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Background: Driving pressure (DP) represents tidal volume normalised to respiratory system compliance (C RS) and is a novel parameter to target ventilator settings. We conducted a study to determine whether C RS and DP reflect aerated lung volume and dynamic strain during general anaesthesia. Methods: Twenty non-obese patients undergoing open abdominal surgery received three PEEP levels (2, 7, or 12 cm H 2 O) in random order with constant tidal volume ventilation. Respiratory mechanics, lung volumes, and alveolar recruitment were measured to assess end-expiratory aerated volume, which was compared with the patient's individual predicted functional residual capacity in supine position (FRCp). Results: C RS was linearly related to aerated volume and DP to dynamic strain at PEEP of 2 cm H 2 O (intraoperative FRC) (r¼0.72 and r¼0.73, both P<0.001). These relationships were maintained with higher PEEP only when aerated volume did not overcome FRCp (r¼0.73, P<0.001; r¼0.54, P¼0.004), with 100 ml lung volume increases accompanied by 1.8 ml cm H 2 O À1 (95% confidence interval [1.1e2.5]) increases in C RS. When aerated volume was greater or equal to FRCp (35% of patients at PEEP 2 cm H 2 O, 55% at PEEP 7 cm H 2 O, and 75% at PEEP 12 cm H 2 O), C RS and DP were independent from aerated volume and dynamic strain, with C RS weakly but significantly inversely related to alveolar dead space fraction (r¼e0.47, P¼0.001). PEEP-induced alveolar recruitment yielded higher C RS and reduced DP only at aerated volumes below FRCp (P¼0.015 and 0.008, respectively). Conclusions: During general anaesthesia, respiratory system compliance and driving pressure reflect aerated lung volume and dynamic strain, respectively, only if aerated volume does not exceed functional residual capacity in supine position, which is a frequent event when PEEP is used in this setting.

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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...