No

Beta Blocker, Beta₁ Selective; Ophthalmic Agent, Antiglaucoma

Treatment of chronic open-angle glaucoma and ocular hypertension; management of hypertension

C (per manufacturer); D (in 2nd and 3rd trimester, based on expert analysis)

Hypersensitivity to betaxolol 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 trimester)

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 with concurrent use of beta-blockers and either verapamil or diltiazem; bradycardia or heart block can occur. Use caution in patients with PVD (can aggravate arterial insufficiency). In general, beta-blockers should be avoided in patients with bronchospastic disease. Betaxolol, 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 required in severe renal impairment and those on dialysis. Use care with anesthetic agents which decreases myocardial function.

Ophthalmic:

>10%: Ocular: Conjunctival hyperemia

1% to 10%:

Ocular: Anisocoria, corneal punctate keratitis, keratitis, corneal staining, decreased corneal sensitivity, eye pain, vision disturbances

Systemic:

>10%:

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 discomfort

Respiratory: Bronchospasm

Miscellaneous: Cold extremities

<1% (Limited to important or life-threatening symptoms): Chest pain, thrombocytopenia

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 V_d, long half-life, or low intrinsic clearance (acebutolol, atenolol, nadolol, sotalol)

CYP1A2 and 2D6 enzyme substrate

Clonidine; Hypertensive crisis after or during withdrawal of either agent.

Drugs which slow AV conduction (digoxin): Effects may be additive with beta-blockers.

Glucagon: Betaxolol may blunt the hyperglycemic action of glucagon.

Insulin and oral hypoglycemics: 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.

Verapamil or diltiazem may have synergistic or additive pharmacological effects when taken concurrently with beta-blockers.

Avoid freezing

Competitively blocks beta₁-receptors, with little or no effect on beta₂-receptors; ophthalmic reduces intraocular pressure by reducing the production of aqueous humor

Onset of action: Ophthalmic: 30 minutes; Oral: 1-1.5 hours

Duration: Ophthalmic: greater than or equal to 12 hours

Absorption: Systemically absorbed

Metabolism: Hepatic (multiple metabolites)

Half-life: 12-22 hours

Time to peak: Within 2 hours

Elimination: Renal

Adults:

Oral: 10 mg/day; may increase dose to 20 mg/day after 7-14 days if desired response is not achieved. Initial dose in elderly: 5 mg/day.

Dosage adjustment in renal impairment: Administer 5 mg/day. Can increase every 2 weeks up to a maximum of 20 mg/day.

Cl_cr <10 mL/minute: Administer 50% of usual dose.

Ophthalmic: Intraocular pressure. Systemic: Blood pressure, pulse

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 used.

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.

May cause drowsiness; rare reports of depression and hallucinations

Has been used to treat akathisia; propranolol preferred

No information available to require special precautions

Noncardioselective beta-blockers (ie, propranolol, nadolol) enhance the pressor response to epinephrine, resulting in hypertension and bradycardia. This has not been reported for betaxolol, a cardioselective beta-blocker. Therefore local anesthetic with vasoconstrictor can be safely used in patients medicated with betaxolol. 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.

Oral: Use as directed; do not increase dose unless directed by prescriber. You may experience dizziness or blurred vision (use caution when driving engaging in tasks requiring alertness until response to drug is known); nausea or vomiting (small frequent meals, frequent mouth care, sucking lozenges, or chewing gum may help). Report persistent GI response (nausea, vomiting, diarrhea, or constipation); chest pain or palpitations; unusual cough, difficulty breathing, swelling or coolness of extremities; or unusual mental depression. Pregnancy/breast-feeding precautions: Inform prescriber if you are or intend to be pregnant. Consult prescriber if breast-feeding.

Ophthalmic: Shake well before using. Tilt head back and instill in eye. Keep eye open; do not blink for 30 seconds. Apply gentle pressure to corner of eye for 1 minute. Wipe away excess from skin. Do not touch applicator to eyes or contaminate tip of applicator. Report if condition does not improve or if you experience eye pain, vision disturbances, or other adverse eye response.

Monitor for systemic effect of beta-blockade

Solution, ophthalmic, as hydrochloride (Betoptic®): 0.5% (2.5 mL, 5 mL, 10 mL)

Suspension, ophthalmic, as hydrochloride (Betoptic® S): 0.25% (2.5 mL, 10 mL, 15 mL)

Tablet, as hydrochloride (Kerlone®): 10 mg, 20 mg

Ball S, "Congestive Heart Failure From Betaxolol," Arch Ophthalmol, 1987, 105(3):320.

Foster CA and Aston SJ, "Propranolol-Epinephrine Interaction: A Potential Disaster," Plast Reconstr Surg, 1983, 72(1):74-8.

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.

Wynn RL, "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.