Department of Translational Physiology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, Amsterdam, The Netherlands.
Curr Vasc Pharmacol. 2013 Mar 1;11(2):161-9.
Microcirculatory dysfunction has been recently recognized as a key pathophysiologic process in the evolution of sepsis. In the present review, we discuss fundamental aspects of microcirculatory abnormalities during septic shock, including pathogenic mechanisms, technological assessment, clinical correlates and potential therapies. The most important function of the microcirculation is the regulation and distribution of flow within the different organs. In septic shock, microcirculatory dysfunction may arise as a result of several factors such as endothelial dysfunction, leukocyte-endothelium interactions, coagulation and inflammatory disorders, hemorheologic abnormalities, and functional shunting. Severity and persistence of these microcirculatory abnormalities are associated with bad prognosis and are not necessarily predicted by systemic variables. The introduction of bedside techniques that allow evaluation of the microcirculation into clinical practice has opened up a new field of functional hemodynamic monitoring. Recent data suggest that microcirculatory abnormalities can be staged in severity. Some microcirculatory indices are more accurately related to morbidity and mortality, and thus a definition of clinically relevant microcirculatory abnormalities is feasible. On the other hand, although several systemic variables do not predict microcirculatory status, high norepinephrine (NE) requirements and hyperlactatemia are associated with a much higher prevalence of relevant microcirculatory derangements. Therefore, severe septic shock patients could represent a more precise target for interventions, particularly in microcirculation-oriented clinical trials. Clinical research has identified various therapeutic approaches that are successful in modifying the microcirculation. Future research must determine whether some of these approaches are successful in improving outcome of critically ill patients by recruiting the microcirculation.
微循环功能障碍最近被认为是脓毒症演变过程中的一个关键病理生理过程。在本综述中，我们讨论了脓毒性休克期间微循环异常的基本方面，包括发病机制、技术评估、临床相关性和潜在治疗方法。微循环的最重要功能是调节和分配不同器官内的血流。在脓毒性休克中，微循环功能障碍可能是由于内皮功能障碍、白细胞-内皮相互作用、凝血和炎症紊乱、血液流变学异常以及功能性分流等多种因素引起的。这些微循环异常的严重程度和持续时间与预后不良有关，并且不一定可以通过全身变量预测。将允许评估微循环的床边技术引入临床实践开辟了功能血流动力学监测的新领域。最近的数据表明，微循环异常可以根据严重程度进行分期。一些微循环指标与发病率和死亡率更密切相关，因此可以定义临床上相关的微循环异常。另一方面，尽管一些全身变量不能预测微循环状态，但高去甲肾上腺素 (NE) 需求和高乳酸血症与相关微循环紊乱的更高发生率相关。因此，严重脓毒性休克患者可能代表更精确的干预目标，特别是在以微循环为导向的临床试验中。临床研究已经确定了各种成功改变微循环的治疗方法。未来的研究必须确定这些方法中的一些是否通过募集微循环来成功改善危重症患者的预后。
