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P wave triggered pacemakers can produce complicated arrhythmias during normal function. A ventricular, R wave inhibited pacemaker and an atrial sensing pacemaker were both present and functioning normally in the patient reported here. A premature paced beat was observed every 12th beat which resulted from discharge of the atrial sensing pacemaker. This arrhythmia appeared because a "P" wave occurred during the noise sampling period of the atrial sensing pacemaker, disabling the demand function and resulting in generator discharge on or near the T wave of a preceding unsensed beat while the pacemaker was in the asynchronous mode.

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.