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  In a cohort of multisystem trauma patients with femur fractures, greater injury severity and depth of shock, as measured by LacTW24h, were associated with late operative fixation. Late fixation was also associated with MOF. Strategies to reduce the burden of MOF in this population require further investigation.
 In a cohort of multisystem trauma patients with femur fractures, greater injury severity and depth of shock, as measured by LacTW24h, were associated with late operative fixation. Late fixation was also associated with MOF. Strategies to reduce the burden of MOF in this population require further investigation.Cardioprotection encompasses a variety of strategies protecting the heart against myocardial injury that occurs during and after inadequate blood supply to the heart during myocardial infarction. While restoring reperfusion is crucial for salvaging myocardium from further damage, paradoxically, it itself accounts for additional cell death-a phenomenon named ischemia/reperfusion injury. Therefore, therapeutic strategies are necessary to render the heart protected against myocardial infarction. Ischemic pre- and postconditioning, by short periods of sublethal cardiac ischemia and reperfusion, are still the strongest mechanisms to achieve cardioprotection. However, it is highly impractical and far too invasive for clinical use. Fortunately, it can be mimicked pharmacologically, for example, by volatile anesthetics, noble gases, opioids, propofol, dexmedetomidine, and phosphodiesterase inhibitors. These substances are all routinely used in the clinical setting and seem promising candidates for successful translation of cardioprotection from experimental protocols to clinical trials. This review presents the fundamental mechanisms of conditioning strategies and provides an overview of the most recent and relevant findings on different concepts achieving cardioprotection in the experimental setting, specifically emphasizing pharmacological approaches in the perioperative context.Perioperative cardioprotection aims to minimize the consequences of myocardial ischemia-reperfusion injury. In isolated tissue and animal experiments, several treatments have been identified providing cardioprotection. Some of these strategies have been confirmed in clinical proof-of-concept studies. However, the final translation of cardioprotective strategies to really improve clinical outcome has been disappointing large randomized controlled clinical trials mostly revealed inconclusive, neutral, or negative results. This review provides an overview of the currently available evidence regarding clinical implications of perioperative cardioprotective therapies from an anesthesiological perspective, highlighting nonpharmacological as well as pharmacological strategies. We discuss reasons why translation of promising experimental results into clinical practice and outcome improvement is hampered by potential confounders and suggest future perspectives to overcome these limitations.Despite substantial advances in anesthesia safety within the past decades, perioperative mortality remains a prevalent problem and can be considered among the top causes of death worldwide. Acute organ failure is a major risk factor of morbidity and mortality in surgical patients and develops primarily as a consequence of a dysregulated inflammatory response and insufficient tissue perfusion. Neurological dysfunction, myocardial ischemia, acute kidney injury, respiratory failure, intestinal dysfunction, and hepatic impairment are among the most serious complications impacting patient outcome and recovery. Pre-, intra-, and postoperative arrangements, such as enhanced recovery after surgery programs, can contribute to lowering the occurrence of organ dysfunction, and mortality rates have improved with the advent of specialized intensive care units and advances in procedures relating to extracorporeal organ support. However, no specific pharmacological therapies have proven effective in the prevention or reversal of perioperative organ injury. Therefore, understanding the underlying mechanisms of organ dysfunction is essential to identify novel treatment strategies to improve perioperative care and outcomes for surgical patients. This review focuses on recent knowledge of pathophysiological and molecular pathways leading to perioperative organ injury. Additionally, we highlight potential therapeutic targets relevant to the network of events that occur in clinical settings with organ failure.In the past, it was common practice to use a high tidal volume (VT) during intraoperative ventilation, because this reduced the need for high oxygen fractions to compensate for the ventilation-perfusion mismatches due to atelectasis in a time when it was uncommon to use positive end-expiratory pressure (PEEP) in the operating room. Convincing and increasing evidence for harm induced by ventilation with a high VT has emerged over recent decades, also in the operating room, and by now intraoperative ventilation with a low VT is a well-adopted approach. There is less certainty about the level of PEEP during intraoperative ventilation. Evidence for benefit and harm of higher PEEP during intraoperative ventilation is at least contradicting. While some PEEP may prevent lung injury through reduction of atelectasis, higher PEEP is undeniably associated with an increased risk of intraoperative hypotension that frequently requires administration of vasoactive drugs. The optimal level of inspired oxygen fraction (FIO2) during surgery is even more uncertain. The suggestion that hyperoxemia prevents against surgical site infections has not been confirmed in recent research. In addition, gas absorption-induced atelectasis and its association with adverse outcomes like postoperative pulmonary complications actually makes use of a high FIO2 less attractive. Based on the available evidence, we recommend the use of a low VT of 6-8 mL/kg predicted body weight in all surgery patients, and to restrict use of a high PEEP and high FIO2 during intraoperative ventilation to cases in which hypoxemia develops.  https://www.selleckchem.com/products/camostat-mesilate-foy-305.html  Here, we prefer to first increase FIO2 before using high PEEP.