Figure 4.

Mechanisms for shock failure, for shocks far below (A) and near (B) the DFT. In (A), arrhythmia is induced right after the shock, initiated by a post-shock activation (typically a break excitation wave) that reenters in the heart. In (B), the presence of only intramural excitable areas results in propagation of post-shock activations initiated in these areas deep in the ventricular wall (‘tunnel propagation’). These intramural wavefronts cannot make a breakthrough on the ventricular surface because of the post-shock depolarization of the surfaces. Only when the surfaces recover from this depolarization, the intramural wavefronts propagating in the mid-wall tunnel are able to make a breakthrough on the wall surfaces, marking the end of the isoelectric window, and becoming the earliest propagated post-shock activations propagating globally (and thus on the ventricular surfaces). Image based on figure published in Trayanova et al.¹⁵