Acute Effect of Pulmonary Desufflation on Cardiac Performance in COPD Patients
Status:
Completed
Trial end date:
2014-10-01
Target enrollment:
Participant gender:
Summary
Chronic Obstructive Pulmonary disease (COPD) is one of the major clinical entities that
causes thousands of deaths every year all over the world and weights a lot on the health care
system of every country in terms of direct and indirect costs. The physiopathological
modifications that characterise COPD are represented by irreversible (sometimes partially
reversible) airflow obstruction, and bronchiolar inflammation. Lungs that develop emphysema
lack of elastic recoil and imply increased resistances and airflow obstruction due to loss of
lung parenchyma and supporting elastic structures. All these modifications produce air
trapping and so lung hyperinflation. The latter is precisely the cause of the symptoms and
particularly dyspnoea which is often heavily perceived by COPD patients and that drives to
the limitation of daily activities. Lung hyperinflation and the other alterations that occur
in COPD imply gas retention and increase in pulmonary vascular resistances. Considering that
the rib cage has limited elastic properties, the effects of gas trapping and lung parenchymal
damage on mediastinum and particularly on heart mechanics is indisputable. Together with
alveolar hypoxia, lung hyperinflation is responsible for the development, as the disease
progresses, of the cor pulmonale. Tha latter causes pulmonary hypertension and increased
mechanic load during right heart chambers contraction and relaxation. Those alterations may
effect left heart chambers too.
Airflow obstruction in COPD is usually treated by inhaled bronchodilators and
corticosteroids. The main and most used bronchodilators are represented by beta 2 agonists
(short, long and ultra-long acting) and anticholinergic inhalatory drugs, which can be also
short, long and ultra long acting. Among ultra long acting beta 2 agonists, indacaterol is
characterised by quick onset of action (5 minutes), and guarantees an effective
bronchodilation duration of 24 hours. It is also known that it has an important effect on
reducing lung hyperinflation decreasing residual volume and consequently allowing an increase
of inspiratory capacity. The purpose of our study is to evaluate the effects of indacaterol
on lung hyperinflation in COPD subjects of any stage and with lung air trapping, and the
consequent potential effects on heart performance evaluated by cardiac trans thoracic echo
color doppler.