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Analysis of cardiopulmonary function after subarachnoid hemorrhage

蛛网膜下腔出血后心肺功能分析

基本信息

批准号：
20592117
负责人：
ISOTANI Eiji
金额：
$ 2.5万
依托单位：
Tokyo Medical and Dental University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2008
资助国家：
日本
起止时间：
2008 至 2009
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20592117/
关键词：
subarachnoid hemorrhage pulmonary edema triple H therapy cerebral vasospasm extravasucular lung water index 脳神経疾患 PiCCO plus 肺血管外水分量胸腔内血液量心機能くも膜下出血カテコラミン BNP 神経原性肺水腫 CSWS 血管内容量の再分布

项目摘要

Objectives : Volume management is crucial in intensive care, however, in some patients it is very hard to achieve optimal water balance. Subarachnoid hemorrhage (SAH) patient is a representative example. Cardiopulmonary complications are common after SAH : neurogenic pulmonary edema, cardiac failure, and so on. We have started the multicenter controlled trial about cardiopulmonary function after SAH. In this study we will present the effects of PiCCO plus monitoring after SAH. Methods : We analyzed the cardiopulmonary functions of 62 patients monitored by PiCCO plus during two weeks after SAH. Results : Output, contractility and afterload were essentially normal after SAH. Intrathoracic blood volume was slightly elevated and this fluid redistribution causes hydrostatic fluid retention in lung tissues on PiCCO monitoring after SAH. Conclusions : Persistent catecholamine release and the different sensitivity of blood vessels to catecholamine cause the blood volume redistribution and hydrostatic pulmonary edema. The cardiac preload due to catecholamine release leads to BNP release resulted in natriuresis. This is the underlying mechanism of so-called cerebral salt wasting syndrome.

目的：容量管理在重症监护中至关重要，然而，在某些患者中，很难达到最佳的水平衡。蛛网膜下腔出血（SAH）患者就是一个典型的例子。SAH后常见的心肺并发症有：神经源性肺水肿、心力衰竭等，我们已经开展了SAH后心肺功能的多中心对照试验。在本研究中，我们将介绍PiCCO加SAH后监测的效果。方法：对62例SAH患者在术后2周内应用PiCCO plus监测心肺功能进行分析。结果：SAH后输出量、收缩力和后负荷基本正常。胸腔内血容量略微升高，并且在SAH后PiCCO监测中，这种液体再分布导致肺组织中的流体静力学液体潴留。结论：持续的儿茶酚胺释放和血管对儿茶酚胺的不同敏感性导致血容量重新分布和流体静力性肺水肿。由于儿茶酚胺释放导致的心脏前负荷导致BNP释放，从而导致钠尿。这就是所谓的脑性盐耗综合征的潜在机制。