Chest
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Disorders of elevated body temperature may be classified as either fever or hyperthermia. Fever is caused by a pyrogen-mediated upward adjustment of the hypothalamic thermostat; hyperthermia results from a loss of physiologic control of temperature regulation. Fever in the ICU can be due to infectious or noninfectious causes. ⋯ Both high fever and prolonged fever have been associated with increased mortality; however, a causal role for fever as a mediator of adverse outcomes during non-neurologic critical illness has not been established. Outside the realm of acute brain injury, the practice of treating fever remains controversial. To generate high-quality, evidence-based guidelines for the management of fever, large, prospective, multicenter trials are needed.
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This is the first of a two-part series that reviews advanced critical care echocardiography (CCE) techniques designed for critical care physicians. In this section, we review training in basic and advanced CCE. ⋯ This section ends with a review of the quantitative and semiquantitative measurements of stroke volume, as well as problems with measurement of stroke volume in the ICU and its useful clinical applications. Video-based examples will help demonstrate the techniques that are described in the text.
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Sphingolipids comprise a class of bioactive lipids that are involved in a variety of pathophysiologic processes, including cell death and survival. Ceramide and sphingosine-1-phosphate (S1P) form the center of sphingolipid metabolism and determine proapoptotic and antiapoptotic balance. Findings in animal models suggest a possible pathophysiologic role of ceramide and S1P in COPD, cystic fibrosis, and asthma. ⋯ Ceramides and S1P also regulate endothelial permeability through cortical actin cytoskeletal rearrangement, which is relevant for the pathogenesis of ARDS. On the basis of these observations, the feasibility of pharmacologic intervention in the sphingolipid pathway to influence disease development and progression is presently explored, with promising early results. The prospect of new strategies to prevent and repair lung disease by interfering with sphingolipid metabolism is exciting and could potentially reduce morbidity and mortality in patients with severe lung disorders.