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

Introduction Vascular calcifi cation is a regulated process, which associates with coronary artery disease (CAD) and occurs through an increase in transcription factor expression such as RUNX2, MSX2 and alkaline phosphatase (ALP), then inducing calcium deposition. Bone morphogenetic protein-2 (BMP2) is a potent osteochondrogenic mediator, which is expressed in CAD. Endothelin-1 (ET1) and leptin have a role in regulating infl ammation and CAD. We hypothesized that BMP2, leptin or both increase ROS formation in C57BL/6 vascular smooth muscle cells (SMC), stimulating osteochondrogenic diff erentiation. We also investigated the eff ect of ET1 in SMC osteochondrogenesis. Our objectives were: to investigate ROS production in SMC after BMP2 (50 ng/ml) and/or leptin (10 ng/ml) incubation for 6 hours; and to assess osteochondrogenic gene expression and calcifi cation of SMC stimulated with BMP2, leptin or ET1 (10 nM). Methods We assessed 2-hydroxyethidium, more specifi c for superoxide, and ethidium which refl ects hydrogen peroxide through HPLC analysis in SMC after stimulation. SMC cells were incubated with these stimuli for 48 to 96 hours and RUNX2, MSX2, ALP mRNA and protein expression were assessed using qPCR and western blotting. We quantifi ed SMC calcifi cation after 14 days of stimulation through Alizarin Red staining. Results The results are shown as mean ± SD and were statistically signifi cant when pHydrogen peroxide and superoxide production increased both in BMP2 and in leptin-incubated SMC (3.77 ± 0.32 and 3.26 ± 0.26) versus control (n = 6); pBMP2 and leptin alone increased SMC calcifi cation (1.25 ± 0.08 and 1.28 ± 0.14) versus control after 14 days (n = 6); pET1 alone did not stimulate osteocondrogenic mRNA expression vs. control. Conclusion We showed that BMP2 and leptin increased ROS formation in SMC, which stimulated osteocondrogenic mRNA/protein expression to induce SMC calcifi cation. ET1 alone did not increase osteochondrogenesis in SMC. P2 Eff ects of rapid repetition of a vascular occlusion test on near-infrared spectroscopy-derived variables in healthy subjects and in critically ill patients

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Introduction Vascular calcifi cation is a regulated process, which associates with coronary artery disease (CAD) and occurs through an increase in transcription factor expression such as RUNX2, MSX2 and alkaline phosphatase (ALP), then inducing calcium deposition. Bone morphogenetic protein-2 (BMP2) is a potent osteochondrogenic mediator, which is expressed in CAD. Endothelin-1 (ET1) and leptin have a role in regulating infl ammation and CAD. We hypothesized that BMP2, leptin or both increase ROS formation in C57BL/6 vascular smooth muscle cells (SMC), stimulating osteochondrogenic diff erentiation. We also investigated the eff ect of ET1 in SMC osteochondrogenesis. Our objectives were: to investigate ROS production in SMC after BMP2 (50 ng/ml) and/or leptin (10 ng/ml) incubation for 6 hours; and to assess osteochondrogenic gene expression and calcifi cation of SMC stimulated with BMP2, leptin or ET1 (10 nM). Methods We assessed 2-hydroxyethidium, more specifi c for superoxide, and ethidium which refl ects hydrogen peroxide through HPLC analysis in SMC after stimulation. SMC cells were incubated with these stimuli for 48 to 96 hours and RUNX2, MSX2, ALP mRNA and protein expression were assessed using qPCR and western blotting. We quantifi ed SMC calcifi cation after 14 days of stimulation through Alizarin Red staining. Results The results are shown as mean ± SD and were statistically signifi cant when pHydrogen peroxide and superoxide production increased both in BMP2 and in leptin-incubated SMC (3.77 ± 0.32 and 3.26 ± 0.26) versus control (n = 6); pBMP2 and leptin alone increased SMC calcifi cation (1.25 ± 0.08 and 1.28 ± 0.14) versus control after 14 days (n = 6); pET1 alone did not stimulate osteocondrogenic mRNA expression vs. control. Conclusion We showed that BMP2 and leptin increased ROS formation in SMC, which stimulated osteocondrogenic mRNA/protein expression to induce SMC calcifi cation. ET1 alone did not increase osteochondrogenesis in SMC. P2 Eff ects of rapid repetition of a vascular occlusion test on near-infrared spectroscopy-derived variables in healthy subjects and in critically ill patients

Introduction Vascular calcifi cation is a regulated process, which associates with coronary artery disease (CAD) and occurs through an increase in transcription factor expression such as RUNX2, MSX2 and alkaline phosphatase (ALP), then inducing calcium deposition. Bone morphogenetic protein-2 (BMP2) is a potent osteochondrogenic mediator, which is expressed in CAD. Endothelin-1 (ET1) and leptin have a role in regulating infl ammation and CAD. We hypothesized that BMP2, leptin or both increase ROS formation in C57BL/6 vascular smooth muscle cells (SMC), stimulating osteochondrogenic diff erentiation. We also investigated the eff ect of ET1 in SMC osteochondrogenesis. Our objectives were: to investigate ROS production in SMC after BMP2 (50 ng/ml) and/or leptin (10 ng/ml) incubation for 6 hours; and to assess osteochondrogenic gene expression and calcifi cation of SMC stimulated with BMP2, leptin or ET1 (10 nM). Methods We assessed 2-hydroxyethidium, more specifi c for superoxide, and ethidium which refl ects hydrogen peroxide through HPLC analysis in SMC after stimulation. SMC cells were incubated with these stimuli for 48 to 96 hours and RUNX2, MSX2, ALP mRNA and protein expression were assessed using qPCR and western blotting. We quantifi ed SMC calcifi cation after 14 days of stimulation through Alizarin Red staining. Results The results are shown as mean ± SD and were statistically signifi cant when pHydrogen peroxide and superoxide production increased both in BMP2 and in leptin-incubated SMC (3.77 ± 0.32 and 3.26 ± 0.26) versus control (n = 6); pBMP2 and leptin alone increased SMC calcifi cation (1.25 ± 0.08 and 1.28 ± 0.14) versus control after 14 days (n = 6); pET1 alone did not stimulate osteocondrogenic mRNA expression vs. control. Conclusion We showed that BMP2 and leptin increased ROS formation in SMC, which stimulated osteocondrogenic mRNA/protein expression to induce SMC calcifi cation. ET1 alone did not increase osteochondrogenesis in SMC. P2Eff ects of rapid repetition of a vascular occlusion test on near-infrared spectroscopy-derived variables in healthy subjects and in critically ill patients DO Cortes, F Pufl ea, K Donadello, D de Backer, J-L Vincent, J Creteur Erasme Hospital, Universite Libre de Bruxelles, Anderlecht, Bruxelles, Belgium Critical Care 2013, 17(Suppl 3):P2 (doi: 10.1186/cc12618) Introduction Transient ischemia modifi es cellular metabolism and microvascular physiology in order to limit damage from future hypoxic episodes, a phenomenon called preconditioning. Near-infrared spectroscopy (NIRS) is a non-invasive technique that, when coupled to a vascular occlusion test (VOT), provides an indirect measurement of muscle oxygen consumption (VO 2 ) and microvascular reactivity. We hypothesized that: rapid repetition of a VOT may alter VOTinduced NIRS-derived variables and these changes could refl ect preconditioning; and these alterations would be diff erent in healthy volunteers and critically ill patients. Methods Continuous non-invasive measurements of thenar tissue oxygen saturati...