Critical Care 2017, 21(Suppl 1):P349 Introduction Imbalance in cellular energetics has been suggested to be an important mechanism for organ failure in sepsis and septic shock. We hypothesized that such energy imbalance would either be caused by metabolic changes leading to decreased energy production or by increased energy consumption. Thus, we set out to investigate if mitochondrial dysfunction or decreased energy consumption alters cellular metabolism in muscle tissue in experimental sepsis. Methods We submitted anesthetized piglets to sepsis (n = 12) or placebo (n = 4) and monitored them for 3 hours. Plasma lactate and markers of organ failure were measured hourly, as was muscle metabolism by microdialysis. Energy consumption was intervened locally by infusing ouabain through one microdialysis catheter to block major energy expenditure of the cells, by inhibiting the major energy consuming enzyme, N+/K + -ATPase. Similarly, energy production was blocked infusing sodium cyanide (NaCN), in a different region, to block the cytochrome oxidase in muscle tissue mitochondria. Results All animals submitted to sepsis fulfilled sepsis criteria as defined in Sepsis-3, whereas no animals in the placebo group did. Muscle glucose decreased during sepsis independently of N+/K + -ATPase or cytochrome oxidase blockade. Muscle lactate did not increase during sepsis in naïve metabolism. However, during cytochrome oxidase blockade, there was an increase in muscle lactate that was further accentuated during sepsis. Muscle pyruvate did not decrease during sepsis in naïve metabolism. During cytochrome oxidase blockade, there was a decrease in muscle pyruvate, independently of sepsis. Lactate to pyruvate ratio increased during sepsis and was further accentuated during cytochrome oxidase blockade. Muscle glycerol increased during sepsis and decreased slightly without sepsis regardless of N+/K + -ATPase or cytochrome oxidase blocking. There were no significant changes in muscle glutamate or urea during sepsis in absence/presence of N+/K + -ATPase or cytochrome oxidase blockade. ConclusionsThese results indicate increased metabolism of energy substrates in muscle tissue in experimental sepsis. Our results do not indicate presence of energy depletion or mitochondrial dysfunction in muscle and should similar physiologic situation be present in other tissues, other mechanisms of organ failure must be considered. , and long-term follow up has shown increased fracture risk [2]. It is unclear if these changes are a consequence of acute critical illness, or reduced activity afterwards. Bone health assessment during critical illness is challenging, and direct bone strength measurement is not possible. We used a rodent sepsis model to test the hypothesis that critical illness causes early reduction in bone strength and changes in bone architecture. Methods 20 Sprague-Dawley rats (350 ± 15.8g) were anesthetised and randomised to receive cecal ligation and puncture (CLP) (50% cecum length, 18G needle single pass through anterior and posterior wa...

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Introduction Noninvasive ventilation is a safe and eff ective method to treat acute respiratory failure, minimizing the respiratory workload and oxygenation. Few studies compare the effi cacy of diff erent types of noninvasive ventilation interfaces and their adaptation. Objective To identify the most frequently noninvasive ventilation interfaces used and eventual problems related to their adaptation in critically ill patients. Methods We conducted an observational study, with patients older than 18 years old admitted to the intensive care and step-down units of the Albert Einstein Jewish Hospital that used noninvasive ventilation. We collected data such as reason to use noninvasive ventilation, interface used, scheme of noninvasive ventilation used (continuously, periods or nocturnal use), adaptation, and reasons for nonadaptation. Results We evaluated 245 patients with a median age of 82 years (range of 20 to 107 years). Acute respiratory failure was the most frequent cause of noninvasive ventilation used (71.3%), followed by pulmonary expansion (10.24%), after mechanical ventilation weaning (6.14%) and sleep obstructive apnea (8.6%). The most frequently used interface was total face masks (74.7%), followed by facial masks in 24.5% of the patients, and 0.8% used performax masks. The use of noninvasive ventilation for periods (82.4%) was the most common scheme of use, with 10.6% using it continuously and 6.9% during the nocturnal period only. Interface adaptation occurred in 76% of the patients; the 24% that did not adapt had their interface changed to improve adaptation afterwards. The total face mask had 75.5% of interface adaptation, the facial mask had 80% and no adaptation occurred in patients that used the performax mask. The face format was the most frequent cause of nonadaptation in 30.5% of the patients, followed by patient's related discomfort (28.8%), air leaking (27.7%), claustrophobia (18.6%), noncollaborative patient (10.1%), patient agitation (6.7%), facial trauma or lesion (1.7%), type of mask fi xation (1.7%), and 1.7% patients with other causes. Conclusion Acute respiratory failure was the most frequent reason for noninvasive ventilation use, with the total face mask being the most frequent interface used. The most common causes of interface nonadaptation were face format, patient-related discomfort and air leaking, showing improvement of adaptation after changing the interface used. P2 Exercise training reduces oxidative damage in skeletal muscle of septic rats

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reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. carbon dioxide 30 [27][28][29][30][31][32][33][34][35] mmHg and median temperature 37.1 [36.8-37.3]°C. After removal of artefacts, the mean monitoring time was 22 h08 (8 h54). All patients had impaired cerebral autoregulation during their monitoring time. The mean IAR index was 17 (9.5) %. During H 0 H 6 and H 18 H 24 , the majority of our patients; respectively 53 and 71 % had an IAR index > 10 %. Conclusion According to our data, patients with septic shock had impaired cerebral autoregulation within the first 24 hours of their admission in the ICU. In our patients, we described a variability of distribution of impaired autoregulation according to time. ReferencesSchramm P, Klein KU, Falkenberg L, et al. Impaired cerebrovascular autoregulation in patients with severe sepsis and sepsis-associated delirium. Crit Care 2012; 16: R181. Aries MJH, Czosnyka M, Budohoski KP, et al. Continuous determination of optimal cerebral perfusion pressure in traumatic brain injury. Crit. Care Med. 2012.