Convertino Victor A, Koons Natalie J, Suresh Mithun R
Battlefield Healthy & Trauma Center for Human Integrative Physiology, United States Army Institute of Surgical Research, JBSA San Antonio, Texas, USA.
Compr Physiol. 2021 Feb 12;11(1):1531-1574. doi: 10.1002/cphy.c200016.
Hemorrhage is a leading cause of death following traumatic injuries in the United States. Much of the previous work in assessing the physiology and pathophysiology underlying blood loss has focused on descriptive measures of hemodynamic responses such as blood pressure, cardiac output, stroke volume, heart rate, and vascular resistance as indicators of changes in organ perfusion. More recent work has shifted the focus toward understanding mechanisms of compensation for reduced systemic delivery and cellular utilization of oxygen as a more comprehensive approach to understanding the complex physiologic changes that occur following and during blood loss. In this article, we begin with applying dimensional analysis for comparison of animal models, and progress to descriptions of various physiological consequences of hemorrhage. We then introduce the complementary side of compensation by detailing the complexity and integration of various compensatory mechanisms that are activated from the initiation of hemorrhage and serve to maintain adequate vital organ perfusion and hemodynamic stability in the scenario of reduced systemic delivery of oxygen until the onset of hemodynamic decompensation. New data are introduced that challenge legacy concepts related to mechanisms that underlie baroreflex functions and provide novel insights into the measurement of the integrated response of compensation to central hypovolemia known as the compensatory reserve. The impact of demographic and environmental factors on tolerance to hemorrhage is also reviewed. Finally, we describe how understanding the physiology of compensation can be translated to applications for early assessment of the clinical status and accurate triage of hypovolemic and hypotensive patients. © 2021 American Physiological Society. Compr Physiol 11:1531-1574, 2021.
在美国，出血是创伤性损伤后导致死亡的主要原因。此前，在评估失血背后的生理学和病理生理学方面的许多工作都集中在血液动力学反应的描述性指标上，如血压、心输出量、每搏输出量、心率和血管阻力，以此作为器官灌注变化的指标。最近的研究工作已将重点转向理解对全身氧气输送减少和细胞利用减少的代偿机制，这是一种更全面的方法，用于理解失血后及失血过程中发生的复杂生理变化。在本文中，我们首先应用量纲分析来比较动物模型，然后描述出血的各种生理后果。接着，我们通过详细阐述从出血开始就被激活的各种代偿机制的复杂性和整合情况，来介绍代偿的另一面，这些机制有助于在全身氧气输送减少的情况下维持重要器官的充足灌注和血液动力学稳定性，直至血液动力学失代偿开始。文中引入了新的数据，这些数据挑战了与压力感受性反射功能基础机制相关的传统概念，并为测量对中枢性低血容量的代偿综合反应（即代偿储备）提供了新的见解。我们还回顾了人口统计学和环境因素对出血耐受性的影响。最后，我们描述了如何将对代偿生理学的理解转化为对低血容量和低血压患者临床状态的早期评估及准确分诊的应用。© 2021美国生理学会。《综合生理学》11:1531 - 1574, 2021。
