title: Variable tidal volumes improve lung protective ventilation strategies in experimental lung injury.
abstract: BACKGROUND
  Noisy ventilation with variable Vt may improve respiratory function in acute lung injury.
  
  
  OBJECTIVE
  To determine the impact of noisy ventilation on respiratory function and its biological effects on lung parenchyma compared with conventional protective mechanical ventilation strategies.
  
  
  METHODS
  In a porcine surfactant depletion model of lung injury, we randomly combined noisy ventilation with the ARDS Network protocol or the open lung approach (n = 9 per group).
  
  
  RESULTS
  Respiratory mechanics, gas exchange, and distribution of pulmonary blood flow were measured at intervals over a 6-hour period. Postmortem, lung tissue was analyzed to determine histological damage, mechanical stress, and inflammation. We found that, at comparable minute ventilation, noisy ventilation (1) improved arterial oxygenation and reduced mean inspiratory peak airway pressure and elastance of the respiratory system compared with the ARDS Network protocol and the open lung approach, (2) redistributed pulmonary blood flow to caudal zones compared with the ARDS Network protocol and to peripheral ones compared with the open lung approach, (3) reduced histological damage in comparison to both protective ventilation strategies, and (4) did not increase lung inflammation or mechanical stress.
  
  
  CONCLUSIONS
  Noisy ventilation with variable Vt and fixed respiratory frequency improves respiratory function and reduces histological damage compared with standard protective ventilation strategies.
authors.affiliation: Department of Anesthesiology and Intensive Care Therapy, University Hospital Dresden, Fetscherstrasse 74, 01307 Dresden, Germany.
authors.forename: Peter M
authors.initials: PM
authors.lastname: Spieth
authors.forename: Alysson R
authors.initials: AR
authors.lastname: Carvalho
authors.forename: Paolo
authors.initials: P
authors.lastname: Pelosi
authors.forename: Catharina
authors.initials: C
authors.lastname: Hoehn
authors.forename: Christoph
authors.initials: C
authors.lastname: Meissner
authors.forename: Michael
authors.initials: M
authors.lastname: Kasper
authors.forename: Matthias
authors.initials: M
authors.lastname: Hübler
authors.forename: Matthias
authors.initials: M
authors.lastname: von Neindorff
authors.forename: Constanze
authors.initials: C
authors.lastname: Dassow
authors.forename: Martina
authors.initials: M
authors.lastname: Barrenschee
authors.forename: Stefan
authors.initials: S
authors.lastname: Uhlig
authors.forename: Thea
authors.initials: T
authors.lastname: Koch
authors.forename: Marcelo Gama
authors.initials: MG
authors.lastname: de Abreu
mesh_terms: D055371:Acute Lung Injury / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D000818:Animals; D004195:Disease Models, Animal; D006439:Hemodynamics; D008168:Lung / Q000098:blood supply; D010100:Oxygen / Q000378:metabolism; D010101:Oxygen Consumption / Q000502:physiology; D010313:Partial Pressure; D011650:Pulmonary Alveoli / Q000473:pathology; D011659:Pulmonary Gas Exchange / Q000502:physiology; D011897:Random Allocation; D012121:Respiration, Artificial / Q000009:adverse effects / Q000379:methods*; D012128:Respiratory Distress Syndrome / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D015656:Respiratory Mechanics / Q000502:physiology; D018709:Statistics, Nonparametric; D013552:Swine; D013990:Tidal Volume / Q000502:physiology
chemical_list: D010100:Oxygen