High Frequency Oscillation for Acute Respiratory Failure in Adults

Abstract

In the acute respiratory distress Syndrome (ARDS), major mechanisms of ventilator-induced lung injury (VILI) include barotrauma, volutrauma, atelectrauma, and biotrauma [1, 2]. In an excellent review, Gattinoni et al. [2], argue that during conventional mechanical ventilation, lung stress and strain are the major determinants of VILI. Alveolar stress (i.e., transmural pressure) is the ratio of alveolar wall tension to thickness [3]. Overall lung parenchymal stress is reflected by plateau and peak transpulmonary pressures [1, 2]. Lung strain refers to the deformation of the lung parenchyma induced by the distending force applied by the ventilator. Strain is reflected by the tidal volume to end-expiratory lung volume ratio [3]. Early and severe ARDS is characterized by non-homogeneously distributed and frequently diffuse lung damage [4], with intra-alveolar and interstitial edema and hyaline membrane formation. The absolute reduction in ventilatable lung parenchyma supports the “baby lung” concept [5]. According to this simplified and theoretical description, the ARDS lung is “small but not stiff” [2, 5]. Consequently, the use of a high tidal volume should cause mechanical harm, ultimately resulting in increased mortality [2, 5–8].