Post-Countershock Arrhythmias in Untreated and Digitalized Dogs

Abstract

Recent studies suggest that countershock can stimulate cardiac autonomic nerves and that the resulting release of norepinephrine contributes to postcountershock (PCS) arrhythmias. /J-Adrenergic receptor blocking agents, reserpine, cocaine, and cardiac-denervated preparations were used to evaluate this hypothesis in dogs under pentobarbital anesthesia. The suitability of the dog as an experimental system was examined. In the normal dog, the duration of PCS arrhythmia caused by a countershock of given energy was increased 100% by ouabain (0.05 mg/kg iv). In both normal dogs and dogs given ouabain (0.05 mg/kg iv), dicbloroisoproterenol, pronethalol, and propranolol reduced the duration of PCS arrhythmia; reserpine, a norepinephrine depletor, reduced the duration of PCS arrhythmia; cocaine, a norepinephrine-uptake inhibitor possessing antiarrhythmic properties, increased the duration of PCS arrhythmia; denervation of the heart reduced the duration of PCS arrhythmia. Ouabain (0.05 mg/kg iv) reduced the duration of PCS arrhythmia in dogs with denervated hearts. These findings indicate that PCS arrhythmia in dogs is norepinephrine dependent. Evidence indicated that ouabain has an antiadrenergic action on the heart also is presented.From the Studies on the physiology of countershock, in preparation. LEAD I FROM DOGA -I5v Trigger input B -Sawtooth output C " Sowtooth input D " Pulse output E -Gate output ELECTRONICS FOR MEDICINE FIGURE 1A block diagram of the electronic circuitry used. This apparatus can be assembled from standard eQuipment which is available in most laboratories. A is the "trigger in" (15 v) of a Tektronix waoeform generator (WFC) operated in the "triggered" mode. The triggering pulse is a 4 msec, 15 v, square wave supplied by the Schmitt trigger. B is the "sawtooth out"; C is the "sawtooth input" of a pulse generator (PC); D is the "pulse output" of a pulse generator; and E is the "gate output" of a pulse generator.

Ventricular Arrhythmias Induced hy Electrical Cardioversion in Digitalised Patients

“…The report of Castellanos et al [7], which remains the only controlled study in this field, showed that none of 16 patients developed arrhythmia with a 20-watt shock prior to digitalisation, whereas 4 of the 16 had ventricular ectopic activity with the same shock when digitalised. Animal studies confirmed that digitalis 'sensitised' the heart to electric shock [8,9], In dogs ns CCF = Congestive cardiac failure; HR = heart rate; ns = not significant. Dose of quinidine was 500 mg daily in 72% of cases and > 500 mg in 38%.…”

“…(2) The type and time course of the arrhyth mias documented are similiar to those described in the early clinical reports [3,[5][6][7] which were sometimes associated with ventricular fibrillation. (3) Animal stud ies show ventricular ectopic activity is the early sign of digoxin/shock interaction [8]. (4) The type of arrhythmia…”

“…Therefore we now report our results with 50 consecutive cardioversions in digitalised patients who showed no clinical or ECG evidence of toxicity com pared to 33 cardioversions performed in non-digitalised patients over the same time period. Because the inci dence of actual life-threatening arrhythmia following cardioversion is rare, the main endpoint of this study was the occurrence of lesser ventricular arrhythmia -the approach used in previous clinical [7,12,13] and animal studies [8][9][10][11]. …”

“…The use of digoxin was the only variable found to be independently associated with the occurrence of arrhythmia (p < 0.05). With the cardioversion protocol used in this study digitalised patients had an increased incidence of post-cardioversion ventricular arrhythmias, even in the absence of clinical and elec trocardiographic features of digoxin toxicity, and these arrhythmias may represent an increased risk of ventricular fibrillation.transthoracic shocks above a certain threshold induced ventricular ectopics and progressive shock increments caused a corresponding increase in the duration and severity of ventricular ectopic activity with the eventual induction of ventricular tachycardia [8]. The addition of digoxin reduced the thresholds for the onset of ventricu lar ectopics [8] and ventricular tachycardia [9].…”

“…The addition of digoxin reduced the thresholds for the onset of ventricu lar ectopics [8] and ventricular tachycardia [9]. How ever, many of the patients reported in the clinical studies had electrocardiogrphic (ECG) evidence of digoxin tox icity [3,5,6] and toxic doses of digoxin were often used in the animal studies [9], therefore the relationship between 'therapeutic' digoxin levels and electic counter shock remained unclear.…”