uinidine It is clear that the elevation of digoxin levels by concurrent quinidine administration results in enhanced electro physiologic effects demon started on the surface electrocardiogram as a prolongation of the PR interval , by central nervous system manifestation s of toxicity such as anorexia , nausea and vomiting also by enhanced ventricular ectopic activity . The elevated serum digoxin levels induced by concurrent administration of digoxin and quinidine have been reported not to show an enhanced inotropic effect as measured by systolic time intervals . Clinical evidence indicates that there are increased electro physiologic and inotropic effects associated with the elevation of serum digoxin as a result of concurrent quinidine administration . In 1978, Ejvinsson reported that the concurrent administration of quinidine to 12 patients increased average serum digoxin concentrations from 0.9 to 1.6 ng/ml. Decisive evidence for a decrease in the nonretail excretion of digoxin under the influence of quinidine was established by comparing the kinetics of digoxin in anuric patients on chronic hemodialysis when given digoxin alone and concomitantly with quinidine . However, in patients with a glomerular filtration rate of less than 50 ml/rnin , the time required for digoxin to reach a new steady state with the addition of quinidine may be considerably longer. , however, measured inotropic effects of digoxin at steady state during digoxin administration alone and during digoxin and quinidine administration . Since glornerular filtration rate is unchanged during concurrent digoxin quinidine administration, it is clear that the decreased renal elimination of digoxin in human beings results from a quinidine- induced decrease in tubular secretion of digoxin . If the dose of quinidine is increased, one can anticipate a further increase in serum digoxin levels. They then gave sufficient digoxin to achieve a serum digoxin concentration similar to that obtained when digoxin and quinidine were given concomitantly.