Pulmonary Gas Exchange in Chronic Obstructive Lung Diseases

Chronic obstructive pulmonary disease, which by this point we define COPD, is understood as a situation of progressive airflow limitation, sometimes reversible, whose pathogenetic mechanisms responsible are to be attributed, on the one hand, to the progressive obstruction of the central and peripheral airways, with structural modification of their histological status and, secondly, to a progressive destruction of the elastic component of the parenchymal tissue, with loss of alveoli and pulmonary capillaries . It follows that such a combination of inflammatory insults at the level of the bronchial and bronchiolar airways and loss of alveoli and capillaries, inevitably, leads to a progressive inefficiency of intrapulmonary gas exchange . This inefficiency is initially reflected in evidences of slight reduction in arterial oxygen tension (hypoxia) and carbon dioxide (hypocapnia) . If the disease progresses, it can reach a level where it is established respiratory failure characterized by severe hypoxemia associated with hypoor hypercapnia [1]. The alterations in gas exchange, even in the early stages of the disease, are supported primarily by the presence of a growing unequal distribution of ventilation, which is to be supported by pathological phenomena that increase airway resistance and increase the time of filling and emptying of the alveoli. To the unequal distribution of ventilation is associated also a progressive alteration of the distribution of perfusion, which in the phases of onset of the disease, may represent a sort of compensation reactive but that in the long run leads to an altered transfer of oxygen and carbon dioxide from side to another side of the alveolar-capillary membrane resulting in inefficiency of exchange [2].