• Jacopo Fumagalli, Lorenzo Berra, Changsheng Zhang, Massimiliano Pirrone, Roberta R De Santis Santiago, Susimeire Gomes, Federico Magni, Glaucia A B Dos Santos, Desmond Bennett, Vinicius Torsani, Daniel Fisher, Caio Morais, Marcelo B P Amato, and Robert M Kacmarek.
• 1Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA.2Dipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti, Universita' degli Studi di Milano, Milan, Italy.3Pulmonary Division, Heart Institute, School of Medicine, University of São Paulo, São Paulo, Brazil.4Dipartimento di Medicina e Chirurgia, Universita' degli Studi di Milano-Bicocca, Milan, Italy.5Hospital das Clínicas da Faculdade de Medicina da USP (HCFMUSP)-Instituto de Radiologia (InRad), Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.6Respiratory Care Department, Massachusetts General Hospital, Boston, MA.
• Crit. Care Med. 2017 Aug 1; 45 (8): 1374-1381.

ObjectivesAtelectasis develops in critically ill obese patients when undergoing mechanical ventilation due to increased pleural pressure. The current study aimed to determine the relationship between transpulmonary pressure, lung mechanics, and lung morphology and to quantify the benefits of a decremental positive end-expiratory pressure trial preceded by a recruitment maneuver.DesignProspective, crossover, nonrandomized interventional study.SettingMedical and Surgical Intensive Care Units at Massachusetts General Hospital (Boston, MA) and University Animal Research Laboratory (São Paulo, Brazil).Patients/SubjectsCritically ill obese patients with acute respiratory failure and anesthetized swine.InterventionsClinical data from 16 mechanically ventilated critically ill obese patients were analyzed. An animal model of obesity with reversible atelectasis was developed by placing fluid filled bags on the abdomen to describe changes of lung mechanics, lung morphology, and pulmonary hemodynamics in 10 swine.Measurements And Main ResultsIn obese patients (body mass index, 48 ± 11 kg/m), 21.7 ± 3.7 cm H2O of positive end-expiratory pressure resulted in the lowest elastance of the respiratory system (18.6 ± 6.1 cm H2O/L) after a recruitment maneuver and decremental positive end-expiratory pressure and corresponded to a positive (2.1 ± 2.2 cm H2O) end-expiratory transpulmonary pressure. Ventilation at lowest elastance positive end-expiratory pressure preceded by a recruitment maneuver restored end-expiratory lung volume (30.4 ± 9.1 mL/kg ideal body weight) and oxygenation (273.4 ± 72.1 mm Hg). In the swine model, lung collapse and intratidal recruitment/derecruitment occurred when the positive end-expiratory transpulmonary pressure decreased below 2-4 cm H2O. After the development of atelectasis, a decremental positive end-expiratory pressure trial preceded by lung recruitment identified the positive end-expiratory pressure level (17.4 ± 2.1 cm H2O) needed to restore poorly and nonaerated lung tissue, reestablishing lung elastance and oxygenation while avoiding increased pulmonary vascular resistance.ConclusionsIn obesity, low-to-negative values of transpulmonary pressure predict lung collapse and intratidal recruitment/derecruitment. A decremental positive end-expiratory pressure trial preceded by a recruitment maneuver reverses atelectasis, improves lung mechanics, distribution of ventilation and oxygenation, and does not increase pulmonary vascular resistance.

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