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Online ISSN 1827-1596
SMART 2006 - Milan, May 10-12, 2006
Almac E. 1, Siegemund M. 2, Demirci C.3, Ince C.1
1 Department of Physiology Academic Medical Center University of Amsterdam Amsterdam, The Netherlands
2 Department of Anaesthesia and Intensive Care University Hospital University of Basel, Basel, Switzerland.
3 Department of Biology Faculty of Science University of Istanbul, Instanbul, Turkey
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.