Eleff S M, Sugimoto H, Shaffner D H, Traystman R J, Koehler R C
Department of Anesthesiology, Johns Hopkins University School of Medicine, Baltimore, Md, USA.
Stroke. 1995 Jun;26(6):1028-34. doi: 10.1161/01.str.26.6.1028.
Cardiopulmonary resuscitation (CPR) generating low perfusion pressures and beginning immediately after cardiac arrest maintains cerebral ATP but not cerebral pH or arterial pH. We tested the hypothesis that preventing severe arterial acidemia prevents cerebral acidosis, whereas augmenting arterial acidemia augments cerebral acidosis.
In dogs anesthetized with pentobarbital and fentanyl, cerebral pH and ATP were measured with 31P MR spectroscopy and blood flow was measured with radiolabeled microspheres. A pneumatically controlled vest was placed around the thorax, and chest compressions were begun immediately after electrically induced cardiac arrest. Cerebral perfusion pressure was maintained with epinephrine at 30 mm Hg for 90 minutes. The arterial acidemia observed during CPR was untreated in a control group, corrected to a pH of 7.3 with the use of sodium bicarbonate, or maintained below pH 6.5 with intravenous lactic acid after 14 minutes of CPR.
At 10 minutes of CPR, cerebral ATP (99 +/- 1.5%, control), blood flow (35 +/- 3 mL/min per 100 g), O2 consumption (4.0 +/- 0.2 mL/min per 100 g), and cerebral pH (7.05 +/- .03) were unchanged from prearrest values (mean +/- SEM). After 10 minutes of CPR in the control group, cerebral pH progressively fell (6.43 +/- 0.10 at 90 minutes) in parallel with cerebral venous pH. In the bicarbonate group cerebral pH was maintained higher (6.91 +/- 0.08). Cerebral blood flow, O2 consumption, and ATP were sustained near prearrest values in both groups. In the lactate group, however, the rate of decrease of cerebral pH was augmented (6.47 +/- 0.06 by 30 minutes), and cerebral blood flow and metabolism were significantly reduced.
Cerebral pH decreased in parallel with blood pH when resuscitation was started immediately upon arrest even when cerebral O2 consumption and blood flow were near normal. Although cerebral metabolism was near normal during the first hour of CPR, systemic bicarbonate administration ameliorated the cerebral acidosis. This finding indicates that the blood-brain pH gradient is important at the subnormal cerebral perfusion pressures seen in CPR.
心肺复苏（CPR）在心脏骤停后立即开始，产生低灌注压，可维持脑ATP，但不能维持脑pH值或动脉pH值。我们检验了以下假设：预防严重动脉酸血症可预防脑酸中毒，而加重动脉酸血症则会加重脑酸中毒。
在戊巴比妥和芬太尼麻醉的犬中，用31P磁共振波谱测量脑pH值和ATP，用放射性微球测量血流量。在胸部周围放置气动控制背心，在电诱导心脏骤停后立即开始胸外按压。用肾上腺素将脑灌注压维持在30 mmHg 90分钟。在对照组中，对心肺复苏期间观察到的动脉酸血症不予治疗，使用碳酸氢钠将pH值纠正至7.3，或在心肺复苏14分钟后用静脉注射乳酸将pH值维持在6.5以下。
心肺复苏10分钟时，脑ATP（99±1.5%，对照组）、血流量（35±3 mL/min per 100 g）、耗氧量（4.0±0.2 mL/min per 100 g）和脑pH值（7.05±0.03）与心脏骤停前的值（平均值±标准误）无变化。对照组心肺复苏10分钟后，脑pH值与脑静脉pH值平行逐渐下降（90分钟时为6.43±0.10）。在碳酸氢盐组中，脑pH值维持在较高水平（6.91±0.08）。两组的脑血流量、耗氧量和ATP均维持在接近心脏骤停前的值。然而，在乳酸盐组中，脑pH值下降速率加快（30分钟时为6.47±0.06），脑血流量和代谢显著降低。
即使脑耗氧量和血流量接近正常，在心脏骤停后立即开始复苏时，脑pH值与血液pH值平行下降。尽管在心肺复苏的第一个小时内脑代谢接近正常，但全身给予碳酸氢盐可改善脑酸中毒。这一发现表明，在心肺复苏中所见的低于正常的脑灌注压下，血脑pH梯度很重要。
