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      Mechanical Power during Veno-Venous Extracorporeal Membrane Oxygenation Initiation: A Pilot-Study

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          Abstract

          Mechanical power (MP) represents a useful parameter to describe and quantify the forces applied to the lungs during mechanical ventilation (MV). In this multi-center, prospective, observational study, we analyzed MP variations following MV adjustments after veno-venous extra-corporeal membrane oxygenation (VV ECMO) initiation. We also investigated whether the MV parameters (including MP) in the early phases of VV ECMO run may be related to the intensive care unit (ICU) mortality. Thirty-five patients with severe acute respiratory distress syndrome were prospectively enrolled and analyzed. After VV ECMO initiation, we observed a significant decrease in median MP (32.4 vs. 8.2 J/min, p < 0.001), plateau pressure (27 vs. 21 cmH 2O, p = 0.012), driving pressure (11 vs. 8 cmH 2O, p = 0.014), respiratory rate (RR, 22 vs. 14 breaths/min, p < 0.001), and tidal volume adjusted to patient ideal body weight (V T/IBW, 5.5 vs. 4.0 mL/kg, p = 0.001) values. During the early phase of ECMO run, RR (17 vs. 13 breaths/min, p = 0.003) was significantly higher, while positive end-expiratory pressure (10 vs. 14 cmH 2O, p = 0.048) and V T/IBW (3.0 vs. 4.0 mL/kg, p = 0.028) were lower in ICU non-survivors, when compared to the survivors. The observed decrease in MP after ECMO initiation did not influence ICU outcome. Waiting for large studies assessing the role of these parameters in VV ECMO patients, RR and MP monitoring should not be underrated during ECMO.

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          Acute respiratory distress syndrome: the Berlin Definition.

          The acute respiratory distress syndrome (ARDS) was defined in 1994 by the American-European Consensus Conference (AECC); since then, issues regarding the reliability and validity of this definition have emerged. Using a consensus process, a panel of experts convened in 2011 (an initiative of the European Society of Intensive Care Medicine endorsed by the American Thoracic Society and the Society of Critical Care Medicine) developed the Berlin Definition, focusing on feasibility, reliability, validity, and objective evaluation of its performance. A draft definition proposed 3 mutually exclusive categories of ARDS based on degree of hypoxemia: mild (200 mm Hg < PaO2/FIO2 ≤ 300 mm Hg), moderate (100 mm Hg < PaO2/FIO2 ≤ 200 mm Hg), and severe (PaO2/FIO2 ≤ 100 mm Hg) and 4 ancillary variables for severe ARDS: radiographic severity, respiratory system compliance (≤40 mL/cm H2O), positive end-expiratory pressure (≥10 cm H2O), and corrected expired volume per minute (≥10 L/min). The draft Berlin Definition was empirically evaluated using patient-level meta-analysis of 4188 patients with ARDS from 4 multicenter clinical data sets and 269 patients with ARDS from 3 single-center data sets containing physiologic information. The 4 ancillary variables did not contribute to the predictive validity of severe ARDS for mortality and were removed from the definition. Using the Berlin Definition, stages of mild, moderate, and severe ARDS were associated with increased mortality (27%; 95% CI, 24%-30%; 32%; 95% CI, 29%-34%; and 45%; 95% CI, 42%-48%, respectively; P < .001) and increased median duration of mechanical ventilation in survivors (5 days; interquartile [IQR], 2-11; 7 days; IQR, 4-14; and 9 days; IQR, 5-17, respectively; P < .001). Compared with the AECC definition, the final Berlin Definition had better predictive validity for mortality, with an area under the receiver operating curve of 0.577 (95% CI, 0.561-0.593) vs 0.536 (95% CI, 0.520-0.553; P < .001). This updated and revised Berlin Definition for ARDS addresses a number of the limitations of the AECC definition. The approach of combining consensus discussions with empirical evaluation may serve as a model to create more accurate, evidence-based, critical illness syndrome definitions and to better inform clinical care, research, and health services planning.
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            Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network.

            Traditional approaches to mechanical ventilation use tidal volumes of 10 to 15 ml per kilogram of body weight and may cause stretch-induced lung injury in patients with acute lung injury and the acute respiratory distress syndrome. We therefore conducted a trial to determine whether ventilation with lower tidal volumes would improve the clinical outcomes in these patients. Patients with acute lung injury and the acute respiratory distress syndrome were enrolled in a multicenter, randomized trial. The trial compared traditional ventilation treatment, which involved an initial tidal volume of 12 ml per kilogram of predicted body weight and an airway pressure measured after a 0.5-second pause at the end of inspiration (plateau pressure) of 50 cm of water or less, with ventilation with a lower tidal volume, which involved an initial tidal volume of 6 ml per kilogram of predicted body weight and a plateau pressure of 30 cm of water or less. The primary outcomes were death before a patient was discharged home and was breathing without assistance and the number of days without ventilator use from day 1 to day 28. The trial was stopped after the enrollment of 861 patients because mortality was lower in the group treated with lower tidal volumes than in the group treated with traditional tidal volumes (31.0 percent vs. 39.8 percent, P=0.007), and the number of days without ventilator use during the first 28 days after randomization was greater in this group (mean [+/-SD], 12+/-11 vs. 10+/-11; P=0.007). The mean tidal volumes on days 1 to 3 were 6.2+/-0.8 and 11.8+/-0.8 ml per kilogram of predicted body weight (P<0.001), respectively, and the mean plateau pressures were 25+/-6 and 33+/-8 cm of water (P<0.001), respectively. In patients with acute lung injury and the acute respiratory distress syndrome, mechanical ventilation with a lower tidal volume than is traditionally used results in decreased mortality and increases the number of days without ventilator use.
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              Acute respiratory distress syndrome

              The acute respiratory distress syndrome (ARDS) is a common cause of respiratory failure in critically ill patients and is defined by the acute onset of noncardiogenic pulmonary oedema, hypoxaemia and the need for mechanical ventilation. ARDS occurs most often in the setting of pneumonia, sepsis, aspiration of gastric contents or severe trauma and is present in ~10% of all patients in intensive care units worldwide. Despite some improvements, mortality remains high at 30–40% in most studies. Pathological specimens from patients with ARDS frequently reveal diffuse alveolar damage, and laboratory studies have demonstrated both alveolar epithelial and lung endothelial injury, resulting in accumulation of protein-rich inflammatory oedematous fluid in the alveolar space. Diagnosis is based on consensus syndromic criteria, with modifications for under-resourced settings and in paediatric patients. Treatment focuses on lung-protective ventilation; no specific pharmacotherapies have been identified. Long-term outcomes of patients with ARDS are increasingly recognized as important research targets, as many patients survive ARDS only to have ongoing functional and/or psychological sequelae. Future directions include efforts to facilitate earlier recognition of ARDS, identifying responsive subsets of patients and ongoing efforts to understand fundamental mechanisms of lung injury to design specific treatments.
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                Author and article information

                Journal
                Membranes (Basel)
                Membranes (Basel)
                membranes
                Membranes
                MDPI
                2077-0375
                02 January 2021
                January 2021
                : 11
                : 1
                : 30
                Affiliations
                [1 ]2nd Intensive Care Unit, UOC Anestesia e Rianimazione II Cardiopolmonare, Fondazione IRCCS Policlinico San Matteo, 27100 Pavia, Italy; m.belliato@ 123456gmail.com
                [2 ]Department of Clinical-Surgical, Diagnostic and Paediatric Sciences, Unit of Anaesthesia and Intensive Care, University of Pavia, 27100 Pavia, Italy; doc.cremascoli@ 123456gmail.com (L.C.); magiqu@ 123456gmail.com (M.G.Q.)
                [3 ]1st Intensive Care Unit, UOC Anestesia e Rianimazione I, Fondazione IRCCS Policlinico San Matteo, 27100 Pavia, Italy; fioreferrari28@ 123456gmail.com
                [4 ]International Renal Research Institute of Vicenza (IRRIV) and Department of Nephrology, Dialysis and Transplantation, 36100 Vicenza, Italy
                [5 ]Department of Internal Medicine II, Cardiology and Pneumology, Intensive Care, University Hospital Regensburg, 93053 Regensburg, Germany; christoph.fisser@ 123456ukr.de (C.F.); maxmalfertheiner@ 123456gmail.com (M.V.M.)
                [6 ]Department of Intensive Care, Erasme Hospital, Université Libre de Bruxelles, Cliniques Universitaires de Brussels, 1070 Brussels, Belgium; ftaccone@ 123456ulb.ac.be
                [7 ]Pediatric Intensive Care, Bambino Gesù Children’s Hospital, IRCCS, 00165 Rome, Italy; matteo.dinardo@ 123456opbg.net
                [8 ]ECMO Centre Karolinska, Astrid Lindgren Children’s Hospital, Karolinska University Hospital, and Department of Physiology and Pharmacology, Karolinska Institutet, 171 64 Solna (Stockholm), Sweden; lars.broman@ 123456sll.se
                [9 ]Department of Cardio-Thoracic Surgery, Heart and Vascular Centre, Maastricht University Medical Centre (MUMC), 6229 HX Maastricht, The Netherlands; roberto.lorussobs@ 123456gmail.com
                [10 ]Cardiovascular Research Institute Maastricht (CARIM), 6229 ER Maastricht, The Netherlands
                Author notes
                [* ]Correspondence: francesco.epis01@ 123456gmail.com ; Tel.: +39-0382-503524
                Author information
                https://orcid.org/0000-0002-3411-6293
                https://orcid.org/0000-0002-8926-7873
                https://orcid.org/0000-0001-8978-9551
                https://orcid.org/0000-0001-6001-7072
                https://orcid.org/0000-0001-5833-1230
                https://orcid.org/0000-0003-0051-8080
                https://orcid.org/0000-0003-4124-4581
                Article
                membranes-11-00030
                10.3390/membranes11010030
                7824596
                33401668
                6a86bc25-05dd-43ab-ab7c-f09e5e657509
                © 2021 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 18 November 2020
                : 29 December 2020
                Categories
                Article

                veno-venous extracorporeal membrane oxygenation,acute respiratory distress syndrome,ventilator-induced lung injury,mechanical ventilation,mechanical power,respiratory rate

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