title: Intratidal Overdistention and Derecruitment in the Injured Lung: A Simulation Study.
abstract: Ventilated patients with the acute respiratory distress syndrome (ARDS) are predisposed to cyclic parenchymal overdistention and derecruitment, which may worsen existing injury. We hypothesized that intratidal variations in global mechanics, as assessed at the airway opening, would reflect such distributed processes.
  
  
  
  We developed a computational lung model for determining local instantaneous pressure distributions and mechanical impedances continuously during a breath. Based on these distributions and previous literature, we simulated the within-breath variability of airway segment dimensions, parenchymal viscoelasticity, and acinar recruitment in an injured canine lung for tidal volumes( VT) of 10, 15, and 20 mL·kg-1and positive end-expiratory pressures (PEEP) of 5, 10, and 15 cm H2O. Acini were allowed to transition between recruited and derecruited states when exposed to stochastically determined critical opening and closing pressures, respectively.
  
  
  
  For conditions of low VTand low PEEP, we observed small intratidal variations in global resistance and elastance, with a small number of cyclically recruited acini. However, with higher VTand PEEP, larger variations in resistance and elastance were observed, and the majority of acini remained open throughout the breath. Changes in intratidal resistance, elastance, and impedance followed well-defined parabolic trajectories with tracheal pressure, achieving minima near 12 to 16 cm H2O.
  
  
  
  Intratidal variations in lung mechanics may allow for optimization of ventilator settings in patients with ARDS, by balancing lung recruitment against parenchymal overdistention.
  
  
  
  Titration of airway pressures based on variations in intratidal mechanics may mitigate processes associated with injurious ventilation.
authors.forename: Reza
authors.initials: R
authors.lastname: Amini
authors.forename: Jacob
authors.initials: J
authors.lastname: Herrmann
authors.forename: David W
authors.initials: DW
authors.lastname: Kaczka
mesh_terms: D000403:Airway Resistance; D000818:Animals; D003198:Computer Simulation; D004285:Dogs; D055119:Elastic Modulus; D006801:Humans; D008170:Lung Compliance; D008954:Models, Biological; D011175:Positive-Pressure Respiration; D012128:Respiratory Distress Syndrome / Q000503:physiopathology* / Q000628:therapy*; D015656:Respiratory Mechanics; D013990:Tidal Volume; D055397:Ventilator-Induced Lung Injury / Q000209:etiology / Q000503:physiopathology*