Gastrointestinal stasis is most commonly seen in right heart failure due to various cardiovascular diseases and in portal hypertension due to various causes. Gastrointestinal stasis can be seen in various causes of portal hypertension, where gastrointestinal venous blood does not flow smoothly through the portal vein to the liver, resulting in gastrointestinal stasis. It can be seen in various causes of portal hypertension, where the venous blood of the gastrointestinal tract does not flow smoothly through the portal vein to the liver, thus causing gastrointestinal stasis. Venous reflux disorders at any site can cause esophageal varices, the latter being an important complication of portal hypertension because of the formation of collateral circulation between the portal vein and superior vena cava in portal hypertension. The specific collateral circulation pathways are as follows: portal vein – gastric coronary vein – esophageal venous plexus – odd vein – superior vena cava. The following diseases may also be the cause of gastrointestinal stasis: 1. Pediatric congestive heart failure Congestive heart failure is referred to as heart failure. Heart failure is a cardiac dysfunction in which the cardiac output is reduced to meet the needs of the body. Clinically, heart failure is a syndrome consisting of 4 parts: cardiac dysfunction, reduced exercise tolerance, congestion in the pulmonary circulation, and the late development of arrhythmias. Cardiac dysfunction is required to constitute heart failure, and the other three components are clinical manifestations of the compensatory mechanisms of cardiac insufficiency. The early stage is compensated by accelerating the heart rate, myocardial hypertrophy and heart enlargement, when the blood displacement to meet the needs of the body only cardiac dysfunction, and there are no signs of heart failure yet, called the compensatory period of cardiac function. During this period, the disease progresses with pulmonary and/or body circulation stasis, shortness of breath, superficiality, cough and perioral cyanosis, jugular venous anger, hepatosplenomegaly, and edema in children. The clinical manifestation is congestive heart failure. Heart failure is a serious health hazard for children, and it is a common pediatric emergency that should be rescued in time. 2, chronic heart failure Heart failure is due to myocardial infarction, cardiomyopathy, hemodynamic overload, inflammation and other causes of various chronic myocardial disease and long-term ventricular overload (pressure or volume overload), resulting in primary or secondary weakening of myocardial contractility, so that the heart can not beat the blood supply commensurate with the venous return and the metabolic needs of the body’s tissues, called chronic heart failure. Chronic heart failure is also called congestive heart failure because it is almost always accompanied by significant obstructive congestion (bruising) of the organs. Chronic heart failure is mostly a result of organic cardiovascular disease that undergoes a compensatory process of varying length. When myocardial contractility is severely impaired and the heart and blood circulation lose their compensatory capacity, symptoms of reduced cardiac output, inadequate perfusion of organs and tissues, and stasis in the body circulation gradually appear. The goal of treating heart failure is not only to improve symptoms and quality of life, but also to target the mechanisms of myocardial remodeling, delay and prevent the development of myocardial remodeling, and reduce the rate of hospitalization and mortality in heart failure. 3, portal hypertension Portal hypertension is a group of syndromes caused by a persistent increase in portal pressure. Most of them are caused by cirrhosis, but a few are secondary to obstruction of the main portal vein or hepatic veins and other factors of unknown origin. Increased portal venous pressure occurs when portal blood does not flow smoothly back through the liver into the inferior vena cava. This is manifested by the opening of the portal-body venous communication branches, and a large amount of portal blood enters the body circulation directly through the communication branches before entering the liver, resulting in dilatation of the abdominal wall and esophageal veins, splenomegaly and hypersplenism, hepatic dysfunction, and ascites. The most serious is the dilatation of the veins at the junction of the esophagus and stomach, which can cause severe acute upper gastrointestinal bleeding and endanger life once it ruptures. 4.refractory heart failure Heart failure can often improve rapidly with proper etiological treatment and conventional anti-heart failure treatment (rest, salt restriction, diuretics, digitalis, ACEI, etc.), but if the symptoms and signs of heart failure persist for a long time without change or are progressively aggravated under conventional heart failure treatment, it is called refractory heart failure. 5, tricuspid stenosis tricuspid stenosis (tricuspid stenosis) is mostly seen in women, most of them are caused by rheumatic fever, but rheumatic tricuspid stenosis alone is extremely rare, almost always accompanied by mitral and/or aortic valve lesions, and also tricuspid valve closure insufficiency. The pathologic changes are fibrotic thickening of the valve with redundant growths at the edges and adherence or fusion of the three valves to form a triangular stenotic orifice. The lesion may also extend to the tendon cords and papillary muscles. After stenosis formation, blood flow from the right atrium to the right ventricle is obstructed, resulting in enlargement of the right atrium and increased pressure. Due to obstruction of vena cava return, venous pressure is chronically elevated, showing signs such as jugular vein anger, hepatomegaly, ascites, and swelling of the extremities. The right ventricle is atrophied due to reduced blood flow. In the presence of mitral valve lesions, the right ventricle can be hypertrophic. 6, tricuspid insufficiency tricuspid insufficiency or tricuspid regurgitation, most of them are functional tricuspid insufficiency secondary to mitral valve lesions, and a few are caused by organic lesions of the tricuspid valve itself.