Diastolic Field Stimulation: the Role of Shock Duration in Epicardial Activation and Propagation

Abstract

Detailed knowledge of tissue response to both systolic and diastolic shock is critical for understanding defibrillation. Diastolic field stimulation has been much less studied than systolic stimulation, particularly regarding transient virtual anodes. Here we investigated high-voltage-induced polarization and activation patterns in response to strong diastolic shocks of various durations and of both polarities, and tested the hypothesis that the activation versus shock duration curve contains a local minimum for moderate shock durations, and it grows for short and long durations. We found that 0.1-0.2-ms shocks produced slow and heterogeneous activation. During 0.8-1 ms shocks, the activation was very fast and homogeneous. Further shock extension to 8 ms delayed activation from 1.55 ± 0.27 ms and 1.63 ± 0.21 ms at 0.8 ms shock to 2.32 ± 0.41 ms and 2.37 ± 0.3 ms (N = 7) for normal and opposite polarities, respectively. The traces from hyperpolarized regions during 3-8 ms shocks exhibited four different phases: beginning negative polarization, fast depolarization, slow depolarization, and after-shock increase in upstroke velocity. Thus, the shocks of >3 ms in duration created strong hyperpolarization associated with significant delay (P < 0.05) in activation compared with moderate shocks of 0.8 and 1 ms. This effect appears as a dip in the activation-versus-shock-duration curve.

Electrical Pacing of Cardiac Tissue Including Potassium Inward Rectification

“…We have studied the effect of the I K1 inward-rectifying potassium current on an anisotropic two dimensional sheet of cardiac tissue using the bidomain model. Experiments reveal little or no hyperpolarization at a virtual anode when a shock is applied to resting tissue [ 6 – 8 ]. Another experiment showed that hyperpolarization appeared at the beginning of a shock but disappeared within 1 ms [ 17 ].…”

“…Experiments in which a stimulus is applied to refractory tissue produce results similar to the predictions of the passive bidomain model, with adjacent regions of depolarization and hyperpolarization [ 3 – 5 ]. However, when a stimulus is applied to resting (diastolic) tissue, hyperpolarization is rarely seen [ 6 – 8 ]. One reason for this behavior might be that the shock excited an action potential resulting in active depolarization that masks any hyperpolarization.…”