title: Experimental blunt chest trauma--cardiorespiratory effects of different mechanical ventilation strategies with high positive end-expiratory pressure: a randomized controlled study.
abstract: BACKGROUND
  Uncertainty persists regarding the optimal ventilatory strategy in trauma patients developing acute respiratory distress syndrome (ARDS). This work aims to assess the effects of two mechanical ventilation strategies with high positive end-expiratory pressure (PEEP) in experimental ARDS following blunt chest trauma.
  
  
  METHODS
  Twenty-six juvenile pigs were anesthetized, tracheotomized and mechanically ventilated. A contusion was applied to the right chest using a bolt-shot device. Ninety minutes after contusion, animals were randomized to two different ventilation modes, applied for 24 h: Twelve pigs received conventional pressure-controlled ventilation with moderately low tidal volumes (VT, 8 ml/kg) and empirically chosen high external PEEP (16 cmH2O) and are referred to as the HP-CMV-group. The other group (n = 14) underwent high-frequency inverse-ratio pressure-controlled ventilation (HFPPV) involving respiratory rate of 65 breaths · min(-1), inspiratory-to-expiratory-ratio 2:1, development of intrinsic PEEP and recruitment maneuvers, compatible with the rationale of the Open Lung Concept. Hemodynamics, gas exchange and respiratory mechanics were monitored during 24 h. Computed tomography and histology were analyzed in subgroups.
  
  
  RESULTS
  Comparing changes which occurred from randomization (90 min after chest trauma) over the 24-h treatment period, groups differed statistically significantly (all P values for group effect <0.001, General Linear Model analysis) for the following parameters (values are mean ± SD for randomization vs. 24-h): PaO2 (100% O2) (HFPPV 186 ± 82 vs. 450 ± 59 mmHg; HP-CMV 249 ± 73 vs. 243 ± 81 mmHg), venous admixture (HFPPV 34 ± 9.8 vs. 11.2 ± 3.7%; HP-CMV 33.9 ± 10.5 vs. 21.8 ± 7.2%), PaCO2 (HFPPV 46.9 ± 6.8 vs. 33.1 ± 2.4 mmHg; HP-CMV 46.3 ± 11.9 vs. 59.7 ± 18.3 mmHg) and normally aerated lung mass (HFPPV 42.8 ± 11.8 vs. 74.6 ± 10.0 %; HP-CMV 40.7 ± 8.6 vs. 53.4 ± 11.6%). Improvements occurring after recruitment in the HFPPV-group persisted throughout the study. Peak airway pressure and VT did not differ significantly. HFPPV animals had lower atelectasis and inflammation scores in gravity-dependent lung areas.
  
  
  CONCLUSIONS
  In this model of ARDS following unilateral blunt chest trauma, HFPPV ventilation improved respiratory function and fulfilled relevant ventilation endpoints for trauma patients, i.e. restoration of oxygenation and lung aeration while avoiding hypercapnia and respiratory acidosis.
authors.affiliation: Helios Park Clinic, Department of Intensive Care Medicine, Leipzig, Germany. Dierk.Schreiter@herzzentrum-leipzig.de.
authors.forename: Dierk
authors.initials: D
authors.lastname: Schreiter
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, University Hospital Leipzig, Liebigstr. 20, D-04103, Leipzig, Germany. cristinnecarvalho@gmail.com.|Department of Electronic Engineering, Federal University of Minas Gerais, Belo Horizonte, Brazil. cristinnecarvalho@gmail.com.
authors.forename: Nadja C
authors.initials: NC
authors.lastname: Carvalho
authors.affiliation: Sana Kliniken Leipziger Land, Department of Orthopedic, Trauma and Hand Surgery, Borna, Germany. sebastian.katscher@kliniken-leipziger-land.de.
authors.forename: Sebastian
authors.initials: S
authors.lastname: Katscher
authors.affiliation: Intensive Care Unit, Sana Kliniken Leipziger Land, Borna, Germany. ludger.mende@kliniken-leipziger-land.de.
authors.forename: Ludger
authors.initials: L
authors.lastname: Mende
authors.affiliation: Anesthesiology and Intensive Care Medicine, Fachkrankenhaus Coswig, Coswig, Sachsen, Germany. alexander.reske@me.com.
authors.forename: Alexander P
authors.initials: AP
authors.lastname: Reske
authors.affiliation: Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Dresden, Germany. peter.spieth@uniklinikum-dresden.de.
authors.forename: Peter M
authors.initials: PM
authors.lastname: Spieth
authors.affiliation: Carlos Chagas Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. roncally.carvalho@gmail.com.
authors.forename: Alysson R
authors.initials: AR
authors.lastname: Carvalho
authors.affiliation: Department of Electronic Engineering, Federal University of Minas Gerais, Belo Horizonte, Brazil. ale.beda@gmail.com.
authors.forename: Alessandro
authors.initials: A
authors.lastname: Beda
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, Charité, Berlin Medical University, Berlin, Germany. burkhard.lachmann@gmail.com.
authors.forename: Burkhard
authors.initials: B
authors.lastname: Lachmann
authors.affiliation: Cardio-Pulmonary Department, Pulmonary Division, Hospital das Clínicas, University of São Paulo, São Paulo, Brazil. marcelo.amato@limpneumo.fm.usp.br.
authors.forename: Marcelo B P
authors.initials: MB
authors.lastname: Amato
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, University Hospital Leipzig, Liebigstr. 20, D-04103, Leipzig, Germany. Hermann.Wrigge@medizin.uni-leipzig.de.
authors.forename: Hermann
authors.initials: H
authors.lastname: Wrigge
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, University Hospital Leipzig, Liebigstr. 20, D-04103, Leipzig, Germany. andreas.reske@medizin.uni-leipzig.de.
authors.forename: Andreas W
authors.initials: AW
authors.lastname: Reske
mesh_terms: D000818:Animals; D011175:Positive-Pressure Respiration / Q000379:methods; D011897:Random Allocation; D012121:Respiration, Artificial / Q000379:methods*; D012128:Respiratory Distress Syndrome / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D015656:Respiratory Mechanics / Q000502:physiology*; D013552:Swine; D013898:Thoracic Injuries / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D014949:Wounds, Nonpenetrating / Q000150:complications / Q000503:physiopathology / Q000628:therapy*