Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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In the intensive care unit (ICU) of our tertiary care university medical center, central venous pressure (CVP) measurements derived from bedside monitors differ considerably from measurements by trained intensivists using paper tracings. To quantify these differences, printed CVP tracings and concurrent respiratory waveforms were collected from 100 consecutive critically ill patients along with the corresponding monitor-displayed CVP. Four blinded intensivists interpreted the tracings. ⋯ To determine the potential clinical impact of these differences, we used the original Surviving Sepsis Campaign Guidelines for fluid administration based upon the measurement of CVP. For individual physicians, protocol-driven fluid management strategy would have differed in 19.2% to 25.3% of cases, dependent upon which measured value was chosen. Although protocol-driven strategies to direct fluid infusion therapy may improve outcomes, these interventions in a specific patient are dependent upon the method by which the CVP is measured.
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There are only few strategic and therapeutic options to improve the functional outcome of patients after cardiac arrest and resuscitation (CPR). The pathophysiology of reperfusion injury after global ischemia is not completely understood. We present here a murine model of cardiac arrest and resuscitation that allows an analysis of the pathophysiology of reperfusion injury, especially focusing on survival, tissue damage, and functional neurological parameters. ⋯ Histological examinations and blood analyses of CPR animals revealed significant leukocyte tissue infiltration and morphological damage of brain, lung, and kidneys. In summary, mice undergoing CPR after cardiac arrest present distinct neurological deficits, marked organ damage, and a 54% mortality rate. Our highly standardized and reproducible model of mice resuscitation provides a means for a better understanding of the post-CPR pathophysiology and thus opens new perspectives to develop relevant therapeutic approaches to minimize global I/R injury.
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Identification of occult shock is a major clinical problem compounded by inadequate criteria for assessing the efficacy of fluid resuscitation. We suggest that these problems may be resolved in part by understanding both the physiological mechanisms underlying oxygen debt accumulation and, more importantly, the debt repayment schedule during resuscitation. We present a simplified tutorial that incorporates the concept of the oxygen supply-delivery relationship with that of oxygen debt and show how this is relevant to the understanding of shock and resuscitation. ⋯ Because of difficulties inherent in measuring oxygen debt in the prehospital and emergency settings, various metabolic end points such as lactate and base deficit have been proposed as surrogates. We demonstrate the heuristic value of this model in providing a predictive framework for both the optimum therapeutic time window and optimum fluid loadings before critical transitions to an irreversible shock state can occur. The model also provides an unambiguous and objective standard for quantifying the behavior of various postulated shock "markers".
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The present study was designed to find out whether SB431542, an inhibitor of transforming growth factor beta1 activin receptor-like kinase, could protect the lung from LPS-induced injury. Inflammatory lung injury model was induced by intratracheal administration of LPS. C57BL/6 mice were randomly divided into the sham control group (S group), the LPS stimulation group (L group), the LPS + early SB431542 treatment group (Ie group), and the LPS + delayed SB431542 treatment group (Id group). ⋯ Those parameters were further aggravated in the Ie group whereas relieved significantly in the Id group. These data suggest that SB431542 therapy for inflammatory lung injury could be harmful if performed during early-phase inflammatory response. However, the therapy would prevent lung from inflammatory injury and fibrosis if it was initiated late.