Adrenergically mediated variations in the energy required to defibrillate the heart: observations in closed-chest, nonanesthetized dogs.

Abstract

The day-to-day variations in epicardial defibrillation threshold (DFT) were examined in closed-chest, unanesthetized dogs. In 11 animals, DFT decreased from 15.8 -+-2.1 J (mean SE) at the beginning of the study (day 1), to 7.4 + 1.7 J on day 2 (p < .0001). DFT measured daily for 5 consecutive days in seven dogs decreased from 22.1 + 3.1 J on day 1 to 9.3 + 2.3 J on day 2 (p < .01) and remained stable from day 2 to day 5. Transcardiac impedance, measured in six dogs, decreased from 112 + 6 Q on day 1 to 100 + 6 Q on day 2 (p = NS). Propranolol given on day 2 in 14 dogs increased DFT from 12.0 + 2.2 to 18.0 ± 3.1 J (p < .05). The effects on DFT of sequential administration of isoproterenol and propranolol were examined in 10 dogs. Isoproterenol decreased DFT from 10. O + 1. 9 to 5.5 + 1. 5 J when given before propranolol (p < .001, n = 10), and from 1 1. 7 -+ 3.0 to 9.7 + 3.1 J when given after propranolol (p < .05, n = 9). Propranolol increased DFT from 10.6 + 3.0 to 14.6 + 3.9 J when given before isoproterenol (p < .02, n = 9), and from 10.7 + 1.4 to 14.4 + 1.5 J when given after isoproterenol (p < .01, n = 10). These experiments demonstrate a sustained cardiac effect of epicardial defibrillation reflected by a decrease in DFT that is partially reversible by propranolol. A similar decrease was produced by /3-adrenergic stimulation, an effect that was partially blocked by propranolol. Thus, variations in the autonomic state of the heart may be an important modulator of cardiac DFT. extends these initial observations to a closed-chest, nonanesthetized preparation, and examines the pattern of DFT measurements repeated daily over several days. Material and methodsDogs weighing between 11 and 19 kg were anesthetized with 22.5 mg/kg pentobarbital and ventilated with a Harvard respirator using room air. A left thoracotomy was performed on each, and the left ventricular free wall was exposed. A 2.5 cm diameter cupped electrode (Parsonnet Porous Epicardial Electrode) was sutured on the anteroapical surface of the left ventricle, and its cable was extended through the rib cage and tunneled under the skin onto the left infrascapular area. The thoracotomy was closed in layers, the skin was sutured, and the dogs were taken back to their cages. Several days after thoracotomy, and after the dogs' complete recovery from the operation, experiments were begun. Each animal was sedated with 2.25 mg/kg subcutaneous morphine sulfate and placed on a rubber thermal blanket to prevent current leakage. This amount of morphine sulfate produced enough sedation to allow placement of the dogs on their sides, loosely restrained, for the duration of the experiment. The animals, however, were awake, responsive, and did not require respiratory support.

Interação entre drogas antiarrítmicas e limiares de desfibrilação em pacientes portadores de cardioversor desfibrilador implantável

“…Os efeitos dos betabloqueadores sobre a desfibrilação ventricular parecem ser variáveis, de acordo com o tipo de droga utilizada. O propranolol foi responsável por elevação de limiares em dois estudos 19,20 . Os autores atribuíram este efeito mais à sua ação estabilizadora de membrana do que à sua atividade bloqueadora betadrenérgica.…”

Does Acute Volume Overloading in the Setting of Left Ventricular Dysfunction and Pulmonary Hypertension Affect the Defibrillation Threshold?

“…The present study's objective was to document whether acutely elevated pulmonary capillary wedge pressures (PCWPs) significantly affect the DFT in the setting of impaired left ventricular function. In particular, the DFT was determined and compared at baseline, with both mildly elevated PCWP (12)(13)(14)(15)(16)(17)(18)(19), and with grossly elevated PCWP (> 19 mmHg) in a canine model of acute volume overload with moderate left ventricular dysfunction.…”

Racing to the flatline: heart rate and β-adrenergic stimulation quicken the pace

“…Do ␤-blockers prolong the maintenance of adequate levels of metabolic reserve during ischemia to maintain VF while also reducing defibrillation threshold? Could ␤-blockers alter mechanisms that maintain VF during ischemia and shorten the time to asystole (10) or increase defibrillation threshold (14)? Answers to these questions, and many others, will likely have significant impact on improving therapy for OHCA.…”