Still no room to breathe: insights on supine lung mechanics from oscillometry in COPD

Although COPD is characterised by the presence of airflow obstruction during forced expiration, it is the downstream consequences of airflow obstruction that result in many of the symptoms of COPD. In particular, airflow obstruction leads to pulmonary hyperinflation, which in turn reduces inspiratory capacity (IC), increases work of breathing and produces dyspnoea [1]. These problems are compounded when the mechanical load on the respiratory system of the patient with COPD increases as it does during exercise [2] or when patients lie down [3]. In healthy people, lying down results in a slight drop in end-expiratory lung volume (EELV) [4], which is associated with a higher end-expiratory position of the diaphragm [5]. The lower EELV in the face of preserved total lung capacity (TLC) results in an increase in IC. In people with COPD and hyperinflation, lying down results in less of a fall in EELV [4] and the diaphragm remains in a more flattened position at the end of expiration [5], resulting in a reduced ability to increase IC. These events are accompanied by the onset of expiratory flow limitation which can be detected during tidal breathing by the negative expiratory pressure manoeuvre [6] or the within-breath reactance change on oscillometry [7]. In addition, the neural drive to breathe is increased in patients with COPD when supine, but this signalling is relatively ineffective and results in neuromechanical uncoupling, further increasing the sensation of dyspnoea [8]. However, the link between these neuromechanical events and overall respiratory system dynamic elastance, which reflects lung stiffness, has not been previously demonstrated.