Failure of defibrillation by direct current (DC) shocks is the result in pa
rt of new ventricular tachyarrhythmias induced by the shocks. We investigat
ed the arrhythmogenic substrate produced by the shocks. Fluorescent action
potential (AP) signals were recorded from rabbit hearts perfused in vitro w
ith the use of our original optical recording system. Localized application
of 10-ms shocks (S2) during the plateau phase of APs by basic stimuli (S1)
caused field intensity (FI)-dependent changes in APs: (a) S2 > 7 V/cm caus
ed additional depolarization, giving rise to a prolongation of AP duration
(APD); (b) With S2 > 20 V/cm, terminal repolarization was inhibited, and su
bsequent postshock S1 APs for 1 to 5 min were characterized by decreases in
the maximum diastolic potential and amplitude of APs; and (c) S2 > 30 V/cm
often resulted in a prolonged refractoriness, oscillation of membrane pote
ntial leading to ventricular tachycardia or fibrillation (VT/VF). The right
ventricle was more susceptible than other regions for the aftereffects of
high-intensity shocks. Using an 8-channel recording system, we compared the
effect of IO-ms monophasic (M) and 5/5-ms biphasic (B) shocks applied to t
he whole ventricles with FI of 1 to 20 V/cm at the signal recording sites.
B shocks were less potent than M shocks in the FI-dependent action potentia
l duration (APD) prolongation, and in the shock-induced enhancement of APD
dispersion. Incidence and duration of VT/VF induced by M shocks were signif
icantly greater than those by B shocks. These findings suggest that DC shoc
ks will cause two types of arrhythmogenic substrate: one induced at sites o
f high FI, and the other at sites with moderate FI. The former would produc
e local block or focal repetitive excitation due to prolonged depolarizatio
n and oscillation of membrane potential, and the latter circuitous movement
of wavefronts through an enhancement of spatial inhomogeneity of repolariz
ation.