Microcirculatory and mitochondrial hypoxia in sepsis, XXXX , and resuscitation.

@entity1 @entity1457 @entity26 @entity3124
UNASSIGNED: After @entity1457 , persistent @entity26 extraction deficit despite the apparent adequate recovery of systemic hemodynamic and @entity26 -derived variables has been a source of uncertainty and controversy. Dysfunction of @entity26 transport pathways during intensive care underlies the sequelae that lead to organ failure, and the limitations of techniques used to measure tissue oxygenation in vivo have contributed to the lack of progress in this area. Novel techniques have provided detailed quantitative insight into the determinants of microcirculatory and mitochondrial oxygenation. These techniques, which are based on the @entity26 -dependent quenching of phosphorescence or delayed luminescence are briefly reviewed. The application of these techniques to animal models of @entity1457 and resuscitation revealed the heterogeneous nature of @entity26 distributions and the alterations in @entity26 distribution in the microcirculation and in mitochondria. These studies identified functional shunting in the microcirculation as an underlying cause of @entity26 extraction deficit observed in states of @entity1457 and resuscitation. The translation of these concepts to the bedside has been enabled by our development and clinical introduction of hand-held microscopy. This tool facilitates the direct observation of the microcirculation and its alterations at the bedside under the conditions of @entity1457 and resuscitation. Studies identified loss of coherence between the macrocirculation and the microcirculation, in which resuscitation successfully restored systemic circulation but did not alleviate microcirculatory perfusion alterations. Various mechanisms responsible for these alterations underlie the loss of hemodynamic coherence during unsuccessful resuscitation procedures. Therapeutic resolution of persistent heterogeneous microcirculatory alterations is expected to improve outcomes in @entity3124 @entity1 .
