R V Ditchey — Page 2 | PubMed Health

PubMed1981

Safety of electrical cardioversion in patients without digitalis toxicity.

To ascertain whether electrical cardioversion increases ventricular ectopy in patients receiving nontoxic doses of digitalis, we recorded continuous electrocardiograms in 21 patients for at least 1 hour before and immediately after direct-current countershock. Seventeen patients also received specific antiarrhythmic therapy. There were no consistent differences in the frequency of severity of ventricular ectopy before and after cardioversion despite a wide range of serum digoxin levels (0.1 to 3.0 ng/mL; mean, 1.6 ng/mL). No patient had ventricular tachycardia after cardioversion, and all eight patients with serum digoxin levels greater than 2.0 ng/mL had the same or fewer ventricular ectopic beats per hour and the same or lower ectopy grades after cardioversion when pre- and postshock recordings were compared. These findings suggest that patients receiving digoxin without clinical evidence of digitalis toxicity are at low risk for serious postcardioversion ventricular arrhythmias, even when serum digoxin levels are modestly elevated. The extent to which this low risk is due to concomitant antiarrhythmic therapy is unknown

Adult↗

PubMed1981

Effects of apparently nontoxic doses of digoxin on ventricular ectopy after direct-current electrical shocks in dogs.

To determine whether nontoxic doses of digoxin increase the risk of serious ventricular arrhythmias after d.c. cardioversion, studies were made of the effects of different doses of digoxin on the incidence and severity of ventricular arrhythmias after graded, external d.c. shocks in 14 closed-chest dogs. Electrocardiograms were recorded continuously for 20 min before and 10 min immediately after sequential QRS-synchronized shocks of 10, 100 and 150 joules. Ventricular premature beats were counted and their severity was graded. Digoxin (0.01--0.05 mg/kg) was then given i.v. to 12 dogs. Despite a wide range of serum digoxin concentrations (1.3--12.5 ng/ml), electrocardiographic signs of digitalis toxicity did not develop in any of these animals. The same sequence of d.c. shocks was repeated after 2 hr in nine dogs and after more than 24 hr in three dogs. Neither the total number of ventricular ectopic beats nor the arrhythmia grade postshock differed significantly before and after digoxin. Furthermore, more dogs developed ventricular ectopy at each energy level after control shocks than following shocks after digoxin administration. Two additional dogs were given repeated digoxin doses until electrocardiographic evidence of digitalis toxicity was apparent. Both developed sustained ventricular tachycardia after electrical shocks at all energy levels. Whereas overt digitalis toxicity predisposes to serious ventricular arrhythmias after d.c. shocks, we conclude that the risk of postshock ventricular ectopy is not increased by pretreatment with apparently nontoxic digoxin doses.

Animals↗