Primary Causes and Pathophysiological Mechanisms of Hyperinflated Lungs

Pathophysiological Mechanisms of Lung Hyperinflation

The European Respiratory Society suggests that COPD is the most common cause of pathological lung hyperinflation, characterized by airflow limitation, reduced elastic recoil, and destruction of lung parenchyma 1, 2
Emphysema leads to destruction of alveolar walls, resulting in loss of lung elastic recoil, decreased carbon monoxide transfer capacity, increased static lung compliance, and increased total lung capacity, as reported by the European Respiratory Society 2
Intrinsic positive end-expiratory pressure (PEEPi) acts as an inspiratory threshold load that must be overcome by respiratory muscles, according to the European Respiratory Society 1
Reduction in elastic recoil of the lung due to parenchymal destruction (emphysema) leads to static hyperinflation, with two major patterns of emphysema contributing to hyperinflation: panacinar and centriacinar, as described by the European Respiratory Society 2

The British Thoracic Society notes that signs of chronic overinflation include loss of cardiac dullness, decreased cricosternal distance, and increased anterior-posterior diameter of the chest 3, 4
Rhonchi (wheezes), especially on forced expiration, are a common finding, as reported by the British Thoracic Society 4
Abnormal FEV1 (<80% of predicted) with an FEV1/VC ratio of <70% strongly suggests COPD with hyperinflation, according to the British Thoracic Society 4
Chest radiography may show flattened diaphragms, increased retrosternal airspace, and hyperlucent lung fields, as noted by the British Thoracic Society 5

Increased energy consumption of inspiratory muscles at any given level of minute ventilation is a consequence of hyperinflation, as reported by the European Respiratory Society 1
Ventilation/perfusion (V'/Q') inequality is the major mechanism impairing gas exchange and leading to arterial hypoxemia, according to the European Respiratory Society 1
Right ventricular afterload increases, potentially leading to right heart dysfunction, as noted by the European Respiratory Society 1