Several different patterns of wave break have been described by mapping of
the tissue surface during fibrillation. However, it is not clear whether th
ese surface patterns are caused by multiple distinct mechanisms or by a sin
gle mechanism. To determine the mechanism by which wave breaks are generate
d during ventricular fibrillation, we conducted optical mapping studies and
single cell transmembrane potential recording in six isolated swine right
ventricles (RV). Among 763 episodes of wave break (0.75 times.s(-1).cm(-2))
, optical maps showed three patterns: 80% due to a wave front encountering
the refractory wave back of another wave, 11.5% due to wave fronts passing
perpendicular to each other, and 8.5% due to a new (target) wave arising ju
st beyond the refractory tail of a previous wave. Computer simulations of s
croll waves in three-dimensional tissue showed that these surface patterns
could be attributed to two fundamental mechanisms: head-tail interactions a
nd filament break. We conclude that during sustained ventricular fibrillati
on in swine RV, surface patterns of wave break are produced by two fundamen
tal mechanisms: head-tail interaction between waves and filament break.