Quinidine, Serum or Plasma

Serum or plasma

1 mL

0.3 mL

Red-top tube or green-top (heparin) tube. Do not use a gel-barrier tube. The use of gel-barrier tubes is not recommended due to slow absorption of the drug by the gel. Depending on the specimen volume and storage time, the decrease in drug level due to absorption may be clinically significant.

This Class 1A drug is useful in both supraventricular and ventricular arrhythmias. It major uses are to maintain sinus rhythm after conversion of atrial flutter or fibrillation, to prevent ventricular tachycardia, and for long-term prophylaxis in patients with AV nodal reentrant tachycardia and automatic atrial tachycardia. Quinidine also has been used to prevent symptomatic premature supraventricular and ventricular complexes. Because it slows conduction and prolongs the refractory period of the accessory pathway and suppresses automaticity of ectopic pacemakers, quinidine may prevent recurrences of paroxysmal supraventricular tachycardia caused by reentry over a concealed pathway or AV reciprocating tachycardia associated with the Wolff-Parkinson-White syndrome. It also may slow the ventricular response to atrial flutter or fibrillation in the preëxcitation syndrome. Quinidine is often preferred to procainamide for long-term therapy because elevated antinuclear antibody titers and drug-induced lupus are common during prolonged therapy with procainamide.

Immunoassay (IA)

Therapeutic: 2.0−5.0 μg/mL

Optimal resampling time after change in dosage is one to two days. Biologic half-life is about six to eight hours. Doses of quinidine >250 mg/day result in increased serum digoxin concentrations about 2.5 times the digoxin concentration before quinidine was added. The new steady-state of digoxin concentration occurs in 7 to 14 days, with signs of toxicity beginning to appear in three to seven days after initiation of quinidine therapy. Therefore, serum digoxin concentrations should be measured before initiation of quinidine therapy and again in four to six days. Measure trough because of variability of peak interval. Renal failure prolongs apparent half-life, perhaps through accumulation of fluorescent metabolites. Severe heart failure also prolongs half-life, as does liver disease. Concomitant administration of phenytoin increases hepatic metabolism, and therefore decreases half-life and serum quinidine concentrations. Clearance may be diminished in the elderly.¹