Critical care : the official journal of the Critical Care Forum
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We review key research papers in cardiology and intensive care published during 2008 in Critical Care. We quote studies on the same subject published in other journals if appropriate. Papers have been grouped into three categories: (a) cardiovascular biomarkers in critical illness, (b) haemodynamic management of septic shock, and (c) haemodynamic monitoring.
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Original research contributions published in Critical Care in 2008 in the fields of respirology and critical care medicine are summarized. Eighteen articles were grouped into the following categories: acute lung injury and acute respiratory distress syndrome, mechanical ventilation, mechanisms of ventilator-induced lung injury, and tracheotomy decannulation and non-invasive ventilation.
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Review
Monitoring trauma and intensive care unit resuscitation with tissue hemoglobin oxygen saturation.
The purpose of the present review is to review our experience with near-infrared spectroscopy (NIRS) monitoring in shock resuscitation and predicting clinical outcomes. ⋯ StO2 is an important tool in identifying high-risk patients in septic and hemorrhagic shock. It is a non-invasive means of obtaining vital information regarding outcome and adequacy of resuscitation.
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High mobility group box nuclear protein 1 (HMGB1) is a DNA nuclear binding protein that has recently been shown to be an early trigger of sterile inflammation in animal models of trauma-hemorrhage via the activation of the Toll-like-receptor 4 (TLR4) and the receptor for the advanced glycation endproducts (RAGE). However, whether HMGB1 is released early after trauma hemorrhage in humans and is associated with the development of an inflammatory response and coagulopathy is not known and therefore constitutes the aim of the present study. ⋯ The results of this study demonstrate for the first time that HMGB1 is released into the bloodstream early after severe trauma in humans. The release of HMGB1 requires severe injury and tissue hypoperfusion, and is associated with posttraumatic coagulation abnormalities, activation of complement and severe systemic inflammatory response.
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In septic patients increased central drive and increased metabolic demands combine to increase energy demands on the ventilatory muscles. This occurs at a time when energy supplies are limited and energy production hindered, and it leads to an energy supply-demand imbalance and often ventilatory failure. ⋯ In this review I discuss factors related to ventilatory muscle failure, giving emphasis to mechanical and supply demand aspects. I also review the implications of changes in ventilatory patterns for heart-lung interactions.