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微循环复苏策略可纠正脓毒症时的组织二氧化碳异常。

Microcirculatory recruitment maneuvers correct tissue CO2 abnormalities in sepsis.

作者信息

Almac E, Siegemund M, Demirci C, Ince C

机构信息

Department of Physiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

出版信息

Minerva Anestesiol. 2006 Jun;72(6):507-19.

Abstract

The rises in tissue partial pressure of carbon dioxide have been observed in critically ill patients with shock and sepsis for a long time and have been proposed to be an earlier and more reliable marker of tissue hypoxia than traditional markers. However, the mechanisms leading to those increases, especially in sepsis and endotoxemia, are not well understood. Recent studies provided further data, supporting the idea that the origin of those increases in partial pressure of CO2 in sepsis as being caused by microcirculatory perfusion deficit resulting in mitochondrial depression by time. Previously, we have termed this condition where despite correction of systemic oxygen delivery variables, regional hypoxia and oxygen extraction deficit persist as microcirculatory and mitochondrial distress syndrome (MMDS). Recent findings support the idea that the progression from early to severe sepsis is accompanied or possibly even caused by microcirculatory dysfunction, which leads to mitochondrial dysfunction by time. Therefore early identification of microcirculatory dysfunction and correction with microcirculatory recruitment maneuvers are needed to ensure adequate microcirculatory perfusion and tissue oxygenation. Microcirculatory imaging, such as SDF imaging technique, appears to be a very useful tool for this task and its combination together with other systemic and regional tissue oxygenation measurements may provide more information regarding the tissue oxygenation and will be a very promising tool for microcirculatory researchers and the management of critically ill patients at the bedside.

摘要

长期以来,在患有休克和脓毒症的重症患者中观察到组织二氧化碳分压升高,并且有人提出这是比传统标志物更早且更可靠的组织缺氧标志物。然而,导致这些升高的机制,尤其是在脓毒症和内毒素血症中,尚未完全了解。最近的研究提供了进一步的数据,支持这样一种观点,即脓毒症中二氧化碳分压升高的原因是微循环灌注不足,随着时间的推移导致线粒体功能抑制。此前,我们将这种尽管全身氧输送变量得到纠正,但局部缺氧和氧摄取不足仍然持续的情况称为微循环和线粒体窘迫综合征(MMDS)。最近的研究结果支持这样一种观点,即从早期脓毒症发展到严重脓毒症是伴随着微循环功能障碍,甚至可能是由微循环功能障碍引起的,随着时间的推移会导致线粒体功能障碍。因此,需要早期识别微循环功能障碍并通过微循环恢复策略进行纠正,以确保足够的微循环灌注和组织氧合。微循环成像,如SDF成像技术,似乎是完成这项任务的非常有用的工具,并且它与其他全身和局部组织氧合测量方法相结合可能会提供更多关于组织氧合的信息,对于微循环研究人员和床边重症患者的管理来说将是一个非常有前景的工具。

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