Shaffner D H, Eleff S M, Brambrink A M, Sugimoto H, Izuta M, Koehler R C, Traystman R J
Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins Medical Institutions, Baltimore, MD, USA.
Crit Care Med. 1999 Jul;27(7):1335-42. doi: 10.1097/00003246-199907000-00026.
To test the hypothesis that greater cerebral perfusion pressure (CPP) is required to restore cerebral blood flow (CBF), oxygen metabolism, adenosine triphosphate (ATP), and intracellular pH (pHi) levels after variable periods of no-flow than to maintain them when cardiopulmonary resuscitation (CPR) is started immediately.
Prospective, randomized, comparison of three arrest times and two perfusion pressures during CPR in 24 anesthetized dogs.
University cerebral resuscitation laboratory.
We used radiolabeled microspheres to determine CBF and magnetic resonance spectroscopy to derive ATP and pHi levels before and during CPR. Ventricular fibrillation was induced, epinephrine administered, and thoracic vest CPR adjusted to provide a CPP of 25 or 35 mm Hg after arrest times of O, 6, or 12 mins.
When CPR was started immediately after arrest with a CPP of 25 mm Hg, CBF and ATP were 57 +/- 10% and 64 +/- 14% of prearrest (at 10 mins of CPR). In contrast, CBF and ATP were minimally restored with a CPP at 25 mm Hg after a 6-min arrest time (23 +/- 5%, 16 +/- 5%, respectively). With a CPP of 35 mm Hg, extending the no-flow arrest time from 6 to 12 mins reduced reflow from 71 +/- 11% to 37 +/- 7% of pre-arrest and reduced ATP recovery from 60 +/- 11% to 2 +/- 1% of pre-arrest. After 6- or 12-min arrest times, brainstem blood flow was restored more than supratentorial blood flow, but cerebral pHi was never restored.
A CPP of 25 mm Hg maintains supratentorial blood flow and ATP at 60% to 70% when CPR starts immediately on arrest, but not after a 6-min delay. A higher CPP of 35 mm Hg is required to restore CBF and ATP when CPR is delayed for 6 mins. After a 12-min delay, even the CPP of 35 mm Hg is unable to restore CBF and ATP. Therefore, increasing the arrest time at these perfusion pressures increases the resistance to reflow sufficient to impair restoration of cerebral ATP.
验证这样一个假设，即与心肺复苏（CPR）立即开始时维持脑血流量（CBF）、氧代谢、三磷酸腺苷（ATP）和细胞内pH（pHi）水平相比，在不同时长的无血流期后恢复这些指标需要更高的脑灌注压（CPP）。
对24只麻醉犬进行前瞻性、随机研究，比较CPR期间三个停搏时间点和两种灌注压。
大学脑复苏实验室。
我们在CPR前和期间使用放射性微球测定CBF，并用磁共振波谱法测定ATP和pHi水平。诱发室颤，给予肾上腺素，并调整胸段背心式CPR，在停搏0、6或12分钟后提供25或35 mmHg的CPP。
停搏后立即开始CPR，CPP为25 mmHg时，CPR 10分钟时CBF和ATP分别为停搏前的57±10%和64±14%。相比之下，停搏6分钟后，CPP为25 mmHg时CBF和ATP的恢复程度极低（分别为23±5%和16±5%）。CPP为35 mmHg时，无血流停搏时间从6分钟延长至12分钟，再灌注血流从停搏前的71±11%降至37±7%，ATP恢复率从停搏前的60±11%降至2±1%。停搏6或12分钟后，脑干血流的恢复程度超过幕上血流，但脑pHi从未恢复。
停搏后立即开始CPR时，25 mmHg的CPP可使幕上血流和ATP维持在60%至70%，但延迟6分钟后则不能。CPR延迟6分钟时，需要更高的35 mmHg的CPP来恢复CBF和ATP。延迟12分钟后，即使35 mmHg的CPP也无法恢复CBF和ATP。因此，在这些灌注压下延长停搏时间会增加再灌注阻力，足以损害脑ATP的恢复。
