Section: Chronic Heart Failure

The cardiovascular system consists of the heart and blood vessels, with blood vessels divided into arteries, veins, and capillaries connecting arteries and veins. The heart serves as the hub linking arteries and veins and is the driving organ that propels blood circulation within the cardiovascular system. Arteries are blood vessels that carry blood away from the heart; starting from the ventricles, they repeatedly branch along their course, dividing into large arteries, medium arteries, small arteries, and micro-arteries, with gradual transitions between these types without clear boundaries. As they branch further, they become increasingly fine until finally transforming into capillaries. Veins are blood vessels that guide blood back to the atria; micro-veins originate from the venous ends of capillaries and gradually merge into small veins, medium veins, and large veins on their way back to the atria before finally emptying into the atria. Capillaries are tiny blood vessels interwoven like a network between micro-arteries and micro-veins, serving as the site of substance exchange between blood and tissue fluid.
The incidence of cardiovascular diseases has been increasing year by year, with common conditions including coronary heart disease, hypertension, arrhythmias, and rheumatic heart disease. Diseases of the cardiovascular system, especially heart diseases, undoubtedly severely affect the function of all organs in the body, posing a serious threat to human health and life. According to traditional Chinese medicine, “the heart is the sovereign organ” and “the heart governs the blood vessels,” indicating that the “heart” is the most important organ in the human body and its relationship with the blood vessels is crucial.
Section: Chronic Heart Failure
Heart failure refers to a group of clinical syndromes caused by various structural or functional heart diseases that impair the ventricular filling and/or ejection capacity. Due to decreased ventricular contractility and impaired ejection function, the cardiac output cannot meet the body’s metabolic needs, resulting in insufficient blood perfusion to various organs and tissues, accompanied by pulmonary and/or systemic congestion, mainly manifested as dyspnea, fatigue, limitation of physical activity, and edema. Cardiac dysfunction or impairment is a broader concept; when cardiac dysfunction is accompanied by clinical symptoms, it is termed heart failure, whereas having cardiac dysfunction does not necessarily mean having heart failure. Chronic heart failure (CHF) is the ultimate outcome of most cardiovascular diseases and also the leading cause of death.
Causes (---) Basic Causes
Almost all types of heart and major vascular diseases can lead to heart failure. Heart failure reflects a dysfunction in the heart’s pumping ability, namely an incomplete contraction and relaxation of the myocardium.
Pathophysiology
It is now recognized that heart failure is a progressive disease; once heart failure occurs, even if there is no new damage to the heart, under the influence of various pathophysiological changes, cardiac dysfunction will continue to worsen. When underlying heart disease damages the heart and impairs cardiac function, the body first activates multiple compensatory mechanisms. These mechanisms can maintain cardiac function at a relatively normal level for a certain period, but they also have negative effects. When compensation fails and heart failure occurs, the pathophysiological changes become even more complex.
Clinical Manifestations
Clinically, left heart failure is the most common, while right heart failure is less frequent. It is more common for left heart failure to subsequently lead to right heart failure, resulting in global heart failure, or for severe widespread myocardial disease to simultaneously affect both the left and right hearts, causing global heart failure.
(---) Left Heart Failure
Mainly characterized by pulmonary congestion and reduced cardiac output. 1. Symptoms
(1) Dyspnea
Primarily varying degrees of dyspnea, such as dyspnea after exertion, orthopnea, and paroxysmal nocturnal dyspnea; in severe cases, acute pulmonary edema may occur, which is the most serious form of dyspnea in left heart failure.
(2) Cough, sputum, hemoptysis
Cough appears early in left heart failure, often occurring at night. Coughing may ease when sitting or standing, with white, serous, foamy sputum being characteristic. Occasionally, blood streaks may appear in the sputum. When pulmonary edema occurs, the sputum becomes pink and foamy. (3) Symptoms of insufficient cardiac output
Fatigue, tiredness, dizziness, palpitations, insomnia, decreased urine output, pallor, cyanosis, etc. These are the main symptoms caused by insufficient organ and tissue perfusion and compensatory tachycardia.
2. Signs
Cardiac enlargement, mainly left ventricular enlargement. Increased second heart sound in the pulmonic valve area and diastolic gallop heard at the apex. Moist rales at both lung bases are the main signs of left heart failure in the lungs; patients lying on their side will have more rales on the lower side.
(II) Right Heart Failure

1. Symptoms
   Mainly characterized by systemic congestion.
   (1) Gastrointestinal symptoms
   Abdominal distension, loss of appetite, nausea, and vomiting caused by gastrointestinal and hepatic congestion are the most common symptoms of right heart failure.
   (2) Dyspnea on exertion
   Dyspnea due to right heart failure secondary to left heart failure already exists. Simple right heart failure is often caused by congenital heart defects with shunt or lung diseases, also presenting obvious dyspnea.
2. Signs
   (1) Edema
   Characterized by first appearing in the lowest parts of the body, often symmetrical pitting edema. In severe cases, it affects the whole body, even leading to pleural effusion and ascites.
   (2) Jugular vein signs
   Increased pulsation, fullness, and distention of the jugular veins are the main signs of right heart failure; positive hepatojugular reflux sign is even more characteristic.
   (3) Hepatic enlargement
   Hepatic enlargement due to congestion is often accompanied by tenderness; prolonged chronic right heart failure can lead to cardiogenic cirrhosis, with jaundice, impaired liver function, and massive ascites in the later stages.
   (4) Cardiac signs
   In addition to the corresponding signs of underlying heart disease, right heart failure can also present regurgitant murmurs due to significant right ventricular enlargement and tricuspid insufficiency.
   (III) Global Heart Failure
   Simultaneously exhibits clinical manifestations of both left and right heart failure; however, because right heart failure reduces right ventricular output, it can alleviate the load on the left heart, thereby reducing the manifestations of left heart failure.
3. Western Medical Diagnosis
   Western medical diagnosis of heart failure is made based on a comprehensive assessment of etiology, medical history, symptoms, signs, and objective examinations. First, there must be a clear diagnosis of organic heart disease. Symptoms and signs of heart failure are important bases for diagnosing heart failure. Fatigue and weakness caused by reduced cardiac output are non-specific and have little diagnostic value, whereas pulmonary congestion in left heart failure causes varying degrees of dyspnea, and systemic congestion in right heart failure leads to jugular vein distention, hepatomegaly, and edema—these are important bases for diagnosing heart failure.
4. Western Medical Treatment (---) Treatment Principles
   Includes early treatment of various basic causes and contributing factors that can impair cardiac function, such as coronary heart disease, hypertension, and diabetes; regulation of compensatory mechanisms in heart failure to reduce their negative effects, such as antagonizing excessive activation of neurohumoral factors and preventing myocardial remodeling; for patients with clinical heart failure, in addition to alleviating symptoms, efforts should also be made to achieve…

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Objective: ① Improve exercise tolerance and quality of life. ② Prevent or delay further worsening of myocardial damage. ③ Reduce mortality.
(2) Treatment Measures

1. Etiological Treatment
   (1) Treatment of Underlying Causes
   For patients with heart failure, the underlying cause should be carefully identified and effectively treated. For example, early control of hypertension and diabetes; pharmacological, interventional, and surgical treatments to improve myocardial ischemia in coronary artery disease; interventional procedures or valve replacement/correction surgery for chronic valvular heart disease and congenital defects—all should be performed before clinical symptoms of heart failure develop. For a small number of diseases with unknown causes, such as primary dilated cardiomyopathy, early intervention is also necessary to slow down ventricular remodeling at the pathophysiological level. The biggest obstacle to etiological treatment is late detection and treatment. Many patients are often satisfied with short-term symptomatic relief, delaying treatment until severe heart failure develops, making them unable to tolerate surgery and ultimately missing the opportunity for effective therapy.
   (2) Elimination of Triggers
   Control respiratory infections by actively using appropriate antibacterial agents. Correct arrhythmias, especially atrial fibrillation; for rapid ventricular response in atrial fibrillation, the ventricular rate should be controlled as quickly as possible, and cardioversion should be performed promptly if feasible. Potential hyperthyroidism and anemia are also causes of worsening heart failure and should be screened for and corrected.
2. General Treatment
   (1) Rest
   Limit physical activity, avoid psychological stress, and reduce cardiac workload to facilitate recovery of cardiac function. However, prolonged bed rest can easily lead to venous thrombosis and even pulmonary embolism, while also reducing digestive function and causing muscle atrophy. Therefore, patients with heart failure should be encouraged to engage in active exercise, gradually increasing aerobic activities such as walking based on the severity of their condition, starting from sitting at the bedside.
   (2) Sodium Restriction
   Patients with heart failure have increased blood volume and fluid retention, so reducing sodium intake helps alleviate edema and other symptoms. However, when using potent diuretics, excessive salt restriction can lead to hyponatremia.
3. Pharmacological Treatment
   (1) Diuretics
   Diuretics are the most commonly used drugs in the treatment of heart failure. By promoting sodium and water excretion, they reduce the volume load on the heart and improve left ventricular function, with very significant effects in relieving congestion and reducing edema. Thiazide diuretics are generally preferred, with potassium-sparing diuretics added when necessary. Potent diuretics are mainly used for acute pulmonary edema and refractory heart failure. Key principles: ① Intermittent use. ② Small doses, with careful monitoring of fluid intake/output and weight changes. ③ For mild cases, thiazides can be taken intermittently; for moderate cases, potassium-sparing diuretics can be used continuously. ④ Potassium-sparing diuretics are contraindicated in patients with renal insufficiency. Electrolyte levels should be monitored regularly to prevent electrolyte disturbances.
   (2) Vasodilators
   Vasodilators dilate peripheral arterioles, reducing resistance to cardiac ejection and lowering afterload; they also dilate peripheral veins, decreasing venous return and reducing preload. When using vasodilators, close monitoring of the patient’s condition and changes in heart rate and blood pressure before and after medication is required to prevent excessive vasodilation, inadequate cardiac filling, hypotension, and tachycardia. At the same time, attention should be paid to potential side effects of the drugs.
   (3) Angiotensin-Converting Enzyme (ACEI) Inhibitors
   The main mechanism of action of ACEI inhibitors in heart failure is: ① Inhibition of the renin-angiotensin system (RAS). In addition to vasodilation and suppression of sympathetic nervous system excitation achieved through inhibition of the circulating RAS, more importantly, inhibition of the RAS within cardiac tissue improves and delays ventricular remodeling. ② Inhibition of bradykinin degradation increases the production of prostaglandins with vasodilatory effects, while also exerting anti-proliferative effects on tissues. In summary, through ACEI inhibitors, in addition to their vasodilatory effects that improve hemodynamics and relieve congestion in heart failure, more importantly, they reduce the adverse effects of compensatory neurohumoral responses in heart failure patients, limit remodeling of the myocardium and small vessels, thereby maintaining myocardial function, delaying the progression of heart failure, and reducing long-term mortality.
   (4) Positive Inotropic Drugs
   ① Digitalis preparations: These can enhance myocardial contractility, increasing stroke volume, reducing end-diastolic pressure and volume, alleviating venous and organ congestion, and increasing blood perfusion throughout the body. Digitalis preparations can directly or indirectly reduce sinoatrial node automaticity by stimulating the vagus nerve, slowing atrioventricular conduction and thus reducing heart rate, while shortening the refractory period and repolarization period of atrial and ventricular myocardium, without increasing oxygen consumption in failing myocardium.
   ② Sympathomimetic drugs: Such as dopamine and dobutamine.
   ③ Phosphodiesterase inhibitors: These are only used in end-stage heart failure or for short-term support prior to heart transplantation.
   VI. Prevention