Influence of postshock epicardial activation patterns on initiation of ventricular fibrillation by upper limit of vulnerability shocks.

BACKGROUND Shocks of identical strength and timing sometimes induce ventricular fibrillation (VFI) and other times do not (NoVFI). To investigate this probabilistic behavior, a shock strength near the upper limit of vulnerability, ULV(50), was delivered to yield equal numbers of VFI and NoVFI episodes. METHODS AND RESULTS In 6 pigs, a 504-electrode sock was pulled over the ventricles. ULV(50) was determined by scanning the T wave. S(1) pacing was from the right ventricular apex. Ten S(2) shocks of approximate ULV(50) strength were delivered at the same S(1)-S(2) coupling interval. Intercycle interval (ICI) and wave front conduction time (WCT) were determined for the first 5 postshock cycles. ICI and the WCT of cycle 1 were not different for VFI versus NoVFI episodes (P=0.3). Beginning at cycle 2, ICI was shorter and WCT was longer for VFI than NoVFI episodes (P<0.05). CONCLUSIONS The first cycle after shocks of the same strength (ULV(50)) delivered at the same time has the same activation pattern regardless of shock outcome. During successive cycles, however, a progressive decrease in ICI and increase in WCT occur during VFI but not NoVFI episodes. These findings suggest shock outcome is (1) deterministic but exquisitely sensitive to differences in electrophysiological state at the time of the shock that are too small to detect or (2) probabilistic and not determined until after the first postshock cycle.

[1]  T. Sano Mechanism of cardiac fibrillation. , 1976, Pharmacology & therapeutics. Part B: General & systematic pharmacology.

[2]  G. Moe,et al.  Nonuniform Recovery of Excitability in Ventricular Muscle , 1964, Circulation research.

[3]  Carl J. Wiggers,et al.  VENTRICULAR FIBRILLATION DUE TO SINGLE, LOCALIZED INDUCTION AND CONDENSER SHOCKS APPLIED DURING THE VULNERABLE PHASE OF VENTRICULAR SYSTOLE , 1940 .

[4]  P. Wolf,et al.  Mechanism of Ventricular Vulnerability to Single Premature Stimuli in Open‐Chest Dogs , 1988, Circulation research.

[5]  T. Sawanobori,et al.  Mechanism Initiating Ventricular Fibrillation Demonstrated in Cultured Ventricular Muscle Tissue , 1970, Circulation research.

[6]  By David,et al.  Extrasystoles and Allied Arralythmias , 1953, The Indian Medical Gazette.

[7]  R. Ideker,et al.  Effects of transvenous electrode polarity and waveform duration on the relationship between defibrillation threshold and upper limit of vulnerability. , 1997, Circulation.

[8]  P D Wolf,et al.  Activation during ventricular defibrillation in open-chest dogs. Evidence of complete cessation and regeneration of ventricular fibrillation after unsuccessful shocks. , 1986, The Journal of clinical investigation.

[9]  P. Wolf,et al.  Influence of shock strength and timing on induction of ventricular arrhythmias in dogs. , 1988, The American journal of physiology.

[10]  José Jalife,et al.  Cardiac electrophysiology and arrhythmias , 1985 .

[11]  D. Rosenbaum,et al.  Mechanism linking T-wave alternans to the genesis of cardiac fibrillation. , 1999, Circulation.

[12]  W. M. Smith,et al.  The effects of ventricular fibrillation duration and site of initiation on the defibrillation threshold during early ventricular fibrillation. , 1998, Journal of the American College of Cardiology.

[13]  R. Ideker,et al.  Locally propagated activation immediately after internal defibrillation. , 1998, Circulation.

[14]  Samuel D. Stearns,et al.  Signal processing algorithms using Fortran and C , 1992 .

[15]  D. T. Kaplan,et al.  Chaos in Cardiology , 1991 .