Critical care : the official journal of the Critical Care Forum
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Review
Bench-to-bedside review: hypercapnic acidosis in lung injury--from 'permissive' to 'therapeutic'.
Modern ventilation strategies for patients with acute lung injury and acute respiratory distress syndrome frequently result in hypercapnic acidosis (HCA), which is regarded as an acceptable side effect ('permissive hypercapnia'). Multiple experimental studies have demonstrated advantageous effects of HCA in several lung injury models. To date, however, human trials studying the effect of carbon dioxide per se on outcome in patients with lung injury have not been performed. ⋯ The underlying mechanisms by which HCA exerts its protective effects are complex, but dampening of the inflammatory response seems to play a pivotal role. After briefly summarizing the physiological effects of HCA, a critical analysis of the available evidence on the potential beneficial effects of therapeutic HCA from in vitro, ex vivo and in vivo lung injury models and from human studies will be reviewed. In addition, the potential concerns in the clinical setting will be outlined.
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Comparative Study
The use of a blood conservation device to reduce red blood cell transfusion requirements: a before and after study.
Anaemia and the associated need for packed red blood cell (PRBC) transfusions are common in patients admitted to the intensive care unit (ICU). Among many causes, blood losses from repeated diagnostic tests are contributory. ⋯ The use of a blood conservation device is associated with 1) reduced PRBC transfusion requirements and 2) a smaller decrease in Hb levels in the ICU.
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Novel insights into the metabolic alterations of critical illness were published in Critical Care in 2009. The association between early hypoglycaemia/high glycemic variability and poor outcome was confirmed. ⋯ The relationship between the achievement of nutritional goals and outcomes was further investigated. Finally, understanding of some critical-illness-related endocrine and neuromuscular disorders improved through new experimental and clinical findings.
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In sepsis, inflammation and thrombosis are both the cause and the result of interactions between circulating (for example, leukocytes and platelets), endothelial and smooth muscle cells. Microparticles are proinflammatory and procoagulant fragments originating from plasma membrane generated after cellular activation and released in body fluids. In the vessel, they constitute a pool of bioactive effectors pulled from diverse cellular origins and may act as intercellular messengers. ⋯ Microparticles may participate in the pathogenesis of sepsis through multiple ways. They are able to regulate vascular tone and are potent vascular proinflammatory and procoagulant mediators. Microparticles' abilities are of increasing interest in deciphering the mechanisms underlying the multiple organ dysfunction of septic shock.
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Randomized Controlled Trial Comparative Study
Role of selective V2-receptor-antagonism in septic shock: a randomized, controlled, experimental study.
V(2)-receptor (V(2)R) stimulation potentially aggravates sepsis-induced vasodilation, fluid accumulation and microvascular thrombosis. Therefore, the present study was performed to determine the effects of a first-line therapy with the selective V(2)R-antagonist (Propionyl(1)-D-Tyr(Et)(2)-Val(4)-Abu(6)-Arg(8,9))-Vasopressin on cardiopulmonary hemodynamics and organ function vs. the mixed V(1a)R/V(2)R-agonist arginine vasopressin (AVP) or placebo in an established ovine model of septic shock. ⋯ Selective V(2)R-antagonism may represent an innovative therapeutic approach to attenuate multiple organ dysfunction in early septic shock.