"Having close biological relatives with heart disease can increase your risk of developing this disease. Family health history offers important information to help you and your family members understand health risks and prevent disease.
Inappropriate infusion rate
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 β–receptor blocking agent.
Exacerbated bradycardia in sick sinus syndrome
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).
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.
In patients without implanted pacemakers who are at high risk of complete atrioventricular block (eg, those with digitalis intoxication, second–degree atrioventricular block, or severe intraventricular conduction defects), quinidine should be used only with caution.
Carcinogenesis, mutagenesis, impairment of fertility
Animal studies to evaluate quinidine's carcinogenic or mutagenic potential have not been performed. Similarly, there are no animal data as to quinidine's potential to impair fertility.
Pregnancy Category C
Animal reproductive studies have not been conducted with quinidine. There are no adequate and well–controlled studies in pregnant women. Quinidine should be given to a pregnant woman only if clearly needed.
In one neonate whose mother had received quinidine throughout her pregnancy, the serum level of quinidine was equal to that of the mother, with no apparent ill effect. The level of quinidine in amniotic fluid was about three times higher than that found in serum.
Labor and Delivery
Quinine is said to be oxytocic in humans, but there are no adequate data as to quinidine's effect (if any) on human labor and delivery.
Quinidine is present in human milk at levels slightly lower than those in maternal serum; a human infant ingesting such milk should (scaling directly by weight) be expected to develop serum quinidine levels at least an order of magnitude lower than those of the mother. On the other hand, the pharmacokinetics and pharmacodynamics of quinidine in human infants have not been adequately studied, and neonates' reduced protein binding of quinidine may increase their risk of toxicity at low total serum levels. Administration of quinidine should (if possible) be avoided in lactating women who continue to nurse.
In antimalarial trials, quinidine was as safe and effective in pediatric patients as in adults. Notwithstanding the known pharmacokinetic differences between pediatric patients and adults (see Pharmacokinetics and Metabolism), pediatric patients in these trials received the same doses (on a mg/kg basis) as adults.
Safety and effectiveness of antiarrhythmic use in pediatric patients have not been established.
Safety and efficacy of quinidine in elderly patients has not been systematically studied. Clinical studies of quinidine did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. The reported clinical experience has not identified differences in responses between the elderly and younger patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal or cardiac function and of concomitant disease or other drug therapy.
Last reviewed on RxList: 5/21/2009
This monograph has been modified to include the generic and brand name in many instances.
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