Bronchoalveolar breath sounds can be heard in the region of normal alveolar breath sounds. When lower airway resistance increases, inspiration and expiration are both difficult. Since the alveoli in the inspiratory phase are dilated and the airway diameter is relatively large, the airway resistance in the inspiratory phase is smaller than that in the expiratory phase, so the increased airway resistance is mainly manifested by prolonged expiration time. The strength of alveolar breath sounds in normal subjects is related to the depth of breathing, the size of the elasticity of the lung tissue, the thickness of the chest wall, and the age and gender of the subject. What are the clinical examination symptoms of prolonged expiratory sounds? 1, hyperplastic hypertrophy of glands, hypersecretory function: chronic bronchitis mucus glandular alveoli are significantly increased, the ducts are dilated, plasma glands and mixed glands are correspondingly reduced, and some glands are almost entirely occupied by mucus glands. The Reid index (ratio of gland thickness to bronchial wall thickness) in chronic bronchitis increases to more than 0.55-0.79 (normal is less than 0.4). The larger the Reid index, the more severe the inflammation, the more hypertrophic the glands and the narrower the bronchial lumen. The hyperplastic and hypertrophied glands are hypersecretory, and mucus secretion increases, so the daily sputum volume of patients increases. 2. Changes of mucosal epithelial cells: due to repeated inflammation, focal necrosis of epithelium and squamous epithelial metaplasia are caused, ciliated epithelial cells are damaged to varying degrees, and cilia become shorter, uneven or sparse and fall off. 3. Changes in bronchial wall: The bronchial wall has various inflammatory cell infiltration, congestion, edema and fibroplasia. The bronchial mucosa is ulcerated and granulation tissue is proliferated. In severe cases, the bronchial smooth muscle and elastic fibers are also damaged and mechanized, causing luminal narrowing. In a few cases, the bronchial cartilage is atrophied and degenerated and partially replaced by connective tissue. Mucus plugs may be found in the lumen. Due to mucosal swelling or mucus retention and obstruction, the local tube wall is easily collapsed, twisted and deformed or dilated. 4. Electron microscopy: The following changes in the alveolar wall are seen in cases of chronic bronchitis: ① swelling and thickening of type I alveolar epithelial cells, in which the mitochondria are swollen and the endoplasmic reticulum is dilated in the form of vacuoles, and hyperplasia of type II alveolar epithelial cells. (ii) thickening of capillary basement membrane, endothelial cell injury, thrombosis and luminal fibrosis and occlusion. (iii) Diffuse hyperplasia of fibrous tissue in the alveolar wall. These changes are particularly significant in those with concomitant emphysema and pulmonary heart disease. 5, respiratory function changes: chronic bronchitis early lesions are mainly in the small airways with an inner diameter <2mm, clinical symptoms are not obvious, most of the routine lung function tests are normal, but the closed air volume test is seen to increase. When the inflammation spreads to larger bronchi, during the acute exacerbation period, the airway narrows, resistance increases, and conventional ventilation function tests such as maximum ventilation volume, 1-second expiratory volume, and maximum mid-expiratory flow rate are mildly reduced. Residual air volume was mildly increased, but spirometry was normal. In remission, all changes in lung function return to normal. The impairment of respiratory function is mostly irreversible after the complication of obstructive pulmonary emphysema.