Kern K B, Hilwig R W, Rhee K H, Berg R A
Department of Medicine, University of Arizona, Tucson 85724, USA.
J Am Coll Cardiol. 1996 Jul;28(1):232-40. doi: 10.1016/0735-1097(96)00130-1.
This study investigated the effect of prolonged cardiac arrest and subsequent cardiopulmonary resuscitation on left ventricular systolic and diastolic function.
Cardiac arrest from ventricular fibrillation results in cessation of forward blood flow, including myocardial blood flow. During cardiopulmonary resuscitation, myocardial blood flow remains suboptimal. Once the heart is defibrillated and successful resuscitation achieved, reversible myocardial dysfunction, or "stunning," may occur. The magnitude and time course of myocardial stunning from cardiac arrest is unknown.
Twenty-eight domestic swine (26 +/- 1 kg) were studied with both invasive and noninvasive measurements of ventricular function before and after 10 or 15 min of untreated cardiac arrest. Contrast left ventriculograms, ventricular pressures, cardiac output, isovolumetric relaxation time (tau) and transthoracic Doppler-echocardiographic studies were obtained.
Twenty-three of 28 animals were successfully resuscitated and postresuscitation data obtained. Left ventricular ejection fraction showed a significant reduction 30 min after resuscitation (p < 0.05). Regional wall motion analysis revealed diffuse, global left ventricular systolic dysfunction. Left ventricular end-diastolic pressure increased significantly in the postresuscitation period (p < 0.05). Isovolumetric relaxation time (tau) was significantly increased over baseline by 2 h after resuscitation (p < 0.05). Similar findings were noted with the Doppler-echocardiographic analysis, including a reduction in fractional shortening (p < 0.05), a reduction in mitral valve deceleration time (p < 0.05) and an increase in left ventricular isovolumetric relaxation time at 5 h after resuscitation (p < 0.05> By 24 h, these invasive and noninvasive variables of systolic and diastolic left ventricular function had begun to improve. At 48 h, all measures of left ventricular function had returned to baseline levels.
Myocardial systolic and diastolic dysfunction is severe after 10 to 15 min of untreated cardiac arrest and successful resuscitation. Full recovery of this postresuscitation myocardial stunning is seen by 48 h in this experimental model of ventricular fibrillation cardiac arrest.
本研究调查了长时间心脏骤停及随后的心肺复苏对左心室收缩和舒张功能的影响。
室颤导致的心脏骤停会使包括心肌血流在内的前向血流停止。在心肺复苏期间，心肌血流仍不理想。一旦心脏除颤并成功复苏，可能会发生可逆性心肌功能障碍，即“心肌顿抑”。心脏骤停所致心肌顿抑的程度和时间进程尚不清楚。
对28头家猪（体重26±1千克）进行研究，在未经处理的心脏骤停10或15分钟前后，采用有创和无创方法测量心室功能。获得了对比左心室造影、心室压力、心输出量、等容舒张时间（tau）和经胸多普勒超声心动图研究结果。
28只动物中有23只成功复苏并获得复苏后数据。复苏后30分钟左心室射血分数显著降低（p<0.05）。局部室壁运动分析显示左心室弥漫性整体收缩功能障碍。复苏后期左心室舒张末期压力显著升高（p<0.05）。复苏后2小时等容舒张时间（tau）较基线显著延长（p<0.05）。多普勒超声心动图分析也有类似发现，包括缩短分数降低（p<0.05）、二尖瓣减速时间缩短（p<0.05）以及复苏后5小时左心室等容舒张时间延长（p<0.05）。到24小时时，这些左心室收缩和舒张功能的有创和无创指标开始改善。在48小时时，左心室功能的所有指标均恢复到基线水平。
在未经处理的心脏骤停10至15分钟并成功复苏后，心肌收缩和舒张功能严重受损。在这个室颤性心脏骤停的实验模型中，复苏后心肌顿抑在48小时内完全恢复。
