1, hemodynamic changes and vascular endothelial function effects The occurrence of pulmonary embolism pulmonary vascular resistance rises, embolus obstruction of pulmonary artery causes mechanical pulmonary capillary anterior arterial hypertension, pulmonary vascular bed reduction causes pulmonary circulation resistance increases, pulmonary artery pressure rises, right ventricular load increases, cardiac output drops. When the disease develops further, it can cause right heart failure and blood pressure drop. Due to the strong reserve capacity of the pulmonary vascular bed, in patients without cardiopulmonary anomalies, pulmonary artery elevation occurs only after 30-50% blockage of the pulmonary vascular cut-off area. In patients with blockage of more than 50% of pulmonary artery pressure, the right ventricular afterload is significantly higher, and sudden death can occur if the blockage area is more than 85%. Pulmonary artery pressure changes are more pronounced in patients with pre-existing cardiopulmonary disease. At the same time, the opening of collateral vessels in the closed state, the major bronchopulmonary artery anastomoses and intrapulmonary venous shunts reduce oxygenated blood. In addition to the vascular mechanical factors, neurohumoral factors and circulating endocrine hormones also play an important role in the rise of pulmonary vascular resistance, as pulmonary embolism occurs when the pulmonary vascular endothelium is damaged, releasing a large number of contractile substances such as endothelin and angiotensin II. Vasoactive substances, such as adenosine diphosphate, histamine, 5-hydroxytryptamine, a variety of prostaglandins, etc., all of which lead to widespread constriction of small pulmonary arteries, while reflexively causing sympathetic release of catecholamines, causing a contraction effect at the pulmonary vessels to form the first vicious circle. Some experiments suggest that thrombus interrupts pulmonary artery blood flow causing hypoxia as well as platelet adhesion and aggregation, causing the endothelium to secrete excessive ET (plasma endothelin), and the excessive increase in ET may cause vasospasm at the blockage site, preventing the emboli from moving to the next level of blood vessels. Increased ET may cause a rise in pulmonary artery pressure and an acceleration of blood flow to regulate hyperventilation that occurs in response to definite oxygenation. Experiments also suggest that plasma NO concentration is significantly higher after acute PE than before embolism, and increased NO can diastole the pulmonary vasculature, reduce pulmonary resistance, and maintain the pulmonary circulation pressure and low resistance state. In massive pulmonary embolism, pulmonary artery pressure rises, right ventricular myocardial work and oxygen consumption increase, right ventricular pressure increases, aortic and right ventricular pressure step difference decreases, and coronary perfusion decreases. In addition, the concentration of endothelin in the body increases significantly during acute pulmonary embolism, and the amount of endothelin converted locally in the coronary arteries also increases significantly, resulting in coronary artery spasm, causing insufficient coronary artery perfusion and myocardial ischemia, and forming a second malignant loop at the coronary arteries of the heart. Therefore, some patients with pulmonary embolism may show myocardial ischemia such as V1–4 conduction, II, III, AVF conduction T-wave inversion on ECG. 2.Pathophysiological changes of respiratory system The most important symptom of pulmonary embolism is dyspnea, and almost all symptomatic pulmonary embolism have different degrees of respiratory dysfunction. Pulmonary embolism embolism site has ventilation but no blood perfusion, so pulmonary embolism can lead to a serious imbalance of pulmonary ventilation/perfusion ratio. In addition, a large pulmonary embolism can cause reflex pulmonary vasospasm, and 5-hydroxytryptamine, histamine, platelet-activating factor and sympathetic excitation can also cause tracheospasm, increase airway resistance, and cause poor ventilation. Chemical mediators such as 5-hydroxytryptamine, histamine, and thromboxane A2 can also cause changes in vascular permeability. When pulmonary capillary blood flow is severely reduced or terminated for 24 h, alveolar surface active substances decrease, alveolar atrophy occurs, and pulmonary atelectasis occurs, while alveolar epithelial permeability increases and a large amount of inflammatory mediators are released, causing local diffuse pulmonary edema and pulmonary hemorrhage. Decreased alveolar cell function in turn causes decreased synthesis and loss of surface active substances, resulting in decreased lung compliance and further decrease in pulmonary ventilation-diffusion function. In conclusion, pulmonary embolism, especially acute massive pulmonary embolism, alters the distribution of ventilation/perfusion in the lung, increases cardiac and pulmonary vascular resistance, leads to right heart failure, hypoxemia and hypocapnia, and causes a series of pathophysiological changes in the body, resulting in different clinical manifestations.