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Mechanism of formation of pulmonary hypertension in chronic pulmonary heart disease.
(1) anatomical factors: chronic inflammation of the bronchial tubes and their surrounding tissues often involves the small pulmonary arteries, causing inflammation of the small pulmonary arteries and thickening of the vascular wall with spasm or fibrosis, resulting in narrowing or occlusion of the lumen. In addition, emphysema-induced increase in intra-alveolar pressure compression of alveolar capillaries, so that the lumen is narrowed or occluded, increasing the resistance of the pulmonary circulation. Severe emphysema may also cause destruction and fusion of the alveolar walls, destruction of the capillary network, and reduction of the vascular bed. In addition, primary pulmonary hypertension, repeated pulmonary vascular embolism, interstitial fibrosis, pneumoconiosis, etc., can also cause an increase in pulmonary resistance.

(2) Functional factors: hypoxia, hypercapnia and respiratory acidosis, through the neurohumoral mechanism, causing pulmonary vasoconstriction, spasm, and increased pulmonary resistance. Long-term persistent pulmonary vasospasm, increased pulmonary circulatory resistance can cause arterial muscular layer hypertrophy, focal necrosis of the intima, scar fibroplasia and vitreous changes and other anatomical changes, so that the narrowing of the vascular bed, pulmonary arterial pressure is further increased.

(3) Increased blood volume and blood viscosity: chronic hypoxia causes secondary erythrocytosis, increased blood viscosity; hypoxia, hypercapnia makes sympathetic nerve excitation, contraction of small renal arteries, decreased renal blood flow, resulting in sodium retention, increased blood volume, increased pulmonary artery pressure.