Locally propagated activation immediately after internal defibrillation.

BACKGROUND Electrical mapping studies indicate an interval of 40 to 100 ms between a defibrillation shock and the earliest activation that propagates globally over the ventricles (globally propagated activation, GPA). This study determined whether activation occurs during this interval but propagates only locally before being blocked (locally propagated activation, LPA). METHODS AND RESULTS In five anesthetized pigs, the heart was exposed and a 504-electrode sock with 4-mm interelectrode spacing was pulled over the ventricles. Ten biphasic shocks of a strength near the defibrillation threshold (DFT) were delivered via intracardiac catheter electrodes, and epicardial activation sequences were mapped before and after attempted defibrillation. Local activation was defined as dV/dt < or =-0.5 V/s. Postshock activation times and wave-front interaction patterns were determined with an animated display of dV/dt at each electrode in a computer representation of the ventricular epicardium. LPAs were observed after 40 of the 50 shocks. A total of 173 LPA regions were observed, each of which involved 2+/-2 (mean+/-SD) electrodes. LPAs were observed after both successful and failed shocks but occurred earlier (P<.0001) after failed (35+/-8 ms) than successful (41+/-16 ms) shocks, although the times at which the GPA appeared were not significantly different. On reaching the LPA region, the GPA front either propagated through it (n=135) or was blocked (n=38). The time from the onset of the LPA until the GPA front propagated to reach the LPA region was shorter (P<.01) when the GPA front was blocked (32+/-12 ms) than when it propagated through the LPA region (63+/-20 ms). CONCLUSIONS LPAs exist after successful and failed shocks near the DFT. Thus, the time from the shock to the GPA is not totally electrically silent.

[1]  A. C. Young,et al.  Spread of Excitation During Premature Ventricular Systoles , 1955, Circulation research.

[2]  Directional Difference of Conduction Velocity in the Cardiac Ventricular Syncytium Studied by Microelectrodes , 1959 .

[3]  A. Castellanos,et al.  The Role of Canine Superficial Ventricular Muscle Fibers in Endocardial Impulse Distribution , 1978, Circulation research.

[4]  On-line cardiac mapping: an analog approach using video and multiplexing techniques. , 1982, The American journal of physiology.

[5]  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.

[6]  P D Wolf,et al.  Epicardial activation after unsuccessful defibrillation shocks in dogs. , 1988, The American journal of physiology.

[7]  P D Wolf,et al.  Comparison of activation during ventricular fibrillation and following unsuccessful defibrillation shocks in open-chest dogs. , 1990, Circulation research.

[8]  R Plonsey,et al.  Mechanism of cardiac defibrillation in open-chest dogs with unipolar DC-coupled simultaneous activation and shock potential recordings. , 1990, Circulation.

[9]  W.M. Smith,et al.  Activation in unipolar cardiac electrograms: a frequency analysis , 1990, IEEE Transactions on Biomedical Engineering.

[10]  P. Wolf,et al.  Strength-duration and probability of success curves for defibrillation with biphasic waveforms. , 1990, Circulation.

[11]  Cary Laxer,et al.  A graphical display system for animating mapped cardiac potentials , 1990, [1990] Proceedings. Third Annual IEEE Symposium on Computer-Based Medical Systems.

[12]  R. Sweeney,et al.  Characterization of Refractory Period Extension by Transcardiac Shock , 1991, Circulation.

[13]  S M Dillon,et al.  Optical recordings in the rabbit heart show that defibrillation strength shocks prolong the duration of depolarization and the refractory period. , 1991, Circulation research.

[14]  Capelle,et al.  Dispersion of refractoriness in canine ventricular myocardium. Effects of sympathetic stimulation. , 1991, Circulation research.

[15]  P D Wolf,et al.  Three‐dimensional Potential Gradient Fields Generated by Intracardiac Catheter and Cutaneous Patch Electrodes , 1992, Circulation.

[16]  Y. Cha,et al.  Effects of Lidocaine on Relation Between Defibrillation Threshold and Upper Limit of Vulnerability in Open‐Chest Dogs , 1992, Circulation.

[17]  W. M. Smith,et al.  Effect of field stimulation on cellular repolarization in rabbit myocardium. Implications for reentry induction. , 1992, Circulation research.

[18]  P Lander,et al.  Ambiguities of epicardial mapping. , 1992, Journal of electrocardiology.

[19]  S. Dillon Synchronized Repolarization After Defibrillation Shocks: A Possible Component of the Defibrillation Process Demonstrated by Optical Recordings in Rabbit Heart , 1992, Circulation.

[20]  P. Wolf,et al.  Epicardial mapping of ventricular defibrillation with monophasic and biphasic shocks in dogs. , 1993, Circulation research.

[21]  P D Wolf,et al.  Effects of monophasic and biphasic shocks on action potentials during ventricular fibrillation in dogs. , 1993, Circulation research.

[22]  Halina Podbielska,et al.  Clinical Applications of Modern Imaging Technology II , 1993 .

[23]  B. Roth,et al.  Electrical stimulation of cardiac tissue: a bidomain model with active membrane properties , 1994, IEEE Transactions on Biomedical Engineering.

[24]  R E Ideker,et al.  An automated technique for identification and analysis of activation fronts in a two-dimensional electrogram array. , 1994, Computers and biomedical research, an international journal.

[25]  J.L. Jones,et al.  Refractory period prolongation by biphasic defibrillator waveforms is associated with enhanced sodium current in a computer model of the ventricular action potential , 1994, IEEE Transactions on Biomedical Engineering.

[26]  Eric A. Sobie,et al.  Near-field and far-field stimulation of cardiac muscle , 1994, Photonics West - Lasers and Applications in Science and Engineering.

[27]  J. Wikswo,et al.  Virtual electrodes in cardiac tissue: a common mechanism for anodal and cathodal stimulation. , 1995, Biophysical journal.

[28]  P D Wolf,et al.  Regional capture of fibrillating ventricular myocardium. Evidence of an excitable gap. , 1995, Circulation research.

[29]  R. Ideker,et al.  Impedance to Defibrillation Countershock: Does an Optimal Impedance Exist? , 1995, Pacing and clinical electrophysiology : PACE.

[30]  S M Dillon,et al.  Shock-induced depolarization of refractory myocardium prevents wave-front propagation in defibrillation. , 1996, Circulation research.

[31]  Intracardiac defibrillation-strength shocks produce large regions of hyperpolarization and depolarization , 1996 .

[32]  V. Fast,et al.  Spatial changes in transmembrane potential during extracellular electrical shocks in cultured monolayers of neonatal rat ventricular myocytes. , 1996, Circulation research.

[33]  R. Ideker,et al.  Epicardial Sock Mapping Following Monophasic and Biphasic Shocks of Equal Voltage with an Endocardial Lead System , 1996, Journal of cardiovascular electrophysiology.

[34]  P. Tchou,et al.  Transmembrane Voltage Changes Produced by Real and Virtual Electrodes During Monophasic Defibrillation Shock Delivered by an Implantable Electrode , 1997, Journal of cardiovascular electrophysiology.

[35]  M. Fishbein,et al.  Cellular graded responses and ventricular vulnerability to reentry by a premature stimulus in isolated canine ventricle. , 1997, Circulation.

[36]  G P Walcott,et al.  Effect of Electrode Polarity on Internal Defibrillation with Monophasic and Biphasic Waveforms Using an Endocardial Lead System , 1997, Journal of cardiovascular electrophysiology.