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脑灌注压升高是否总是意味着大脑氧合改善?一项针对头部受伤患者的研究。

Does an increase in cerebral perfusion pressure always mean a better oxygenated brain? A study in head-injured patients.

作者信息

Sahuquillo J, Amoros S, Santos A, Poca M A, Panzardo H, Domínguez L, Pedraza S

机构信息

Department of Neurosurgery, Vall d'Hebron University Hospitals, Barcelona, Spain.

出版信息

Acta Neurochir Suppl. 2000;76:457-62. doi: 10.1007/978-3-7091-6346-7_95.

Abstract

The adequate management of cerebral perfusion pressure (CPP) continues to be a controversial issue in head-injured patients. The purpose of our study was to test two hypotheses. The first was that in patients with a CPP below 70 mm Hg, oxygen delivery is compromised and that therefore signs of tissue hypoxia would be reflected in low PtiO2 measurements. The second hypothesis was that manipulating mean arterial blood pressure to increase CPP improves oxygen delivery, particularly in patients with a CPP below 70 mm Hg. Twenty-five moderately or severely head-injured patients were included in the study. In all of them PtiO2 was monitored in the non-injured hemisphere using the Licox system (GMS, Kiel-Mielkendorf, Germany). Arterial hypertension was induced with phenylephrine 29 times. To quantify the effect of increasing mean arterial blood pressure (MABP) on oxygen delivery to the brain, the PtiO2-BP index was calculated (PtiO2-BP index = delta PtiO2/delta MABP). In 16 tests (55%) baseline CPP was above or equal to 70 mm Hg and in the remaining 13 (45%) it was below 70 mm Hg. Mean increase in MABP after phenylephrine was 23.7 +/- 10.2 mm Hg. Mean PtiO2 was 29.5 +/- 14.7 mm Hg in patients with a basal CPP of below 70 mm Hg and 28.9 +/- 10.6 mm Hg in patients in the high CPP group. These differences being not statistically significant. The PtiO2-BP index was 0.29 +/- 0.23 in patients with a basal CPP of below 70 mm Hg and in patients with a CPP of above 70 mm Hg this index was 0.16 +/- 0.11 Hg. These differences were not statistically significant (Student's t-test, P = 0.09). In our study a low PtiO2 was not observed in patients with marginally low CPPs (48-70 mm Hg) and readings below 15 mm Hg were observed in cases with both normal or supranormal CPPs. We conclude that episodes of low PtiO2 could not be predicted on the basis of CPP alone. On the other hand, raising CPP did not increase oxygen availability in the majority of cases, even if the CPP was markedly improved.

摘要

在颅脑损伤患者中,脑灌注压(CPP)的恰当管理仍是一个存在争议的问题。我们研究的目的是验证两个假设。第一个假设是,在CPP低于70mmHg的患者中,氧输送会受到影响,因此组织缺氧的迹象会在低PtiO2测量值中体现出来。第二个假设是,通过调节平均动脉血压来提高CPP可改善氧输送,尤其是在CPP低于70mmHg的患者中。本研究纳入了25例中度或重度颅脑损伤患者。所有患者均使用Licox系统(德国基尔 - 米尔肯多夫的GMS公司)在未受伤的半球监测PtiO2。使用去氧肾上腺素诱导动脉高血压29次。为了量化平均动脉血压(MABP)升高对脑氧输送的影响,计算了PtiO2 - BP指数(PtiO2 - BP指数 = ΔPtiO2 / ΔMABP)。在16次测试(55%)中基线CPP高于或等于70mmHg,其余13次(45%)低于70mmHg。使用去氧肾上腺素后MABP的平均升高为23.7±10.2mmHg。基础CPP低于70mmHg的患者平均PtiO2为29.5±14.7mmHg,高CPP组患者为28.9±10.6mmHg。这些差异无统计学意义。基础CPP低于70mmHg的患者PtiO2 - BP指数为0.29±0.23,CPP高于70mmHg的患者该指数为0.16±0.11mmHg。这些差异无统计学意义(学生t检验,P = 0.09)。在我们研究中,轻度低CPP(48 - 70mmHg)的患者未观察到低PtiO2,而在CPP正常或超常的病例中观察到读数低于15mmHg的情况。我们得出结论,不能仅根据CPP预测低PtiO2发作。另一方面,即使CPP显著改善,在大多数情况下提高CPP也不会增加氧供应。

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