Eleff S M, Schleien C L, Koehler R C, Shaffner D H, Tsitlik J, Halperin H R, Rogers M C, Traystman R J
Department of Anesthesiology/Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205.
Anesthesiology. 1992 Jan;76(1):77-84. doi: 10.1097/00000542-199201000-00012.
Cardiac arrest causes a rapid loss of cerebral adenosine triphosphate [corrected] (ATP) and a decrease in cerebral intracellular pH (pHi). Depending on the efficacy of cardiopulmonary resuscitation (CPR), cerebral blood flow levels (CBF) ranging from near zero to near normal have been reported experimentally. Using 31P magnetic resonance spectroscopy, the authors tested whether experimental CPR with normal levels of cerebral blood flow can rapidly restore cerebral ATP and pHi despite the progressive systemic acidemia associated with CPR. After 6 min of ventricular fibrillation in six dogs anesthetized with fentanyl and pentobarbital, ATP was reduced to undetectable concentrations and pHi decreased from 7.11 +/- 0.02 to 6.28 +/- 0.09 (+/- SE) as measured by 31P magnetic resonance spectroscopy. Application of cyclic chest compression by an inflatable vest placed around the thorax and infusion of epinephrine (40 micrograms/kg bolus plus 8 micrograms/kg/min, intravenously) maintained cerebral perfusion pressure greater than 70 mmHg for 50 min with the dog remaining in the magnet. Prearrest cerebral blood flows were generated. Cerebral pHi recovered to 7.03 +/- 0.03 by 35 min of CPR, whereas arterial pH decreased from 7.41 +/- 0.4 to 7.08 +/- 0.04 and cerebral venous pH decreased from 7.29 +/- 0.03 to 7.01 +/- 0.04. Cerebral ATP levels recovered to 86 +/- 7% (+/- SE) of prearrest concentration by 6 min of CPR. There was no further recovery of ATP, which remained significantly less than control. Therefore, in contrast to hyperemic reperfusion with spontaneous circulation and full ATP recovery, experimental CPR may not be able to restore ATP completely after 6 min of global ischemia despite restoration of CBF and brain pHi to prearrest levels.
心脏骤停会导致脑内三磷酸腺苷(ATP)迅速流失,脑内细胞内pH值(pHi)降低。根据心肺复苏(CPR)的效果,实验报道脑血流水平(CBF)范围从接近零到接近正常。作者使用31P磁共振波谱法,测试了尽管CPR会导致进行性全身酸中毒,但具有正常脑血流水平的实验性CPR是否能迅速恢复脑ATP和pHi。在用芬太尼和戊巴比妥麻醉的6只狗发生室颤6分钟后,通过31P磁共振波谱法测量,ATP降至无法检测的浓度,pHi从7.11±0.02降至6.28±0.09(±标准误)。通过围绕胸部放置的可充气背心进行循环胸外按压,并静脉注射肾上腺素(40微克/千克推注加8微克/千克/分钟),在狗保持在磁体中的情况下,维持脑灌注压大于70 mmHg达50分钟。产生了心脏骤停前的脑血流。CPR 35分钟时,脑pHi恢复到7.03±0.03,而动脉pH从7.41±0.4降至7.08±0.04,脑静脉pH从7.29±0.03降至7.01±0.04。CPR 6分钟时,脑ATP水平恢复到心脏骤停前浓度的86±7%(±标准误)。ATP没有进一步恢复,仍显著低于对照组。因此,与自发循环和ATP完全恢复的充血性再灌注不同,尽管CBF和脑pHi恢复到心脏骤停前水平,但在全脑缺血6分钟后,实验性CPR可能无法完全恢复ATP。