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Microcirculation versus Macrocirculation for the Management of Septic Shock: Is Hyperoxia any Good?

机译:微循环与大循环治疗败血性休克:高氧症有好处吗?

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Macrovascular indices such as hemodynamic parameters and conventional cardiovascular support measures are commonly, yet mistakenly used, for the clinical management of septic shock. Nevertheless, it is the microcirculatory dysfunction that contributes immensely to the development of septic shock. Approaches focusing on macrocirculation rather than microcirculation utterly neglect 'what lies beneath' in the microcirculation (1). The most important known mechanisms contributing to the pathophysiology of severe sepsis are but not limited to"microcirculatory and mitochondrial distress syndrome" (MMDS) (2), global tissue rather than arterial hypoxia (3), generalized endothelial cell injury (4), and activation of the coagulation cascade (5). Therefore, setting macrocirculation parameters such as arterial oxygen saturation as the ultimate goal of resuscitation in septic patients (6) not only would not be associated with any benefits but also harm the patients. Moreover, it might falsely reassure the clinicians that the patients are in clinically stable state and overlook ‘what lies beneath' . Hyperoxia was initially believed to exert vasoconstrictor properties, thus potentially allowing for haemodynamic stabilisation in vasodilatory shock. Nevertheless, it has been shown that normobaric hyperoxia decreases the capillary perfusion and VO2 max (the maximum rate of oxygen consumption) and increases the heterogenisity of perfusion (7). Accordingly, some studies revealed that hyperoxia increases the risk of multi-organ failure in sepsis (8). Microcirculatory and cellular factors and tissue diffusion influence oxygen status of cells and supranormal O 2 delivery can compensate for neither the diffusion impairment existing between capillaries and cells, nor for the intracellular metabolic dysfunction (9). Therefore, oxygen therapy should be managed cautiously during sepsis to minimize its probable deleterious effects (8). This might be achieved through personalized oxygenation based on the repeated assessments of ongoing oxygen requirements and implementation of strategies reducing metabolic rate and improving tissue oxygenation.
机译:诸如血流动力学参数和常规心血管支持措施之类的大血管指标通常被误用于败血性休克的临床管理。然而,正是微循环功能障碍极大地导致了败血性休克的发展。专注于大循环而不是微循环的方法完全忽略了微循环中的“底层”。导致严重脓毒症病理生理的最重要的已知机制包括但不限于“微循环和线粒体窘迫综合征”(MMDS)(2),整体组织而非动脉缺氧(3),广泛性内皮细胞损伤(4)和激活凝血级联反应(5)。因此,在脓毒症患者中设置大循环参数(如动脉血氧饱和度)作为复苏的最终目标(6)不仅不会带来任何好处,而且还会损害患者。此外,这可能会错误地使临床医生确信患者处于临床稳定状态,而忽略了“下面的东西”。最初认为高氧血症具有血管收缩特性,因此可能使血管舒张性休克的血流动力学稳定。然而,已显示常压高氧会降低毛细血管灌注和最大摄氧量(VO2 max),并增加灌注的异质性(7)。因此,一些研究表明,高氧血症会增加败血症中多器官衰竭的风险(8)。微循环和细胞因子以及组织扩散影响细胞的氧状态,超常的O 2递送既不能补偿毛细血管和细胞之间存在的扩散障碍,也不能补偿细胞内代谢功能障碍(9)。因此,在败血症期间应谨慎管理氧疗,以最大程度地减少其可能的有害作用(8)。这可以通过基于对持续需氧量的反复评估以及实施降低代谢率和改善组织氧合的策略的个性化氧合来实现。

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