BACKGROUND: Drugs that prolong cardiac refractoriness can decrease def
ibrillation energy requirements. In particular, barium, a relatively s
elective blocker of cardiac Ik1 channels, produces marked decreases in
defibrillation energy. The mechanism of this effect is unknown, and m
ay relate to modulation of the effect of defibrillatory shocks, or an
alternation of the pattern of ventricular fibrillation (VF) by the dru
g. METHODS AND RESULTS: Accordingly, the effect of barium chloride was
examined, 1.1 mg/kg followed by 0.1 mg/kg/min intravenously, or salin
e control, on the pattern of unipolar electrograms using a 120 electro
de array, during 73 episodes of VF (37 after saline, 36 after barium).
For each episode of VF, peak -dV/dt associated with local activations
and mean activation-activation (ACT-ACT) intervals for the last 2 s o
f a 10 s episode of VF were measured for each electrodes. 'Organizatio
n' in VF was measured by the variability in ACT-ACT intervals, their v
isually assessed pattern, and the relation between local activations o
n adjacent electrodes. Voltage gradients were measured at each of 40 e
picardial sites for each defibrillation shock, delivered at voltages,
ranging from 20% to 100% successful in defibrillation. At identical vo
ltage shocks (400 V), mean voltage gradients before and after barium w
ere similar: 18+/-9 and 19+/-1.2 V/cm, respectively. Mean peak -dV/dt
for all activations was -8.7+/-0.5 V/s before and -7.7+/-2.8 V/s after
barium, suggesting no apparent change in local conduction velocity. W
hen the lowest voltage gradient at any site was less than 3.5 V/cm, de
fibrillation was successful 1.4% of the time (two of 14) during contro
l, but 88% of the time (14 of 16) after barium infusion (P<0.01). Mean
ACT-ACT intervals after barium for all episodes over all electrodes w
as 107.5+/-14.1 ms, significantly longer than 89.7+/-3.9 ms after sali
ne, indicating a 20% increase in the cycle length of fibrillation. Dur
ing saline control, local epicardial electrogram patterns showed irreg
ular, variable morphology electrograms and a mean lowest SD of ACT-ACT
intervals over any electrode of 5.1+/-1.5 ms, compared with 1.2+/-0.7
ms after barium (P<0.0001). Following barium, most unipolar epicardia
l electrograms showed regular, phasic activations that appear to refle
ct an organized, uniformly repetitive local activation pattern, sugges
ting spatially homogeneous and temporally regular activation wavefront
s. CONCLUSIONS: During VF after barium, despite and apparently disorga
nized surface electrocardiographic pattern, epicardial electrogram pat
terns are altered and reflect a more 'ordered', homogeneous and regula
r local activation. This increased order may be in part responsible fo
r the decreased defibrillation energy requirements observed after bari
um.