ABSTRACT
Chronic obstructive pulmonary disease (COPD) is one of the few respiratory disorders including an assertion about lung function in the definition, which indeed contains the statement on the reduction of forced expiratory flows [1]. The pathophysiology of COPD is a complex and attractive subject [2]. It includes abnormalities in lung and chest wall mechanics, in pulmonary gas exchanges, in respiratory and skeletal muscles structure and function and so on [3]. COPD is a heterogeneous disease in terms of clinical, physiological, and pathological presentation [4]. Probably the starting point is the inflammation of the airways [5,6] and the final events are severe physical disability and premature death. In this complexity, airflow limitation is a central element, and to some extent the bridge, connecting biological defects with clinical phenotypes. Definitely, airflow limitation is a key mechanism determining dyspnoea, progressive disability and ventilatory failure in patients with COPD [7].
