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正常血容量性高血压疗法用于蛛网膜下腔出血后脑血管痉挛的治疗

Normovolaemic induced hypertension therapy for cerebral vasospasm after subarachnoid haemorrhage.

作者信息

Otsubo H, Takemae T, Inoue T, Kobayashi S, Sugita K

机构信息

Department of Neurosurgery, Shinshu University, School of Medicine, Matsumoto, Japan.

出版信息

Acta Neurochir (Wien). 1990;103(1-2):18-26. doi: 10.1007/BF01420187.

DOI:10.1007/BF01420187
PMID:2360462
Abstract

We showed that normovolaemic induced hypertension therapy was effective in reducing ischaemic symptoms attributed to cerebral vasospasm in 41 patients after subarachnoid haemorrhage. By inducing hypertension to 25% to 50% above normal systolic arterial blood pressure, we observed that in 17 of 24 cases (71%) neurological deficits improved. In four cases of haemorrhagic infarction, the blood pressure rose to over 50% of systolic arterial pressure, and a low density area was confirmed on computerized tomography (CT) scan prior to vasospasm. Induced hypertension was therefore not considered when a low density area was revealed on CT scan. Restriction of fluid input is usually a factor in producing hypovolaemia after a neurosurgical operation. Intravascular volume expansion has been reported effective in reversing ischaemic deficits. However, according to Poiseuille's equation, increasing blood volume to a state of hypervolaemia can not enhance flow. The cerebral blood flow (CBF) was raised by increasing perfusion pressure, reducing viscosity, or increasing blood vessel diameter. Intravascular volume expansion elevates not only systemic arterial pressure, but also pulmonary artery wedge pressure over 18 mmHg and cardiac index over 2.2. Since pulmonary oedema and congestive heart failure may develop, one should monitor haemodynamic parameters with the Swan-Ganz catheter as a preventive measure. We emphasize that normovolaemic induced hypertension, maintaining haemodynamics subset 1 of the comparable haemodynamic subsets, is effective in raising perfusion pressure of CBF.

摘要

我们发现,对于41例蛛网膜下腔出血后的患者,等容性诱导高血压疗法在减轻因脑血管痉挛所致的缺血症状方面是有效的。通过将血压升高至高于正常收缩期动脉血压25%至50%,我们观察到24例中有17例(71%)神经功能缺损得到改善。在4例出血性梗死病例中,血压升至超过收缩期动脉压的50%,并且在血管痉挛之前通过计算机断层扫描(CT)证实有低密度区。因此,当CT扫描显示有低密度区时,不考虑采用诱导高血压疗法。限制液体输入通常是神经外科手术后导致低血容量的一个因素。据报道,血管内容量扩充在逆转缺血性缺损方面是有效的。然而,根据泊肃叶方程,将血容量增加至高血容量状态并不能增加血流量。脑血流量(CBF)可通过增加灌注压、降低血液黏度或增加血管直径来提高。血管内容量扩充不仅会升高体动脉压,还会使肺动脉楔压升高至超过18 mmHg以及使心脏指数超过2.2。由于可能会发生肺水肿和充血性心力衰竭,作为一项预防措施,应使用Swan-Ganz导管监测血流动力学参数。我们强调,等容性诱导高血压,维持可比血流动力学亚组中的血流动力学亚组1,在提高CBF的灌注压方面是有效的。

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Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension.通过血管内容量扩张和诱导性动脉高血压治疗血管痉挛引起的缺血性缺陷。
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