Schiller Alicia M, Howard Jeffrey T, Convertino Victor A
U. S. Army Institute of Surgical Research, Houston, TX 78234-6315, USA.
Exp Biol Med (Maywood). 2017 Apr;242(8):874-883. doi: 10.1177/1535370217694099. Epub 2017 Jan 1.
The ability to quickly diagnose hemorrhagic shock is critical for favorable patient outcomes. Therefore, it is important to understand the time course and involvement of the various physiological mechanisms that are active during volume loss and that have the ability to stave off hemodynamic collapse. This review provides new insights about the physiology that underlies blood loss and shock in humans through the development of a simulated model of hemorrhage using lower body negative pressure. In this review, we present controlled experimental results through utilization of the lower body negative pressure human hemorrhage model that provide novel insights on the integration of physiological mechanisms critical to the compensation for volume loss. We provide data obtained from more than 250 human experiments to classify human subjects into two distinct groups: those who have a high tolerance and can compensate well for reduced central blood volume (e.g. hemorrhage) and those with low tolerance with poor capacity to compensate.We include the conceptual introduction of arterial pressure and cerebral blood flow oscillations, reflex-mediated autonomic and neuroendocrine responses, and respiration that function to protect adequate tissue oxygenation through adjustments in cardiac output and peripheral vascular resistance. Finally, unique time course data are presented that describe mechanistic events associated with the rapid onset of hemodynamic failure (i.e. decompensatory shock). Impact Statement Hemorrhage is the leading cause of death in both civilian and military trauma. The work submitted in this review is important because it advances the understanding of mechanisms that contribute to the total integrated physiological compensations for inadequate tissue oxygenation (i.e. shock) that arise from hemorrhage. Unlike an animal model, we introduce the utilization of lower body negative pressure as a noninvasive model that allows for the study of progressive reductions in central blood volume similar to those reported during actual hemorrhage in conscious humans to the onset of hemodynamic decompensation (i.e. early phase of decompensatory shock), and is repeatable in the same subject. Understanding the fundamental underlying physiology of human hemorrhage helps to test paradigms of critical care medicine, and identify and develop novel clinical practices and technologies for advanced diagnostics and therapeutics in patients with life-threatening blood loss.
快速诊断出血性休克的能力对于患者获得良好预后至关重要。因此，了解在血容量丢失期间活跃且有能力避免血流动力学崩溃的各种生理机制的时间进程和参与情况非常重要。本综述通过开发一种使用下体负压的出血模拟模型，提供了关于人类失血和休克基础生理学的新见解。在本综述中，我们通过利用下体负压人体出血模型展示了对照实验结果，这些结果为对血容量丢失代偿至关重要的生理机制整合提供了新见解。我们提供了从250多次人体实验中获得的数据，将人类受试者分为两个不同的组：那些具有高耐受性且能很好地代偿中心血容量减少（如出血）的人，以及耐受性低且代偿能力差的人。我们纳入了动脉压和脑血流振荡、反射介导的自主神经和神经内分泌反应以及呼吸的概念性介绍，这些通过调整心输出量和外周血管阻力来保护充足的组织氧合。最后，展示了独特的时间进程数据，描述了与血流动力学衰竭（即失代偿性休克）快速发作相关的机制性事件。影响声明出血是 civilian 和军事创伤中死亡的主要原因。本综述中提交的工作很重要，因为它推进了对因出血导致组织氧合不足（即休克）的总体综合生理代偿机制的理解。与动物模型不同，我们引入了下体负压的利用作为一种非侵入性模型，该模型允许研究中心血容量的逐渐减少，类似于清醒人类实际出血期间报告的情况，直至血流动力学失代偿发作（即失代偿性休克的早期阶段），并且在同一受试者中可重复。了解人类出血的基本基础生理学有助于测试重症监护医学的范式，并识别和开发针对危及生命失血患者的先进诊断和治疗的新临床实践和技术。
