Acute respiratory distress syndrome (ARDS) was characterised by Ashbaugh and colleagues1 nearly half a century ago, and yet, to the casual observer, it might appear that little progress has been made since. Clinicians are still struggling with how best to define and treat ARDS.2 ,3 A major advance was the recognition that mechanical ventilation may induce further lung injury and the application of so-called lung protective ventilation (6 ml/kg ideal body weight tidal volumes and plateau pressures <30 cm H₂O) reduces mortality.4 High-frequency oscillatory ventilation (HFOV) is an attractive mode of ventilation because it combines improved lung recruitment with small tidal volumes, often below anatomical dead space, applied at very high frequency. Thus, it theoretically provides ultra-lung protective ventilation, limiting atelectrauma (caused by cyclical alveolar opening and closing) and volutrauma (alveolar over-distension). For those not familiar with this mode of ventilation, it should be noted that, unlike conventional ventilation, increasing the frequency of HFOV reduces CO₂ elimination. HFOV has often been used as a rescue therapy for severe ARDS and refractory hypoxaemia; however, uncertainty remains over its role in early ARDS. Although there is substantial experimental data, clinical studies are limited to case series and two small trials5 ,6 where controls did not receive what is now accepted as standard lung protective ventilation following the ARDSNet study.4

Two recently randomised clinical trials sought to establish if HFOV could reduce mortality in early ARDS.7 ,8 The UK-based OSCAR study7 randomised 795 patients to receive either HFOV or conventional ventilation. No difference was observed in 30 day mortality between groups (41.7% vs 41.1%, respectively). The larger OSCILLATE study8 planned to recruit 1200 patients but was stopped after 548 patients on recommendation from the data monitoring committee, as in-hospital mortality was significantly higher …