Acute heart failure (heart failure) is clinically most common in acute left heart failure, while acute right heart failure is less common. Acute left heart failure refers to the acute onset or aggravation of left heart function abnormalities caused by a significant reduction in myocardial contractility, increased cardiac load, resulting in acute cardiac output, sudden increase in pulmonary circulatory pressure, increased peripheral circulatory resistance, causing pulmonary congestion and acute pulmonary stasis, pulmonary edema and may be accompanied by tissue and organ perfusion deficiency and cardiogenic shock clinical syndrome. Acute right heart failure is a clinical syndrome in which the contractility of the right ventricular myocardium decreases sharply or the anterior and posterior loads of the right ventricle increase suddenly for some reasons, resulting in a rapid decrease in right heart blood output. Acute heart failure can be sudden or acute exacerbation of existing chronic heart failure, mostly systolic heart failure, but also diastolic heart failure; most patients have combined organic cardiovascular disease before the onset of heart failure. For acute heart failure occurring on the basis of chronic heart failure, the condition is stable after treatment and should no longer be called acute heart failure. Acute heart failure is often life-threatening and must be rescued and treated urgently. In the past 10 years, although basic and clinical research on chronic heart failure has made great progress, clinical work on acute heart failure still has the following problems: 1. Clinical studies, especially large sample prospective randomized controlled trials, are rare and clinical evidence is scarce, making most of the current recommendations on treatment in national guidelines based on experience or expert opinion, lacking sufficient evidence to support them; 2. There is a lack of clinical data and even basic epidemiological material is not complete; the management of acute heart failure lacks standardization everywhere, and the morbidity and mortality rate of acute heart failure, although declining, is still an important cause of cardiogenic death and has become a weak link in the treatment of cardiovascular emergencies in China. In view of the above reasons, the Chinese Society of Cardiovascular Diseases decided to compile the “Guidelines for the diagnosis and treatment of acute heart failure” in China to improve the clinical management of this cardiac emergency. The Heart Failure Specialty Group of the Cardiovascular Disease Branch of the Chinese Medical Association formed a writing group and an expert group for this work, and established the basic principles for the preparation of the guidelines: 1. New technologies and methods, drawing on the various guidelines developed and promulgated by major foreign academic cardiovascular organizations in recent years; 2. To be based on China’s national conditions and traditional habits of clinical management and proven effective methods and experience, including the guidelines and expert consensus on heart failure and related diseases prepared by China in recent years, so that they load China’s national conditions; 3. To provide basic units and hospital clinicians at all levels with guidelines that can be accepted A guideline document that they are happy to use. This guideline indicates the recommended categories and evidence level grading for the application of drugs and various therapeutic methods in an internationally accepted manner. Recommendation categories: Category I is proven and/or unanimously considered beneficial and effective: Category II is where the evidence for efficacy is inconsistent or controversial, with category IIa where the relevant evidence tends to be effective and category IIb where it is not yet sufficient; Category III is where the evidence is proven or unanimously considered useless and ineffective, or even potentially harmful. Level of evidence grading: evidence from multiple randomized controlled clinical trials or multiple meta-analyses for Class A; evidence from single randomized controlled clinical trials or non-randomized studies for Class B; evidence from small studies or expert consensus for Class C. I. Common causes of acute left heart failure 1. Acute exacerbation of chronic heart failure. 2, acute myocardial necrosis and/or injury: (1) acute coronary syndromes such as acute myocardial infarction or unstable angina, acute myocardial infarction with mechanical complications, right ventricular infarction; (2) acute severe myocarditis; (3) perinatal cardiomyopathy; (4) drug-induced myocardial injury and necrosis, such as antineoplastic drugs and toxic agents. (3) Acute hemodynamic disturbances: (1) acute massive regurgitation of valves and/or aggravation of existing valve regurgitation, such as mitral and/or aortic valve perforation due to infective endocarditis, mitral tendon cord and/or papillary muscle rupture, valve tears (e.g., traumatic aortic valve tears), and acute damage to prosthetic valves; (2) hypertensive crisis; (3) severe aortic or mitral valve stenosis (4) aortic coarctation; (5) pericardial compression; (6) acute diastolic left heart failure, mostly in elderly patients with poorly controlled hypertension. 1. Acute myocardial injury and necrosis: ischemic heart disease combined with acute heart failure mainly has the following three conditions: (1) acute myocardial infarction: mainly in view of large myocardial infarction; sometimes acute myocardial infarction can also first manifest as acute left heart failure symptoms, especially in elderly patients and diabetic patients; (2) acute myocardial ischemia: large ischemic area and severe ischemia can also induce acute heart failure. (2) acute myocardial ischemia: large ischemic area and severe ischemia can also induce acute heart failure, which can be seen in elderly patients with small infarcts, although the infarct area is small, but the ischemic area is large; (3) pre-existing chronic cardiac insufficiency, such as old myocardial infarction or chronic ischemic heart disease patients with no history of infarction, can develop acute heart failure under ischemic attack or other triggers. In addition, some patients with acute left heart failure as the main manifestation may not have obvious symptoms of chest pain, but it may be due to ischemic heart disease when appropriate risk factors are present. Myocardial ischemia and the resulting myocardial damage leave part of the myocardium in a state of myocardial stasis and myocardial hibernation, and lead to cardiac insufficiency. When coronary blood flow and oxygenation are restored, hibernating myocardial function improves rapidly, while myocardial insufficiency in the dormant myocardium continues for some time, when responding to positive inotropic drugs. Severe and prolonged myocardial ischemia will certainly cause irreversible damage to the myocardium. Acute myocardial infarction or acute severe myocarditis, etc. can cause myocardial necrosis, which reduces the contractile units of the heart. Hypertensive emergencies or severe arrhythmias can increase the load on the heart. These changes can produce hemodynamic disturbances and also activate the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system, promoting the exacerbation and worsening of the condition in patients with heart failure. The above pathophysiological process can progress due to the underlying lesion redundancy, or rapidly occur under the excitation of multiple triggers and produce acute heart failure. 2, hemodynamic disorders: The main hemodynamic disorders in acute heart failure are: (1) decreased cardiac output (CO), absolute or relative decrease in blood pressure and insufficient perfusion of peripheral tissues and organs, resulting in organ dysfunction and peripheral circulatory disorders, and cardiogenic shock. (2) Elevated left ventricular end-diastolic pressure and pulmonary capillary wedge pressure (PCWP), which can lead to hypoxemia, metabolic acidosis and acute pulmonary edema. (3) Elevated right ventricular filling pressure, resulting in increased venous pressure in the body circulation, stasis of the body circulation and major organs, water and sodium retention, and edema. 3, neuroendocrine activation: sympathetic nervous system and RAAS hyperexcitation is a protective compensatory mechanism of the body in acute heart failure, when long-term hyperexcitation will produce adverse effects, so that a variety of endogenous neuroendocrine and cytokine activation, aggravating myocardial injury, decreased cardiac function and hemodynamic disorders, which in turn stimulates the excitation of the sympathetic nervous system and RAAS, forming a vicious circle. 4, cardio-renal syndrome: heart failure and renal failure often coexist and are mutually causal clinically this state is called cardio-renal syndrome. Cardiorenal syndrome can be divided into five types; type 1 is characterized by rapidly deteriorating cardiac function leading to acute renal impairment; type 2 is characterized by chronic heart failure leading to progressive chronic kidney disease; type 3 is a primary, rapid deterioration of renal function leading to acute cardiac insufficiency; type 4 is characterized by chronic kidney disease leading to decreased cardiac function and/or increased risk of adverse cardiovascular events; type 5 is characterized by acute or chronic systemic disease leading to simultaneous cardiac and renal failure. leading to simultaneous failure of cardiac and renal function. Obviously, both type 3 and type 4 cardiorenal syndrome can cause heart failure, where type 3 can cause acute heart failure. type 5 cardiorenal syndrome can also induce heart failure or even acute heart failure. 5, acute decompensation of chronic heart failure: stable chronic heart failure can deteriorate sharply within a short period of time, with cardiac function decompensation, manifesting as acute heart failure. The contributing factors are lack of compliance with drug therapy, severe myocardial ischemia, severe infection, severe hemodynamic arrhythmias, pulmonary embolism and renal impairment. The etiology and pathophysiological mechanisms of acute right heart failure Acute right heart failure is most commonly associated with right ventricular infarction, acute massive pulmonary embolism, and right-sided heart valve disease. Right ventricular infarction rarely occurs alone and is often combined with inferior left ventricular wall infarction. Patients often have varying degrees of right ventricular dysfunction, and about 10-15% of them may have significant hemodynamic disturbances. The site of vascular occlusion in these patients is usually at the opening of the right coronary artery or prior to the emanation of the proximal right ventricular side branch. Impaired right ventricular diastolic activity due to right ventricular infarction increases right ventricular filling pressure and right atrial pressure; reduced right ventricular excretion leads to decreased left ventricular end-diastolic volume and lower PCWP. Acute massive pulmonary embolism causes obstruction of pulmonary blood flow and persistent severe pulmonary hypertension, which increases and dilates the right ventricular afterload and leads to right heart failure; reduced right ventricular blood displacement leads to changes in body circulation and cardiac function, with decreased blood pressure, tachycardia, and inadequate coronary perfusion; the effect on the respiratory system is mainly impaired gas exchange; the release of various vasoactive drugs constricts the extensive small pulmonary arteries, increasing The release of various vasoactive drugs constricts the extensive small pulmonary arteries, which increases the degree of hypoxia, and radiologically promotes the increase of pulmonary artery pressure, forming a vicious circle.