Analysis of cardiopulmonary function after subarachnoid hemorrhage

目的：容量管理在重症监护中是至关重要的，但在一些患者中，很难达到最佳的水量平衡。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。我们已经开始了关于SAH后心肺功能的多中心对照试验。在这项研究中，我们将介绍SAH后PICCO PLUS监测的效果。方法：对62例SAH患者在PICCO PLUS监测下两周内的心肺功能进行分析。结果：SAH后心输出量、收缩能力和后负荷基本正常。根据Picco监测，SAH后胸腔内血容量轻微增加，这种液体重新分布导致肺组织内液体滞留。结论：儿茶酚胺的持续释放和血管对儿茶酚胺的敏感性不同，可引起血容量再分配和静水性肺水肿。儿茶酚胺释放引起的心脏前负荷导致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。

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.