title: Low tidal volume pressure support versus controlled ventilation in early experimental sepsis in pigs.
abstract: BACKGROUND
  In moderate acute respiratory distress syndrome (ARDS) several studies support the usage of assisted spontaneous breathing modes. Only limited data, however, focus on the application in systemic sepsis and developing lung injury. The present study examines the effects of immediate initiation of pressure support ventilation (PSV) in a model of sepsis-induced ARDS.
  
  
  METHODS
  18 anesthetized pigs received a two-staged continuous lipopolysaccharide infusion to induce lung injury. The animals were randomly assigned to PSV or volume controlled (VCV) lung protective ventilation (tidal volume each 6 ml kg-1, n = 2x9) over six hours. Gas exchange parameters, hemodynamics, systemic inflammation, and ventilation distribution by multiple inert gas elimination and electrical impedance tomography were assessed. The post mortem analysis included histopathological scoring, wet to dry ratio, and alveolar protein content.
  
  
  RESULTS
  Within six hours both groups developed a mild to moderate ARDS with comparable systemic inflammatory response and without signs of improving gas exchange parameters during PSV. The PSV group showed signs of more homogenous ventilation distribution by electrical impedance tomography, but only slightly less hyperinflated lung compartments by multiple inert gas elimination. Post mortem and histopathological assessment yielded no significant intergroup differences.
  
  
  CONCLUSIONS
  In a porcine model of sepsis-induced mild ARDS immediate PSV was not superior to VCV. This contrasts with several experimental studies from non-septic mild to moderate ARDS. The present study therefore assumes that not only severity, but also etiology of lung injury considerably influences the response to early initiation of PSV.
authors.forename: Alexander
authors.initials: A
authors.lastname: Ziebart
authors.forename: Erik K
authors.initials: EK
authors.lastname: Hartmann
authors.forename: Rainer
authors.initials: R
authors.lastname: Thomas
authors.forename: Tanghua
authors.initials: T
authors.lastname: Liu
authors.forename: Bastian
authors.initials: B
authors.lastname: Duenges
authors.forename: Arno
authors.initials: A
authors.lastname: Schad
authors.forename: Marc
authors.initials: M
authors.lastname: Bodenstein
authors.forename: Serge C
authors.initials: SC
authors.lastname: Thal
authors.forename: Matthias
authors.initials: M
authors.lastname: David
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006439:Hemodynamics; D008070:Lipopolysaccharides; D008168:Lung / Q000473:pathology / Q000503:physiopathology*; D011659:Pulmonary Gas Exchange; D012121:Respiration, Artificial / Q000379:methods*; D012128:Respiratory Distress Syndrome / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D018805:Sepsis / Q000139:chemically induced / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D034421:Sus scrofa; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D013990:Tidal Volume; D013997:Time Factors
chemical_list: D008070:Lipopolysaccharides