Impedance and alveolar instability in VILI

The mechanical derangements in the acutely injured lung have long been ascribed, in large part, to altered mechanical function at the alveolar level. This has not been directly demonstrated, however, so we investigated the issue in a rat model of over-inflation injury. Following thoracotomy, rats were mechanically ventilated with either 1) high tidal volume (Vt), or 2) low Vt with periodic deep inflations (DIs). Forced oscillations were used to measure pulmonary impedance every min, from which elastance (H) and hysterisivity (η) were derived. Subpleural alveoli were imaged every 15 min using in vivo video microscopy. Cross-sectional areas of individual alveoli were measured at peak inspiration (I) and end-exhalation (E), and the percent change was used as an index of alveolar instability (%I-E∆). Low Vt never lead to an increase in %I-E∆ but did result in progressive atelectasis that coincided with an increase in H but not η. DI reversed atelectasis due to low Vt, returning H to baseline. %I-E∆, H and η all began to rise by 30 min of high Vt and were not reduced by DI. We conclude that simultaneous increases in both H and η are reflective of lung injury in the form of alveolar instability, while an isolated and reversible increase in H during low Vt reflects merely derecruitment of alveoli.