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Digoxin concentrations in serum, myocardium, 3 separate skeletal muscles, kidney, liver, and 5 sites in the brain were measured in 26 dogs given 12-alpha 3 H-digoxin. Ten of the dogs also received 200 mg of quinidine sulfate orally 3 times daily for 3 days, and 6 others received 240 mg of quinidine gluconate intravenously every 3 hours for 24 hours. Mean serum quinidine concentration was 6.7 ± 1.5 μ g/ml in the dogs treated with quinidine for 24 hours and 3.6 ± 2.3 in the dogs treated with quinidine for 3 days (p Thus, in contrast to the findings in a previous study, there is no evidence of increased concentration of digoxin in the brain or of decreased digoxin concentration in the myocardium when quinidine is given to dogs receiving digoxin. The relationship of serum-to-tissue digoxin concentration changes in some tissues after 24 hours of quinidine administration. The decrease in the ratio of renal-to-serum digoxin concentration suggests that the decrease in renal digoxin clearance with quinidine is due to failure of digoxin to enter the kidney rather than to a block in the excretion of digoxin present in the kidney.

1. 206 upper-arm block procedures were performed with a failure rate of 20 per cent. 2. Although the efficiency and reliability of upper-arm block anesthesia are sometimes disappointing, its safety recommends it strongly. 3. Even in the failures, the need for supplemental anesthesia was markedly decreased.

Creatine kinase (CK), lactic dehydrogenase (LDH), and more recently their isoenzyme determinations (CK-MB and LDH1) have been useful adjuncts in verification of myocardial injury. To determine whether DC cardioversion affects these serum enzyme levels, we recorded total CK, total LDH, CK-MB, and LDH1levels serially during 24 hours following elective DC cardioversion in 18 patients without cardiac ischemia. New postcardioversion elevations in total CK and total LDH levels were small and occasional: CK (one of 18 patients), LDH (four of 18 patients). Elevations of CK-MB or LDH1following cardioversion did not develop in any of the patients. Therefore, new CK-MB or LDH1elevations associated with arrhythmias must result from myocardial damage to DC cardioversion. (JAMA239:122-124, 1978)

Excerpt The treatment of ventricular arrhythmias remains a major challenge. Ventricular arrhythmias may be symptomatic; ventricular arrhythmias after myocardial infarction have recently been correl...

The time course of the rise in serum digoxin concentration was followed in 18 patients treated with digoxin as quinidine treatment was started with a loading dose. The mean serum digoxin levels rose significantly during the first 24 hours after administration of quinidine was begun, and reached a new steady state concentration after about 48 hours. Digoxin kinetics were studied in two groups of normal volunteers: Group I (n = 7) received a small dose of quinidine, 800 mg/day, and group II (n = 8) received 1,600 mg/day. There was no significant mean change in the apparent volume of distribution of digoxin in either group. In group I (small dose), quinidine reduced the digoxin clearance values: total clearance by 30 percent, renal clearance by 32 percent and nonrenal clearance by 29 percent. In group II (large dose), quinidine reduced digoxin total clearance by 36 percent, renal clearance by 54 percent and nonrenal clearance by 22 percent. The reductions in digoxin volume of distribution and renal clearance during quinidine treatment were a function of the serum quinidine concentration. The change in nonrenal clearance of digoxin was independent of serum quinidine concentration.

Two of the most important treatable causes of death in patients with coronary artery disease are the cardiac arrhythmias and conduction abnormalities. They may be associated with acute myocardial infarction (AMI) or chronic ischemia. Detection of such rhythm and conduction abnormalities has been discussed in chapter 5, and their pathophysiology was commented on in chapter 2. For the purpose of discussing therapeutic approaches, AMI can be divided into four phases: (1) the prehospital phase, (2) the CCU phase, (3) the post-CCU phase, and (4) the post-hospital phase. The cardiac arrhythmias and conduction defects encountered in each of these phases will be discussed, as will their therapy. The management of arrhythmias encountered in the setting of chronic ischemic heart disease will also be discussed.

Below-knee amputations are commonly performed for peripheral vascular disease. To be successful, the technic must be exacting, and it is crucial to bevel carefully the anterior and medial tibial surfaces to permit successful prosthetic rehabilitation.

We compared the effects of quinidine and three alternate antiarrhythmic drugs on serum digoxin concentration in 63 patients before and during administration of quinidine, procainamide, disopyramide, or mexiletine. Quinidine increased digoxin concentration by at least 0.5 nmol/L in 21 of 22 patients: Mean serum digoxin rose from 1.2 nmol/L to 2.4 nmol/L (P less than 0.001). Procainamide, disopyramide, or mexiletine increased serum digoxin by 0.5 nmol/L in one of 41 patients. Anorexia, nausea, and vomiting develop soon after starting quinidine therapy in 10 of the 22 patients who received quinidine but in only five of the 41 patients who received procainamide, disopyramide, or mexiletine (P less than 0.01). Quinidine prolonged the PR intervals from 160 +/- 14 ms to 183 +/- 26 ms, but procainamide, disopyramide, and mexiletine did not change the PR interval (P less than 0.005). In digitalized patients, quinidine increases serum digoxin concentration, increases digoxin's effect on atrioventricular conduction, and produces more adverse gastrointestinal effects than procainamide, disopyramide, or mexiletine.

The serum digoxin concentration increased in 25 of 27 study patients (93%), and the mean serum digoxin concentration rose from 1.4 ng/ml to 3.2 ng/ml during quinidine therapy. Anorexia, nausea, or vomiting developed in 16 patients (59%) but disappeared in all ten patients for whom the digoxin dose alone was reduced, suggesting that digoxin excess caused these symptoms. Ventricular premature depolarizations developed in three patients after starting quinidine therapy; ventricular tachycardia developed in one patient, and another died suddenly. When starting quinidine therapy in patients who are taking digoxin, the clinical course, ECG, and serum digoxin level should be followed closely. (JAMA240:533-534, 1978)

We would like to reply to the comments by Matzke and Burkle and those by Cisneros. Matzke and Burkle have reservations regarding the incidence of the interaction. We have made no attempt to state the actual incidence of this interaction; a retrospective study of hospitalized cardiac patients cannot possibly establish a true incidence. We have simply reported the finding of 25 cases in a single medical center in a single year, which suggests to us that the interaction must be common. Based on their mathematical model, Drs Matzke and Burkle expected higher serum digoxin concentrations than we found. The implication of this comment is that serum digoxin concentration may have risen merely from institution of a higher dose, enforced patient compliance in the hospital, or increased absorption from changes in other medications. We do not belive this to be the case for the following reasons: First, the baseline

Excerpt Quinidine has been the prototype of antiarryhthmic drug since it was introduced into clinical practice in 1918, and it is widely used for treatment of both atrial and ventricular arrhythmia...

Quinidine causes an increase in the serum digoxin concentration. Three patients were studied to determine if the increase in serum concentration is paralleled by an increase in the cardiac effect of digoxin. Each patient's clinical condition and serum digoxin concentration were stable when quinidine administration was begun. In all three patients, serum digoxin concentrations increased significantly after beginning quinidine, and decreased when quinidine was discontinued. While taking quinidine, all three patients had ECG findings that suggested enhanced digitalis effect and one patient had clinical evidence of an increased hemodynamic effect. These effects paralleled the increases in serum digoxin concentration. Our findings suggest that the increase in serum digoxin concentration, which occurs after beginning quinidine, is associated with an increase in the effect of digoxin on the heart. ( Arch Intern Med 139:519-521, 1979)