The influence of sodium channel blockade on the defibrillation energy requirements of biphasic versus monophasic shocks.

The sodium channel-blocking actions of some Class I antiarrhythmic agents can increase the defibrillation energy requirements (DER) of monophasic shock waveforms. The influence of sodium channel blockade on biphasic shocks is less certain. The purpose of this study was to compare, in a randomized, placebo controlled study, the influence of lidocaine on the DER of biphasic and monophasic shock waveforms in a canine model of transvenous internal defibrillation. The DER was determined by the iterative increment-decrement protocol. Monophasic and biphasic shock DERs were tested at baseline and during lidocaine infusion (group A) or saline control (group B). Group A biphasic shock DERs increased significantly from a baseline of 12.1 +/- 3.6 J to 19.1 +/- 9.3 J when compared to group B (P = 0.005). In group A, the mean DER during lidocaine was significantly higher with monophasic shocks than biphasic shocks (29.6 +/- 11.8 J vs 19.1 +/- 9.3 J, respectively; P < 0.003), but the magnitude of change in biphasic versus monophasic shock DERs was not significantly different (F = 1.78; p = 0.193). There was a linear relationship between the baseline DER and the DER during lidocaine (r2 = 0.63, P < 0.0001). Sodium channel blockade with lidocaine increases the DER of both monophasic and biphasic shocks. However, the DER of biphasic shocks during lidocaine are significantly lower than monophasic shock DERs, a finding that can be explained by the linear relationship between the baseline DER and the DER during lidocaine. These results may have favorable implications for the use of Class I antiarrhythmics with biphasic shock defibrillators.