Quinidine

Quinidine is a generic medication for the drug :

Quinidine medication comes in several different strengths; click on the strength you need to view prices from pharmacies competing to earn your business.

Quinidine 200 mg	Quinidine Sulfate ER 300 mg	Quinidine Sulfate 300 mg
Quinidine Gluconate CR 324 mg

Technical Information

Pharmacology

Pharmacokinetics

Each salt dissociates in the gastrointestinal tract to release quinidine base, which is rapidly and almost completely absorbed from the small intestine. Extended-release formulations and the different salts of the drug are absorbed at different rates. Quinidine concentrations are generally higher and appear earlier when the drug is administered on an empty stomach, but the amount of drug absorbed is not diminished by the presence of food in the digestive tract. Extended-release preparations are generally preferred as the plasma concentration profile is smoother, and doses can be given at 8- to 12-hour intervals compared to the usual 6-hour dosing schedule for regular-release formulations.

All salts and formulations have approximately the same bioavailability of 70%. Peak plasma levels will vary among individuals primarily as a result of individual variations in first pass metabolism. Quinidine is widely distributed to all tissues except the brain. Quinidine crosses the placenta and is distributed into breast milk. At therapeutic plasma concentrations, the plasma protein binding of quinidine is 70 to 90% in adults and older children, but in infants and neonates it may be as low as 50 to 70%.

The onset of action of quinidine is 1 to 3 hours, with therapeutic cardiovascular effects lasting for 6 to 8 hours following an immediate-release formulation.

The elimination half-life is approximately 6 to 8 hours in adults and 3 to 4 hours in children but varies considerably among individuals. Quinidine is metabolized in the liver by the cytochrome P450 isoenzyme, CYP3A4. Some of its metabolites may be therapeutically active. Decreased liver function does not seem to significantly affect the plasma clearance of the drug. Approximately 10 to 50% is excreted unchanged in the urine within 24 hours. Renal excretion is by glomerular filtration and secretion by proximal renal tubules. Renal clearance diminishes as urinary pH increases. Fecal excretion accounts for less than 5% of the oral dose.

Traditionally, the average therapeutic range for quinidine has been 6 to 15 µmol/L (2 to 5 µg/mL). Toxicity was generally associated with serum quinidine levels above 15 µmol/L (5 µg/mL). However, levels differ based on the assay method used. Currently available methods which are more specific than older methods report lower serum quinidine concentrations.

The concentration necessary to produce a therapeutic effect will depend on the individual as well as the type, severity and duration of the arrhythmia. When efficacy is established, a serum drug concentration should be determined against which future levels should be compared if arrhythmia recurs or modifications made to the formulation or salt. Sampling is usually done just prior to the next dose.

Small amounts of quinidine are removed by hemodialysis; the drug is not removed by peritoneal dialysis.

Quinidine

Comparison of Available Salts

Quinidine Salt	Equivalent Dose (mg)	% Quinidine Base
Quinidine bisulfate	250	66
Quinidine gluconate	267	62
Quinidine sulfate	200	83

Indications

No antiarrhythmic drug has been shown to reduce the incidence of sudden death in patients with asymptomatic ventricular arrhythmias. Most antiarrhythmic drugs have the potential to cause dangerous arrhythmias; some have been shown to be associated with an increased incidence of sudden death. In light of the above, physicians should carefully consider the risks and benefits of antiarrhythmic therapy for all patients with ventricular arrhythmias.

Supraventricular Arrhythmias: Quinidine is used in the treatment of new onset (less than 1 year) atrial fibrillation or flutter when direct current cardioversion is undesirable. Quinidine is also used for maintenance of sinus rhythm after cardioversion in patients with atrial fibrillation or flutter and for prevention of recurrent atrial fibrillation or flutter although this latter role is being re-evaluated.

Quinidine may also be used for prevention of paroxysmal atrial tachycardia due to AV nodal re-entry in patients with structural heart disease when digoxin or beta-blockers have failed or cannot be used.

Quinidine is more likely to maintain normal sinus rhythm in patients with recent onset atrial fibrillation or flutter, than in patients with an enlarged left atrium or in patients with long-standing atrial fibrillation or flutter.

Ventricular Arrhythmias: For the treatment of documented life-threatening ventricular arrhythmias, such as sustained ventricular tachycardia. Quinidine may also be used for the treatment of patients with documented symptomatic ventricular arrhythmias when the symptoms are of sufficient severity to require treatment. Because of the proarrhythmic effects of quinidine, its use should be reserved for patients in whom the benefit of treatment clearly outweighs the risks.

For patients with sustained ventricular tachycardia, quinidine therapy should be initiated in a hospital. Hospitalization may also be required for certain other patients depending on their cardiac status and underlying cardiac disease.

Quinidine can have proarrhythmic effects in patients who have survived cardiac arrest or had previous MI and is not recommended in these patients.

Parenterally, quinidine may be used when oral therapy is not feasible or when rapid therapeutic effect is required.

P. falciparum Malaria: IV quinidine gluconate is indicated for the treatment of life-threatening P. falciparum malaria. For more information, consult the 2000 Canadian Recommendations for the Prevention and Treatment of Malaria Among International Travellers, available at www.hc-sc.gc.ca/pphb-dgspsp/publicat/ccdr-rmtc/04vol30/30s1/index.html. Quinidine gluconate injection is available in Canada through the Special Access Programme (see Appendix 2).

Precautions

Lactation

Children

Pregnancy

Quinidine

Drug Interactions

Interacting Drug	Potential Effect
Amiloride	Increased prolongation of QRS interval.
Amiodarone	Increased quinidine levels and prolonged cardiac conduction.
Antiarrhythmics (e.g., disopyramide, flecainide, mexiletine)	Increased serum concentrations of several antiarrhythmics; enhanced cardiac depressant effects and potential toxicity.
Anticholinergics	Additive anticholinergic effect.
Antihypertensives	Enhancement of hypotensive effect.
β-blockers	Decreased metabolism of some β-blockers; additive cardiac depressant effects.
Cholinergic drugs (e.g., neostigmine, edrophonium, pyridostigmine)	Quinidine may antagonize cholinergic effects. May result in failure of quinidine to terminate PSVT.
Cimetidine	Increased half-life and plasma levels of quinidine.
Codeine, hydrocodone^a	Blocked analgesic effect of codeine or hydrocodone.
Digoxin	Markedly increased digoxin levels (see Warnings).
Erythromycin, clarithromycin	Increased quinidine levels, possible arrhythmias.
Hepatic enzyme inducers (e.g., barbiturates, phenytoin, rifampin)	Enhanced hepatic metabolism and decreased levels of quinidine.
Neuromuscular blockers (e.g., tubocurarine, succinylcholine, pancuronium)	Potentiation of neuromuscular blockade.
Nifedipine	Decreased quinidine levels.
Potassium	Quinidine effects enhanced by potassium and reduced by hypokalemia.
Quinine	Additive effects of both drugs.
Tricyclic antidepressants	Decreased clearance of some tricyclic antidepressants; additive QT prolongation.
Urinary alkalinizers (e.g., acetazolamide, sodium bicarbonate, some antacids)	Decreased renal excretion of quinidine and increased blood levels.
Verapamil	Increased quinidine levels, hypotension.
Warfarin	Enhanced hypoprothrombinemic effect and bleeding.

^a.Codeine's analgesic effect is mainly due to its metabolism by the hepatic isoenzyme CYP2D6 to morphine. Quinidine inhibits this enzyme. Hydrocodone may depend on the same isoenzyme for conversion to active metabolites.

Supplied

Not currently available for CPhA monographs. Please consult individual product monographs.

Contraindications

Second-degree or complete atrioventricular block, junctional or idioventricular conduction disturbance that might be aggravated by quinidine, uncompensated heart failure, digitalis intoxication, prolonged QT interval (see also Warnings); patients manifesting clinical signs or having a past history of idiosyncrasy or hypersensitivity to quinidine or other cinchona derivatives (e.g., febrile reactions, skin eruptions, thrombocytopenic purpura, systemic lupus erythematosus-like syndrome); history of drug-induced torsades de pointes; myasthenia gravis.

Warnings

Mortality: The results of the Cardiac Arrhythmia Suppression Trial (CAST) in postmyocardial infarction patients with asymptomatic ventricular arrhythmias showed a significant increase in mortality and in nonfatal cardiac arrest rate in patients treated with certain antiarrhythmic agents compared with a matched placebo group. Whether these results apply to other patient populations, or to other antiarrhythmic agents such as quinidine, is uncertain, but it is prudent to consider these results when using any antiarrhythmic agent.

Quinidine should be used with extreme caution in the presence of: incomplete AV block (since a complete block and asystole may result); digitalized patients (quinidine may cause unpredictable abnormalities of rhythm); partial bundle branch block; severe congestive heart failure, cardiogenic shock, severe bradycardia and hypotensive states (quinidine may have a depressant effect on myocardial contractility and arterial pressure); hepatic and renal insufficiency (especially renal tubular acidosis, because of the potential for quinidine accumulation).

In the treatment of atrial fibrillation or flutter, conversion to sinus rhythm may be preceded by an extremely rapid ventricular rate as the degree of AV block is progressively reduced. Agents that inhibit AV node conduction such as digoxin, beta-blockers or verapamil should be used prior to the initiation of quinidine therapy for atrial fibrillation or flutter.

Conversion of atrial fibrillation may be associated with embolism; therefore, anticoagulant treatment may be necessary before administration of quinidine.

Cardiotoxicity: Quinidine cardiotoxicity may be manifested by increased PR and QT intervals, 50% widening of QRS, ventricular ectopic beats or tachycardia. Appearance of these toxic signs during quinidine administration mandates immediate discontinuation of the drug and close clinical and ECG monitoring.

Digitalis Intoxication: Quinidine slows the elimination of digoxin and simultaneously reduces digoxin's apparent volume of distribution. As a result, serum digoxin levels may double or even triple. When used concurrently, digoxin dosage should be reduced by approximately 50%, plasma concentrations should be monitored and patients observed closely for digoxin toxicity.

Hepatotoxicity: A few cases of hepatotoxicity, including granulomatous hepatitis, due to quinidine hypersensitivity have been reported. Unexplained fever and/or elevation of hepatic enzymes, particularly in the early stages of therapy, warrant consideration of possible hepatotoxicity. Cessation of quinidine in these cases usually results in the disappearance of toxicity.

Syncopal Episodes: Quinidine syncope may occur as a complication of long-term therapy. It is manifested by sudden loss of consciousness and ventricular arrhythmias with bizarre QRS complexes of the torsades de pointes type. This syndrome does not appear to be related to dose or plasma levels, but occurs more often with prolonged QT intervals. Syncopal episodes frequently terminate spontaneously, but sometimes are fatal. If quinidine-induced syncope occurs, the drug should be discontinued immediately.

Vagal Stimulation: Because quinidine antagonizes the effect of vagal excitation upon the atrium and the AV node, the administration of parasympathomimetic drugs or the use of any other procedure to enhance vagal activity may fail to terminate paroxysmal supraventricular tachycardia in patients receiving quinidine.

Adverse Effects

Gastrointestinal

Hypersensitivity

Hematologic

Musculoskeletal

Cardiac

Central Nervous System

Hearing

Miscellaneous

Ophthalmic

Hepatic

Overdose

Symptoms

Treatment

Dosage

Equivalent doses for each of the available quinidine salts can be found in Table 1.

Oral: Dosage based on quinidine sulfate equivalent. Quinidine is available in Canada through the Special Access Programme (see Appendix 2). Administer a preliminary test dose of a single tablet of quinidine sulfate to determine whether the patient has a quinidine idiosyncrasy. Continuous or frequent ECG monitoring is desirable when quinidine therapy is initiated, especially if using large doses, i.e., >2 g quinidine sulfate daily. Gastrointestinal symptoms such as nausea, vomiting, diarrhea and colic may be minimized by giving the drug with food.

Premature Atrial and Ventricular Contractions: 200 to 300 mg of quinidine sulfate 3 or 4 times daily. Alternatively, a loading dose of 12 mg/kg, followed by a maintenance dose of 6 mg/kg every 4 to 6 hours has been recommended.

Paroxysmal Supraventricular Tachycardia: 400 to 600 mg of quinidine sulfate every 2 or 3 hours until the paroxysm is terminated.

Atrial Fibrillation or Flutter: Various schedules of quinidine administration have been utilized. One widely used technique is to give 200 mg of quinidine sulfate orally every 2 or 3 hours for up to 8 doses, with subsequent daily increase of the individual dose until sinus rhythm is restored or toxic effects occur. Most clinicians recommend, however, that 300 to 400 mg of quinidine sulfate be given every 6 hours for conversion of atrial fibrillation. The total daily dose should not exceed 3 to 4 g of quinidine sulfate in any regimen.

The patient should be anticoagulated before conversion of atrial fibrillation. Ventricular rate should be brought under control with digoxin, verapamil or β blockers. Congestive heart failure should be controlled if present. Patients should be digitalized before quinidine administration for atrial flutter.

Maintenance Therapy: 200 to 300 mg of quinidine sulfate 3 or 4 times daily. Extended-release tablets may be given every 8 to 12 hours.

Individual product monographs should be consulted for specific recommendations.

Parenteral: Quinidine injection is available in Canada through the Special Access Programme (see Appendix 2).

Specialized references should be consulted for information on the use of parenteral quinidine in the treatment of arrhythmias or malaria.

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