No

Beta Blocker (with Intrinsic Sympathomimetic Activity)

Management of hypertension

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

Hypersensitivity to pindolol or any component; sinus bradycardia; heart block greater than first degree (except in patients with a functioning artificial pacemaker); sinus node dysfunction; cardiogenic shock; uncompensated cardiac failure; bronchospastic disease; 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. 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 or hepatic dysfunction. Use care with anesthetic agents which decrease myocardial function. Beta-blockers with intrinsic sympathomimetic activity (including pindolol) do not appear to be of benefit in congestive heart failure.

1% to 10%:

Cardiovascular: Chest pain (3%), edema (6%)

Central nervous system: Nightmares/vivid dreams (5%), dizziness (9%), insomnia (10%), fatigue (8%), nervousness (7%)

Dermatologic: Rash, itching (4%)

Gastrointestinal: Nausea (5%), abdominal discomfort (4%)

Neuromuscular & skeletal: Weakness (4%), paresthesia (3%), arthralgia (7%), muscle pain (10%)

Respiratory: Dyspnea (5%)

<1% (Limited to important or life-threatening symptoms): Bradycardia, CHF, palpitations, claudication, hypotension

Central nervous system: Confusion, mental depression, hallucinations, anxiety (<2%), impotence, thrombocytopenia, dry eyes, wheezing

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

CYP2D6 enzyme substrate

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

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

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

Epinephrine (including local anesthetics with epinephrine) - pindolol may cause hypertension.

Glucagon: Pindolol may blunt the hyperglycemic action.

Insulin and oral hypoglycemics: May mask symptoms of hypoglycemia.

NSAIDs (ibuprofen, indomethacin, naproxen, piroxicam) may reduce the antihypertensive effects of beta-blockers.

Pindolol increases antipyrine's half-life.

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.

Protect from light

Blocks both beta₁- and beta₂-receptors and has mild intrinsic sympathomimetic activity; pindolol has negative inotropic and chronotropic effects and can significantly slow A-V nodal conduction. Augmentive action of antidepressants thought to be mediated via a serotonin 1A autoreceptor antagonism.

Duration: ~12 hours

Absorption: Oral: Rapid, 50% to 95%

Protein binding: 50%

Metabolism: In the liver (60% to 65%) to conjugates

Half-life: 2.5-4 hours; increased with renal insufficiency, age, and cirrhosis

Time to peak serum concentration: Within 1-2 hours

Elimination: In urine (35% to 50% unchanged drug)

Oral:

Hypertension: Initial: 5 mg twice daily; increase as necessary by 10 mg/day every 3-4 weeks; maximum daily dose: 60 mg.

Antidepressant augmentation: 2.5 mg 3 times/day

Elderly: Initial: 5 mg once daily; increase as necessary by 5 mg/day every 3-4 weeks.

Dosing adjustment in renal and hepatic impairment: Reduction is necessary in severely impaired.

May be administered without regard to meals

Blood pressure, standing and sitting/supine, pulse, respiratory function

This drug possesses intrinsic sympathomimetic activity. While beta-blockers with intrinsic sympathomimetic activity induce fewer side effects, the cardiovascular benefits listed below are less clear than for beta-blockers without intrinsic sympathomimetic activity.

Withdrawal: Beta-blocker therapy should not be withdrawn abruptly, but gradually tapered to avoid acute tachycardia and hypertension.

Insomnia is common; may cause dizziness, fatigue, nervousness, or nightmares; may rarely cause depression or hallucinations

Has been used as an augmentive agent to the SSRIs for the treatment of depression; barbiturates may decrease the effects of beta-blockers

Use with caution; epinephrine has interacted with nonselective beta-blockers to result in initial hypertensive episode followed by bradycardia

Noncardioselective beta-blockers (ie, propranolol, nadolol, pindolol) 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 as directed; do not discontinue without consulting prescriber. Avoid alcohol and do not take with antacids. You may experience nervousness, dizziness, or fatigue; use caution when driving or engaging in hazardous activities until response to drug is known. Frequent small meals may reduce incidence of nausea; adequate fluids and fiber intake may reduce constipation. Diabetic patients should monitor serum glucose regularly. Report chest pain, rapid heartbeat or palpitations, difficulty breathing, sudden increase in weight, swelling in ankles or hands, persistent dizziness or fatigue, trembling, increased anxiety, or sleeplessness. Pregnancy/breast-feeding precautions: Consult prescriber if pregnant or breast-feeding.

Evaluate blood pressure, apical and radial pulses; do not discontinue abruptly

Tablet: 5 mg, 10 mg

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

Gretzer I, Alvan G, Duner H, et al, "Beta-Blocking Effect and Pharmacokinetics of Pindolol in Young and Elderly Hypertensive Patients," Eur J Clin Pharmacol, 1986, 31(4):415-8.

Meier J, "Pharmacokinetic Comparison of Pindolol With Other Beta-Adrenoceptor-Blocking Agents," Am Heart J, 1982, 104(2 Pt 2):364-73.

Offenstadt G, Hericord PH, and Amstrutz PH, "Voluntary Poisoning With Pindolol," Nouv Presse Med, 1976, 5(24):1539.

Thorpe P, "Pindolol in Hypertension," Med J Aust, 1971, 1(23):1242.

Weinstein RS, "Recognition and Management of Poisoning With Beta-Adrenergic Blocking Agents," Ann Emerg Med, 1984, 13(12):1123-31.

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.