Dworschak Martin, Franz Maximilian, Czerny Martin, Gorlitzer Michael, Blaschek Marieluise, Grubhofer Georg, Haider Wolfram
Division of Cardiothoracic Anesthesia and Intensive Care, University Hospital, Vienna, Austria.
Crit Care Med. 2003 Aug;31(8):2085-9. doi: 10.1097/01.CCM.0000079610.88771.62.
Repeated induction of ventricular fibrillation with ensuing alterations in electroencephalogram and jugular venous oxygen saturation is common practice during insertion of transvenous implantable cardioverters/defibrillators. We investigated whether these functional changes are also associated with cerebral injury.
Prospective study.
University hospital.
We studied 45 patients undergoing implantable cardioverter/defibrillator insertion. Eleven patients with cardiac pacemaker implantation, which was performed in the same manner yet without the necessity to induce ventricular fibrillation, served as controls.
Serum neuron-specific enolase and S100 were determined before, immediately postoperatively, and 2 hrs postoperatively. In a randomly composed subgroup, neuron-specific enolase was also determined 6 and 24 hrs after surgery. Implantable cardioverter/defibrillator patients only showed an increase of both markers postoperatively. Median neuron-specific enolase values climbed from a preoperative 9.9 to 12.3 and 14.4 microg/L at 2 and 24 hrs after surgery, respectively. This increase was associated with the number of shocks and the cumulative time in circulatory arrest. The highest median S100 level (0.075 microg/L) was reached 2 hrs after the procedure. Neuron-specific enolase and S100 were extremely elevated (13.7 and 0.970 microg/L, respectively) in one patient after an extended episode of ventricular fibrillation. Plasma hemoglobin levels were in the normal range in implantable cardioverter/defibrillator patients throughout the observation period.
Apparently, even brief successive periods of global cerebral ischemia cause neuronal damage without obvious severe neurologic deficits. However, they may be related to subtle postoperative neurologic or cognitive dysfunctions that a number of implantable cardioverter/defibrillator patients exhibit after implantation.
在植入经静脉植入式心脏复律除颤器过程中，反复诱发室颤并伴随脑电图和颈静脉血氧饱和度的改变是常见操作。我们研究了这些功能变化是否也与脑损伤有关。
前瞻性研究。
大学医院。
我们研究了45例接受植入式心脏复律除颤器植入术的患者。11例接受心脏起搏器植入术的患者作为对照，起搏器植入术以相同方式进行，但无需诱发室颤。
在术前、术后即刻和术后2小时测定血清神经元特异性烯醇化酶和S100。在一个随机组成的亚组中，术后6小时和24小时也测定了神经元特异性烯醇化酶。植入式心脏复律除颤器患者术后仅显示这两种标志物升高。术后2小时和24小时，神经元特异性烯醇化酶的中位数分别从术前的9.9上升至12.3和14.4μg/L。这种升高与电击次数和循环骤停的累计时间有关。术后2小时达到最高中位数S100水平（0.075μg/L）。一名患者在长时间室颤发作后，神经元特异性烯醇化酶和S100极度升高（分别为13.7和0.970μg/L）。在整个观察期内，植入式心脏复律除颤器患者的血浆血红蛋白水平均在正常范围内。
显然，即使是短暂连续的全脑缺血期也会导致神经元损伤，而无明显严重神经功能缺损。然而，它们可能与一些植入式心脏复律除颤器患者术后出现的细微神经或认知功能障碍有关。
