Department of Intensive Care, CHIREC Hospitals, Université Libre de Bruxelles, Belgium.
Department of Intensive Care, Fundación Valle del Lili - Universidad Icesi, Cali, Columbia.
Curr Opin Anaesthesiol. 2021 Apr 1;34(2):85-91. doi: 10.1097/ACO.0000000000000957.
The aim of this study was to discuss the implication of microvascular dysfunction in septic shock.
Resuscitation of sepsis has focused on systemic haemodynamics and, more recently, on peripheral perfusion indices. However, central microvascular perfusion is altered in sepsis and these alterations often persist despite normalization of various macro haemodynamic resuscitative goals. Endothelial dysfunction is a key element in sepsis pathophysiology. It is responsible for the sepsis-induced hypotension. In addition, endothelial dysfunction is also implicated involved in the activation of inflammation and coagulation processes leading to amplification of the septic response and development of organ dysfunction. It also promotes an increase in permeability, mostly at venular side, and impairs microvascular perfusion and hence tissue oxygenation.Microvascular alterations are characterized by heterogeneity in blood flow distribution, with adequately perfused areas in close vicinity to not perfused areas, thus characterizing the distributive nature of septic shock. Such microvascular alterations have profound implications, as these are associated with organ dysfunction and unfavourable outcomes. Also, the response to therapy is highly variable and cannot be predicted by systemic hemodynamic assessment and hence cannot be detected by classical haemodynamic tools.
Microcirculation is a key element in the pathophysiology of sepsis. Even if microcirculation-targeted therapy is not yet ready for the prime time, understanding the processes implicated in microvascular dysfunction is important to prevent chasing systemic hemodynamic variables when this does not contribute to improve tissue perfusion.
本研究旨在探讨微血管功能障碍在感染性休克中的意义。
脓毒症的复苏一直集中于全身血液动力学,最近则集中于外周灌注指数。然而,脓毒症会改变中心微血管灌注,尽管各种宏观血液动力学复苏目标得到了纠正,这些改变通常仍会持续存在。内皮功能障碍是脓毒症病理生理学的一个关键因素。它是导致脓毒症性低血压的原因。此外,内皮功能障碍还涉及炎症和凝血过程的激活,导致脓毒症反应的放大和器官功能障碍的发展。它还促进了通透性的增加,主要在静脉侧,并损害了微血管灌注,从而影响了组织氧合。微血管改变的特征是血流分布的异质性,在适当灌注的区域附近存在未灌注的区域,因此表现出感染性休克的分布性质。这些微血管改变具有深远的意义,因为它们与器官功能障碍和不良结局有关。此外,对治疗的反应差异很大,不能通过全身血液动力学评估来预测,因此不能用传统的血液动力学工具来检测。
微循环是脓毒症病理生理学的一个关键因素。即使微循环靶向治疗还没有准备好成为主流治疗方法,但了解微血管功能障碍所涉及的过程对于防止在不能改善组织灌注时追逐全身血液动力学变量是很重要的。