title: Peripheral airways injury in acute lung injury/acute respiratory distress syndrome.
abstract: OBJECTIVE
  Peripheral airways are less than 2 mm in diameter and comprise a relatively large cross-sectional area, which allows for slower, laminar airflow. They include both membranous bronchioles and gas exchange ducts, and have been referred to in the past as the 'quiet zone', partly because these structures were felt to contribute little to lung mechanics, and partly because they are difficult to study directly.
  
  
  RESULTS
  Recent studies suggest that peripheral airway dysfunction plays a significant role in acute respiratory distress syndrome, which may be exacerbated by injurious mechanical ventilation strategies. The presence of elevated airways resistance, intrinsic positive end-expiratory pressure or a lower inflection point on a pressure-volume curve of the respiratory system may indicate presence of impaired peripheral airway function. In-vitro animal and human studies have begun to elucidate the signaling mechanisms responsible for stretch and shear mediated cellular injury.
  
  
  CONCLUSIONS
  Understanding the pathophysiology of peripheral airway dysfunction in acute respiratory distress syndrome and mechanical ventilation continues to evolve. Greater insight into the signaling mechanisms involved in cellular injury and repair will lead to further alterations in mechanical ventilation strategies, and may lead to specific treatment options.
authors.affiliation: Division of Pulmonary and Critical Care, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA. m-jan@northwestern.edu
authors.forename: Manu
authors.initials: M
authors.lastname: Jain
authors.forename: J Iasha
authors.initials: JI
authors.lastname: Sznajder
mesh_terms: D001980:Bronchi / Q000503:physiopathology; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D008168:Lung / Q000503:physiopathology*; D012121:Respiration, Artificial / Q000009:adverse effects; D012128:Respiratory Distress Syndrome / Q000209:etiology / Q000503:physiopathology*; D015656:Respiratory Mechanics; D015398:Signal Transduction; D013990:Tidal Volume
chemical_list: D016207:Cytokines