I. Composition and physiology of cardiovascular system The cardiovascular system consists of heart, arteries, capillaries and veins, in which blood flows. The heart is the hub connecting the arteries and veins and the “power pump” of the cardiovascular system, mainly composed of the heart muscle, and has endocrine functions. The heart is divided internally into two unconnected halves, each divided into atria and ventricles, so the heart has four chambers: left atrium, left ventricle, right atrium, and right ventricle. The ipsilateral atria and ventricles are connected through the atrioventricular port. The atria receive veins and the ventricles give off arteries. There are valves at the atrioventricular and arterial openings, which act like valves in a pump, opening and closing with and against the flow, ensuring a directed flow of blood. The arteries are the tubes that carry the blood centrifugally. The arteries branch out during their journey, becoming finer and finer, eventually moving into capillaries. Capillaries are the tubes connecting the arteriovenous endings and are generally 6 to 8 microns in diameter. Capillaries anastomose with each other to form a network and spread throughout the body. Capillaries are numerous, with thin walls, high permeability and slow flow, and are the place where blood and tissue fluids exchange substances. Veins are the vessels that carry blood back to the heart. The small veins are formed by the confluence of capillaries, which continuously receive branches in the process of cardiac return, gradually converging into medium veins, and finally the large veins flow into the atria. Compared with the corresponding arteries, veins have thin walls, large lumen, low elasticity and high capacity. Under neurohumoral regulation, blood circulates continuously along the cardiovascular system. Blood is pumped from the left ventricle, through the aorta and its branches to the capillaries of the province, where it exchanges substances and gases with the surrounding tissues and cells, then through the veins at all levels, and finally returns to the right atrium via the superior and inferior vena cava, a circulatory pathway known as the great circulation (body circulation). Blood is pulsed out of the right ventricle, through the pulmonary artery trunk and its various branches to the alveolar capillaries for gas exchange, and then through the pulmonary veins to the left atrium, a circulatory pathway called the lesser circulation (pulmonary circulation). The body circulation and the pulmonary circulation are carried out at the same time. The body circulation has a long path and a wide range of flow, nourishing all parts of the body with arterial blood and transporting metabolites and carbon dioxide from all parts of the body back to the heart. The pulmonary circulation travels a short distance through the lungs only and transforms mainly venous blood into oxygen-saturated arterial blood. The rhythmic systole and diastole of the heart drive blood, called the pumping or pumping function of the heart, which is the main function of the heart. When the heart contracts, it shoots blood into the arteries and distributes it to all tissues of the body through the arterial system; when the heart diastolic, it returns blood to the heart through the venous system in preparation for the next shot. One contraction and one diastole of the heart constitute a cycle of mechanical activity called the cardiac cycle. During a cardiac cycle, the mechanical activity of both atria and ventricles can be divided into systolic and diastolic phases. The amount of blood ejected from one ventricle in one beat is the output per beat, or beat volume. In the quiet state of a normal adult, the end-diastolic volume of the left ventricle is about 125 mL and the end-systolic volume is about 55 mL. The difference between the two is the beat-to-beat volume, which is about 70 mL. This shows that the ventricle does not eject all the blood that fills the ventricle during each ejection. The percentage of the stroke volume to the end-diastolic volume of the ventricle is called the ejection fraction. Compared to stroke volume, ejection fraction is a more accurate reflection of the heart’s pumping function and is important for early detection of abnormalities in cardiac pumping. The pressure of blood flowing in a blood vessel against the side walls of the vessel, i.e., the pressure per unit area, is called blood pressure. The term blood pressure is usually used to refer to arterial blood pressure. Arterial blood pressure can be expressed as systolic, diastolic, pulse pressure and mean arterial pressure. Systolic pressure is the highest blood pressure achieved during mid-systole of the ventricles. Diastolic blood pressure is the blood pressure at the end of ventricular diastole when the arterial pressure reaches its lowest value. Pulse pressure (abbreviated as pulse pressure) is the difference between systolic and diastolic pressures. Mean arterial pressure, on the other hand, is the average of arterial pressure at each instant in a cardiac cycle, roughly estimated to be about diastolic pressure plus 1/3 of pulse pressure. In the quiet state, the systolic pressure of our healthy young people is 100~120 mmHg, diastolic pressure is 60~80 mmHg, and pulse pressure is 30~40 mmHg. Overview of heart failure Heart failure (abbreviated as heart failure) is a group of clinical syndromes caused by any cause of initial myocardial injury (such as myocardial infarction, cardiomyopathy, hemodynamic overload, inflammation, etc.), resulting in changes in myocardial structure and function, and finally leading to low ventricular pumping and (or) filling function. The main clinical manifestations are dyspnea and weakness (limited activity tolerance), as well as fluid retention (pulmonary stasis and peripheral edema). Heart failure is not an independent disease, but a serious stage of impaired cardiac function due to multiple etiologies, and is the last terminal stage of cardiovascular disease, for doctors treating heart failure is the last battlefield of cardiovascular disease. The high incidence of heart failure, the difficulty of treatment, the high death rate, and the lack of effective treatment methods impose a huge burden on society and the economy, making it one of the major problems in the treatment of cardiovascular diseases today. Third, the etiology of heart failure primary myocardial myogenic fiber contractile dysfunction leads to heart failure, when the pump dysfunction is primary. Heart failure occurs when the myocardial contraction is weak and cannot eject enough blood to the peripheral vasculature to meet the metabolic needs of systemic tissues. The most common cause of heart failure is a lesion of the heart muscle itself, such as a myocardial infarction. In myocardial infarction, part of the heart muscle is necrotic and cannot contract, so the heart loses its “blood supply” function. Long-term hypertension, myocarditis, cardiomyopathy, rheumatic heart disease, etc. can eventually cause heart failure. Less common and easily overlooked causes include pericardial disease, hyper- and hypothyroidism, anemia, foot disease, arteriovenous fistula, atrial mucinous tumors and other cardiac tumors, connective tissue diseases, plateau disease and rare endocrine diseases. According to the speed of heart failure development, there are two types of heart failure: acute and chronic, with chronic being the most common. Acute cases are more common with left heart failure, mainly manifested as acute pulmonary edema; 2. Left heart failure is characterized by pulmonary circulation stasis; right heart failure is mainly manifested by body circulation stasis; 3. Clinical manifestations and symptoms of heart failure Left heart failure is characterized by pulmonary stasis and reduced cardiac output; right heart failure is characterized by body venous stasis; total heart failure is characterized by both left-sided and right-sided heart failure. The most typical symptoms of left heart failure are varying degrees of dyspnea, which is aggravated by activity, and in severe cases, seated breathing, coughing with large amounts of white fluffy pink foamy sputum; the most typical symptoms of right heart failure are decreased appetite, swelling of both lower extremities, swelling and pain in the liver area, liver enlargement, abdominal distension, nausea, vomiting, and oliguria. In addition to the original heart disease signs, in right heart failure, if the right ventricle is significantly enlarged to form functional tricuspid valve closure insufficiency, there may be systolic murmur; signs of venous stasis in the body circulation such as jugular vein anger and/or positive hepatic-jugular venous reflux sign, sunken edema at the site of prolapse; pleural fluid and/or ascites; hepatomegaly with pressure pain, jaundice and ascites in the late stage. VI. Diagnosis of heart failure The manifestation of early heart failure is not typical. Some patients may experience shortness of breath when performing more strenuous activities, chest tightness and shortness of breath when going upstairs, which can be relieved after rest. Some have chest tightness and breath-holding after falling asleep at night, requiring several pillows for comfort, bilateral lower limb edema, fatigue and weakness, dizziness, and memory loss every night. In addition to the clinical manifestations mentioned above, BNP (B-type brain natriuretic peptide) test is an accurate and easy way to diagnose heart failure, and blood BNP test can diagnose or exclude heart failure and detect heart failure patients early. It is difficult to diagnose early heart failure patients with traditional testing methods, and BNP is of considerable value in screening patients with asymptomatic heart failure. VII. Treatment of heart failure At the current stage, conventional treatment of heart failure includes cardiotonic, diuretic and vasodilator drugs to relieve patients’ symptoms and neuroendocrine blockers to improve the prognosis of heart failure. In the last decade, there has been a fundamental change in the treatment strategy of heart failure. Volume load management in heart failure is the basis of treatment, and traditional diuretics are the cornerstone of heart failure treatment at this stage, but diuretics have many problems and drawbacks. 90% of acute episodes of heart failure hospitalization are due to fluid overload, and one third of these patients have diuretic resistance. Moreover, diuretic therapy is ineffective, meaning that the sodium and water retention state is not effectively curbed in most patients. Statistics show that 88% of heart failure patients are treated with diuretics alone or in combination, but this traditional treatment, while relieving sodium and water retention, activates the neuroendocrine system, worsening the long-term prognosis and increasing morbidity and mortality, while the current pharmacological treatments that can improve the long-term survival of patients are all neuroendocrine blocking agents. Although diuretics have been in clinical use for more than 60 years, their efficacy remains uncertain. Therefore in recent years there has been a growing call to question diuretic therapy. Medicine has been explored for nearly 20 years to achieve mechanical dehydration through blood ultrafiltration to correct volume overload and thus relieve heart failure symptoms. Especially in recent years, the introduction of heart failure-specific ultrafiltration devices has set off an international craze for heart failure ultrafiltration therapy. A series of large-scale trials have demonstrated that ultrafiltration therapy can rapidly relieve symptoms, shorten hospitalization time, and reduce rehospitalization rates.