TY - JOUR
T1 - Adrenergically mediated variations in the energy required to defibrillate the heart
T2 - Observations in closed-chest, nonanesthetized dogs
AU - Ruffy, R.
AU - Schechtman, K.
AU - Monje, E.
AU - Sandza, J.
PY - 1986
Y1 - 1986
N2 - 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 Ω on day 1 to 100 ± 6 Ω 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 of DFT of sequential administration of isoproterenol and propranolol were examined in 10 dogs. Isoproterenol decreased DFT from 10.0 ± 1.9 to 5.5 ± 1.5 J when given before propranolol (p < .001, n = 10), and from 11.7 ± 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 β-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 cardial DFT. These findings, however, are experimental, and do not support the use of isoproterenol alone in traditional clinical defibrillation.
AB - 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 Ω on day 1 to 100 ± 6 Ω 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 of DFT of sequential administration of isoproterenol and propranolol were examined in 10 dogs. Isoproterenol decreased DFT from 10.0 ± 1.9 to 5.5 ± 1.5 J when given before propranolol (p < .001, n = 10), and from 11.7 ± 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 β-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 cardial DFT. These findings, however, are experimental, and do not support the use of isoproterenol alone in traditional clinical defibrillation.
UR - http://www.scopus.com/inward/record.url?scp=0022652764&partnerID=8YFLogxK
U2 - 10.1161/01.CIR.73.2.374
DO - 10.1161/01.CIR.73.2.374
M3 - Article
C2 - 2867836
AN - SCOPUS:0022652764
SN - 0009-7322
VL - 73
SP - 374
EP - 380
JO - Circulation
JF - Circulation
IS - 2
ER -