precautions: Inform prescriber if you are or intend
to be pregnant. Consult prescriber if breast-feeding.
Modify dosage in patients with renal insufficiency
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; monitor for CNS side
Tablet, as fumarate: 5 mg, 10 mg
Foster CA and Aston SJ,
"Propranolol-Epinephrine Interaction: A Potential Disaster," Plast Reconstr
Surg, 1983, 72(1):74-8.
Lancaster SG and Sorkin EM,
"Bisoprolol: A Preliminary Review of Its Pharmacodynamic and Pharmacokinetic Properties, and Therapeutic Efficacy in Hypertension and Angina Pectoris,"
Drugs, 1988, 36(3):256-85.
Wong DG, Spence JD, Lamki L, et al,
"Effect of Nonsteroidal Anti-inflammatory Drugs on Control of Hypertension of Beta-Blockers and Diuretics,"
Lancet, 1986, 1(8488):997-1001.
"Dental Nonsteroidal Anti-inflammatory Drugs and Prostaglandin-Based Drug Interactions, Part Two,"
Gen Dent, 1992, 40(2):104, 106, 108.
Wynn RL, "Epinephrine Interactions With Beta-Blockers," Gen Dent,
1994, 42(1):16, 18.
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