bubble_chart Overview

It refers to chronic primary cardiomyopathy and ventricles that, due to long-term pressure or volume overload, weaken myocardial contractility and fail to maintain cardiac output. It is classified into left-sided, right-sided, and total heart failure. Common disease causes include rheumatic heart disease, hypertension, ischemic heart disease, myocarditis, aortic valve stenosis or insufficiency, ventricular septal defect, pulmonary heart disease, and pulmonary valve stenosis. It can occur at any age, symptoms can generally be controlled, frequent relapses are common, and some patients may achieve a cure.

bubble_chart Etiology

According to pathophysiology, heart failure can be classified into the following four categories.

(1) Ventricular overload

Includes ventricular pressure overload (afterload) and volume overload (preload), which lead to secondary myocardial contractility decline and heart failure.

1. Increased pressure overload: i.e., systolic overload, where resistance encountered during systolic ejection increases. (1) Left ventricular afterload overload is seen in hypertension, aortic valve stenosis, aortic coarctation, and in adolescents, acute nephritis is a common cause of left ventricular afterload overload leading to left heart failure; (2) Right ventricular afterload overload is seen in pulmonary hypertension caused by mitral stenosis, pulmonary edema, cor pulmonale, pulmonary valve stenosis, etc.
2. Volume overload: i.e., diastolic overload, where increased venous return raises ventricular diastolic volume, leading to excessive filling. (1) Left ventricular volume overload is seen in valvular regurgitation diseases such as mitral or aortic valve insufficiency; (2) Right ventricular volume overload is seen in tricuspid or pulmonary valve insufficiency; systemic blood volume increase such as hyperthyroidism, anemia, vitamin B1 deficiency, etc., where reduced peripheral vascular resistance, increased circulating blood volume, and elevated venous return lead to right ventricular volume overload.

(2) Insufficient venous return

1. Mechanical obstruction—pericardial tamponade, pericardial constriction, tricuspid stenosis, mitral stenosis, restrictive cardiomyopathy;
2. Systemic blood volume deficiency, blood loss, vomiting, diarrhea, profuse sweating, burns, diuresis, etc.

(3) Myocardial lesions causing weakened myocardial contractility

1. Myocardial hypoxia, ischemia, infarction, myocardial fibrosis;
2. Primary cardiomyopathies including dilated, hypertrophic, and restrictive types, hypothyroidism, cardiac amyloidosis, tumors;
3. Infectious and toxic cardiomyopathies.

(4) Arrhythmias

Such as atrial fibrillation, tachyarrhythmias, and bradyarrhythmias, all of which can reduce stroke volume and cardiac output.

Precipitating factors

Common ones are as follows:

1. Infections can directly or indirectly reduce myocardial contractility and precipitate heart failure. Among infections, viral or bacterial upper respiratory infections, lung inflammation, and rheumatic activity are the most common. In elderly patients, respiratory infections rank first among precipitating factors, with 9% of elderly pneumonia patients dying from heart failure.
2. Physical exertion and emotional stress.
3. Acute myocardial infarction, chronic myocardial ischemia, and coronary insufficiency under various stress conditions.
4. Arrhythmias, especially tachyarrhythmias such as supraventricular tachycardia, atrial fibrillation, and flutter. Bradyarrhythmias such as sick sinus syndrome and high-grade atrioventricular block.
5. Excessive blood transfusion, fluid infusion, or dietary sodium intake.
6. Discontinuation, insufficient dosage, or overdose of digitalis therapy.
7. Pregnancy and childbirth—late-stage pregnancy (especially weeks 28–32) significantly increases metabolic rate and blood volume; postpartum uterine contraction increases venous return, and the exertion during childbirth can all increase cardiac load.
8. Severe anemia, hyperthyroidism.
9. Pulmonary embolism is a common precipitating factor for heart failure in the elderly.
10. Use of myocardial depressants such as beta-blockers, lidocaine, quinidine, procainamide, verapamil, etc.; broad-spectrum antitumor drugs like doxorubicin.

bubble_chart Pathogenesis

Various cardiac pathologies leading to decreased cardiac output trigger the body's compensatory mechanisms through the cardiovascular and neurohumoral systems, mobilizing reserve capacity to maintain the required cardiac output. At this stage, cardiac function remains in the compensatory phase. As the condition progresses and compensation exceeds its limits, the cardiac function enters the decompensated phase. In acute scenarios, some compensatory mechanisms may fail to activate promptly and effectively, resulting in acute heart failure. In chronic conditions, the compensatory mechanisms involve the following five aspects:

1. **Increased preload to enhance stroke volume** According to the Frank-Starling law, within the optimal length of ventricular muscle fibers (2.2 μm), the greater the stretch, the stronger the myocardial contraction and the higher the stroke volume. This compensatory mechanism is termed diastolic reserve.
2. **Enhanced sympathetic activity** Reduced cardiac output stimulates the aortic arch and carotid sinus baroreceptors, as well as the Bainbridge reflex, increasing sympathetic activity. This strengthens myocardial contractility, raises heart rate, and induces venous constriction to augment venous return. This compensation primarily relies on systolic reserve.
3. **Activation of the renin-angiotensin system** This increases water and sodium retention, expanding blood volume and preload.
4. **Myocardial hypertrophy** This reduces ventricular wall tension and improves myocardial contractility. Increased pressure load elevates ventricular wall tension, stimulating myocardial protein synthesis and parallel sarcomere replication, leading to concentric hypertrophy. According to Laplace's law, wall tension is inversely proportional to wall thickness. Early hypertrophy can normalize wall tension without cardiac dilation. However, persistent pressure overload may render hypertrophy insufficient to maintain wall tension, further worsening cardiac function.
5. **Increased oxygen extraction by peripheral tissues** This improves oxygen delivery per unit of cardiac output, widening the arteriovenous oxygen difference.

When these compensatory mechanisms exceed their limits, they become ineffective, leading to heart failure.

bubble_chart Clinical Manifestations

For patients with heart failure, achieving early diagnosis and timely treatment is the key to improving prognosis and prolonging life. Therefore, great attention should be paid to the early symptoms and signs of heart failure.

Early manifestations

(1) Symptoms The early symptoms of heart failure may be subtle and easily overlooked.

1. Manifestations of sympathetic nervous system excitation, such as sinus tachycardia, excessive sweating, and pale complexion.
2. Dyspnea or cardiac colicky pain during heavy physical labor or intense exercise, as well as manifestations of hypoxia due to increased oxygen demand caused by myocardial hypertrophy. In the early stages of left heart failure, patients may only experience atypical symptoms such as poor sleep at night, waking up breathless, or episodic chest tightness, which are easily ignored.
3. Easy fatigue and exhaustion during activity are the results of decreased myocardial contractility, reduced cardiac output, and insufficient blood supply to the systemic circulation.
4. In the early stages of right heart failure, there may only be epigastric distending pain caused by hepatic congestion and enlargement, which is easily mistaken for digestive system diseases.

(2) Signs Early signs are often more obvious than symptoms. For patients without obvious complaints, careful examination is necessary to detect heart failure early. Apart from cardiac enlargement, the main early signs include:

1. Diastolic gallop rhythm is an early sign of heart failure, commonly seen in myocardial damage, decreased ventricular tension, and cardiac enlargement. If an early diastolic gallop rhythm is audible, it is strong evidence of heart failure.
2. Pulsus alternans is characterized by alternating strong and weak radial pulses, more noticeable in the sitting position. Palpation requires patience and careful attention.
3. Jugular vein distension appears earlier than hepatomegaly and lower limb edema and is an early sign of right heart failure. When the liver begins to congest and enlarge, pressing on the liver may reveal deep internal jugular vein pulsation above the clavicle. When assessing hepatomegaly, the size of the liver should be measured from the upper border of liver dullness to the lower border along the midclavicular line on the right side. A distance greater than 11 cm is considered hepatomegaly.
4. Interstitial pulmonary edema When left atrial or left ventricular failure occurs, interstitial pulmonary edema may develop, presenting as dyspnea and inability to lie flat. An early diastolic gallop rhythm is often audible during examination, while lung auscultation may reveal no dry or wet rales or only weakened breath sounds.

Manifestations of left heart failure

Mainly characterized by pulmonary circulation congestion. This is caused by reduced left cardiac output leading to pulmonary congestion and insufficient blood supply to vital organs such as the brain and kidneys. It is commonly seen in hypertensive heart disease, coronary heart disease, aortic valve disease, and mitral regurgitation.

(1) Symptoms

1. Dyspnea is a fundamental clinical manifestation of left heart failure, resulting from pulmonary congestion and reduced lung capacity. As the severity increases, it may present as exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and acute pulmonary edema.
   (1) Exertional dyspnea: In the early stages of heart failure, exertional dyspnea may only manifest as panting, which can also occur in healthy individuals during activity. When taking a medical history, it is important to clarify whether the level of exertion that triggers dyspnea has changed. Patients often report that a specific level of exertion (e.g., climbing three flights of stairs), which previously caused no difficulty, now leads to significantly more noticeable dyspnea or requires brief pauses to rest midway. As left heart failure progresses, the level of exertion that induces dyspnea progressively decreases. It should be noted that exertional dyspnea only occurs in patients who are physically active; if the patient is at rest, exertional dyspnea will not manifest, thereby masking the presence of heart failure.
   (2) Orthopnea: Dyspnea that occurs in a supine position and is relieved by elevating the head is termed orthopnea. When taking a medical history, comparisons with past experiences should be made. Orthopnea develops rapidly, often within 1–2 minutes of lying down. The patient remains conscious, and orthopnea is an important symptom of left heart failure. The primary mechanism of orthopnea is the gravitational effect of sitting, which shifts approximately 15% of the blood volume to the dependent parts of the body, thereby reducing pulmonary congestion. Additionally, the descent of the diaphragm increases lung capacity.
   (3) Paroxysmal nocturnal dyspnea: This is an early manifestation of left heart failure. It may occur intermittently or consecutively over several nights, typically 1–2 hours after falling asleep. The patient suddenly wakes due to chest tightness and breathlessness, forced to sit up, accompanied by paroxysmal coughing, wheezing, or frothy sputum. In mild cases, the dyspnea subsides on its own after sitting for 10 minutes to an hour, allowing the patient to lie down and sleep again without discomfort during the day. In severe cases, the episode may persist with frequent coughing, pink frothy sputum, or even progression to acute pulmonary edema. Bronchospasm is a common complicating factor in paroxysmal nocturnal dyspnea, caused by bronchial mucosal congestion, which exacerbates ventilation difficulties and increases respiratory effort. Unlike orthopnea, which is relieved immediately by sitting with legs dangling, paroxysmal nocturnal dyspnea may take 30 minutes or longer to subside. The mechanisms underlying nocturnal episodes of paroxysmal nocturnal dyspnea may include: (1) reduced sympathetic cardiac stimulation during sleep; (2) increased intrathoracic blood volume and elevated diaphragm in the supine position; (3) slow reabsorption of interstitial fluid from dependent body parts, increasing blood volume; and (4) the normal inhibitory effect on the respiratory center at night. If paroxysmal nocturnal dyspnea is accompanied by a sensation of chest pressure, it should be considered as cardiac colicky pain caused by myocardial ischemia.
   (4) Acute pulmonary edema: This is the most severe form of left heart failure. For details, refer to acute heart failure.
2. Cough and hemoptysis: Cough often worsens during physical activity or when lying flat at night. Hemoptysis is a severe manifestation of pulmonary congestion, typically presenting as blood-streaked sputum.
3. Other symptoms: Due to reduced cardiac output, patients often experience fatigue and lack of strength. Insufficient cerebral oxygenation can lead to drowsiness, dysphoria, confusion, and psychiatric symptoms.

(2) Signs: In addition to the signs of the underlying heart disease, there is often an increased heart rate. An early diastolic gallop rhythm may be heard at the cardiac apex. In cases of significant left ventricular dilation, a blowing systolic murmur may be audible at the apex, caused by relative mitral valve insufficiency. Moist rales may be heard at the lung bases. A few patients may have pleural effusion, mostly on the right side, and some cases may present with pulsus alternans. Severe cases may exhibit cyanosis.

Manifestations of right heart failure

The primary clinical features are systemic edema caused by venous congestion and elevated venous pressure.

(1) Symptoms: Chronic and persistent congestion in multiple organs, such as the gastrointestinal tract, kidneys, and central nervous system, may lead to loss of appetite, nausea, vomiting, abdominal distension and fullness. Liver enlargement and stretching of the liver capsule can cause abdominal pain. Severe cases may present with jaundice (cardiac jaundice). Renal congestion can result in oliguria and increased nocturia. In severe right heart failure, cerebral hypoxia often manifests as dysphoria, restlessness, vertigo, forgetfulness, or personality changes.

(2) Signs

1. Jugular vein distension is the earliest sign of right heart failure. If the patient is in a 30° reclining or sitting position, distended external jugular veins may be visible above the clavicle. Pressing the liver may exacerbate jugular vein distension or engorgement, indicating elevated jugular venous pressure.
2. Hepatomegaly is the earliest and most important sign of right heart failure, occurring before subcutaneous edema. When right heart failure leads to excessive right atrial filling and elevated venous pressure, the inferior vena cava return is obstructed, causing hepatic congestion and enlargement. Applying gentle pressure to the right upper abdomen may intensify jugular vein distension.
3. Edema is a significant sign of right heart failure, often occurring in dependent areas such as the lower limbs and medial ankles. In supine patients, it is most prominent in the sacral region. Severe cases may progress to generalized edema, scrotal edema, pleural effusion, and ascites. Pleural effusion is more common on the right side, though bilateral effusion may occasionally occur. Ascites is a manifestation of advanced heart failure. Long-term right heart failure can lead to hepatic congestion, cardiac cirrhosis, liver hardening, often accompanied by jaundice, impaired liver function, and refractory ascites.
4. Cyanosis is more pronounced in right heart failure than in left heart failure, though dyspnea is relatively milder. Peripheral cyanosis is observed in dependent areas and peripheral body regions, such as the extremities (fingers and toes), cheeks, and earlobes. The affected areas are cold, and massage or warming can alleviate the cyanosis. The mechanism involves insufficient systemic perfusion, venous congestion with slowed blood flow, increased tissue oxygen extraction, and elevated levels of reduced hemoglobin in venous blood.
5. Cardiac signs: In addition to the signs of the underlying heart disease, an increased heart rate may be present. A diastolic gallop rhythm may be audible at the left 3rd–4th intercostal spaces near the sternum. A blowing systolic murmur may be heard at the tricuspid area, caused by right ventricular dilation leading to relative tricuspid insufficiency.

Total heart failure

Clinical manifestations of both left and right heart failure coexist. In right heart failure, reduced cardiac output may alleviate or obscure the pulmonary congestion symptoms of left heart failure.

bubble_chart Auxiliary Examination

1. X-ray examination of the heart's shape and the size of its chambers aids in the diagnosis of primary heart disease. The cardiothoracic ratio can serve as an indicator for tracking changes in heart size. The degree of pulmonary congestion can assess the severity of left heart failure. In cases of pulmonary interstitial edema, dense, short horizontal lines (Kerley B lines) may be observed in the lower lung fields near the costophrenic angles. With alveolar pulmonary edema, the hilar shadows take on a butterfly-like appearance. Chest X-rays also allow observation of the occurrence, progression, and resolution of pleural effusion.
2. Electrocardiography may reveal left ventricular hypertrophy and strain, right ventricular enlargement, and an increased terminal negative P-wave force in lead V1 (PtfV1 ≥ 0.04 mm·s), among other findings.
3. Echocardiography, using M-mode, two-dimensional, or Doppler ultrasound techniques, can measure left ventricular systolic and diastolic function. (1) Measuring left ventricular end-systolic and end-diastolic dimensions (reflecting systolic and diastolic volumes) and calculating the ejection fraction, left ventricular fractional shortening, and mean circumferential shortening rate can assess left ventricular systolic function. (2) The ratio of end-systolic wall stress (radius-to-thickness ratio) to end-systolic volume index (ESWS/ESVI) is a more precise echocardiographic measure of overall left ventricular function, reflecting performance under varying preload and afterload conditions. For left ventricular diastolic function, the mitral valve early diastolic closure rate (EF slope) and pulsed Doppler techniques can measure the ratio of early to late diastolic mitral inflow velocities (E/A) or velocity-time integrals (ETVI/ATVI). In healthy individuals, the E/A ratio exceeds 1. With left ventricular diastolic dysfunction, the EF slope decreases, and the E/A ratio is often less than 1.
4. Radionuclide and magnetic resonance imaging (MRI) studies: Radionuclide angiography can measure left and right ventricular end-systolic and end-diastolic volumes and ejection fractions. By recording radioactive activity-time curves, the maximum filling rate and filling fraction of the left ventricle can be calculated to evaluate diastolic function. Radionuclide myocardial scanning can detect abnormal wall motion and perfusion defects, aiding in etiological diagnosis. MRI, as a three-dimensional imaging technique, is less affected by ventricular geometry, allowing more accurate calculation of end-systolic and end-diastolic volumes, stroke volume, and ejection fraction. MRI's three-dimensional visualization clearly delineates myocardial and endocardial borders, enabling quantitative measurement of left ventricular mass. MRI also provides high-resolution imaging of right ventricular myocardium, yielding similar parameters for the right ventricle. Additionally, it can compare right and left ventricular stroke volumes to assess mitral and aortic regurgitation, helping evaluate the severity of underlying disease.
5. Exercise tolerance and peak oxygen consumption (VO2max) measurement: Exercise tolerance tests (maximal duration, maximal workload) can reflect cardiac reserve capacity to some extent—defined as the heart's ability to increase cardiac output in response to metabolic demands. However, exercise tolerance depends more on peripheral circulatory changes than central hemodynamics. In heart failure, peripheral vasoconstriction means increased cardiac output may not correlate with improved exercise tolerance. Oxygen consumption during exercise is the product of arteriovenous oxygen difference and cardiac output. With normal hemoglobin and no intrinsic lung disease, arteriovenous oxygen difference remains constant, so peak VO2 reflects maximal cardiac output during exercise. It is currently the best noninvasive quantitative measure of cardiac reserve, with established grading criteria: Grade A: >20 mL/kg·min; Grade B: 10–20 mL/kg·min; Grade C: 10–15 mL/kg·min; Grade D: <10 mL/kg·min.
6. Traumatic hemodynamic examination using a floating catheter and thermodilution method can measure pulmonary capillary wedge pressure (PCWP), cardiac output (CO), and cardiac index (CI). In the absence of mitral stenosis or pulmonary vascular disease, PCWP can reflect left ventricular end-diastolic pressure.

bubble_chart Diagnosis

1. Diagnostic Basis
   1. Acute left heart failure: (1) Commonly seen in severe acute myocardial infarction, hypertensive heart disease, myocarditis, grade III mitral stenosis, etc., often triggered by respiratory infections, rapid arrhythmias, excessive or rapid fluid infusion, etc.; (2) Sudden severe dyspnea, orthopnea, dysphoria, cyanosis, paroxysmal cough with wheezing, often accompanied by the expectoration of large amounts of pink frothy sputum, which may gush from the mouth and nose in severe cases. (3) Moist rales and wheezing sounds are heard throughout both lungs, with rapid heart rate and a diastolic gallop at the apex. In severe cases, cardiogenic shock may occur. (4) Chest X-ray shows blurred pulmonary vasculature, deepened hilar shadows extending butterfly-like, and decreased lung field transparency resembling a misty appearance.
   2. Acute right heart failure: (1) Often associated with a history of acute or chronic pulmonary heart disease; (2) Clinical manifestations mainly include subcutaneous edema, jugular vein distension, hepatomegaly with tenderness, cyanosis, ascites, and pleural effusion; (3) Venous pressure is significantly elevated; (4) X-ray shows marked enlargement of the cardiac shadow and widening of the superior and inferior vena cava shadows; ECG reveals features of right atrial and ventricular hypertrophy.
2. Assessment of Heart Failure Severity Clinically, heart function is still classified into four grades.
   Grade I: No limitation in physical activity; ordinary activities do not cause symptoms.
   Grade II: Slight limitation in physical activity (grade I); general activities may cause symptoms such as lack of strength, palpitation, and dyspnea.
   Grade III: Marked limitation in physical activity; grade I activities elicit the aforementioned symptoms.
   Grade IV: Severe limitation in physical activity (grade III); the patient cannot perform any physical activity and experiences symptoms even at rest.
3. Diagnosis of Early Heart Failure In addition to the early clinical manifestations mentioned above, the following auxiliary examinations may serve as references.
   (1) Chest X-ray shows venous congestion and dilation in the upper lung fields, indicating a pulmonary capillary wedge pressure (PCWP) above 2.0 kPa (15 mmHg), suggesting the presence of heart failure.
   (2) The terminal P-wave vector in lead V1 (V1Ptf) on ECG correlates to some extent with PCWP and indirectly reflects the load on the left atrium and ventricle. A V1Ptf value less than -0.03 mm·sec suggests early heart failure. For example, a positive V1Ptf value after acute myocardial infarction is a reference indicator for concurrent latent heart failure.
   (3) Hemodynamic changes precede clinical symptoms. If the left ventricular end-diastolic pressure (LVEDP) is greater than or equal to 2.0 kPa, left heart failure can be diagnosed.

bubble_chart Treatment Measures

Principles of Treatment:

1. Eliminate the initiating mechanisms of the development and progression of congestive heart failure, i.e., the prevention and treatment of the primary disease.
2. Stabilize the adaptive or compensatory mechanisms of heart failure to prevent progression to the maladaptive or decompensated stage. For example, counteract the activation of neuroendocrine systems to prevent further myocardial cell death and progressive left ventricular dilation.
3. Alleviate ventricular dysfunction, such as reducing cardiac load and increasing cardiac output.

Treatment Goals: Previous treatment strategies were largely limited to relieving symptoms caused by hemodynamic abnormalities. However, it has now been demonstrated that hemodynamic abnormalities do not correlate with prognosis. Therefore, any treatment measures should achieve the following objectives:

1. Correct hemodynamic abnormalities and alleviate symptoms;
2. Improve exercise tolerance and quality of life;
3. Prevent further aggravation of myocardial damage;
4. Reduce mortality.

Treatment Methods:

(1) Remove or limit the underlying disease cause and eliminate precipitating factors

For example, control hypertension; use medications or interventional methods to improve myocardial ischemia in coronary heart disease. For valvular heart disease, surgical treatment should be performed promptly before myocardial damage and cardiac function progress to an irreversible stage. Correct congenital heart defects and treat hyperthyroidism. Eliminate precipitating factors such as controlling infections and arrhythmias, correcting anemia, electrolyte imbalances, and acid-base disturbances. Respiratory infections are very common in heart failure patients, but clinical signs of infection such as fever and leukocytosis are often not obvious. In principle, antibiotic therapy should be routinely administered for 3–5 days. Atrial fibrillation, especially when combined with a rapid ventricular rate, can suddenly induce heart failure or even pulmonary edema. Conversely, heart failure can trigger atrial fibrillation due to elevated left atrial pressure, creating a vicious cycle. Therefore, rapid conversion of atrial fibrillation or slowing the ventricular rate is particularly important for heart failure patients.

(2) Reduce cardiac load

1. Restrict physical activity but do not emphasize complete bed rest. Provide psychological therapy or adjunctive medication if necessary.
2. Control sodium intake: In the past, strict sodium restriction was emphasized. However, since currently used diuretics have strong sodium-excreting effects, sodium restriction need not be overly strict to avoid hyponatremia.
3. Application of Diuretics Diuretics inhibit the reabsorption of sodium and water, thereby eliminating edema, reducing circulating blood volume, alleviating pulmonary congestion, and decreasing preload to improve left ventricular function. Diuretics can be divided into two major categories: potassium-excreting and potassium-sparing. The former includes loop diuretics and agents acting on the proximal distal convoluted tubule. Potassium-sparing diuretics include agents acting on the distal distal convoluted tubule and collecting duct. The doses and effects of commonly used diuretics are shown in the following table: **Commonly Used Diuretics** | Diuretic | Site of Action in Kidney | Daily Dose (mg) | Duration of Action (h) | |------------------------|--------------------------------|----------------|-----------------------| | **Potassium-Excreting:** | | | | | Hydrochlorothiazide | Distal convoluted tubule | 25–100 (oral) | 12–18 | | Chlorothalidone | Distal convoluted tubule | 25–100 (oral) | 24–72 | | Furosemide | Ascending limb of Henle's loop | 20–1000 (oral/IV) | 4–6 | | Bumetanide | Ascending limb of Henle's loop | 0.5–20 (oral) | 4–6 | | **Potassium-Sparing:** | | | | | Spironolactone | Collecting duct (aldosterone antagonist) | 25–100 (oral) | 24–96 | | Triamterene | Collecting duct | 100–300 (oral) | 12–16 | | Amiloride | Collecting duct | 5–10 (oral) | 12–18 | Persistent and excessive diuresis can lead to severe electrolyte disturbances and acid-base imbalances. Over-diuresis may also cause hypovolemia, hypotension, circulatory failure, and azotemia.

The clinical use of diuretics should avoid abuse and focus on rational application:

1. Potassium-excreting diuretics have strong potassium and sodium excretion effects and should be used intermittently to allow the body's electrolytes to restore balance. Potassium-sparing diuretics have a slower onset and weaker effect, so they should be used continuously.
2. When potassium-excreting and potassium-sparing diuretics are used together, potassium supplementation is generally unnecessary. Potassium-sparing diuretics should not be combined with potassium salts.
3. Selection should be based on the severity of the condition. Grade I patients can use thiazides or loop diuretics intermittently, such as hydrochlorothiazide 25mg twice a week or oral furosemide 20–40mg twice a week. Grade II patients should use potassium-sparing diuretics continuously combined with intermittent use of thiazides or loop diuretics, with the latter administered as furosemide 20–40mg intramuscularly once. For severe patients unresponsive to the above treatments, a combination of potassium-sparing diuretics and one potassium-excreting diuretic can be used continuously, along with intermittent use of another potassium-excreting diuretic. For example, hydrochlorothiazide can be combined with triamterene, supplemented by furosemide injections twice a week. If necessary, aminophylline 0.25–0.5g can be slowly administered intravenously to enhance diuresis by increasing glomerular filtration rate.
4. Selection should also consider renal function. In cases of renal insufficiency, loop diuretics should be chosen as their diuretic effect is unaffected by changes in acid-base balance. Potassium-sparing diuretics are contraindicated as they may cause severe hyperkalemia.
5. Adjust the dose based on therapeutic response. Adverse effects of loop diuretics are often due to their strong diuretic action. Therefore, if 20mg of furosemide already produces a diuretic effect, the dose should not be increased further. If no diuretic effect is observed, the dose can be increased, as furosemide's dose-effect relationship is linear. Hydrochlorothiazide reaches its maximum effect at 100mg/day (the dose-effect curve plateaus), and further increases are ineffective. Once the patient's rales disappear, edema subsides, and weight stabilizes, the diuretic dose should be reduced to maintenance levels.
6. Monitor for water and electrolyte imbalances, particularly hypokalemia, hypomagnesemia, and hyponatremia. Severe hypokalemia often requires simultaneous magnesium supplementation for correction. For example, 25% magnesium sulfate 10–20ml can be diluted in 500–1000ml of glucose solution for intravenous infusion. Differentiate between sodium-depletion hyponatremia and dilutional hyponatremia, as their treatment principles differ. Sodium-depletion hyponatremia occurs after excessive diuresis and is a hypovolemic hyponatremia, characterized by orthostatic hypotension, low urine output with high specific gravity. Treatment involves sodium salt supplementation—mild cases can consume salty foods, while severe cases require saline infusion. Dilutional hyponatremia, also called refractory edema, involves sodium and water retention with water retention exceeding sodium retention, resulting in hypervolemic hyponatremia. Patients exhibit low urine output with low specific gravity and, in severe cases, may experience water intoxication leading to spasms or unconsciousness. Treatment requires strict fluid restriction and focuses on water elimination. Most diuretics excrete more sodium than water and are not suitable. Short-term glucocorticoid use may be attempted, but efficacy is often poor. In cases of water intoxication, hypertonic saline can be administered as needed to relieve symptoms.
7. Be aware of drug interactions. For example, furosemide can increase the nephrotoxicity of aminoglycosides and cephalosporins. Indomethacin can counteract the effects of furosemide.
8. Thiazides adversely affect lipid and glucose metabolism and may cause hyperuricemia, which should be noted.

Application of vasodilators:

Vasodilators reduce cardiac preload and afterload by dilating capacitance and resistance vessels, decreasing myocardial oxygen consumption, and improving ventricular function. Multicenter clinical trials have shown that they can improve patient survival rates.

1. Indications:
   1. Patients with moderate to grade III chronic heart failure (primarily left heart failure) can use vasodilators if no contraindications exist.
   2. It is particularly suitable for valvular regurgitant heart disease (mitral valve, aortic valve insufficiency) and ventricular septal defects, which can reduce regurgitation or shunting and increase forward cardiac output.
2. Non-adaptation indications:
   1. Not suitable for patients with obstructive valvular diseases, such as mitral valve stenosis, aortic valve stenosis, and other left ventricular outflow tract obstructions. In these cases, the maintenance of stroke volume depends on the elevation of left ventricular filling pressure.
   2. Use with caution in patients with severe coronary artery stenosis, especially during acute myocardial infarction or episodes of acute myocardial ischemia, as a reduction in coronary perfusion pressure may exacerbate myocardial ischemia.
3. Contraindications: Hypovolemia, hypotension, renal failure.
4. Selection of preparations: Venous dilators reduce venous return and lower pulmonary capillary wedge pressure (PWP), thereby alleviating pulmonary congestion, but do not increase cardiac output. Small arterial dilators reduce afterload, facilitating myocardial contraction and increasing cardiac output. Balanced vasodilators (which dilate both arteries and veins) combine the effects of reducing pulmonary congestion and increasing cardiac output. Clinically, the choice of treatment can be based on pulmonary congestion (or PWP), arterial blood pressure, and pulse pressure (or CI). The most significant side effect is hypotension, so blood pressure must be frequently monitored during medication, especially when initiating or adjusting the dose. Both supine and standing blood pressure should be measured.
   1. Sodium nitroprusside: The most commonly used intravenous infusion preparation. It dilates both small arteries and veins simultaneously; the initial dose is 10 μg/min, increased by 5–10 μg/min every 5 minutes until the desired effect or side effects such as hypotension occur. The maximum dose is 300 μg/min.
   2. Nitrates: Primarily dilate veins and pulmonary small arteries, with weaker effects on peripheral small arteries. Sublingual nitroglycerin 0.3–0.6 mg takes effect in 2 minutes, peaks at 8 minutes, and lasts 15–30 minutes. Intravenous infusion starts at 10 μg/min, increased by 10 μg/min every 5 minutes, up to a maintenance dose of 50–100 μg/min. Topical patches are suitable for controlling paroxysmal nocturnal dyspnea. Isosorbide dinitrate sublingual 2.5–5 mg every 2 hours; oral 20–40 mg every 4 hours. Isosorbide mononitrate is the active metabolite of isosorbide dinitrate. Compared to the parent drug, it has higher bioavailability and a longer duration of action. The usual dose is 10–20 mg, 3 times/day. The main issue with long-term use of these preparations is tolerance, which limits efficacy. Intermittent dosing, with several hours of drug-free intervals each day, can reduce the development of tolerance.
   3. Angiotensin-converting enzyme inhibitors (ACE-I): Simultaneously inhibit the RAS and SNS, with effects of dilating both small arteries and veins. Inhibiting the RAS in cardiac tissue may prevent ventricular remodeling. Additionally, they help retain potassium and magnesium, correcting typical edema and electrolyte imbalances. Their mortality-reducing effect is superior to that of pure vasodilators, making them the preferred choice. However, they should not be used in patients with renal disease accompanied by renal failure, bilateral renal artery stenosis, or hypotension. The most significant side effect is hypotension, so blood pressure, renal function, and blood potassium should be closely monitored. Diuretics should be reduced to maintenance doses before adding this medication to avoid hypotension. Generally, they should not be used with potassium salts or potassium-sparing diuretics to prevent hyperkalemia. Common preparations include captopril, with an initial dose of 6.25 mg, gradually increased to 25 mg, 3 times/day. Enalapril starts at 2.5 mg, gradually increased to 10–15 mg, once/day, with effects lasting 12–24 hours.
   4. Other vasodilators: Although the combination of hydralazine and nitrate preparations can improve patient survival rates, its efficacy remains controversial, and long-term use may lead to lupus-like syndrome. Prazosin, despite its favorable acute hemodynamic effects, is highly prone to developing medicinal property tolerance, and its long-term efficacy is no better than a placebo. Calcium antagonists have the effects of dilating small stirred pulse and anti-myocardial ischemia, but their effectiveness has not been confirmed in long-term treatment, and they may even increase complications and mortality. It is advisable not to use them.

(3) Increasing Cardiac Output

Positive inotropic drugs are used to increase cardiac output by enhancing myocardial contractility, thereby shifting the ventricular function curve upward and to the left. During the adaptive or compensatory phase of heart failure, although there is a qualitative change in myocardial contractility (reduced contraction speed and prolonged contraction time), there is no quantitative decline, and the myocardial shortening capacity and ventricular emptying ability remain unimpaired. At this stage, positive inotropic drugs have no practical value. Therefore, positive inotropic drugs are only suitable for patients who already have congestive heart failure.

Digitalis Drugs

1. Mechanism of Action: Digitalis inhibits the Na+-K+-ATPase on myocardial cell membranes, leading to an increase in intracellular Na+ levels. This, in turn, promotes Na+-Ca2+ exchange, resulting in elevated intracellular Ca2+ levels, which produces a positive inotropic effect. No positive lusitropic effect has been observed. Digitalis drugs also reduce the activity of the sympathetic nervous system (SNS) and the renin-angiotensin system (RAS), restoring the baroreceptor's inhibitory effect on sympathetic impulses from the central nervous system, making them more beneficial for treating heart failure.
2. Indications: Suitable for moderate to grade III systolic heart failure patients. Efficacy is less certain for grade I patients. Particularly effective for patients with atrial fibrillation and rapid ventricular rates. Also applicable to patients with sinus rhythm.
3. Contraindications:
   1. Wolff-Parkinson-White syndrome with atrial fibrillation. Digitalis may shorten the refractory period of the accessory pathway, leading to ventricular fibrillation.
   2. Grade II or high-degree atrioventricular block.
   3. Sick sinus syndrome, especially in elderly patients.
   4. Pure diastolic heart failure, such as hypertrophic cardiomyopathy, particularly with outflow tract obstruction. Digitalis not only fails to improve diastolic function but may worsen outflow tract obstruction. For such patients with atrial fibrillation, although digitalis can slow the ventricular rate, beta-blockers, verapamil, or amiodarone are more effective.
   5. Isolated grade III mitral stenosis with sinus rhythm and no right heart failure.
   6. Acute myocardial infarction with heart failure, unless accompanied by atrial fibrillation and/or cardiac chamber enlargement, or if digitalis was already in use before the infarction. Generally, digitalis is not used, especially within the first 24 hours.
4. Selection of Preparations:
   1. Rapid-acting agents: Suitable for acute heart failure or acute exacerbation of chronic heart failure. Commonly used are Lanatoside C (0.2–0.4 mg per dose IV, total 24-hour dose 1–1.6 mg, onset in 5–10 minutes, peak effect in 0.5–2 hours) and Strophanthin K (0.25–0.5 mg per dose IV, onset in 5 minutes, peak effect in 0.5–1 hour).
   2. Intermediate- and slow-acting agents: Suitable for grade II heart failure or maintenance therapy.

bubble_chart Prevention

1. Correction of pre-existing cardiac diseases with clear causes of heart blood vessel diseases, treated with medication or surgical intervention, can prevent the occurrence of heart failure.
2. Careful identification and elimination of triggering factors can prevent the recurrence of heart failure.
3. Pharmacological prevention

bubble_chart Differentiation

1. Differentiating acute cardiogenic asthma from acute bronchial asthma can be difficult when both conditions coexist. In patients with a history of bronchial asthma who develop left heart failure, severe bronchospasm and asthma-like symptoms may occur during episodes of paroxysmal nocturnal dyspnea and pulmonary edema. The presence of pink frothy sputum makes the diagnosis of cardiogenic asthma relatively straightforward. Prolonged arm-to-tongue circulation time can aid in distinguishing between the two conditions.
2. Right heart failure must be differentiated from conditions such as pericardial effusion, constrictive pericarditis, and cirrhosis, which can also cause edema and ascites. Pericardial effusion and constrictive pericarditis may lead to jugular vein distension, elevated venous pressure, hepatomegaly, and ascites, but are characterized by weak apical impulses and pulsus paradoxus. Echocardiography can assist in differentiation. Ascites may also result from cirrhosis, nodular subperitoneal inflammation, or hypothyroidism, but these conditions typically lack jugular vein distension and hepatojugular reflux.