Hyperinflation of the lungs, commonly referred to as emphysema. There are several types of emphysema according to their pathogenesis: senile emphysema, compensatory emphysema, interstitial emphysema, focal emphysema, paracentral emphysema, and obstructive emphysema. Emphysema is a pathological condition in which the airways at the distal end of the terminal fine bronchi (respiratory fine bronchi, alveolar ducts, alveolar sacs and alveoli) are hypoelastic, hyperinflated, inflated and have increased lung volume or are accompanied by destruction of the airway walls. What are the risk factors for lung hyperinflation? What are the specific causes? Risk factors for hyperinflation of the lungs: 1. Individual factors: (1) genetic factors such as antitrypsin deficiency; (2) airway hyperreactivity; (3) lung dysplasia. 2, Environmental factors: (1) smoking; (2) occupational dust and chemicals; (3) respiratory infections; (4) environmental pollution; (5) poor socioeconomic status. Smoking, infection and atmospheric pollution cause inflammation of the fine bronchial tubes and narrowing or obstruction of the lumen. During inspiration, the lumen of the fine bronchus expands and air enters the alveoli; during exhalation, the lumen narrows and air is retained, and the intra-alveolar pressure keeps increasing, leading to over-expansion or even rupture of alveoli. The loss of radial traction around the fine bronchus causes the fine bronchus to contract, resulting in narrowing of the lumen. The thickening of the intima of the pulmonary vessels, the reduction of blood supply to the alveolar wall, and the weakening of alveolar elasticity contribute to the rupture of inflated alveoli. α1 antitrypsin deficient individuals have a weakened ability to inhibit proteases and are therefore more prone to emphysema. Smoking also has a negative effect on the protease-anti-protease balance. In conditions such as infection, protease activity is increased in the body and the activity of the anti-protease system is correspondingly increased in normal subjects to protect lung tissue from damage.