Critical care medicine
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Critical care medicine · Nov 2012
Multicenter StudyActivated protein C and septic shock: a propensity-matched cohort study*.
Septic shock is a highly inflammatory and procoagulant state associated with significant mortality. In a single randomized controlled trial, recombinant human activated protein C (drotrecogin alfa) reduced mortality in patients with severe sepsis at high risk of death. Further clinical trials, including a recently completed trial in patients with septic shock, failed to reproduce these results. ⋯ In this retrospective, propensity-matched, multicenter cohort study of patients with septic shock, early use of recombinant human activated protein C was associated with reduced mortality. Improvements in general quality of care such as speed of antimicrobial delivery leading to decreasing mortality of patients with septic shock may have contributed to the null results of the recently completed trial of recombinant human activated protein C in patients with septic shock.
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Critical care medicine · Nov 2012
Mild hypothermia decreases arrhythmia susceptibility in a canine model of global myocardial ischemia*.
Although the majority of sudden cardiac arrests occur in patients with ischemic heart disease, the effect of therapeutic hypothermia on arrhythmia susceptibility during acute global ischemia is not well understood. While both ischemia and severe hypothermia are arrhythmogenic, patients undergoing therapeutic hypothermia do not have an increase in arrhythmias, despite the fact that most sudden cardiac arrest occur in the setting of ischemia. We hypothesized that mild hypothermia induced prior to myocardial ischemia and reperfusion will have a beneficial effect on ischemia-related arrhythmia substrates. ⋯ Mild hypothermia attenuated ischemia-induced increase in dispersion of repolarization, conduction slowing, and block, which are known mechanisms of arrhythmogenesis in ischemia. These data suggest that therapeutic hypothermia may decrease arrhythmogenesis during myocardial ischemia.
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Critical care medicine · Nov 2012
Association of cystic fibrosis transmembrane conductance regulator gene variants with acute lung injury in African American children with pneumonia*.
The cystic fibrosis transmembrane conductance regulator regulates fluid balance in alveolar epithelial cells and appears to modulate the inflammatory response. To determine whether more severe lung injury in children who develop community-acquired pneumonia is associated with variations known to affect function in the gene coding for cystic fibrosis transmembrane conductance regulator. ⋯ Genetic variation in cystic fibrosis transmembrane conductance regulator is associated with acute lung injury in African American children with community-acquired pneumonia.
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To review the current status of critical care education of medical students, focusing on how early, vigorous undergraduate training may address the needs of the learners and society. ⋯ Undergraduate medical education in critical care would be advanced by consolidation and organization into formal curricula. These would teach biomedical and humanistic skills essential to critical care but valuable in all medical settings. Early, well-planned exposure to critical care as a distinct discipline might increase student interest in careers in the field. The effects of educational interventions on the acquisition of knowledge, attitudes, and skills as well as long-term career choice should be subjected to rigorous study.
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Critical care medicine · Nov 2012
Lung microenvironment contributes to the resistance of alveolar macrophages to develop tolerance to endotoxin*.
Endotoxin tolerance corresponds to reprogramming of mononuclear phagocytes after iterative encounters with toll-like receptor agonists aimed to dampen the inflammatory response. We investigated why this phenomenon cannot be observed with murine alveolar macrophages. ⋯ Our results support the conclusion that at homeostasis in the lungs, constitutive expression of granulocyte-macrophage colony-stimulating factor, interleukin-18, interferon-γ and possibly interleukin-15, and a cross-talk between B lymphocytes and alveolar macrophages create a microenvironment specific to the lungs that prevents alveolar macrophages from becoming tolerant to endotoxin.