title: Spontaneous effort causes occult pendelluft during mechanical ventilation.
abstract: BACKGROUND
  In normal lungs, local changes in pleural pressure (P(pl)) are generalized over the whole pleural surface. However, in a patient with injured lungs, we observed (using electrical impedance tomography) a pendelluft phenomenon (movement of air within the lung from nondependent to dependent regions without change in tidal volume) that was caused by spontaneous breathing during mechanical ventilation.
  
  
  OBJECTIVE
  To test the hypotheses that in injured lungs negative P(pl) generated by diaphragm contraction has localized effects (in dependent regions) that are not uniformly transmitted, and that such localized changes in P(pl) cause pendelluft.
  
  
  METHODS
  We used electrical impedance tomography and dynamic computed tomography (CT) to analyze regional inflation in anesthetized pigs with lung injury. Changes in local P(pl) were measured in nondependent versus dependent regions using intrabronchial balloon catheters. The airway pressure needed to achieve comparable dependent lung inflation during paralysis versus spontaneous breathing was estimated.
  
  
  RESULTS
  In all animals, spontaneous breathing caused pendelluft during early inflation, which was associated with more negative local P(pl) in dependent regions versus nondependent regions (-13.0 ± 4.0 vs. -6.4 ± 3.8 cm H2O; P < 0.05). Dynamic CT confirmed pendelluft, which occurred despite limitation of tidal volume to less than 6 ml/kg. Comparable inflation of dependent lung during paralysis required almost threefold greater driving pressure (and tidal volume) versus spontaneous breathing (28.0 ± 0.5 vs. 10.3 ± 0.6 cm H2O, P < 0.01; 14.8 ± 4.6 vs. 5.8 ± 1.6 ml/kg, P < 0.05).
  
  
  CONCLUSIONS
  Spontaneous breathing effort during mechanical ventilation causes unsuspected overstretch of dependent lung during early inflation (associated with reciprocal deflation of nondependent lung). Even when not increasing tidal volume, strong spontaneous effort may potentially enhance lung damage.
authors.affiliation: 1 Laboratório de Pneumologia LIM-09, Disciplina de Pneumologia, Heart Institute (Incor) Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Yoshida
authors.forename: Vinicius
authors.initials: V
authors.lastname: Torsani
authors.forename: Susimeire
authors.initials: S
authors.lastname: Gomes
authors.forename: Roberta R
authors.initials: RR
authors.lastname: De Santis
authors.forename: Marcelo A
authors.initials: MA
authors.lastname: Beraldo
authors.forename: Eduardo L V
authors.initials: EL
authors.lastname: Costa
authors.forename: Mauro R
authors.initials: MR
authors.lastname: Tucci
authors.forename: Walter A
authors.initials: WA
authors.lastname: Zin
authors.forename: Brian P
authors.initials: BP
authors.lastname: Kavanagh
authors.forename: Marcelo B P
authors.initials: MB
authors.lastname: Amato
mesh_terms: D000328:Adult; D000818:Animals; D006801:Humans; D008168:Lung / Q000503:physiopathology*; D008297:Male; D010992:Plethysmography, Impedance; D010994:Pleura / Q000503:physiopathology*; D011175:Positive-Pressure Respiration; D011312:Pressure; D012119:Respiration; D012128:Respiratory Distress Syndrome / Q000503:physiopathology* / Q000628:therapy; D013552:Swine; D013990:Tidal Volume; D014054:Tomography