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Effect of patient–ventilator asynchrony on lung and diaphragmatic injury in experimental acute respiratory distress syndrome in a porcine model

  • Jakob Wittenstein
  • , Robert Huhle
  • , Mark Leiderman
  • , Marius Möbius
  • , Anja Braune
  • , Sebastian Tauer
  • , Paul Herzog
  • , Giulio Barana
  • , Alessandra de Ferrari
  • , Andrea Corona
  • , Thomas Bluth
  • , Thomas Kiss
  • , Andreas Güldner
  • , Marcus J. Schultz
  • , Patricia R. M. Rocco
  • , Paolo Pelosi
  • , Marcelo Gama de Abreu*
  • , Martin Scharffenberg
  • *Corresponding author for this work
  • Division of Hematology and Hemostaseology, Department of Medicine I, University Hospital Carl Gustav Carus, Dresden, Germany
  • Technische Universität Dresden
  • County Hospital Thurgau
  • San Martino Hospital Genoa
  • Mater Olbia Hospital
  • Universidade Federal do Rio de Janeiro
  • University of Genoa
  • Cleveland Clinic Foundation

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Background: Patient–ventilator asynchrony during mechanical ventilation may exacerbate lung and diaphragm injury in spontaneously breathing subjects. We investigated whether subject–ventilator asynchrony increases lung or diaphragmatic injury in a porcine model of acute respiratory distress syndrome (ARDS). Methods: ARDS was induced in adult female pigs by lung lavage and injurious ventilation before mechanical ventilation by pressure assist–control for 12 h. Mechanically ventilated pigs were randomised to breathe spontaneously with or without induced subject–ventilator asynchrony or neuromuscular block (n=7 per group). Subject–ventilator asynchrony was produced by ineffective, auto-, or double-triggering of spontaneous breaths. The primary outcome was mean alveolar septal thickness (where thickening of the alveolar wall indicates worse lung injury). Secondary outcomes included distribution of ventilation (electrical impedance tomography), lung morphometric analysis, inflammatory biomarkers (gene expression), lung wet-to-dry weight ratio, and diaphragmatic muscle fibre thickness. Results: Subject-ventilator asynchrony (median [interquartile range] 28.8% [10.4] asynchronous breaths of total breaths; n=7) did not increase mean alveolar septal thickness compared with synchronous spontaneous breathing (asynchronous breaths 1.0% [1.6] of total breaths; n=7). There was no difference in mean alveolar septal thickness throughout upper and lower lung lobes between pigs randomised to subject–ventilator asynchrony vs synchronous spontaneous breathing (87.3–92.2 μm after subject–ventilator asynchrony, compared with 84.1–95.0 μm in synchronised spontaneous breathing;). There were also no differences between groups in wet-to-dry weight ratio, diaphragmatic muscle fibre thickness, atelectasis, lung aeration, or mRNA expression levels for inflammatory cytokines pivotal in ARDS pathogenesis. Conclusions: Subject–ventilator asynchrony during spontaneous breathing did not exacerbate lung injury and dysfunction in experimental porcine ARDS.
Original languageEnglish
JournalBritish journal of anaesthesia
DOIs
Publication statusE-pub ahead of print - 2021

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