Since the earliest documented accounts of ventricular fibrillation (VF) >3000 years ago,1 the mechanisms responsible have been the source of ongoing debate. During the early part of the last century, both focal and re-entrant mechanisms were proposed, and more recently the re-entry mechanisms have polarized into the multiple wavelet and mother rotor hypotheses. The multiple wavelet hypothesis, originally put forward by Moe2 to explain atrial fibrillation, implies that VF is sustained by multiple circulating unstable wavelets perpetuated by a sequence of wavebreaks and self-generating re-entry. The mother rotor hypothesis3 proposes that VF is maintained by a single rapid periodic source that is unable to sustain uniform 1:1 conduction throughout the myocardium, resulting in intermittent conduction block with multiple irregular activation patterns. Early studies from several groups across a range of animal species have provided evidence in support of one or other hypothesis. A subsequent study using multielectrode total epicardial mapping in patients undergoing routine surgical procedures showed that both mechanisms appeared to be operative during the first 20–40 s of human VF.4 These findings are now generally accepted, although the relative contributions of focal and rotor activity are still debated. Recently, there has been a revival of interest in focal mechanisms, with studies indicating a role for the Purkinje system both as a trigger and in the maintenance of VF.1,5
