The efficacy of self-adhesive electrode pads for defibrillation and cardioversion was assessed in 80 patients who received 267 shocks from self-adhesive pads. In all but two patients, defibrillation or cardioversion was achieved at least once. The pads were equally effective when used in the apex-anterior or apex-posterior position. The transthoracic impedance using self-adhesive pads was 75 +/- 21 ohms (mean +/- standard deviation), which is similar to previously reported transthoracic impedance in defibrillation, using standard hand-held electrode paddles of 67 +/- 36 ohms. It is concluded that self-adhesive electrode pads are effective for defibrillation and cardioversion.

We compared the success rates and energy requirements of two electrode-paddle positions (anteroposterior vs. anterolateral) and different paddle sizes in the elective cardioversion of atrial arrhythmias. We prospectively studied 173 patients - 111 in atrial fibrillation and 62 in atrial flutter. The anterolateral paddles used were either two standard-size (8.5-cm diameter) paddles or one 13-cm diameter anterior paddle with one standard-size lateral paddle. The anteroposterior paddles used were either a standard-size or a 13-cm anterior paddle with 12-cm posterior paddle. Overall cardioversion success rates with either paddle position were similar (greater than 90 per cent). The larger paddles did not significantly reduce energy requirements for cardioversion of either arrhythmia. We conclude that anterolateral paddles are as effective as anteroposterior paddles for the elective cardioversion of atrial arrhythmias, and that there is no demonstrable advantage to using paddles that are larger than the standard size in either position.

Our purpose was to assess the effect of myocardial ischemia, left ventricular hypertrophy, and systemic hypoxia and acid-base abnormalities on the energy requirements for defibrillation. We determined the defibrillation threshold (DFT), the minimum energy required to defibrillate. DFT was not significantly elevated after left anterior descending coronary occlusion, nor was there a relationship between the size of the occluded coronary distribution area (coronary risk area) and the change in DFT in individual animals. Renal hypertension and left ventricular hypertrophy were induced by unilateral nephrectomy and contralateral renal artery stenosis. DFT in left ventricular hypertrophy dogs was not significantly higher than in dogs without hypertrophy. Finally, we induced systemic hypoxia and acid-base abnormalities. Neither respiratory nor metabolic acid-base disturbances affected DFT, but during systemic hypoxia (O2 tension 45 +/- 2) DFT fell from 83 +/- 49 to 58 +/- 28 J (P less than 0.01). Thus in dogs, myocardial ischemia, left ventricular hypertrophy, and acid-base abnormalities do not elevate defibrillation energy requirements, whereas hypoxia reduces the energy needed to defibrillate.

The purpose of this study was to determine the effect of the antiarrhythmic drugs lidocaine and bretylium on the minimal energy requirement for transthoracic defibrillation--the defibrillation threshold. Closed chest dogs were anesthetized with chloralose or pentobarbital; lidocaine was administered at varying rates for 2 hours and defibrillation threshold periodically redetermined. Similar protocols were followed for bretylium. Serum lidocaine levels from therapeutic to toxic ranges were obtained, and up to a 60% (p less than 0.05) increase in defibrillation threshold in the pentobarbital-anesthetized dogs was demonstrated. In chloralose-anesthetized dogs the lidocaine effect was modest, with only a 10 to 20% rise in defibrillation threshold (p = NS) despite similar increases in serum lidocaine levels. Thus, lidocaine increases the minimal energy requirements for transthoracic defibrillation, but this effect is in part anesthesia-related, indicating a lidocaine-pentobarbital interaction. When phentolamine was administered to chloralose-anesthetized dogs receiving lidocaine, defibrillation threshold rose 13% (p less than 0.05); this suggests that alpha-adrenergic receptor blockade is at least in part the mechanism of the pentobarbital-lidocaine interaction on defibrillation threshold. Bretylium with either anesthetic had no significant effect on defibrillation threshold.

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