title: Impact of Chest Wall Modifications and Lung Injury on the Correspondence Between Airway and Transpulmonary Driving Pressures.
abstract: OBJECTIVE
  Recent interest has arisen in airway driving pressure (DP(AW)), the quotient of tidal volume (V(T)), and respiratory system compliance (C(RS)), which could serve as a direct and easily measured marker for ventilator-induced lung injury risk. We aimed to test the correspondence between DP(AW) and transpulmonary driving pressure (DP(TP))-the quotient of V(T) and lung compliance (C(L)), in response to intra-abdominal hypertension and changes in positive end-expiratory pressure during different models of lung pathology.
  
  
  METHODS
  Well-controlled experimental setting that allowed reversible modification of chest wall compliance (C(CW)) in a variety of models of lung pathology.
  
  
  METHODS
  Large animal laboratory of a university-affiliated hospital.
  
  
  METHODS
  Ten deeply anesthetized swine.
  
  
  METHODS
  Application of intra-abdominal pressures of 0 and 20 cm H2O at positive end-expiratory pressure of 1 and 10 cm H2O, under volume-controlled mechanical ventilation in the settings of normal lungs (baseline), unilateral whole-lung atelectasis, and unilateral and bilateral lung injuries caused by saline lavage.
  
  
  RESULTS
  Pulmonary mechanics including esophageal pressure and calculations of DP(AW), DP(TP), C(RS), C(L), and C(CW). When compared with normal intra-abdominal pressures, intra-abdominal hypertension increased DP(AW), during both "normal lung conditions" (p < 0.0001) and "unilateral atelectasis" (p = 0.0026). In contrast, DP(TP) remained virtually unaffected by changes in positive end-expiratory pressure or intra-abdominal pressures in both conditions. During unilateral lung injury, both DPA(W) and DP(TP) were increased by the presence of intra-abdominal hypertension (p < 0.0001 and p = 0.0222, respectively). During bilateral lung injury, intra-abdominal hypertension increased both DP(AW) (at positive end-expiratory pressure of 1 cm H2O, p < 0.0001; and at positive end-expiratory pressure of 10 cm H2O, p = 0.0091) and DP(TP) (at positive end-expiratory pressure of 1 cm H2O, p = 0.0510; and at positive end-expiratory pressure of 10 cm H2O, p = 0.0335).
  
  
  CONCLUSIONS
  Our data indicate that DP(AW) is influenced by reductions in chest wall compliance and by underlying lung properties. As with other measures of pulmonary mechanics that are based on unmodified P(AW), caution is advised in attempting to attribute hazard or safety to any specific absolute value of DP(AW).
authors.affiliation: 1Department of Internal Medicine, University of Minnesota, Minneapolis, MN. 2Department of Pulmonary and Critical Care Research, Regions Hospital, St. Paul, MN. 3Research Methodology Group, HealthPartners Institute for Education and Research, Bloomington, MN. 4Department of Surgery, Regions Hospital, St. Paul, MN. 5Department of Pulmonary and Critical Care, Regions Hospital, St. Paul, MN.
authors.forename: Gustavo A
authors.initials: GA
authors.lastname: Cortes-Puentes
authors.forename: Joseph C
authors.initials: JC
authors.lastname: Keenan
authors.forename: Alexander B
authors.initials: AB
authors.lastname: Adams
authors.forename: Emily D
authors.initials: ED
authors.lastname: Parker
authors.forename: David J
authors.initials: DJ
authors.lastname: Dries
authors.forename: John J
authors.initials: JJ
authors.lastname: Marini
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D008170:Lung Compliance; D015656:Respiratory Mechanics / Q000502:physiology*; D013552:Swine; D035441:Thoracic Wall / Q000503:physiopathology*; D013990:Tidal Volume; D055397:Ventilator-Induced Lung Injury / Q000503:physiopathology*