Atelectrauma can be avoided if expiration is sufficiently brief: evidence from inverse modeling and oscillometry during airway pressure release ventilation

Airway pressure release ventilation (APRV) has been shown to be protective against atelectrauma if expirations are brief. We hypothesize that this is protective because epithelial surfaces are not given enough time to come together and adhere during expiration, thereby avoiding their highly damaging forced separation during inspiration.

We investigated this hypothesis in a porcine model of ARDS induced by Tween lavage. Animals were ventilated with APRV in 4 groups based on whether inspiratory pressure was 28 or 40 cmH₂O, and whether expiration was terminated when end-expiratory flow reached either 75% (a shorter expiration) or 25% (a longer expiration) of its initial peak value. A mathematical model of respiratory system mechanics that included a volume-dependent elastance term characterized by the parameter \({E}_{2}\) $E_2$ was fit to airway pressure-flow data obtained each hour for 6 h post-Tween injury during both expiration and inspiration. We also measured respiratory system impedance between 5 and 19 Hz continuously through inspiration at the same time points from which we derived a time-course for respiratory system resistance ( \({R}_{rs}\) $R_{\mathit{rs}}$ ).

\({E}_{2}\) $E_2$ during both expiration and inspiration was significantly different between the two longer expiration versus the two shorter expiration groups (ANOVA, p < 0.001). We found that \({E}_{2}\) $E_2$ was most depressed during inspiration in the higher-pressure group receiving the longer expiration, suggesting that \({E}_{2}\) $E_2$ reflects a balance between strain stiffening of the lung parenchyma and ongoing recruitment as lung volume increases. We also found in this group that \({R}_{rs}\) $R_{\mathit{rs}}$ increased progressively during the first 0.5 s of inspiration and then began to decrease again as inspiration continued, which we interpret as corresponding to the point when continuing derecruitment was reversed by progressive lung inflation.

These findings support the hypothesis that sufficiently short expiratory durations protect against atelectrauma because they do not give derecruitment enough time to manifest. This suggests a means for the personalized adjustment of mechanical ventilation.