Cardiac insufficiency in pregnancy is manifested by pulmonary abandonment, acute pulmonary edema, and right heart failure. Heart disease during pregnancy can be divided into two main categories. The first category is pre-existing heart disease, mostly rheumatic and congenital heart disease, while hypertensive heart disease, mitral valve prolapse and hypertrophic heart disease are rare. The second category is heart disease induced by pregnancy, such as hypertensive heart disease and perinatal heart disease. So what are the triggers of pulmonary abandonment of blood? Here’s an explanation. Most of the pregnant women with pulmonary abandonment have predisposing factors, such as pulmonary infection, anemia, pulmonary hypertension, overexertion, extreme emotional changes, hypertension, protein deficiency, atrial fibrillation, etc. Pulmonary infection can lead to heart failure due to the increase of pulmonary circulatory resistance; anemia and hypoproteinemia can aggravate myocardial hypoxia; hyperemesis increases the left ventricular end-diastolic pressure and increases the cardiac afterload due to systemic small artery spasm and increased peripheral resistance, while heart preload increases due to water and sodium retention and increased blood volume, thus predisposing to heart failure. In addition, medical heart failure due to excessive postpartum rehydration cannot be ignored. Therefore, active search for the cause, early diagnosis and timely management are extremely important for the prevention and treatment of pulmonary abandonment. Pathogenesis: Hemodynamic changes occur significantly during pregnancy, and cardiac output can increase by 30% to 40% in a quiet state. At the same time, hemodynamic changes cause neuroendocrine changes and increased sympathetic excitability, leading to contraction and spasm of small pulmonary arteries and surrounding small vessels, especially when accompanied by anemia, infection and hypertensive disease during pregnancy, which will further increase the resistance load of the left and right ventricles and reduce cardiac output, triggering or aggravating pulmonary abandonment. or aggravate the pulmonary abandonment of blood, and even myocardial degeneration or cardiac arrest may occur.