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Published on: April 7, 2021
Variable pressure support ventilation vs. biphasic positive airway pressure/airway pressure release ventilation in
Thomas Bluth1, Maren Thiel1,2, Dirk Haufe1
1Department of Anaesthesiology and Intensive Care Medicine, Pulmonary Engineering Group, Faculty of Medicine, University Hospital Carl Gustav Carus, TUD Dresden University of Technology, Fetscherstraße 74, Dresden, 01307, Germany.
Background:
Spontaneous breathing during mechanical ventilation (MV) can improve cardiorespiratory function and lung protection. Biphasic Positive Airway Pressure (BIPAP) and Airway Pressure Release Ventilation (APRV) are common MV modes that combine spontaneous breathing with controlled ventilation. Variable pressure support ventilation (PSV), which varies breath-by-breath pressure support randomly, has been shown to improve gas exchange and reduce lung injury compared to conventional MV modes. This study aimed to compare the short-term effects of variable PSV with BIPAP in a model of acute respiratory failure, hypothesizing that variable PSV would improve lung function without increasing lung damage or inflammation.
Methods:
In an exploratory randomized study with 18 pigs, lung injury was induced by lung lavage. Over 4 h, two lung protective strategies were applied with individually optimized PEEP: (1) BIPAP with non-assisted spontaneous breathing and (2) variable PSV, maintaining a mean tidal volume of 6 ml/kg body weight while varying pressure support. Plasma and bronchoalveolar lavage fluid samples were collected for inflammation markers, and lung damage was assessed histologically. Gene expression of inflammatory cytokines was also measured.
Results:
Variable PSV resulted in slightly improved gas exchange with higher mean tidal volumes and minute ventilation compared to BIPAP, as well as reduced work of breathing. Histopathological analysis showed alveolar damage to be mild, with no significant overall difference between the groups. However, variable PSV caused more alveolar edema, especially in gravity-dependent lung regions, and increased the wet-to-dry ratio compared with BIPAP. Despite these differences, there were no significant changes in systemic or pulmonary inflammatory cytokines or gene expression between the two groups.
Conclusion:
In this model of acute respiratory failure, variable PSV with a protective tidal volume of 6 ml/kg resulted in marginal, but clinically insignificant improvements in gas exchange and reduced work of breathing compared to BIPAP with non-assisted spontaneous breathing. Although inflammatory markers and overall diffuse alveolar damage did not differ between ventilation modes, the findings suggest a possible association between variable PSV and increased pulmonary oedema compared with BIPAP.
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