No

Beta Blocker (with Intrinsic Sympathomimetic Activity); Ophthalmic Agent, Antiglaucoma

Management of hypertension; treatment of chronic open-angle glaucoma and intraocular hypertension

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

Hypersensitivity to carteolol or any component; sinus bradycardia; heart block greater than first-degree (except in patients with a functioning artificial pacemaker); cardiogenic shock; bronchial asthma, bronchospasm, or COPD; uncompensated cardiac failure; pulmonary edema; pregnancy (2nd and 3rd trimesters)

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. Patients with bronchospastic disease should not receive beta-blockers. 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 renal dysfunction. Use care with anesthetic agents that decrease myocardial function. Beta-blockers with intrinsic sympathomimetic activity have not been demonstrated to be of value in congestive heart failure.

Ophthalmic:

>10%: Ocular: Conjunctival hyperemia

1% to 10%:

Ocular: Anisocoria, corneal punctate 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, arrhythmias, orthostatic hypotension, nervousness, headache, depression, hallucinations, confusion (especially in the elderly), psoriasiform eruption, itching, polyuria, 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 V_d, long half-life, or low intrinsic clearance (acebutolol, atenolol, nadolol, sotalol).

Albuterol (and other beta₂ agonists): Effects may be blunted by nonspecific beta-blockers.

Alpha-blockers (prazosin, terazosin): Concurrent use of beta-blockers may increase risk of orthostasis.

Carteolol causes hypertension when used with local anesthetics (tetracaine, lidocaine, or bupivacaine) containing epinephrine.

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

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

Glucagon: Carteolol may blunt the hyperglycemic action of glucagon.

Insulin: Carteolol 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.

Blocks both beta₁- and beta₂-receptors and has mild intrinsic sympathomimetic activity; has negative inotropic and chronotropic effects and can significantly slow A-V nodal conduction

Onset of effect: Oral: 1-1.5 hours

Peak effect: 2 hours

Duration: 12 hours

Absorption: Oral: 80%

Protein binding: 23% to 30%

Metabolism: 30% to 50%

Half-life: 6 hours

Elimination: Renally excreted metabolites

Adults:

Ophthalmic: Instill 1 drop in affected eye(s) twice daily.

Dosing interval in renal impairment:

Cl_cr >60 mL/minute/1.73 m²: Administer every 24 hours.

Cl_cr 20-60 mL/minute/1.73 m²: Administer every 48 hours.

Cl_cr <20 mL/minute/1.73 m²: Administer every 72 hours.

Ophthalmic: Intraocular pressure; Systemic: Blood pressure, pulse, CNS status

Carteolol has mild intrinsic sympathomimetic activity and is a nonspecific beta-blocker. Thus, the cardiovascular benefits of carteolol are less clear compared to other beta-blockers. Furthermore, the beta-2 blocking activity may be accompanied by an increased level of side effects with respect to bronchospasm and peripheral vasoconstriction.

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 fatigue, insomnia, confusion, and nightmares and clinically look like a major depression

Antipsychotics and MAOIs may increase the effects of beta-blockers; conversely beta-blockers may increase the effects of antipsychotics and benzodiazepines

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 carteolol, a cardioselective beta-blocker. Therefore, local anesthetic with vasoconstrictor can be safely used in patients medicated with carteolol. 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: Take exactly as directed. Do not increase, decrease, or adjust dosage without consulting prescriber. Take pulse daily, prior to medication; follow prescriber's instruction about holding medication. Do not take with antacids and avoid alcohol or OTC medications (eg, cold remedies) without consulting prescriber. If diabetic, monitor serum blood glucose 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, when driving, or climbing stairs until response to medication is known. May cause alteration in sexual performance (reversible). Report 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.

Ophthalmic: Wash hands before instilling. Sit or lie down to instill. Open eye, look at ceiling, and instill prescribed amount of medication. Close eye and apply gentle pressure to inner corner of eye. Do not let tip of applicator touch eye or contaminate tip of applicator. Temporary stinging or burning may occur. Report persistent pain, burning, vision disturbances, swelling, itching, or worsening of condition.

Advise against abrupt withdrawal; monitor orthostatic blood pressures, apical and peripheral pulse, and mental status changes (ie, confusion, depression)

Solution, ophthalmic, as hydrochloride (Ocupress®): 1% (5 mL, 10 mL)

Tablet, as hydrochloride (Cartrol®): 2.5 mg, 5 mg

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

Ishizaki T, Ohnishi A, Sasaki T, et al, "Concentration-Effect and Time-Effect Relationships on Carteolol," Eur J Clin Pharmacol, 1983, 25(6):749-57.

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.