Dorian P, Penkoske P A, Witkowski F X
Department of Medicine, University of Toronto, Ontario.
Can J Cardiol. 1996 Apr;12(4):399-406.
Drugs that prolong cardiac refractoriness can decrease defibrillation energy requirements. In particular, barium, a relatively selective blocker of cardiac Ik1 channels, produces marked decreases in defibrillation energy. The mechanism of this effect is unknown, and may relate to modulation of the effect of defibrillatory shocks, or an alteration of the pattern of ventricular fibrillation (VF) by the drug.
Accordingly, the effect of barium chloride was examined, 1.1 mg/kg followed by 0.1 mg/kg/min intravenously, or saline control, on the pattern of unipolar electrograms using a 120 electrode 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 of a 10 s episode of VF were measured for each electrode. 'Organization' in VF was measured by the variability in ACT-ACT intervals, their visually assessed pattern, and the relation between local activations on adjacent electrodes. Voltage gradients were measured at each of 40 epicardial sites for each defibrillation shock, delivered at voltages ranging from to 20% to 100% successful in defibrillation. At identical voltage shocks (400 V), mean voltage gradients before and after barium were 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. When the lowest voltage gradient at any site was less than 3.5 V/cm, defibrillation was successful 14% of the time (two of 14 ) during control, but 88% of the time (14 to 16) after barium infusion (P<0.01). Mean ACT-ACT intervals after barium for all episodes over all electrodes was 107.5+/-14.1 ms, significantly longer than 89.7 +/-3.9 ms after saline, indicating a 20% increase in the cycle length of fibrillation. During saline control, local epicardial electrogram patterns showed irregular, 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 epicardial electrograms showed regular, phasic activations that appear to reflect an organized, uniformly repetitive local activation pattern, suggesting spatially homogeneous and temporally regular activation wavefronts.
During VF after barium, despite an apparently disorganized surface electrocardiographic pattern, epicardial electrogram patterns are altered and reflect a more ¿ordered', homogeneous and regular local activation. This increased order may be in part responsible for the decreased defibrillation energy requirements observed after barium.
延长心脏不应期的药物可降低除颤能量需求。特别是钡，一种相对选择性的心脏Ik1通道阻滞剂，可使除颤能量显著降低。这种效应的机制尚不清楚，可能与调节除颤电击的效果有关，或者与药物改变室颤（VF）模式有关。
因此，研究了静脉注射1.1mg/kg氯化钡继以0.1mg/kg/min或生理盐水对照对73次VF发作（37次在注射生理盐水后，36次在注射钡后）期间使用120电极阵列记录的单极电图模式的影响。对于每次VF发作，测量每个电极在10秒VF发作的最后2秒内与局部激活相关的峰值dV/dt以及平均激活-激活（ACT-ACT）间期。通过ACT-ACT间期的变异性、视觉评估的模式以及相邻电极上局部激活之间的关系来测量VF中的“组织化”程度。在每个除颤电击时，在40个心外膜部位测量电压梯度，电击电压范围为成功除颤所需电压的20%至100%。在相同电压电击（400V）时，钡注射前后的平均电压梯度相似：分别为18±9和19±1.2V/cm。所有激活的平均峰值dV/dt在钡注射前为-8.7±0.5V/s，注射后为-7.7±2.8V/s，表明局部传导速度无明显变化。当任何部位的最低电压梯度小于3.5V/cm时，在对照期间除颤成功的时间为14%（14次中有2次），但在钡输注后为88%（14至16次）（P<0.01）。所有发作所有电极在钡注射后的平均ACT-ACT间期为107.5±14.1ms，显著长于注射生理盐水后的89.7±3.9ms，表明颤动周期长度增加了20%。在生理盐水对照期间，局部心外膜电图模式显示不规则、形态多变的电图，任何电极上ACT-ACT间期的平均最低标准差为5.1±1.5ms，而钡注射后为1.2±0.7ms（P<0.0001）。注射钡后，大多数单极心外膜电图显示规则的、阶段性的激活，似乎反映了一种有组织的、均匀重复的局部激活模式，提示空间上均匀且时间上规则的激活波前。
在注射钡后的VF期间，尽管表面心电图模式明显紊乱，但心外膜电图模式发生改变，反映出更“有序”、均匀且规则的局部激活。这种增加的有序性可能部分解释了注射钡后观察到的除颤能量需求降低的现象。
