title: Comparison of "open lung" modes with low tidal volumes in a porcine lung injury model.
abstract: BACKGROUND
  Ventilator strategies that maintain an "open lung" have shown promise in treating hypoxemic patients. We compared three "open lung" strategies with standard of care low tidal volume ventilation and hypothesized that each would diminish physiologic and histopathologic evidence of ventilator induced lung injury (VILI).
  
  
  METHODS
  Acute lung injury (ALI) was induced in 22 pigs via 5% Tween and 30-min of injurious ventilation. Animals were separated into four groups: (1) low tidal volume ventilation (LowVt -6 mL/kg); (2) high-frequency oscillatory ventilation (HFOV); (3) airway pressure release ventilation (APRV); or (4) recruitment and decremental positive-end expiratory pressure (PEEP) titration (RM+OP) and followed for 6 h. Lung and hemodynamic function was assessed on the half-hour. Bronchoalveolar lavage fluid (BALF) was analyzed for cytokines. Lung tissue was harvested for histologic analysis.
  
  
  RESULTS
  APRV and HFOV increased PaO(2)/FiO(2) ratio and improved ventilation. APRV reduced BALF TNF-α and IL-8. HFOV caused an increase in airway hemorrhage. RM+OP decreased SvO(2), increased PaCO(2), with increased inflammation of lung tissue.
  
  
  CONCLUSIONS
  None of the "open lung" techniques were definitively superior to LowVt with respect to VILI; however, APRV oxygenated and ventilated more effectively and reduced cytokine concentration compared with LowVt with nearly indistinguishable histopathology. These data suggest that APRV may be of potential benefit to critically ill patients but other "open lung" strategies may exacerbate injury.
authors.affiliation: Department of Surgery, Upstate Medical University, Syracuse, New York 13210, USA.
authors.forename: Scott
authors.initials: S
authors.lastname: Albert
authors.forename: Brian D
authors.initials: BD
authors.lastname: Kubiak
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Vieau
authors.forename: Shreyas K
authors.initials: SK
authors.lastname: Roy
authors.forename: Joseph
authors.initials: J
authors.lastname: DiRocco
authors.forename: Louis A
authors.initials: LA
authors.lastname: Gatto
authors.forename: Jennifer L
authors.initials: JL
authors.lastname: Young
authors.forename: Sudipta
authors.initials: S
authors.lastname: Tripathi
authors.forename: Girish
authors.initials: G
authors.lastname: Trikha
authors.forename: Carlos
authors.initials: C
authors.lastname: Lopez
authors.forename: Gary F
authors.initials: GF
authors.lastname: Nieman
mesh_terms: D055371:Acute Lung Injury / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy*; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D002320:Cardiovascular Physiological Phenomena; D045422:Continuous Positive Airway Pressure / Q000379:methods; D004195:Disease Models, Animal; D006612:High-Frequency Ventilation / Q000379:methods; D016209:Interleukin-8 / Q000378:metabolism; D008168:Lung / Q000473:pathology / Q000502:physiology; D011175:Positive-Pressure Respiration / Q000379:methods; D012121:Respiration, Artificial / Q000379:methods*; D034421:Sus scrofa; D013990:Tidal Volume / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha