Hemodynamic and oxygen transport patterns after head trauma and brain death: Implications for management of the organ donor
Hemodynamic and oxygen transport patterns after head trauma and brain death: Implications for management of the organ donor
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DOI：
10.1097/01.ta.0000235995.86162.d2
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发表时间：
2007-11-01
影响因子：
--
通讯作者：
Demetriades, Demetrios
中科院分区：
文献类型：
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作者：
Belzberg, Howard;Shoemaker, William C.;Demetriades, Demetrios
目的：本研究的目的是描述的时间血流动力学和氧运输模式的患者头部受伤，以及那些谁成为脑死亡的模式，以更好地了解潜在的中央调节血流动力学机制的作用，并最终提高率的器官donations.Methods：我们研究了388例连续的非侵入性监测严重的头部创伤患者，其中79成为脑死亡。在急诊科入院后不久开始监测，旨在通过心脏指数（CI）、平均动脉压、心率、脉搏血氧饱和度（Sapo（2））和经皮氧和二氧化碳（Ptco（2）/FIo（2）和PtCCO 2）模式描述心脏、肺和组织灌注功能的顺序。后者被用作组织灌注或氧合的标志物。Resutls：脑损伤患者，随后成为脑死亡最初有低CI与穷人的组织灌注后不久，急诊入院。随后是以高CI（4.43 +/- 1.3 L中心点min（-1）中心点M-2）和增强的组织氧合（Ptco（2）/FIo（2）238 186）为特征的延长期。在脑死亡的晚期或终末期，血流动力学恶化和崩溃迅速导致停搏。在试图保持血液动力学稳定的器官捐赠，各种治疗方法对血液动力学patterns的影响进行了初步描述。结论：脑死亡患者的高动力状态与夸张的外周组织灌注或氧合作用的压力反应的中枢血管收缩机制的损失，导致在不反对的外周代谢血管舒张产生高C1和组织灌注。
Objectives: The aims of the present study were to describe the temporal hemodynamic and oxygen transport patterns of patients with head injuries as well as the patterns of those who became brain dead to better understand the role of underlying central regulatory hemodynamic mechanisms and ultimately to improve rates of organ donation.Methods: We studied 388 consecutive noninvasively monitored patients with severe head trauma; 79 of these became brain dead. Monitoring was started shortly after admission to the emergency department and was designed to describe the sequence of cardiac, pulmonary, and tissue perfusion functions by cardiac index (CI), mean arterial pressure, heart rate, arterial saturation by pulse oximetry (Sapo(2)), and transcutaneous oxygen and carbon dioxide (Ptco(2)/FIo(2) and PtCCO2) patterns. The latter were used as markers of tissue perfusion or oxygenation.Resutls: Patients with head injuries who subsequently became brain dead initially had low CI with poor tissue perfusion beginning shortly after emergency department admission. This was followed by a prolonged period characterized by high CI (4.43 +/- 1.3 L center dot min(-1)center dot M-2) and enhanced tissue oxygenation (Ptco(2)/FIo(2) 238 186). In the late or end stage of brain death, hemodynamic deterioration and collapse led rapidly to arrest. In attempts to maintain hemodynamic stability for organ donation, the effects of various therapies on the hemodynamic patterns were preliminarily described.Conclusions: The hyperdynamic state with exaggerated peripheral tissue perfusion or oxygenation in brain-dead patients associated with loss of central vasoconstrictive mechanisms of the stress response resulted in unopposed peripheral metabolic vasodilatation producing high C1 and tissue perfusion.