Quinidine is an effective antiarrhythmic agent whose therapeutic effects and toxicity have been related to its serum concentrations. Many patients with cardiac arrhythmias also suffer from congestive heart failure. It is well documented that congestive heart failure can reduce blood perfusion to many regions of the body, and could conceivably alter drug pharmacokinetics. A pharmacokinetic evaluation of two sets of quinidine data in congestive heart failure patients indicates that congestive heart failure reduced the rate of absorption and volume of distribution following oral or intramuscular administration of quinidine. Furthermore, the amount of quinidine absorbed following oral administration is reduced, but congestive heart failure does not appear to alter the elimination rate of quinidine. The interpretation of the data presented herein strongly suggests that the site of administration, extent of distribution, and rate of absorption must be considered when determining dosage regimens in congestive heart failure patients since normal dosages in these patients result in abnormally high serum quinidine concentrations.