The incidence of obesity is increasing worldwide, and obese or severely obese patients often present with several comorbidities. Obesity is associated with significant complications, and an increase in the mortality of obese patients after hospital admission compared to non-obese patients is justified [1]. The proportion of obesity in patients presenting with acute respiratory distress syndrome (ARDS) has not been investigated systematically, but data from the influenza A (H1N1) pandemic in 2009 suggested that obese patients were overrepresented compared to the general population [2]. The management of ARDS in patients with obesity is a special challenge, since obesity and severe obesity are associated with marked derangements in lung and chest wall mechanics [3].In clinical studies on obese mechanically ventilated patients without lung injury [4] or with ARDS [5], specific changes in respiratory system mechanics were observed (Table 1). These findings may help develop a better understanding of a suitable ventilation strategy in obesity. In all studies, static respiratory compliance (C st,rs ) was reduced with a rising level of obesity [expressed by body mass index (BMI)], while elastance (the reciprocal of compliance) tended to increase. These changes in C st,rs were due to compliance reduction in both parts of the respiratory system: the lung and the chest wall. In other words, during mechanical ventilation in obese patients, the lungs and predominantly the chest wall become 'stiffer' . This finding-observed in obese lung-healthy patients as well in ARDS patients-deserves attention and interpretation. Physiologically, the chest wall (rib cage and abdomen) is elastic, and the interaction between the lungs and the chest wall is finely balanced under spontaneous breathing [7]. The chest wall tends to expand outward, while the lungs tend to collapse. The 'mediator' between both is the pleural pressure. The reduction of chest wall compliance (C st,w ) in obesity is mainly due to the increase of intraabdominal pressure in these patients [3], which results in a lower lung volume for the same pleural pressure.In a large retrospective analysis of the data of 3562 ARDS patients from nine studies, Amato et al. [8] demonstrated that elevated driving pressure (∆P), a parameter expressing the relation between tidal volume and functional lung size (compliance of the respiratory system) = V T /C st,rs , was an independent ventilation variable strongly associated with increased mortality, while changes in tidal volume or positive end-expiratory pressure were not independent predictors of the outcome. An actual systematic review [9] reconfirmed the retrospective data of Amato et al. [8] by analysing the data of four prospective randomized studies (3252 patients): a higher ∆P was associated with a significantly higher mortality in ARDS patients.