Traditionally, heart failure is a group of clinical syndromes in which the patient experiences dyspnea, fatigue, weakness, abdominal distention or swelling of the extremities due to organic or functional damage to the heart, resulting in decreased filling and/or ejection capacity of the ventricles, resulting in pulmonary and/or body circulation stasis. The diagnosis of heart failure requires evidence of organic cardiac injury in addition to clinical symptoms. Echocardiography and brain natriuretic peptide (BNP) or N-terminal brain natriuretic peptide precursor (NT-ProBNP) tests are important adjuncts. Symptoms of heart failure are the first step in the diagnosis of heart failure. Early manifestations are chest tightness, shortness of breath, dyspnea and weakness during heavy physical activity. If left untreated, the condition tends to worsen year by year, with activity endurance decreasing year by year and even inability to lie down for long periods of time. Some patients may wake up suddenly during sleep at night, and then sit up or stand up to get relief and fall back to sleep. In severe cases, the patient is unable to engage in any physical activity and is in a sitting position. As the disease progresses, patients gradually develop poor appetite, abdominal distension, swelling of the lower limbs, and even ascites. In addition to heart failure, dyspnea and weakness are also common in respiratory diseases (especially emphysema and pulmonary heart disease), obesity, and lack of exercise. Patients with coronary artery disease also often show exertional chest tightness and shortness of breath. Lower extremity swelling can also occur in hypertension, obesity, pulmonary heart disease, lower extremity venous dysfunction or thrombosis, etc. Therefore, heart failure cannot be diagnosed by symptoms alone. There are many causes of heart failure: any factors that increase the burden on the heart, cause myocardial damage or abnormal myocardial metabolism can cause heart failure, such as various congenital heart diseases, valvular heart diseases, various cardiomyopathies, hypertension, diabetes, coronary heart disease, myocardial infarction, myocarditis, anemia, hyperthyroidism, and some connective tissue diseases involving the heart. Therefore, once the diagnosis of heart failure is made, it is important to have an etiological diagnosis. Echocardiography is an important test for the diagnosis of heart failure. It can easily identify precardiac disease, valvular disease, cardiomyopathy, myocardial infarction, hypertensive heart disease, etc. The echocardiogram provides a more accurate definition of the patient’s cardiac function, including systolic and diastolic function. Measurement of left ventricular ejection fraction (EF) is the most commonly used index to assess left ventricular systolic function, but it may be measured inaccurately in many cases: for example, in patients with smoking, advanced age, or pulmonary disease, where the transmittance window is poor and the image is unclear; in atrial fibrillation, especially when the heart rate is too fast, and in myocardial infarction, where there is often error; and in the ultrasound operator’s own proficiency, which has a significant impact on the measured value. Experienced ultrasonographers will estimate EF values more accurately based on the amplitude of myocardial motion. It is important to note that EF values only reflect the motility of the left ventricular myocardium and cannot determine or exclude cardiac insufficiency, i.e., a normal EF cannot be considered as a patient without heart failure. Valvular heart disease cannot be determined from EF values, but once the EF value is below normal, it often indicates deterioration and a poor prognosis. Patients with coronary artery disease, hypertension, diabetes mellitus, and myocardial hypertrophy often present with heart failure with normal EF, due to reduced diastolic function of the heart. A more accurate index for cardiac ultrasound detection of diastolic insufficiency is the E/E’ ratio, which is the ratio of early diastolic blood flow velocity (E) at the mitral valve cusps measured by pulsed Doppler to early diastolic myocardial motion velocity (E’) at the mitral annulus measured by tissue Doppler, and this ratio <8 can exclude diastolic insufficiency; . >=8<15 to be determined clinically; >15 indicates the presence of diastolic insufficiency. Typical heart failure patients do not require BNP or ProBNP measurement to confirm the diagnosis, but the measured values are useful to determine the prognosis and treatment outcome. In cases where the diagnosis cannot be confirmed, BNP or ProBNP testing is of great value. Most patients with heart failure have BNP above 400 pg/ml; BNP <100 pg/ml does not support the diagnosis of heart failure; BNP between 100 and 400 pg/ml should also be considered for other reasons, such as pulmonary embolism, chronic obstructive pulmonary disease, compensated heart failure, etc. NT-proBNP is the inactive N-terminal fragment after BNP hormone prodivision, and compared with BNP It has a longer half-life and is more stable than BNP, and its concentration reflects the release of newly synthesized rather than stored BNP in a short period of time, and therefore better reflects the activation of BNP pathway. The concentrations of plasma BNP and NT-proBNP are similar in normal subjects. In left ventricular dysfunction, plasma NT-proBNP levels exceed BNP levels by up to 4-fold. Plasma NT-proBNP levels are age-, gender- and weight-dependent, elevated in older adults and women, decreased in obese individuals, and elevated in renal insufficiency. The sensitivity and specificity of plasma NT-proBNP levels for the diagnosis of acute heart failure are 93% and 95%, respectively, in adults under 50 years of age with a plasma NT-proBNP concentration of 450 pg/ml. The sensitivity and specificity of plasma concentration of 900 pg/ml for the diagnosis of heart failure in people over 50 years of age were 91% and 80%, respectively. NT-proBNP <300 pg/ml was considered normal and could exclude heart failure, with a negative predictive value of 99%. NT-proBNP <200 pg/ml after heart failure treatment suggests a good prognosis. In renal insufficiency, the sensitivity and specificity of NT-proBNP 1200 pg/ml for the diagnosis of heart failure in glomerular filtration rate <60 ml/min were 85% and 88%, respectively.