Obesity hypoventilation syndrome (OHS) has been conventionally (and to some extent arbitrarily) defined by the combination of obesity (body mass index (BMI) >30 kg/m²), daytime hypercapnia (arterial partial pressure of carbon dioxide (PaCO₂) ≥45 mm Hg or 6 kPa) during wakefulness, and usually (but not always) the presence of ‘sleep disordered breathing’, such as obstructive sleep apnoea, rapid eye movement sleep hypoventilation or both.1 The survival curve for untreated OHS is significantly reduced compared with the non-obese,2 and so early identification and treatment for these patients is likely to be beneficial. Little is currently known about the true prevalence of OHS in ambulatory obese individuals, with estimates range from 0.3–0.4% of the general population,3 to around 30% of hospitalised patients with a BMI >35 kg/m …