Biological Response to Time-Controlled Adaptive Ventilation Depends on Acute Respiratory Distress Syndrome Etiology

Objectives: To compare a time-controlled adaptive ventilation strategy, set in airway pressure release ventilation mode, versus a protective mechanical ventilation strategy in pulmonary and extrapulmonary acute respiratory distress syndrome with similar mechanical impairment. Design: Animal study. Setting: Laboratory investigation. Subjects: Forty-two Wistar rats. Interventions: Pulmonary acute respiratory distress syndrome and extrapulmonary acute respiratory distress syndrome were induced by instillation of Escherichia coli lipopolysaccharide intratracheally or intraperitoneally, respectively. After 24 hours, animals were randomly assigned to receive 1 hour of volume-controlled ventilation (n = 7/etiology) or time-controlled adaptive ventilation (n = 7/etiology) (tidal volume = 8 mL/kg). Time-controlled adaptive ventilation consisted of the application of continuous positive airway pressure 2 cm H2O higher than baseline respiratory system peak pressure for a time (Thigh) of 0.75–0.85 seconds. The release pressure (Plow = 0 cm H2O) was applied for a time (Tlow) of 0.11–0.18 seconds. Tlow was set to target an end-expiratory flow to peak expiratory flow ratio of 75%. Nonventilated animals (n = 7/etiology) were used for Diffuse Alveolar Damage and molecular biology markers analyses. Measurement and Main Results: Time-controlled adaptive ventilation increased mean respiratory system pressure regardless of acute respiratory distress syndrome etiology. The Diffuse Alveolar Damage score was lower in time-controlled adaptive ventilation compared with volume-controlled ventilation in pulmonary acute respiratory distress syndrome and lower in time-controlled adaptive ventilation than nonventilated in extrapulmonary acute respiratory distress syndrome. In pulmonary acute respiratory distress syndrome, volume-controlled ventilation, but not time-controlled adaptive ventilation, increased the expression of amphiregulin, vascular cell adhesion molecule-1, and metalloproteinase-9. Collagen density was higher, whereas expression of decorin was lower in time-controlled adaptive ventilation than nonventilated, independent of acute respiratory distress syndrome etiology. In pulmonary acute respiratory distress syndrome, but not in extrapulmonary acute respiratory distress syndrome, time-controlled adaptive ventilation increased syndecan expression. Conclusion: In pulmonary acute respiratory distress syndrome, time-controlled adaptive ventilation led to more pronounced beneficial effects on expression of biomarkers related to overdistension and extracellular matrix homeostasis. Drs. Silva, Cruz, Samary, and Moraes contributed equally to this work. Drs. Andrews, Habashi, Nieman, and Rocco share senior authorship. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (http://ift.tt/29S62lw). Supported, in part, by the Brazilian Council for Scientific and Technological Development (CNPq), the Rio de Janeiro State Research Foundation (The Carlos Chagas Filho Rio de Janeiro State Research Supporting Foundation [FAPERJ]), the Coordination for the Improvement of Higher Education Personnel, and the Department of Science and Technology—Brazilian Ministry of Health. Dr. Silva received support for article research from FAPERJ and Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq). Drs. de Magalhães and Bose received support for article research from CNPq. Drs. Gatto, Andrews, Nieman, and Habashi have lectured for Intensive Care Online Network (ICON). Dr. Gatto received funding from the Canadian Society of Respiratory Therapists (lecture honorarium). Drs. Andrews, Habashi, and Nieman have presented and received honoraria and/or travel reimbursement at events sponsored by Dräger Medical Systems, outside of the published work. Dr. Andrews received funding from lectures at conferences sponsored by Draeger Medical and ICON (reimbursement for travel expenses and honorarium). Dr. Habashi received funding from lecturing at industry sponsored events including Draeger Medical (travel expenses and honorarium) and disclosed having patents in the area of mechanical ventilation (although no money from stocks, royalties, or license fees have been received); he is the founder of ICON, of which Dr. Andrews is an employee; and he holds patents on a method of initiating, managing, and/or weaning airway pressure release ventilation, as well as controlling a ventilator in accordance with the same, but these patents are not commercialized, licensed, nor royalty producing. Dr. Nieman received funding from Draeger Medical. The remaining authors have disclosed that they do not have any potential conflicts of interest. Address requests for reprints to: Patricia R. M. Rocco, MD, PhD, Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, s/n, Bloco G-014, Ilha do Fundão, 21941-902, Rio de Janeiro, Brazil. E-mail: prmrocco@gmail.com Copyright © by 2018 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.

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