4.6 Article

Impact of different frequencies of controlled breath and pressure-support levels during biphasic positive airway pressure ventilation on the lung and diaphragm in experimental mild acute respiratory distress syndrome

Journal

PLOS ONE
Volume 16, Issue 8, Pages -

Publisher

PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0256021

Keywords

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Funding

  1. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico [421067/2016-0, 443894/2018-3]
  2. Fundacao Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro [E-26/210.910/2016, E-26/010.001488/2019]

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The study found that adjusting the frequency of controlled breaths and the level of pressure support can mitigate lung and diaphragm damage in an animal model of acute respiratory distress syndrome. Increasing pressure support can improve lung mechanics and reduce lung injury, while partitioning inspiratory effort and pressure in spontaneous breathing can minimize lung and diaphragm damage.
Background We hypothesized that a decrease in frequency of controlled breaths during biphasic positive airway pressure (BIVENT), associated with an increase in spontaneous breaths, whether pressure support (PSV)-assisted or not, would mitigate lung and diaphragm damage in mild experimental acute respiratory distress syndrome (ARDS). Materials and methods Wistar rats received Escherichia coli lipopolysaccharide intratracheally. After 24 hours, animals were randomly assigned to: 1) BIVENT-100+PSV0%: airway pressure (P-high) adjusted to V-T = 6 mL/kg and frequency of controlled breaths (f) = 100 bpm; 2) BIVENT-50+PSV0%: P-high adjusted to V-T = 6 mL/kg and f = 50 bpm; 3) BIVENT-50+PSV50% (PSV set to half the P-high reference value, i.e., PSV50%); or 4) BIVENT-50+PSV100% (PSV equal to P-high reference value, i.e., PSV100%). Positive end-expiratory pressure (P-low) was equal to 5 cmH(2)O. Nonventilated animals were used for lung and diaphragm histology and molecular biology analysis. Results BIVENT-50+PSV0%, compared to BIVENT-100+PSV0%, reduced the diffuse alveolar damage (DAD) score, the expression of amphiregulin (marker of alveolar stretch) and muscle atrophy F-box (marker of diaphragm atrophy). In BIVENT-50 groups, the increase in PSV (BIVENT-50+PSV50% versus BIVENT-50+PSV100%) yielded better lung mechanics and less alveolar collapse, interstitial edema, cumulative DAD score, as well as gene expressions associated with lung inflammation, epithelial and endothelial cell damage in lung tissue, and muscle ring finger protein 1 (marker of muscle proteolysis) in diaphragm. Transpulmonary peak pressure (Ppeak,L) and pressure-time product per minute (PTPmin) at P-high were associated with lung damage, while increased spontaneous breathing at P-low did not promote lung injury. Conclusion In the ARDS model used herein, during BIVENT, the level of PSV and the phase of the respiratory cycle in which the inspiratory effort occurs affected lung and diaphragm damage. Partitioning of inspiratory effort and transpulmonary pressure in spontaneous breaths at P-low and P-high is required to minimize VILI.

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