BACKGROUND: Recent studies examining mechanisms of defibrillation have focused on prolongation of graded cellular response duration during refractory period stimulation. This mechanism assumes that defibrillation shocks interact with ventricular cells during the process of repolarization. METHODS AND RESULTS: To test this assumption, we examined monophasic action potentials (MAPs) from 171 episodes of induced ventricular dysrhythmia associated with loss of systemic perfusion pressure in 22 patients undergoing nonthoracotomy defibrillator implantation. Ventricular fibrillation (VF)/polymorphic ventricular tachycardia (PVT), defined by an irregular limb lead I morphology, was present in 156 dysrhythmia episodes. Monomorphic ventricular tachycardia (VT), present in the remaining 15 episodes, was associated with regular limb lead morphology. All episodes were examined for MAP cycle length, variation, fractionation, and repolarization. VF/PVT cycle length was 215 +/- 28 msec, with a 14 +/- 7% (33 +/- 20-msec) cycle length variability. Nonfractionated MAP recordings were found in 122 of 156 VF/PVT episodes. Episodes characterized as VF by ECG criteria (n = 136) showed lack of MAP diastole and had a mean cycle length of 213 +/- 27 msec. Episodes characterized as PVT (n = 20) were associated with amiodarone therapy and had occasional MAP diastole and a significantly longer mean cycle length of 257 +/- 22 msec (p < 0.001). Monomorphic VT had a mean cycle length of 261 +/- 29 msec, minimal cycle length variation (1 +/- 3%), absence of MAP fractionation, and consistent degree of repolarization before restimulation. CONCLUSIONS: These results suggest that human VF cycle length is limited by cellular refractory periods so that defibrillating shocks interact with cells primarily during their refractory period.
BACKGROUND: Recent studies examining mechanisms of defibrillation have focused on prolongation of graded cellular response duration during refractory period stimulation. This mechanism assumes that defibrillation shocks interact with ventricular cells during the process of repolarization. METHODS AND RESULTS: To test this assumption, we examined monophasic action potentials (MAPs) from 171 episodes of induced ventricular dysrhythmia associated with loss of systemic perfusion pressure in 22 patients undergoing nonthoracotomy defibrillator implantation. Ventricular fibrillation (VF)/polymorphic ventricular tachycardia (PVT), defined by an irregular limb lead I morphology, was present in 156 dysrhythmia episodes. Monomorphic ventricular tachycardia (VT), present in the remaining 15 episodes, was associated with regular limb lead morphology. All episodes were examined for MAP cycle length, variation, fractionation, and repolarization. VF/PVT cycle length was 215 +/- 28 msec, with a 14 +/- 7% (33 +/- 20-msec) cycle length variability. Nonfractionated MAP recordings were found in 122 of 156 VF/PVT episodes. Episodes characterized as VF by ECG criteria (n = 136) showed lack of MAP diastole and had a mean cycle length of 213 +/- 27 msec. Episodes characterized as PVT (n = 20) were associated with amiodarone therapy and had occasional MAP diastole and a significantly longer mean cycle length of 257 +/- 22 msec (p < 0.001). Monomorphic VT had a mean cycle length of 261 +/- 29 msec, minimal cycle length variation (1 +/- 3%), absence of MAP fractionation, and consistent degree of repolarization before restimulation. CONCLUSIONS: These results suggest that humanVF cycle length is limited by cellular refractory periods so that defibrillating shocks interact with cells primarily during their refractory period.
Authors: Bokyung Min; Jeffrey Kluger; James S Kalus; Danette Guertin; Brian F McBride; C Michael White Journal: Ann Noninvasive Electrocardiol Date: 2005-07 Impact factor: 1.468