Diagnostic basis: 1. Long-term history of chronic bronchitis-repeated cough and expectoration for 20 years. 2. Physical examination: body temperature is 37.8℃, and heart rate 130 beats/min. Barrel chest, high-definition voice prompts emphysema. Both lungs are full of dry and wet rales. 3 cm below the liver ribs, soft and tender, with positive signs of hepatic jugular vein reflux-suggesting liver congestion, pulmonary hypertension and systemic congestion. Edema of both lower limbs. 3. Chest X-ray results.
Main pathology of chronic pulmonary heart disease;
(1) Bronchial lesions: changes and thickening of bronchial mucositis, hyperplasia of mucous glands, excessive secretion, expansion of acinus with a large number of secretions, inflammatory exudates and mucus secretions remaining in bronchial cavity, forming inflammatory plugs or mucus plugs, and damage of bronchial ciliated epithelium to varying degrees, involving the purification function of ciliated epithelium. The lesion spreads downward to bronchioles, and smooth muscle hypertrophy can occur, which makes the lumen narrow and irregular; In addition, changes such as wall spasm, cartilage destruction, and easy closure of the lumen when breathing gas make the bronchioles incomplete or completely blocked.
(2) Alveolar lesions Due to the above lesions in the bronchi, the residual gas in the alveoli blocked by the exhaust pipe increases, the pressure increases, and the alveoli expand excessively, so that the bubble wall passively expands on the basis of the damage of elastic fibers, and the bubble wall ruptures, so that several small bubbles merge into one big bubble, forming emphysema.
(III) Pulmonary Vascular Disease Chronic obstructive pulmonary disease often recurs, accompanied by inflammation around bronchi and pneumonia. The inflammation spreads to the bronchial artery and the nearby pulmonary artery branches, which makes the bronchial artery thicker to varying degrees, leading to muscular pulmonary arterioles, intima muscle hypertrophy, increased area of type I and II collagen, and fibrous thickening of the intima of pulmonary arterioles. In addition, there may be nonspecific pulmonary vasculitis and pulmonary intravascular thrombosis. About 30% patients have dilated communicating branches, which can produce arteriovenous shunt.
(4) Right ventricle hypertrophy, wall thickening, heart cavity dilatation, pulmonary artery cone dilatation, myocardial fiber hypertrophy and atrophy, interstitial edema, focal necrosis, replaced by fibrous tissue. Some patients may be complicated with coronary atherosclerosis.