The effect of patient-ventilator asynchrony on lung and diaphragmatic injury in experimental acute respiratory distress syndrome: laboratory study.

BJA: British Journal of Anaesthesia(2021)

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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 and/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 12h. Mechanically ventilated pigs were randomised to spontaneously breath with, or without, induced subject-ventilator asynchrony, or neuromuscular blockade (n=7/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 ratio and diaphragmatic muscle fibre thickness. RESULTS Mean alveolar septal thickness was similar in pigs randomised to subject-ventilator asynchrony (mean (SD):29.5% (10.8) asynchronous breaths of total breaths; n=7) compared to synchronous spontaneous breathing (asynchronous breaths 1.8% (2.9) of total breaths; n=7). There was no difference in mean alveolar septal thickness throughout upper and lower lungs lobes between pigs randomised to subject-ventilator asynchrony versus synchronous spontaneous breathing (87.3-92.2μm after subject-ventilator asynchrony, compared to 84.1-95.0 μm in synchronised spontaneous breathing; P=0.956). There were also no differences between groups in wet-to-dry ratio, diaphragmatic muscle fibre thickness, atelectasis, lung aeration, and mRNA expression levels for inflammatory cytokines pivotal in ARDS pathogenesis. CONCLUSION Subject-ventilator asynchrony during spontaneous breathing did not exacerbate lung injury and dysfunction in experimental ARDS.
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