Infection with partial bronchial obstruction may lead to chronic atelectasis and ultimately to chronic pneumonitis because of poor drainage. In the early stages, blood perfuses the airless lung, causing arterial hypoxemia. If capillary and tissue hypoxia results in transudation of fluid and pulmonary edema, the alveolar spaces fill with secretions and cells, preventing complete collapse of the atelectatic lung. Distention of the unaffected surrounding area of the lung may partially compensate for the volume loss. However, in cases of extensive collapse, the diaphragm may become elevated, the chest wall may flatten, and the heart and mediastinum may shift to the affected side.
Dyspnea results from a variety of stimuli affecting the respiratory centers and cerebral cortex.
Pa O2 often improves during and after the first 24 h, presumably as blood flow to the atelectatic area decreases. Pa CO2 is usually normal or low due to hyperventilation of the remaining normal lung parenchyma. If the obstruction is relieved, air enters, any complicating infection subsides, and the lung may eventually return to normal, depending on the magnitude of the infection. If the obstruction remains and infection is present, the lack of air and circulation initiates changes leading to fibrosis and bronchiectasis. Mild to severe disturbances in gas exchange may result.