Delivery of a strong electric shock to the heart remains the only effe
ctive therapy against ventricular fibrillation. Despite significant im
provements in implantable cardioverter defibrillator (ICD) therapy, th
e fundamental mechanisms of defibrillation remain poorly understood. W
e have recently demonstrated that a monophasic defibrillation shock pr
oduces a highly nonuniform epicardial polarization pattern, referred t
o as a virtual electrode pattern (VEP), The VEP consists of large adja
cent areas of strong positive and negative polarization. We sought to
determine whether the VEP may be responsible for defibrillation failur
e by creating dispersion of postshock repolarization and reentry. Trun
cated exponential biphasic and monophasic shocks were delivered from a
bipolar ICD lend in Langendorff-perfused rabbit hearts. Epicardial el
ectrical activity was mapped during and after defibrillation shocks an
d shocks applied at the plateau phase of a normal action potential pro
duced by ventricular pacing. A high-resolution fluorescence mapping sy
stem with 256 recording sites and a voltage-sensitive dye were used. B
iphasic shocks with a weak second phase (<20% lending-edge voltage of
the second phase with respect to the leading-edge voltage of the first
phase) produced VEPs similar to monophasic shocks. Biphasic shocks wi
th a strong second phase (>70%) produced VEPs of reversed polarity. Bo
th of these waveforms resulted in extra beats and arrhythmias. However
, biphasic waveforms with intermediate second-phase voltages (20% to 7
0% of first-phase voltage) produced no VEP, because of an asymmetric r
eversal of the first-phase polarization. Therefore, there was no subst
rate for postshock dispersion of repolarization. Shocks producing stro
ng VEPs resulted in postshock reentrant arrhythmias via a mechanism of
phase singularity. Points of phase singularity were coated by the sho
ck in the intersection of areas of positive, negative, and no polariza
tion, which were set by the shock to excited, excitable, and refractor
y states, respectively. Shock-induced VEPs may reinduce arrhythmias vi
a a phase-singularity mechanism. Strong shocks may overcome the presho
ck electrical activity and create phase singularities, regardless of t
he preshock phase distribution. Optimal defibrillation waveforms did n
ot produce VEPs because of an asymmetric effect of phase reversal on m
embrane polarization.