Quinidine Gluconate Solution
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Questions & Answers
Side Effects & Adverse Reactions
Inappropriate infusion rate — Overly rapid infusion of quinidine (see Dosage and Administration) may cause peripheral vascular collapse and severe hypotension.
Proarrhythmic effects — Like many other drugs (including all other class 1a antiarrhythmics), quinidine prolongs the QTc interval, and this can lead to torsades de pointes, a life–threatening ventricular arrhythmia (see Overdosage). The risk of torsades is increased by any of bradycardia, hypokalemia, hypomagnesemia, and high serum levels of quinidine, but it may appear in the absence of any of these risk factors. The best predictor of this arrhythmia appears to be the length of the QTc interval, and quinidine should be used with extreme care in patients who have preexisting long–QT syndromes, who have histories of torsades de pointes of any cause, or who have previously responded to quinidine (or other drugs that prolong ventricular repolarization) with marked lengthening of the QTc interval. Estimation of the incidence of torsades in patients with therapeutic levels of quinidine is not possible from the available data.
Other ventricular arrhythmias that have been reported with quinidine include frequent extrasystoles, ventricular tachycardia, ventricular flutter, and ventricular fibrillation.
Paradoxical increase in ventricular rate in atrial flutter/fibrillation — When quinidine is administered to patients with atrial flutter/fibrillation, the desired pharmacologic reversion to sinus rhythm may (rarely) be preceded by a slowing of the atrial rate with a consequent increase in the rate of beats conducted to the ventricles. The resulting ventricular rate may be very high (greater than 200 beats per minute) and poorly tolerated. This hazard may be decreased if partial atrioventricular block is achieved prior to initiation of quinidine therapy, using conduction–reducing drugs such as digitalis, verapamil, diltiazem, or a ß–receptor blocking agent.
Exacerbated bradycardia in sick sinus syndrome — In patients with the sick sinus syndrome, quinidine has been associated with marked sinus node depression and bradycardia.
Pharmacokinetic considerations — Renal or hepatic dysfunction causes the elimination of quinidine to be slowed, while congestive heart failure causes a reduction in quinidine’s apparent volume of distribution. Any of these conditions can lead to quinidine toxicity if dosage is not appropriately reduced. In addition, interactions with coadministered drugs can alter the serum concentration and activity of quinidine, leading either to toxicity or to lack of efficacy if the dose of quinidine is not appropriately modified (see Precautions/Drug Interactions).
Vagolysis — Because quinidine opposes the atrial and A–V nodal effects of vagal stimulation, physical or pharmacological vagal maneuvers undertaken to terminate paroxysmal supraventricular tachycardia may be ineffective in patients receiving quinidine.
Legal Issues
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FDA Safety Alerts
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Manufacturer Warnings
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FDA Labeling Changes
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Uses
Treatment of malaria — Quinidine gluconate injection is indicated for the treatment of life–threatening Plasmodium falciparum malaria.
Conversion of atrial fibrillation/flutter — Quinidine gluconate injection is also indicated (when rapid therapeutic effect is required, or when oral therapy is not feasible) as a means of restoring normal sinus rhythm in patients with symptomatic atrial fibrillation/flutter whose symptoms are not adequately controlled by measures that reduce the rate of ventricular response. If this use of quinidine gluconate does not restore sinus rhythm within a reasonable time, then its use should be discontinued.
Treatment of ventricular arrhythmias — Quinidine gluconate injection is also indicated for the treatment of documented ventricular arrhythmias, such as sustained ventricular tachycardia, that in the judgement of the physician are life–threatening. Because of the proarrhythmic effects of quinidine, its use with ventricular arrhythmias of lesser severity is generally not recommended, and treatment of patients with asymptomatic ventricular premature contractions should be avoided. Where possible, therapy should be guided by the results of programmed electrical stimulation and/or Holter monitoring with exercise.
Antiarrhythmic drugs (including quinidine) have not been shown to enhance survival in patients with ventricular arrhythmias.
History
There is currently no drug history available for this drug.
Other Information
Quinidine is an antimalarial schizonticide and an antiarrhythmic agent with class 1a activity; it is the d–isomer of quinine and its molecular weight is 324.43. Quinidine gluconate is the gluconate salt of quinidine; its chemical name is cinchonan–9–ol, 6'–methoxy–, (9S)–, mono–D–gluconate; its structural formula is
its empirical formula is C20H24N2O2•C6H12O7, and its molecular weight is 520.58, of which 62.3% is quinidine base.
Each vial of Quinidine Gluconate Injection contains 800 mg (1.5 mmol) of quinidine gluconate (500 mg of quinidine) in 10 mL of Sterile Water for Injection, 0.005% of edetate disodium, 0.25% phenol, and (as needed) D–gluconic acid δ–lactone to adjust the pH.
Sources
Quinidine Gluconate Solution Manufacturers
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Eli Lilly And Company
![Quinidine Gluconate Solution [Eli Lilly And Company]](/wp-content/themes/bootstrap/assets/img/loading2.gif)
Quinidine Gluconate Solution | Eli Lilly And Company
Because the kinetics of absorption may vary with the patient's peripheral perfusion, intramuscular injection of quinidine gluconate is not recommended.
Treatment of P. falciparum malaria — Two regimens have each been shown to be effective, with or without concomitant exchange transfusion. There are no data indicating that either should be preferred to the other.
In Regimen A, each patient received a loading dose of 15 mg/kg of quinidine base (that is, 24 mg/kg of quinidine gluconate) in 250 mL of normal saline infused over 4 hours. Thereafter, each patient received a maintenance regimen of 7.5 mg/kg of base (12 mg/kg of quinidine gluconate) infused over 4 hours every 8 hours, starting 8 hours after the beginning of the loading dose. This regimen was continued for 7 days, except that in patients able to swallow, the maintenance infusions were discontinued, and approximately the same daily doses of quinidine were supplied orally, using 300–mg tablets of quinidine sulfate.
In Regimen B, each patient received a loading dose of 6.25 mg/kg of quinidine base (that is, 10 mg/kg of quinidine gluconate) in approximately 5 mL/kg of normal saline over 1–2 hours. Thereafter, each patient received a maintenance infusion of 12.5 μg/kg/min of base (that is, 20 μg/kg/min of quinidine gluconate). In patients able to swallow, the maintenance infusion was discontinued, and eight–hourly oral quinine sulfate was administered to provide approximately as much daily quinine base as the patient had been receiving quinidine base (for example, each adult patient received 650 mg of quinine sulfate every eight hours). Quinidine/quinine therapy was continued for 72 hours or until parasitemia had decreased to 1% or less, whichever came first. After completion of quinidine/quinine therapy, adults able to swallow received a single 1500–mg/75–mg dose of sulfadoxine/pyrimethamine (FANSIDAR®, Roche Laboratories) or a seven–day course of tetracycline (250 mg four times daily), while those unable to swallow received seven–day courses of intravenous doxycycline hyclate (VIBRAMYCIN®, Roerig), 100 mg twice daily. Most of the patients described as having been treated with this regimen also underwent exchange transfusion. Small children have received this regimen without dose adjustment and with apparent good results, notwithstanding the known differences in quinidine pharmacokinetics between pediatric patients and adults (see Clinical Pharmacology).
Even in patients without preexisting cardiac disease, antimalarial use of quinidine has occasionally been associated with hypotension, QTc prolongation, and cinchonism; see Warnings.
Treatment of symptomatic atrial fibrillation/flutter — A patient receiving an intravenous infusion of quinidine must be carefully monitored, with frequent or continuous electrocardiography and blood–pressure measurement. The infusion should be discontinued as soon as sinus rhythm is restored: the QRS complex widens to 130% of its pre–treatment duration; the QTc interval widens to 130% of its pre–treatment duration, and is then longer than 500 ms; P waves disappear; or the patient develops significant tachycardia, symptomatic bradycardia, or hypotension.
To prepare quinidine for infusion, the contents of the supplied vial (80 mg/mL) should be diluted to 50 mL (16 mg/mL) with 5% dextrose. The resulting solution may be stored for up to 24 hours at room temperature or up to 48 hours at 4°C (40°F).
Because quinidine may be absorbed to PVC tubing, tubing length should be minimized. In one study (Am J Health Syst Pharm. 1996; 53:655–8), use of 112 inches of tubing resulted in 30% loss of quinidine, but drug loss was less than 3% when only 12 inches of tubing was used.
An infusion of quinidine must be delivered slowly, preferable under control of a volumetric pump, no faster than 0.25 mg/kg/min (that is, no faster than 1 mL/kg/hour). During the first few minutes of the infusion, the patient should be monitored especially closely for possible hypersensitive or idiosyncratic reactions.
Most arrhythmias that will respond to intravenous quinidine will respond to a total dose of less than 5 mg/kg, but some patients may require as much as 10 mg/kg. If conversion to sinus rhythm has not been achieved after infusion of 10 mg/kg, then the infusion should be discontinued, and other means of conversion (eg, direct–current cardioversion) should be considered.
Treatment of life–threatening ventricular arrhythmias — Dosing regimens for the use of intravenous quinidine gluconate in controlling life–threatening ventricular arrhythmias have not been adequately studied. Described regimens have generally been similar to the regimen described just above for the treatment of symptomatic atrial fibrillation/flutter.
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