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Ítem The Endothelium in Sepsis(Lippincott Williams & Wilkins, 2016-03-01) Ince, CanSepsis affects practically all aspects of endothelial cell (EC) function and is thought to be the key factor in the progression from sepsis to organ failure. Endothelial functions affected by sepsis include vasoregulation, barrier function, inflammation, and hemostasis. These are among other mechanisms often mediated by glycocalyx shedding, such as abnormal nitric oxide metabolism, up-regulation of reactive oxygen species generation due to down-regulation of endothelial-associated antioxidant defenses, transcellular communication, proteases, exposure of adhesion molecules, and activation of tissue factor. This review covers current insight in EC-associated hemostatic responses to sepsis and the EC response to inflammation. The endothelial cell lining is highly heterogeneous between different organ systems and consequently also in its response to sepsis. In this context, we discuss the response of the endothelial cell lining to sepsis in the kidney, liver, and lung. Finally, we discuss evidence as to whether the EC response to sepsis is adaptive or maladaptive. This study is a result of an Acute Dialysis Quality Initiative XIV Sepsis Workgroup meeting held in Bogota, Columbia, between October 12 and 15, 2014.
Ítem Understanding the venous–arterial CO2 to arterial–venous O2 content difference ratio(Springer, 2016-11-12) Ospina-Tascón, Gustavo A.Introduction Early identification of tissue hypoperfusion is a cornerstone of shock management [1]. Normal macrohemodynamic and oxygen-derived parameters do not, however, rule out the presence of tissue hypoxia [2]. In this setting, carbon dioxide (CO2)-derived variables may provide information on macroand microvascular blood flow [3] and also on the presence of anaerobic metabolism [4, 5]. Importantly, variations in CO2 occur more rapidly than changes in lactate kinetics, making the former an attractive biomarker for monitoring, especially during the early stages of resuscitation [6, 7].