title: Ventilation with constant versus decelerating inspiratory flow in experimentally induced acute respiratory failure.
abstract: BACKGROUND
  Recognition of the potential for ventilator-associated lung injury has renewed the debate on the importance of the inspiratory flow pattern. The aim of this study was to determine whether a ventilatory pattern with decelerating inspiratory flow, with the major part of the tidal volume delivered early, would increase functional residual capacity at unchanged (or even reduced) inspiratory airway pressures and improve gas exchange at different positive end-expiratory pressure levels.
  
  
  METHODS
  Surfactant depletion was induced by repeated bronchoalveolar lavage in 13 anesthetized piglets. Decelerating and constant inspiratory flow ventilation was applied at positive end-expiratory pressure levels of 22, 17, 13, 9, and 4 cm H(2)O. Tidal volume, inspiration-to-expiration ratio, and ventilatory frequency were kept constant. Airway pressures, gas exchange, functional residual capacity (using a wash-in/washout method with sulfurhexafluoride), central hemodynamics, and extravascular lung water (using the thermo-dye-indicator dilution technique) were measured.
  
  
  RESULTS
  Decelerating inspiratory flow yielded a lower arterial carbon dioxide tension compared to constant flow, that is, it improved alveolar ventilation. There were no differences between the flow patterns regarding end-inspiratory occlusion airway pressure, end-inspiratory lung volume, static compliance, or arterial oxygen tension. No differences were seen in hemodynamics and oxygen delivery.
  
  
  CONCLUSIONS
  The decelerating inspiratory flow pattern increased carbon dioxide elimination, without any reduction of inspiratory airway pressure or apparent improvement in arterial oxygen tension. It remains to be established whether these differences are sufficiently pronounced to justify therapeutic consideration.
authors.affiliation: Department of Anesthesiology and Intensive Care, University Hospital, Uppsala, Sweden.
authors.forename: A M
authors.initials: AM
authors.lastname: Markström
authors.forename: M
authors.initials: M
authors.lastname: Lichtwarck-Aschoff
authors.forename: B A
authors.initials: BA
authors.lastname: Svensson
authors.forename: K A
authors.initials: KA
authors.lastname: Nordgren
authors.forename: U H
authors.initials: UH
authors.lastname: Sjöstrand
mesh_terms: D000208:Acute Disease; D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D006439:Hemodynamics; D011659:Pulmonary Gas Exchange; D012121:Respiration, Artificial / Q000379:methods*; D012131:Respiratory Insufficiency / Q000503:physiopathology / Q000628:therapy*; D013552:Swine
chemical_list: D002245:Carbon Dioxide