• Andreas Güldner, Anja Braune, Lorenzo Ball, Pedro L Silva, Cynthia Samary, Angelo Insorsi, Robert Huhle, Ines Rentzsch, Claudia Becker, Liane Oehme, Michael Andreeff, Vidal Melo Marcos F MF, Tilo Winkler, Paolo Pelosi, Patricia R M Rocco, Jörg Kotzerke, and Gama de Abreu Marcelo M.
• 1Department of Anesthesiology and Intensive Care Medicine, Pulmonary Engineering Group, University Hospital Dresden, Technische Universität Dresden, Dresden, Germany.2IRCCS San Martino IST, Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, Genoa, Italy.3Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.4Institute of Nuclear Medicine, University Hospital Dresden, Dresden, Germany.5Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard University, Boston, MA.
• Crit. Care Med. 2016 Sep 1; 44 (9): e854-65.

ObjectiveVolutrauma and atelectrauma promote ventilator-induced lung injury, but their relative contribution to inflammation in ventilator-induced lung injury is not well established. The aim of this study was to determine the impact of volutrauma and atelectrauma on the distribution of lung inflammation in experimental acute respiratory distress syndrome.DesignLaboratory investigation.SettingUniversity-hospital research facility.SubjectsTen pigs (five per group; 34.7-49.9 kg)Interventions: Animals were anesthetized and intubated, and saline lung lavage was performed. Lungs were separated with a double-lumen tube. Following lung recruitment and decremental positive end-expiratory pressure trial, animals were randomly assigned to 4 hours of ventilation of the left (ventilator-induced lung injury) lung with tidal volume of approximately 3 mL/kg and 1) high positive end-expiratory pressure set above the level where dynamic compliance increased more than 5% during positive end-expiratory pressure trial (volutrauma); or 2) low positive end-expiratory pressure to achieve driving pressure comparable with volutrauma (atelectrauma). The right (control) lung was kept on continuous positive airway pressure of 20 cm H2O, and CO2 was partially removed extracorporeally.Measurements And Main ResultsRegional lung aeration, specific [F]fluorodeoxyglucose uptake rate, and perfusion were assessed using computed and positron emission tomography. Volutrauma yielded higher [F]fluorodeoxyglucose uptake rate in the ventilated lung compared with atelectrauma (median [interquartile range], 0.017 [0.014-0.025] vs 0.013 min [0.010-0.014 min]; p < 0.01), mainly in central lung regions. Volutrauma yielded higher [F]fluorodeoxyglucose uptake rate in ventilator-induced lung injury versus control lung (0.017 [0.014-0.025] vs 0.011 min [0.010-0.016 min]; p < 0.05), whereas atelectrauma did not. Volutrauma decreased blood fraction at similar perfusion and increased normally as well as hyperaerated lung compartments and tidal hyperaeration. Atelectrauma yielded higher poorly and nonaerated lung compartments, and tidal recruitment. Driving pressure increased in atelectrauma.ConclusionsIn this model of acute respiratory distress syndrome, volutrauma promoted higher lung inflammation than atelectrauma at comparable low tidal volume and lower driving pressure, suggesting that static stress and strain are major determinants of ventilator-induced lung injury.

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