Electrophysiologic consequences of hyperkalemic cardioplegia during surgical ischemia.
Electrophysiologic consequences of hyperkalemic cardioplegia during surgical ischemia.
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手术缺血期间高钾心麻痹的电生理后果。
DOI：
10.1016/0003-4975(94)91332-3
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
DamianoJr,RJ
中科院分区：
文献类型：
--
作者：
Cohen,NM;Allen,CA;Hsia,PW;Nixon,TE;Wise,RM;DamianoJr,RJ
心肌保护策略使用心脏停搏液来减轻手术缺血和再灌注引起的损伤。然而，心脏停搏后电生理异常的发生率很高。在猪体外循环模型中，使用计算机心外膜标测系统来测量不同心肌保护技术的电生理结果。比较了温、冷、晶体和血液心脏停搏液。在对照组中检查低温和长时间心肺转流的影响，对照组经历了2小时的低温期，没有心脏停搏液或主动脉阻断，随后进行2小时的常温再灌注。在心脏停搏前和再灌注过程中，测量了等离子体激活图、单极电图、心室不应期和起搏阈值。与对照组相比，晶体心脏停搏液（而不是血心脏停搏液）伴随着心室激动模式的巨大变化，并且持续（> 2小时）且显着减慢完全心室激动所需的时间。这不是缺氧的结果。此外，任何心脏停搏液的有效不应期和起搏阈值都没有变化。我们的数据表明，晶体停搏液增加心肌对电流的阻力，导致电脉冲传播紊乱，可能是心肌梗死的基础。
Myocardial protection strategics use cardioplegic solutions to reduce the injury induced by surgical ischemia and reperfusion. However, there is a high incidence of electrophysiotogic abnormalities after cardioplegic arrest. A computerized epicardial mapping system in a porcine cardiopulmonary bypass model was used to measure the electrophysiologic consequences of different myocardial protection techniques. Both warm and cold, crystalloid and blood cardioplegic solutions were compared. The effects of hypothermia and prolonged cardiopulmonary bypass were examined in a control group that underwent a 2-hour period of hypothermia without cardioplegia or aortic cross-clamping, followed by 2 hours of normothermic reperfusion. Isochronous activation maps, unipolar electrograms, ventricular refractory periods, and pacing thresholds were measured before cardioplegic arrest and during reperfusion. Compared with the control group, crystalloid cardioplegia, but not blood cardioplegia, was accompanied by large changes in the pattern of ventricular activation and by persistent (> 2 hours) and significant slowing of the time required for complete ventricular activation. This was not the result of hypoxia. Moreover, the effective refractory period and the pacing threshold were unchanged by any cardioplegia. Our data suggest that crystalloid cardioplegia increases myocardial resistance to current flow leading to a derangement of electrical impulse propagation that may underlie arrhythmogenesis.