Eleff S M, Kim H, Shaffner D H, Traystman R J, Koehler R C
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Md.
Stroke. 1993 Dec;24(12):2066-73. doi: 10.1161/01.str.24.12.2066.
Cardiopulmonary resuscitation with external chest compression generates low perfusion pressures that may be inadequate for restoring cerebral metabolism and may worsen intracellular pH. We tested the hypothesis that cerebral reperfusion with a low perfusion pressure after arrest restores brain adenosine triphosphate (ATP) and pH to levels attained at the same perfusion pressure without preceding complete ischemia.
Brain ATP and intracellular pH were measured by magnetic resonance spectroscopy, and cerebral blood flow was measured with microspheres in anesthetized dogs. External chest compressions were begun in group A (n = 6) immediately after the onset of arrest (ie, arrest time zero) and in group B (n = 10) after 6 minutes of arrest (ie, arrest time 6 minutes). In both groups, mean cerebral perfusion pressure was regulated at 30 mm Hg for 70 minutes by adjustment of inflation pressure of a pneumatic thoracic vest.
At 12 minutes of resuscitation, cerebral blood flow was 27 +/- 4 mL/min per 100 g in group A and 21 +/- 4 mL/min per 100 g in group B, but ATP in group B (58 +/- 10% of prearrest) was less than in group A (105 +/- 6%). With prolonged resuscitation, ATP deteriorated to near zero levels in dogs in group B, with blood flow less than 15 mL/min per 100 g. Dogs with greater blood flow never achieved complete metabolic recovery. In group B, intracellular pH was unchanged from the 6.3 value at the start of resuscitation, even in those dogs with extremely low blood flows.
Levels of cerebral perfusion pressure sufficient to maintain cerebral oxidative metabolism without complete ischemia during cardiopulmonary resuscitation are not sufficient to restore metabolism after complete ischemia during cardiopulmonary resuscitation. However, low "trickle" blood flow did not worsen intracellular acidosis.
通过外部胸外按压进行心肺复苏所产生的灌注压较低，可能不足以恢复脑代谢，还可能使细胞内pH值恶化。我们检验了这样一个假设，即心脏骤停后以低灌注压进行脑再灌注可将脑三磷酸腺苷（ATP）和pH值恢复到在相同灌注压且无先前完全缺血情况下所达到的水平。
通过磁共振波谱法测量脑ATP和细胞内pH值，并用微球法在麻醉犬中测量脑血流量。A组（n = 6）在心脏骤停开始后立即（即骤停时间为零）开始进行外部胸外按压，B组（n = 10）在心脏骤停6分钟后（即骤停时间为6分钟）开始。在两组中，通过调节气动胸衣的充气压力，将平均脑灌注压维持在30 mmHg 70分钟。
复苏12分钟时，A组脑血流量为每100 g脑组织27±4 mL/分钟，B组为每100 g脑组织21±4 mL/分钟，但B组的ATP（为骤停前的58±10%）低于A组（105±6%）。随着复苏时间延长，B组犬的ATP恶化至接近零水平，血流量低于每100 g脑组织15 mL/分钟。血流量较高的犬从未实现完全的代谢恢复。在B组中，即使是那些血流量极低的犬，细胞内pH值从复苏开始时的6.3值也未发生变化。
在心肺复苏期间足以维持脑氧化代谢而无完全缺血的脑灌注压水平，在心肺复苏期间完全缺血后不足以恢复代谢。然而，低“涓流”血流量并未使细胞内酸中毒恶化。
