Barium decreases defibrillation energy requirements

Certain antiarrhythmic drugs that inhibit myocardial repolarizing currents decrease defibrillation energy, but the effect of blocking particular currents on defibrillation is not well understood. We therefore investigated the effect of barium, a relatively selective blocker of inwardly rectifying potassium current (Ik1) on voltage and energy requirements for defibrillation in an open-chest dog model. Defibrillation energy and voltage requirements were assessed by delivering monophasic shocks through epicardial electrode patches at varying voltages to construct a dose-response curve of energy and voltage versus success in defibrillation. The energy and voltage for 50% success in defibrillation (E 50 and V50, respectively) were determined by logistic regression. Monophasic action potential duration at 90% repolarization (MAPDgo) was measured with a contact electrode, and ventricular refractory period (VERP) was measured. After baseline measurements were obtained of A£so, VJ0, MAPD90, and VERP, saline (control) (n = 6) or barium (1.1 mg/kg/min for 5 min followed by 0.25 mg/kg/min) (n = 11) was administered. Defibrillation voltage and energy requirements and electrophysiologic measures were repeated after 30 and 120 min of barium or saline infusion. In control animals, there was no significant change with time in V50 (2.0 ± 12.4 and -0.2 ± 16.0% at 30 and 120 min, respectively), VERP (+ 3 ± 5 and -2 ± 3% at 30 and 120 min, respectively) or MAPD90 (+1 ± 4 and – 2 ± 6, at 30 and 120 min, respectively). In contrast, after barium infusion, there was a significant decrease in V50 both at 30 and 120 min (-21.8 ± 19.2, -36.2 ± 15.8%, p < 0.001), in E 50 (decrease of -34.2 ± 38 and -59.9 ± 23% at 30 and 120 min, respectively, p < 0.001), and increases in VERP (+ 20 ± 4 and + 22 ± 4% at 30 and 120 min, p < 0.03) and in MAPD90 (+ 15 ± 6 and + 15 ± 4% at 30 and 120 min, p < 0.03). We conclude that relatively specific inhibition of inwardly rectifying potassium current markedly decreases defibrillation voltage and energy requirements at a dose that produces slight increases in ventricular refractoriness and MAPD.