bubble_chart Overview

Congestive heart failure (CHF) occurs when the heart's function is impaired, and despite compensatory mechanisms, the cardiac output is insufficient to meet the metabolic needs of the body at rest or during activity. This leads to blood stasis in related parts of the body, resulting in a series of clinical symptoms and signs, making it a common clinical syndrome. Based on the onset speed, congestive heart failure can be classified into acute and chronic types. Depending on the sequence of ventricular involvement, it can be divided into left ventricular failure and right ventricular failure. According to the hemodynamic changes during heart failure, it can be categorized into low cardiac output and high cardiac output heart failure. The latter, such as in severe anemia or arteriovenous fistula, may present with heart failure even when the heart function is not significantly reduced and the cardiac output is normal or relatively increased, as it still cannot meet the body's needs. Clinically, chronic low cardiac output congestive heart failure is more common.

bubble_chart Etiology

The weakening of heart function can be due to primary myocardial diseases such as myocarditis or cardiomyopathy, or other myocardial metabolic and nutritional disorders, making the myocardium unable to bear the normal load; it may also be secondary to excessive cardiac volume or pressure load, such as congenital septal defects or aortic valve insufficiency, causing blood shunting or regurgitation, increasing ventricular volume load; or such as pulmonary valve or aortic valve stenosis, hypertension, etc., causing excessive ventricular pressure load; or both.

Congestive heart failure can occur during the fetal period and is more common in infancy and childhood. The main disease causes of heart failure in infancy are congenital cardiovascular malformations, commonly including ventricular septal defects, complete transposition of the great vessels, aortic coarctation, patent ductus arteriosus, and endocardial cushion defects. Heart failure occurring immediately after birth is most commonly seen in hypoplastic left heart syndrome and complete transposition of the great arteries. The heart failure caused by the above disease causes mostly presents as chronic congestive heart failure. Myocarditis, severe pneumonia, endocardial fibroelastosis, and paroxysmal supraventricular tachycardia are the main disease causes of acute congestive heart failure in infancy. In recent years, the incidence of Kawasaki disease has increased, becoming one of the disease causes of heart failure in infants and young children. After the age of 4, the main causes of congestive heart failure in children are rheumatic fever and cardiomyopathy: ① acute myocarditis or carditis; ② residual chronic valvular disease. In childhood, the former is predominant.

Myocarditis, such as viral myocarditis, diphtheritic myocarditis, and infectious myocarditis caused by acute streptococcal infection, often leads to acute congestive heart failure. Severe anemia and vitamin B₁ deficiency, among other diseases, can cause heart failure by affecting myocardial function. Keshan disease is a regional cardiomyopathy in China, which can occur in childhood, rarely before the age of 2, and is the main disease cause of heart failure in endemic areas.

Pediatric high-altitude heart disease is more common in high-altitude areas at 3000m and above, and it is initially believed that chronic hypoxia-induced pulmonary hypertension is the cause of this disease.

Other rare disease causes include infective endocarditis, pulmonary heart disease, vitamin B₁ deficiency, cardiac glycogen storage disease, and hypertension. Excessive intravenous fluid volume or rapid infusion can cause acute heart failure, especially in malnourished infants.

Acute pericarditis, pericardial effusion, and chronic constrictive pericarditis can all cause obstruction of venous return, leading to venous stasis, insufficient ventricular diastolic filling, decreased cardiac output, and pericardial tamponade, with symptoms similar to congestive heart failure, but the pathophysiological changes and treatment methods are different, so it does not belong to true congestive heart failure.

Acute cardiac diseases can immediately cause heart failure, but chronic cardiac diseases often have triggers for congestive heart failure, common triggers include: ① infection, especially respiratory infections, congenital cardiovascular malformations with left-to-right shunts often trigger heart failure due to concurrent pneumonia; rheumatic fever is the main trigger for rheumatic heart disease heart failure. ② Excessive fatigue and emotional stress. ③ Anemia and malnutrition can increase cardiac burden and damage the myocardium. ④ Arrhythmias, with paroxysmal supraventricular tachycardia and atrial fibrillation being common. ⑤ Excessive sodium intake. ⑥ Premature discontinuation or overdose of digitalis. Chronic congestive heart failure patients often experience recurrence of heart failure due to discontinuation of digitalis. Toxic reactions caused by digitalis overdose often lead to refractory heart failure. ⑦ Use of cardiac depressants such as propranolol can weaken the sympathetic nerve's role in enhancing myocardial contraction, triggering heart failure.

bubble_chart Pathogenesis

1. Hemodynamic changes in congestive heart failure: Under normal circumstances, the function of the ventricles varies greatly. At rest, cardiac output and ventricular work are at a basal level. Different levels of physical activity increase the body's oxygen demand, requiring varying degrees of blood supply from the heart.

⑴ Regulation of cardiac function or cardiac output: Mainly related to the following five basic factors:

1) Preload: Also known as volume load, it refers to the load borne by the heart before contraction, equivalent to the volume of returning heart blood or the blood volume at the end of ventricular diastole and the pressure it generates. According to the Frank-Starling law, within certain limits, as the end-diastolic volume and pressure of the ventricle increase, so does the cardiac output. The end-diastolic volume of the ventricle is related to the circulating blood volume, venous return blood volume, and ventricular compliance. Preload can be represented by the end-diastolic pressure of the ventricle.

2) Afterload: Also known as pressure load, it refers to the load borne by the ventricle after it begins to contract. It can be represented by the systolic pressure during ventricular ejection or the aortic pulse pressure. It is mainly determined by the resistance of the peripheral circulation, which in turn is mainly determined by the degree of dilation and contraction of the small arteries. According to the following formula.

Cardiac output ∝ (Blood pressure / Peripheral circulation resistance)

When blood pressure is constant, an increase in peripheral resistance decreases cardiac output; conversely, under the action of vasodilators, a decrease in peripheral circulation resistance increases cardiac output accordingly.

3) Myocardial contractility: Refers to the ventricular contraction ability independent of the heart's preload and afterload, related to the concentration of Ca⁺⁺ ions within myocardial cells and the conversion of energy in contractile proteins. It is mainly regulated by the sympathetic nervous system.

4) Heart rate: Cardiac output (L/min) = Stroke volume (L/beat) × Heart rate. Within a certain range, an increase in heart rate increases cardiac output. However, the diastolic period of the ventricle shortens as the heart rate increases. When the heart rate exceeds 150 beats/min, the diastolic period is too short, leading to insufficient filling and a decrease in stroke volume, resulting in a reduction in cardiac output. When the heart rate is significantly slow, below 40 beats/min, although the stroke volume increases, the cardiac output decreases.

5) Coordination of ventricular contraction: The coordinated movement of the ventricular wall during contraction is also one of the important factors in maintaining normal cardiac output. Myocardial ischemia and myocardial infarction can lead to weakened or absent local myocardial movement, asynchronous movement, or even paradoxical movement, causing the ventricular contraction to lose coordination and leading to a decrease in cardiac output.

Among the above factors, the regulatory roles of the first three are more important. Although reduced ventricular contractility is the main cause of heart failure, diastolic dysfunction causing heart failure is not uncommon and should be taken seriously.

⑵ Changes in hemodynamic indicators during heart failure:

1) Cardiac index: That is, cardiac output calculated by body surface area. The normal value for children is 3.5～5.5L/(min﹒m²), which decreases in heart failure.

2) Blood pressure: In heart failure, the stroke volume decreases, reflexively exciting the sympathetic nervous system to increase peripheral resistance, and blood pressure can be maintained at normal levels.

3) Central venous pressure: Normal value 0.59～1.18kPa(6～12cmH₂O). Reflects the end-diastolic pressure of the right ventricle, exceeding 1.18kPa in right heart failure, leading to systemic circulation static blood.

4) Pulmonary capillary wedge pressure: Normal value 0.8～1.6kPa(6～12mmHg). Reflects the end-diastolic pressure of the left ventricle, the earliest hemodynamic change in left heart failure. Reaching 2.0～2.67kPa(15～20mmHg), the heart is in the optimal filling state, and cardiac output increases to the maximum; exceeding 2.67kPa(20mmHg), pulmonary static blood and left heart failure occur.

2. Changes in generation and transformation during congestive heart failure. The heart generates force and consumes energy during the process of beating. The contraction and relaxation of the myocardium are produced by the interaction of the contractile proteins contained in the sarcomere, the basic functional unit of the myocardium, with the participation of calcium ions. The sarcomere contains two contractile proteins, myosin and actin, and two regulatory proteins, tropomyosin and troponin, which are connected to cross-bridges and have ATPase activity, capable of catalyzing ATP breakdown. Actin is present in the thin filaments, lacks independent contractile ability, and has no ATPase activity; it has receptor sites that can react with the cross-bridges. Myosin and actin are arranged in an interdigitating pattern. During myocardial relaxation, tropomyosin blocks the binding of myosin cross-bridges to the receptor sites on actin. When the concentration of Ca⁺⁺ in the sarcoplasm reaches a certain level, Ca⁺⁺ is released from the sarcoplasm to troponin, forming a Ca⁺⁺-troponin-tropomyosin complex with tropomyosin. This causes tropomyosin to contract, exposing the receptor sites on actin to bind with the myosin cross-bridges, forming an actomyosin complex. At this point, the ATPase on myosin is activated, promoting ATP breakdown to provide energy, leading to myocardial contraction. The more Ca⁺⁺-troponin-tropomyosin complexes there are, the greater the myocardial contractile force.

In heart failure, calcium metabolism in myocardial fibers is abnormal. Although the total intracellular calcium is not reduced, a large amount of Ca⁺⁺ is transferred to the mitochondria, and the Ca⁺⁺ in the sarcoplasmic reticulum decreases. The more severe the heart failure, the higher the Ca⁺⁺ content in the mitochondria. Since the affinity of mitochondria for binding Ca⁺⁺ is stronger than that of the sarcoplasmic reticulum, the release of Ca⁺⁺ slows down and decreases when the cell is stimulated, resulting in a significant reduction in Ca⁺⁺ supplied to the contractile proteins during myocardial depolarization, thereby inhibiting myocardial contraction.

In heart failure, the activity of ATPase in the myocardium decreases, affecting the conversion of chemical energy, limiting ATP decomposition and energy production, slowing down the reaction rate, and impairing myocardial contractility. The depletion of myocardial Black Catechu phenethylamine leads to insufficient conversion of ATP to cAMP. cAMP can release Ca⁺⁺ from the calcium pool, and a reduction in cAMP inhibits the release of Ca⁺⁺, further suppressing myocardial contraction.

3. Compensatory mechanisms of congestive heart failure. The various compensatory mechanisms of heart failure aim to regulate cardiac output by directly or indirectly altering preload, afterload, and myocardial contractility, with the ultimate goal of maintaining or approaching normal cardiac output at rest. To some extent, these mechanisms may be hemodynamically beneficial in heart failure, but excessive compensation can be harmful. The main compensatory mechanisms of heart failure are:

(1) Ventricular dilation: After myocardial involvement, ventricular dilation occurs as an initial compensatory mechanism to maintain stroke volume under increased volume or pressure load. According to the Frank-Starling principle, within certain limits, the greater the diastolic volume, the greater the myocardial contractility and stroke volume, thereby maintaining the balance between cardiac output and venous return. However, this compensatory mechanism has limitations, as stroke volume decreases when end-diastolic volume significantly increases.

(2) Ventricular hypertrophy: This increases myocardial contractility by adding more contractile units, thereby enhancing stroke volume. However, myocardial hypertrophy itself can become a factor in heart failure, as the blood supply to hypertrophied myocardium may decrease, and in some cases, it can cause outflow tract obstruction, exacerbating cardiac dysfunction.

(3) Neurohumoral regulation: This is the primary compensatory process in heart failure. It involves the activation of the sympathetic nervous system, renin-angiotensin-aldosterone system, atrial natriuretic peptide, and vasopressin.

1) Sympathetic nervous system: A decrease in cardiac output reflexively increases sympathetic nervous system activity. In heart failure patients, plasma norepinephrine levels can be 2-3 times higher than normal, and 24-hour urinary norepinephrine excretion is significantly elevated. The increase in plasma norepinephrine levels is directly correlated with left ventricular function, pulmonary capillary wedge pressure, and cardiac index. Sympathetic activation increases heart rate, enhances myocardial contractility, and causes peripheral vasoconstriction, leading to increased cardiac output and maintenance of blood pressure, partially compensating for hemodynamic abnormalities in heart failure. However, sustained and excessive sympathetic activation can reduce adenylate cyclase activity mediated by cardiac β₁ receptors, impairing myocardial contractility, and activate the renin-angiotensin-aldosterone system, increasing renin and angiotensin II levels.

2) Renin-angiotensin-aldosterone system: It is a major neurohumoral regulatory process in heart failure. The reduction in renal blood flow perfusion and the stimulation of β₁ adrenergic receptors in the juxtaglomerular apparatus during heart failure are the primary mechanisms for activating the renin-angiotensin-aldosterone system; however, a low-salt diet and the use of diuretics causing hyponatremia during heart failure are also reasons for activating this system. In heart failure patients, plasma renin activity, angiotensin II, and aldosterone levels are all elevated. Angiotensin II has a vasoconstrictive effect on peripheral blood vessels that is 40 times stronger than norepinephrine; it can also promote sympathetic nerve excitation, enhance the release of norepinephrine, and further cause peripheral vasoconstriction. Additionally, angiotensin II promotes the production and release of aldosterone from the adrenal cortex, leading to water and sodium retention. The activation of this system inactivates bradykinin through the action of converting enzymes and can decrease the concentration of prostaglandin E, hindering vasodilation. These changes can compensate for part of the hemodynamic process of heart failure, but excessive activation can further increase the preload and afterload of the heart and cause fluid imbalance. In recent years, the use of converting enzyme inhibitors can inhibit the aforementioned excessive compensation, transforming the pathophysiological changes of heart failure into a benign cycle, and thus, they have been widely used in the treatment of heart failure.

3) Atrial Natriuretic Peptide (ANP): Also known as atrial peptide, it is an important cardiac endocrine hormone discovered in recent years. It is synthesized by atrial myocytes and stored in special granules within the atrial muscle. It acts on target organs such as the kidneys and vascular smooth muscles, producing diuretic, natriuretic, vasodilatory effects, and inhibiting renin and aldosterone. In healthy infants, the blood ANP level is 129-356 pg/ml (average 227 pg/ml) 2-4 days after birth, significantly higher than the 2-109 pg/ml (average 47 pg/ml) in other age groups. Due to postnatal circulatory changes, decreased pulmonary vascular resistance, increased pulmonary blood flow, and increased systemic vascular resistance, these changes may be accompanied by increased atrial pressure and volume, thereby stimulating the atrial wall to release ANP. Patients with congenital cardiopulmonary diseases have blood ANP levels 2-10 times higher than the control group. Factors promoting ANP release include: ① Increased left and right atrial pressure due to heart failure; ② Expanded extracellular fluid volume during heart failure, leading to increased atrial volume. Observations have shown that peripheral blood ANP concentration is positively correlated with the severity of heart failure, and ANP levels decrease as the condition improves. Therefore, ANP measurement can assess the degree of heart failure and the effectiveness of treatment. However, in the late stage of heart failure [third stage], patients with a longer course of the disease may have reduced peripheral blood ANP levels, possibly due to long-term hypersecretion leading to depletion.

During heart failure, ANP secretion increases, producing vasodilatory, natriuretic, and diuretic effects, counteracting the overactivation of the renin-angiotensin-aldosterone system, which is beneficial for curbing the progression of the vicious cycle of heart failure. However, the relative effect of endogenous ANP increase is weak and usually insufficient to counteract the powerful effects of the activated sympathetic nervous system and the renin-angiotensin-aldosterone system. Another reason is the decreased sensitivity of local ANP receptors in the kidneys and other organs during heart failure. Therefore, although peripheral blood ANP levels are significantly elevated in heart failure patients, the natriuretic, diuretic, and vasodilatory effects are usually not observed. In recent years, synthetic ANP has been used intravenously to treat heart failure, and significant reductions in heart rate, right atrial pressure, pulmonary capillary wedge pressure, and peripheral vascular resistance have been observed, along with increased cardiac index and stroke work index, and decreased blood aldosterone and norepinephrine levels. This may open a new pathway for treating heart failure.

4) Vasopressin: Synthesized in the hypothalamus and stored in the posterior pituitary, it is released in small amounts into the bloodstream. Vasopressin has antidiuretic effects, increasing water reabsorption, hence it is also called antidiuretic hormone. In heart failure patients, blood vasopressin levels can be twice the normal level, though the mechanism of this increase is unclear. Increased vasopressin secretion can cause extracellular fluid retention, reduced free water excretion, hyponatremia, and peripheral vasoconstriction. These effects can exacerbate heart failure symptoms.

(4) Changes in Red Blood Cells: In children with heart failure, the concentration of 2,3-diphosphoglycerate in red blood cells increases, helping red blood cells release more oxygen to tissues as they pass through.

The symptoms of congestive heart failure are partly related to the side effects brought about by the aforementioned compensatory mechanisms. Increased end-diastolic pressure accompanying ventricular dilation leads to increased atrial pressure and pulmonary congestion. Increased sympathetic tone causes arteriovenous constriction, redistribution of blood flow, flusteredness, and increased sweating. The contraction of small stirred pulses in most tissues and organs increases peripheral vascular resistance, thereby increasing the heart's afterload. Fluid retention exacerbates edema. Ventricular hypertrophy increases myocardial oxygen consumption, offsetting its beneficial effects due to relative ischemia.

In heart failure, the perfusion of various tissues and organs in the body decreases, along with pulmonary static blood, causing tissues to be in a hypoxic state. Additionally, the clearance of metabolic products is affected, leading to acidemia and hypoxemia. Consequently, the contractility of myocardial cells is inhibited. Furthermore, pancreatic ischemia and insufficient insulin secretion impair the myocardium's ability to utilize glucose as an energy source, further suppressing myocardial function. The generation and transformation in children with heart failure are significantly altered, with most experiencing respiratory and/or metabolic acidosis, and low levels of blood sodium and chloride.

bubble_chart Clinical Manifestations

The beauty and signs of heart failure are mainly caused by the dysfunction of cardiac compensation, sympathetic nerve excitation, venous system congestion, increased blood volume, and sodium and water retention. Due to differences in age, disease causes, and hemodynamic changes, the clinical characteristics vary among different age groups in children.

1. Symptoms in Infants and Toddlers: Newborns often exhibit drowsiness, apathy, lack of strength, refusal to feed, or vomiting, among other non-specific symptoms. The symptoms of heart failure in infants and toddlers are often atypical, generally onsetting acutely and progressing rapidly, potentially presenting as a fulminant course. Acute myocarditis and endocardial fibroelastosis often present with a sudden onset of heart failure. The child may suddenly develop dyspnea within minutes to hours, with suprasternal and intercostal retractions during inspiration, and rapid breathing, often exceeding 60 breaths per minute, even reaching over 100. Concurrently, vomiting, dysphoria, profuse sweating, pallor or cyanosis, cold extremities, rapid and weak pulse, tachycardia, gallop rhythm, and dry rales in the lungs may occur, presenting as acute congestive heart failure. Congenital heart defects such as septal defects often present as chronic congestive heart failure, with a slower onset, primarily manifesting as feeding difficulties, dyspnea after minimal feeding, fatigue, refusal to eat, and failure to gain weight. Dysphoria, profuse sweating, a desire to be held and lean on an adult's shoulder (a manifestation of orthopnea in infants), dyspnea even at rest, frequent coughing, weak crying, and sometimes hoarseness due to the left recurrent laryngeal nerve being compressed by the dilated pulmonary artery. The precordium is prominent, the apical impulse is enhanced, and the cardiac borders are enlarged. Hepatosplenomegaly with rounded edges and tenderness is present. Pulmonary rales are often absent or only wheezing is heard. Jugular vein distension and edema are not obvious and can only be assessed by observing weight gain.

2. Symptoms in Older Children: The manifestations of heart failure in older children are similar to those in adults, with a generally slower onset. Left and right heart failure present as follows:

(1) Left heart failure: Seen in rheumatic mitral valve disease and hypertensive heart disease, the main symptoms are due to acute or chronic pulmonary congestion. Clinical manifestations include: ① Dyspnea: Often the earliest symptom, initially mild and only occurring after activity, the child's activity is limited, easily fatigued, and eventually dyspnea occurs even at rest, with rapid and shallow breathing. The cause of dyspnea is mainly due to increased reflex stimulation of the respiratory center caused by pulmonary congestion. Dyspnea often worsens when lying flat, so the child prefers to sit up, presenting orthopnea, as sitting reduces pulmonary congestion due to gravitational effects on blood pooling in the lower extremities and abdomen, reducing the volume of blood returning to the right ventricle. Additionally, sitting lowers the diaphragm, making thoracic expansion easier. Paroxysmal nocturnal dyspnea is uncommon in children. ② Cough: Due to pulmonary congestion and bronchial mucosal congestion, presenting as a chronic dry cough. ③ Hemoptysis: May occur due to incomplete oxygenation of blood passing through pulmonary vessels. ④ Cyanosis: Generally severe, due to incomplete oxygenation of blood passing through pulmonary vessels. ⑤ Wheezing or moist rales may be heard in the lungs. ⑥ Acute pulmonary edema: Due to acute left heart failure, pulmonary congestion rapidly worsens, and fluid exudes from capillaries into the alveoli. The child experiences extreme dyspnea, orthopnea, pallor or cyanosis of the skin, cyanosis of the lips, cold extremities, rapid and weak or impalpable pulse, occasionally alternating pulse (strong and weak pulses alternately), decreased blood pressure, tachycardia often with gallop rhythm, wheezing and moist rales in both lungs, frequent coughing with frothy sputum, and in severe cases, a large amount of frothy fluid may gush from the mouth and nostrils.

(2) Right heart failure: It can be caused by left heart failure, as pulmonary congestion and increased pulmonary arterial pressure during left heart failure increase the systolic load on the right ventricle; congenital cardiovascular anomalies accompanied by pulmonary arterial hypertension often lead to right heart failure. The symptoms of right heart failure are mainly caused by systemic congestion, with clinical manifestations including: ① Edema: Initially seen in the dependent parts of the body, severe cases have two main causes: one is the increased reabsorption of sodium and water by the kidneys, leading to an increase in extracellular fluid; the other is the elevated systemic venous pressure, causing more fluid to seep into the interstitial space from capillaries than is returned via capillaries and lymphatic vessels. ② Hepatomegaly often accompanied by upper abdominal pain: In acute heart failure, abdominal pain and liver tenderness are more pronounced, with a rounded liver edge; hepatomegaly may appear before edema, making it one of the early symptoms of right heart failure. In chronic heart failure, long-term hepatic congestion can lead to jaundice. ③ Jugular vein distension: Jugular vein distension is more noticeable when sitting and becomes more pronounced when the liver is pressed (hepatojugular reflux sign). ④ Loss of appetite, nausea, vomiting, due to gastrointestinal venous congestion. ⑤ Oliguria, with grade I proteinuria and a few red blood cells, due to renal congestion.

3. Evaluation of Cardiac Function Status In the initial stage [first stage] of general heart failure, it can be mainly left or right heart failure. As the condition progresses, it manifests as total heart failure, with total heart failure being more common clinically. Typically, the cardiac function status of patients is classified into four levels based on the patient's medical history, clinical manifestations, and the degree of exercise tolerance:

Grade I: Only signs of heart disease, no symptoms, unrestricted activity, and compensated cardiac function.

Grade II: Symptoms appear with larger amounts of activity, with Grade I activity restriction.

Grade III: Symptoms appear with slightly more activity, with significantly restricted activity.

Grade IV: Symptoms present even at rest, completely losing the ability to work.

The above cardiac function classification is applicable to adults and children, but not to infants. Some authors believe that most infant heart failure is caused by a large left-to-right shunt leading to increased pulmonary circulation blood volume and congestion, which is different from adults where cardiac pump dysfunction is the main issue. Accurate description of feeding history, respiratory rate, respiratory patterns such as nasal flaring, three depressions sign, and moaning respiration, heart rate, peripheral perfusion, diastolic gallop rhythm, and the degree of liver enlargement should be included in the cardiac function classification. The evaluation of infant cardiac function is classified as follows.

0 line: No manifestations of heart failure.

Grade I: Also known as Grade I heart failure. The indicators are each feeding amount <90ml, or feeding time requires more than 40 minutes, respiratory rate >60 times/min, abnormal respiratory patterns, heart rate >160 times/min, liver enlargement 2-3cm below the rib, and gallop rhythm.

Grade II: Also known as Grade III heart failure. The indicators are each feeding <75ml, or feeding time requires more than 40 minutes, respiratory rate >60 times/min, abnormal respiratory patterns, heart rate >170 times/min, gallop rhythm, liver enlargement more than 3cm below the rib, and poor peripheral perfusion. Based on the above clinical manifestations of heart failure, a grading score for infant heart failure is established, which can be used as a reference for the cardiac function classification of infant heart failure.

bubble_chart Diagnosis

1. Chest X-ray: The heart shadow shows generalized enlargement with weakened cardiac pulsation. Increased lung markings, prominent interlobar pleural membrane, and a small amount of pleural effusion indicate pulmonary static blood. The size of each cardiac chamber and pulmonary blood status can assist in the diagnosis of disease cause. In infants, the normal thymic heart shadow may be misdiagnosed as cardiomegaly, which should be noted.

2. Electrocardiogram (ECG): May show atrial and ventricular hypertrophy, repolarization changes, and rhythm abnormalities, aiding in the diagnosis of disease cause and providing reference for the use of digitalis medications.

3. Echocardiography: Provides precise data on the anatomical structure of the heart and great vessels, hemodynamic changes, cardiac function, and pericardial conditions, aiding in the diagnosis of disease cause and the evaluation of pathophysiological, systolic, and diastolic functions.

4. Blood gas analysis and pH measurement: In pulmonary edema and left heart failure, PaO₂ decreases, and PaCO₂ increases, leading to respiratory acidosis. Severe heart failure with poor tissue perfusion and accumulation of acidic metabolites may result in metabolic acidosis.

5. Blood electrolyte and glucose measurement: Assess serum sodium, potassium, and chloride levels. Neonatal hypoglycemia can lead to heart failure. Additionally, it can detect myocardial ischemia, renal function, and anemia, aiding in the determination of disease cause and guiding treatment. {|108|}

bubble_chart Treatment Measures

The therapeutic goal is to improve cardiac contractility and reduce preload and afterload on the heart. The following measures can be taken.

1. General Treatment: Rest can reduce the burden on the heart and is an extremely important treatment measure. Various methods should be adopted to avoid dysphoria and crying, and to relieve tension. Sedatives such as oral phenobarbital or injection of phenobarbital sodium can be used, and morphine 0.1～0.2mg/(kg·time) can be used subcutaneously if necessary, with a maximum dose not exceeding 10mg. Maintaining a semi-recumbent position can alleviate dyspnea. The diet should be restricted in salt, generally reducing the sodium content in the daily diet to 0.5～1g. Provide easily digestible and nutritious food. It is advisable to eat small, frequent meals. Oxygen inhalation can be decided based on the degree of dyspnea. Keep bowel movements smooth. Appropriate antibiotics can be used in case of bacterial infection.

2. Digitalis Drugs

(1) The effects of Digitalis: Digitalis and other similar drugs are the main drugs for treating heart failure. Their effects are as follows:

1) Effects on the heart: The main benefit of digitalis in congestive heart failure is to increase myocardial contractility, increase stroke volume, complete ventricular emptying, and reduce end-diastolic pressure, thereby alleviating venous congestion symptoms. Digitalis can increase the contractility of both in vivo and isolated, normal and failing hearts, although the mechanism is not fully understood. Some evidence suggests that digitalis inhibits the (Na⁺-K⁺)-ATPase on the myocardial cell membrane, weakening the active transport of Na⁺ and K⁺ during diastole, leading to increased intracellular Na⁺ and decreased K⁺. Increased intracellular Na⁺ can promote the release of Ca⁺⁺ from the sarcoplasmic reticulum calcium pool to the actin, increasing Ca⁺⁺ and thereby enhancing myocardial contractility. Many also believe that digitalis only inhibits (Na⁺-K⁺)-ATPase at toxic doses, thus proposing two receptor theories: one receptor can bind with therapeutic doses of digitalis, promoting Ca⁺⁺ influx during depolarization and releasing Ca⁺⁺ from the sarcoplasmic reticulum calcium pool, thereby enhancing myocardial contractility; toxic doses of digitalis inhibit another receptor on the myocardial cell membrane, namely (Na⁺-K⁺)-ATPase, and it is believed that decreased intracellular K⁺ is the pathophysiological basis for arrhythmias during digitalis toxicity.

The inotropic effect of digitalis on myocardial oxygen consumption varies depending on the functional state of the myocardium. For normal myocardium, it increases total oxygen consumption. Conversely, for failing myocardium, due to the positive inotropic effect of digitalis, end-diastolic pressure is reduced, ventricular volume is decreased, myocardial tension is lowered, and it is often accompanied by a significant slowing of the heart rate. The above effects on reducing myocardial oxygen consumption outweigh the increase in oxygen consumption due to increased myocardial contractility, resulting in a net effect of significantly reduced myocardial oxygen consumption.

2) Effects on peripheral blood vessels: Rehmannia has a tendency to increase the tension of peripheral resistance vessels in normal individuals, thereby leading to an overall increase in peripheral resistance, which exacerbates the afterload on the heart. Therefore, although the contractility of the heart increases in normal individuals taking Rehmannia, the stroke volume does not increase or may even decrease due to the simultaneous increase in afterload. In contrast, in untreated congestive heart failure, the peripheral resistance is initially high due to increased sympathetic tension. However, after effective treatment with Rehmannia, which improves heart failure, the peripheral resistance may remain unchanged or decrease.

There is no consensus on the hemodynamic effects of Digitalis on a heart that is functionally compensated but already enlarged. Most believe that after taking Digitalis, such a heart can improve myocardial work capacity, reduce the end-diastolic pressure of ventricular relaxation to achieve the same stroke work and cardiac output, thereby enhancing myocardial work efficiency and increasing the reserve of contractile energy, and reducing the degree of cardiac enlargement.

3) Slowing heart rate: A secondary effect of Digitalis is to slow the heart rate. On one hand, due to the strengthening of myocardial contractility, venous pressure decreases, thus reflexively eliminating compensatory tachycardia and slowing the sinus rhythm; on the other hand, Digitalis acts on the cardiac conduction system, prolonging the refractory period of the atrioventricular node and slowing conduction, therefore significantly reducing the ventricular rate in cases of atrial fibrillation with a fast ventricular rate.

4) Diuresis: The use of Digitalis in heart failure can induce diuresis, mainly due to increased stroke volume, increased renal blood flow, and increased glomerular filtration rate. Additionally, Digitalis directly acts on the ascending limb of the loop of Henle and the distal tubule, inhibiting sodium reabsorption to produce a diuretic effect, although the direct diuretic effect of Digitalis is mild.

(2) Preparations and usage of Digitalis drugs: Commonly used Digitalis drugs can be divided into two categories, namely slow-acting and fast-acting. The speed of onset is proportional to the speed of disappearance. Commonly used slow-acting drugs include Digitalis glycosides; fast-acting drugs include digoxin (a derivative of Digitalis glycosides), lanatoside C (Cedilanid), and strophanthin K, with dosages shown in Table 1.

Table 1 Clinical Application of Digitalis Drugs

Digitalis Preparations	Administration Method	Total Digitalization Dose (mg/kg)	Average Daily Maintenance Dose	Onset of Effect	Peak Effect	Disappearance of Effect
						Toxic Effects	Complete Disappearance of Effect
Digitalis Glycosides	Oral or Intramuscular Injection	Newborns 0.015～0.03	1/10 of Digitalization Dose	Oral: 2 hours	Oral: 6～9 hours	3～10 days	10～20 days
		Before 2 years old 0.03～0.04
		After 2 years old 0.02～0.03		Intramuscular: 30 minutes	Intramuscular: 2～8 hours
Digoxin (a derivative of Digitalis glycosides)	Oral	premature labor 0.03～0.035	1/4 Rehmannia dose (divided into 2 doses)	Oral: 2 hours	Oral: 4～8 hours	1～2 days	4～7 days
		Full-term infant 0.03～0.05
		Before 2 years old 0.05～0.06
		After 2 years old 0.03～0.05
		Total dose should not exceed 2.0mg
	Intravenous	Before 2 years old 0.03～0.04		Intravenous: 10 minutes	Intravenous: 1～2 hours
		After 2 years old 0.02～0.03
Cedilanid (lanatoside C)	Intravenous	Before 2 years old 0.03～0.04		10～30 minutes	1～2 hours	1 day	2～4 days
		After 2 years old 0.02～0.03
Strophanthin K	Intravenous	Before 2 years old 0.006～0.012		3～5 minutes	1.5～1 hour	6 hours	1 day
		After 2 years old 0.005～0.01

After oral administration, Rehmannia glycosides are almost 100% absorbed in the intestines, so the oral dose is the same as the injection. After oral administration of Rehmannia glycosides, 26% enters the enterohepatic circulation. The half-life is 5 to 7 days. It is mainly metabolized in the liver, hydrolyzed into products without cardiotonic activity, and excreted from the body. The daily excretion of body reserves is 15-20%. After oral administration, about 80% of digoxin is absorbed through the small intestine, so the injection dose should be smaller than the oral dose, approximately 2/3 of the oral dose. 6.8% enters the enterohepatic circulation, and the half-life is about 1.5 days. The daily excretion of body reserves is 33%. Most of it is excreted unchanged by the kidneys, so patients with renal insufficiency are prone to poisoning. Cedilanid is for intravenous injection, oral absorption is irregular, intramuscular absorption is slow, and it cannot achieve rapid effects. It is mainly excreted by the kidneys, and its half-life is consistent with that of digoxin. Strophanthin K begins to take effect 3 to 5 minutes after injection, and its effect completely disappears within 24 hours. It is mainly excreted unchanged by the kidneys. Strophanthin G has a stronger effect than the former, and its dosage should be smaller. The excretion rate of various Rehmannia preparations is proportional to the body reserves, so it is obviously inappropriate to calculate the body reserves based on a fixed daily amount.

The positive inotropic effect of Digitalis is linearly related to its dosage, meaning that even a small dose of Digitalis can increase myocardial contractility. As the dose increases, the positive inotropic effect also increases until toxicity occurs. Therefore, the optimal therapeutic effect achieved with Digitalis can be considered as Digitalization. Subsequently, a certain amount of the drug can be administered daily to compensate for the portion lost through metabolism and excretion. The clinical manifestations of heart failure being essentially controlled include: ① decreased heart rate and respiration; ② reduction in liver size; ③ increased urine output, reduction in edema or weight loss; ④ cardiac retraction; ⑤ improved appetite and mental state.

To reduce the occurrence of Digitalis toxicity, there is a trend towards lowering the digitalizing dose and adopting a daily maintenance dose therapy. The daily excretion of Digitalis is related to the body's storage, meaning that more is cleared if the body stores more, and less is cleared if the body stores less. Initially, instead of giving a "digitalizing dose," a daily maintenance dose is administered. After 4 to 5 half-lives, a stable and effective plasma concentration can be achieved, which is a dynamic equilibrium where the daily oral dose equals the clearance. This plasma concentration is the same as that achieved by first giving a "digitalizing dose" followed by a maintenance dose. For example, the half-life of digoxin is 1.5 days, and after 6 to 8 days of continuous maintenance dosing, the half-life of Digitalis glycosides, which is longer (5 to 7 days), requires about a month to reach a stable plasma concentration. However, infants and young children often experience acute onset of heart failure with rapid progression, so for severe heart failure in children, Digitalization is initially performed to quickly correct heart failure. After satisfactory clinical results are achieved with Digitalization, a daily maintenance dose is used to maintain a stable plasma concentration. Evidence suggests that infants and children are less sensitive to Digitalis than adults, thus their tolerance per unit body weight is greater than that of adults. Sensitivity to Digitalis increases with age, so the dose for children is relatively higher than for adults. The mechanism is unclear, but newborns and premature infants, due to immature liver and kidney function, are more sensitive to Digitalis and prone to toxicity, so the dose should be relatively small. The duration of Digitalis maintenance therapy depends on whether the cause of heart failure can be resolved. If the disease cause can be controlled in a short time, maintenance therapy is often unnecessary or can be stopped after a few days, such as in severe pneumonia complicated by heart failure. If the disease cause is difficult to control and cardiac compensation is poor, long-term Digitalis maintenance therapy may be required, lasting months or years, such as in rheumatic heart disease complicated by heart failure or endocardial fibroelastosis. As the patient's weight and age increase, the maintenance dose should also be adjusted accordingly.

The choice of Digitalis drugs depends on the severity and urgency of the condition. In pediatrics, digoxin is commonly used. For general congestive heart failure, a daily maintenance dose therapy can be adopted, with oral digoxin administered at 8-10 μg/kg for newborns, 10-15 μg/kg for infants, and 8-10 μg/kg for school-age children, divided into two doses. For more severe cases, the initial oral dose of digoxin is half the digitalizing dose, with the remaining half divided into two doses, taken 6 hours apart. For acute congestive heart failure, acute pulmonary edema, critical conditions, or unconsciousness and vomiting preventing oral intake, a rapidly acting Digitalis preparation can be injected intravenously, with half the digitalizing dose of digoxin given initially, and the remaining half divided into two doses, administered 4 to 6 hours apart. If maintenance therapy is needed, oral digoxin maintenance dose can be started 12 hours after the last injection. Recent reports suggest the use of β-methyldigoxin for treating heart failure in children. This drug is completely absorbed orally, takes effect within 15 minutes, and its plasma concentration decreases after 4 hours, with a half-life of 2 to 8 hours, maintaining its effect for 8 days. Its pharmacological effects are similar to digoxin. Due to its complete oral absorption and slightly longer half-life, the dose should be reduced by 1/4 to 1/5 compared to digoxin.

(3) Digitalis toxic reaction: The therapeutic dose of digitalis is close to the toxic dose, approximately 60% of the toxic dose. The more severe the heart failure and the worse the cardiac function, the closer the therapeutic dose is to the toxic dose, making toxicity more likely to occur. Digitalis toxicity is also prone to occur in cases of impaired liver and kidney function, electrolyte disturbances, hypokalemia, hypomagnesemia, hypercalcemia, myocarditis, myocardial metabolic disorders, and after extensive diuresis.

The toxic reactions of Digitalis are as follows: ① Gastrointestinal symptoms include nausea and vomiting. ② Arrhythmias, commonly seen as first-degree atrioventricular block, second-degree type I atrioventricular block (Wenckebach phenomenon), ventricular and atrial premature beats, non-paroxysmal junctional tachycardia, severe sinus bradycardia, and sinoatrial block. Other conditions include paroxysmal supraventricular tachycardia with atrioventricular block and third-degree atrioventricular block. ③ Neurological symptoms such as drowsiness, unconsciousness, and visual disturbances are relatively rare. When using various cardiac glycosides (such as various Digitalis glycosides and strophanthin), gastrointestinal toxic reactions are often absent, and arrhythmias frequently occur. It is advisable to perform an electrocardiogram before and after using Digitalis to promptly detect toxic reactions.

The application of radioimmunoassay to measure serum digoxin concentration can assist in the diagnosis of Digitalis poisoning. Six hours after oral administration or four hours after intravenous injection of digoxin, the ratio of its content in myocardial tissue to serum concentration is relatively constant (e.g., 33:1 for digoxin), and blood should be drawn for measurement at this time. The effective serum concentration of digoxin for general therapeutic doses in children is 1.3 ng/ml, and in infants, it is 2.8 ng/ml. Generally, a serum digoxin concentration of >2 ng/ml in children, >3 ng/ml in infants, and >4 ng/ml in newborns is considered indicative of Digitalis poisoning. Although there is some overlap between therapeutic and toxic serum concentrations, radioimmunoassay of serum concentration is generally considered a valuable method. However, the final determination of Digitalis poisoning should still be based on the combination of disease conditions and clinical circumstances. Measuring serum digoxin concentration can assist in the diagnosis of Digitalis poisoning and also provide the following information: ① Whether the digoxin dosage is adequate; ② Early diagnosis of accidental digoxin ingestion; ③ Monitoring of digoxin dosage in patients with renal failure. Some have found that the serum digoxin concentration in infants not receiving digoxin medication can reach 0.35-1.5 ng/ml when measured by radioimmunoassay, and the explanation for this phenomenon has yet to be concluded.

Once symptoms of poisoning appear, the use of Rehmannia and diuretics should be immediately discontinued. For milder cases, oral potassium chloride at 1-1.5 mmol/(kg·d) [75-100 mg/(kg·d)] can be administered. For severe arrhythmias, potassium chloride solution (20-40 mmol in 500 ml of 5% glucose solution) should be administered intravenously under ECG monitoring at a rate of 0.5 mmol/kg per hour, with the total dose not exceeding 2 mmol/kg. Potassium administration should be stopped immediately once arrhythmia resolves or hyperkalemic ECG changes appear. Intravenous potassium is contraindicated in patients with hyperkalemia or renal failure. In cases of third-degree or near third-degree atrioventricular block caused by Rehmannia poisoning, intravenous potassium chloride is contraindicated to avoid exacerbating conduction disturbances. Intravenous phenytoin is effective for severe ventricular arrhythmias caused by Rehmannia poisoning, with a typical dose of 2-3 mg/(kg·dose), dissolved in 10 ml of 5% glucose solution and administered slowly over 5-10 minutes. For older children, the initial dose is usually 100 mg, which can be repeated after 10-15 minutes if ineffective, up to a maximum of three times. Lidocaine is also effective for correcting ventricular arrhythmias, with an intravenous dose of 1 mg/kg, repeated if necessary after 10-15 minutes, with a total dose not exceeding 5 mg/kg. If effective, a maintenance infusion of 20-30 μg/(kg·min) can be administered. For second-degree and third-degree atrioventricular block, atropine 0.01-0.03 mg/(kg·dose) can be administered intravenously, and a pacemaker may be necessary. Recently, the use of digoxin-specific antibodies has shown good results in treating severe hyperkalemia, central nervous system depression, and third-degree block caused by high-dose digoxin poisoning. The antibody dose is calculated based on the estimated digoxin body load, with approximately 100 mg of digoxin-specific antibody required for every 1 mg of digoxin.

(4) Precautions for using Digitalis injections: ① Understand the child's use of Digitalis in the past 2-3 weeks, including all dosage forms, dosages, and methods of administration. ② Master the usage and dosage of Digitalis, and at least be familiar with the usage and dosage of one oral and one intravenous preparation, as Digitalis poisoning is often caused by improper dosage. ③ The digitalization dose and maintenance dose of Digitalis must be analyzed specifically for each case, and the calculated dose is for reference only. ④ Understand the various causes of Digitalis poisoning, such as electrolyte disturbances. ⑤ Perform an ECG before using Digitalis for comparison. After using Digitalis, the ECG may show Digitalis-type ST-T changes (mainly ST segment oblique descent and T wave decrease or biphasic; in leads with the main QRS wave direction downward, the ST segment rises obliquely and the T wave stands up or becomes biphasic). And the Q-T interval shortens. This Digitalis poisoning and overdose can only be diagnosed as Digitalis poisoning when arrhythmia occurs. A series of ECG examinations before and after medication can be used as a reference for diagnosing Digitalis poisoning. ⑥ Calcium has a synergistic effect with Digitalis, so calcium preparations should be avoided when using Digitalis drugs, but in cases of hypocalcemia, calcium salt injections can still be given as appropriate. ⑦ Measure the serum concentration of Digitalis.

3. Black Catechu Phenolamine drugs β-adrenergic receptor agonists such as adrenaline, isoproterenol, dopamine, dobutamine, etc., act on β-adrenergic receptors, have positive inotropic effects, strengthen myocardial contractility, and increase cardiac output. They are commonly used in emergencies, especially in heart failure with hypotension, and in low cardiac output syndrome after cardiac surgery. Commonly used are:

(1) Dopamine: directly acts on the β₁-adrenergic receptors of the myocardium, strengthens myocardial contractility, and can selectively act on dopamine receptors, dilating renal, mesenteric, cerebral, and coronary vessels. After medication, the cardiac index increases, peripheral vascular resistance decreases, and glomerular filtration rate and renal blood flow increase, producing a diuretic effect. The effect of dopamine is dose-related, small dose 2～5μg/(kg﹒min), excites dopamine receptors, increases urine output; medium dose 5～10μg/(kg﹒min), excites β receptors, enhances myocardial contractility, accelerates heart rate, and dilates renal vessels, increasing urine output; large dose >μg/(kg﹒min), excites α receptors, constricts peripheral vessels, and raises blood pressure. The initial dose should be small, about 1～2μg/(kg﹒min), and then gradually increased, up to 2～10μg/(kg﹒min).

(2) Dobutamine: a newly synthesized dopamine side chain inducer, acts on adrenergic receptors. It has a strong positive inotropic effect on the myocardium. The initial intravenous drip is 2～5μg/(kg﹒min), gradually increasing to 10～15μg/(kg﹒min). Some reports suggest that this drug is more effective than dopamine.

(3) Isoproterenol: has the effect of increasing myocardial contractility, but has the disadvantage of increasing heart rate and lowering blood pressure. The dosage is 0.05～0.5μg/(kg﹒min), intravenous drip.

(4) Epinephrine: can increase cardiac index and blood pressure, dosage 0.05～1.0μg/(kg﹒min), intravenous drip. The above drugs act quickly, have a short duration, and should be continuously infused intravenously. Intravenous injection takes effect in 1～2 minutes, peaks in 10～15 minutes, and the effect disappears 10～15 minutes after stopping the medication.

Isoproterenol and epinephrine are prone to cause rapid arrhythmias and are mostly used in patients with bradycardia.

4. Other drugs that enhance myocardial contractility are a class of positive inotropic drugs that are not Digitalis or β receptor agonists. Those that have been used clinically include:

(1) Amrinone: It may enhance myocardial contractility by inhibiting phosphodiesterase II and increasing cyclic adenosine monophosphate (cAMP) concentration, thereby increasing intracellular calcium ion concentration. It also acts on peripheral blood vessels, causing vasodilation and reducing preload and afterload. It is commonly used for chronic congestive heart failure, such as dilated cardiomyopathy. It is well absorbed orally, with effects appearing within 1 hour and lasting for more than 5 hours. The initial oral dose for adults is 100 mg daily, divided into 3 doses, gradually increasing to 300-600 mg daily. For intravenous injection, the initial dose is 0.25-0.75 mg/kg, injected within 2-3 minutes, with effects appearing within 2 minutes, peaking at 10 minutes, and lasting for 1-1.5 hours. Maintenance is then continued at 5-10 μg/(kg·min). After administration, cardiac output increases, and left ventricular filling pressure and peripheral resistance decrease. Long-term use results in side effects in 40% of patients, including hypotension, arrhythmias, thrombocytopenia, fever, hepatitis, gastrointestinal dysfunction, and nephrogenic diabetes insipidus. For pediatric intravenous injection, the initial dose is 0.5 mg/kg, followed by maintenance at 5-10 μg/(kg·min). Experience with pediatric use is still limited.

(2) Milrinone: It is 10 to 40 times more potent than amrinone, with fewer side effects and good oral efficacy. Adults take 7.5 to 10 mg orally every 6 hours, and long-term use has not revealed the side effects associated with amrinone. After administration, the cardiac index increases, pulmonary capillary wedge pressure decreases, and exercise tolerance improves. It can also be administered intravenously. For children, the initial intravenous dose is 0.01 to 0.5 μg/kg, followed by a maintenance dose of 0.1 to 1.0 μg/(kg·min). Currently, there is limited experience in pediatrics.

5. Diuretics: Increased preload is a significant pathophysiological change in heart failure. Using diuretics to reduce preload is an important measure in treating heart failure. When heart failure is not controlled after general treatment and digitalis use, or in cases of severe edema and acute pulmonary edema, diuretics should be used alongside digitalis. Strong diuretics produce a diuretic effect, reduce blood volume, decrease venous return, lower left ventricular filling pressure, and reduce pulmonary capillary wedge pressure, thereby alleviating preload. For acute left heart failure and pulmonary edema, potent diuretics like ethacrynic acid or furosemide are preferred. These drugs primarily act on the ascending limb of the loop of Henle, inhibiting the reabsorption of sodium and chloride ions. Intravenous administration shows effects within 10 to 20 minutes, peaks at 2 hours, and lasts for 6 to 8 hours. For chronic congestive heart failure, thiazides are typically combined with potassium-sparing diuretics, using intermittent therapy to maintain efficacy—4 days of medication followed by 3 days off—to prevent electrolyte imbalances. Heart failure patients may develop secondary hyperaldosteronism, and adding spironolactone can reduce elevated aldosterone levels and increase urine output. For severe edema and refractory heart failure, ethacrynic acid or furosemide may also be used. Long-term use of any diuretic can easily lead to electrolyte imbalances, so close monitoring is essential.

6. Vasodilators: Vasodilators can improve cardiac function in patients with acute or chronic heart failure, increasing stroke volume. The primary mechanism is the dilation of resistance vessels and venous capacitance vessels, reducing cardiac load, mainly afterload. Vasodilators can be divided into three categories: ① Venous dilators like nitroglycerin and isosorbide dinitrate, which lower elevated left ventricular end-diastolic pressure and reduce pulmonary congestion; ② Arterial dilators like phentolamine and hydralazine, which decrease systemic vascular resistance, thereby increasing cardiac output; ③ Combined arterial and venous dilators, which alleviate pulmonary congestion and increase cardiac output, such as nitroprusside and prazosin. By reducing both preload and afterload, vasodilators enhance stroke volume, reduce pulmonary congestion, improve myocardial energy consumption, and stabilize myocardial electrical activity, thereby reducing ventricular tachyarrhythmias. Blood pressure and heart rate should be closely monitored during vasodilator use. Hemodynamic monitoring is ideal if available. Blood pressure changes depend on the type of drug, dose, administration rate, and the patient's condition. A significant drop in blood pressure should be avoided to prevent worsening myocardial hypoxia. Generally, a systolic blood pressure drop of around 1.33 kPa (10 mmHg) is appropriate. Vasodilators are effective in improving hemodynamics only when they do not significantly affect arterial blood pressure. Low baseline blood pressure is not a contraindication for vasodilators, as hemodynamic improvement may lead to increased stroke volume and a potential rise in blood pressure. Heart rate usually remains stable during vasodilator use. Start with a low dose and slow rate, gradually increasing if the effect is insufficient. Common vasodilators include:

(1) Sodium nitroprusside: Selectively acts directly on vascular smooth muscle, reducing the tension in small stirred pulse and small venous walls, with a stronger effect on the former, thereby reducing preload and afterload. It acts quickly and has a short duration of action, so it needs to be administered by intravenous drip. The usual dosage is 0.25 to 8 μg/(kg·min), starting at 0.25 μg/(kg·min) and gradually increasing until the average stirred pulse pressure drops by 0.667 to 1.333 kPa (5 to 10 mmHg) or clinical symptoms improve, generally around 2.5 μg/(kg·min). When discontinuing the medication, the dosage should also be gradually reduced, or prazosin can be administered orally to maintain efficacy. The infusion of sodium nitroprusside can produce cyanide, which binds to hemoglobin to form cyanomethemoglobin, causing toxic reactions. For those who use the medication for more than 72 hours, blood thiocyanate levels should be monitored; toxic reactions can occur at levels of 5 to 10 mg/dl, including nausea, vomiting, and lack of strength. At higher blood concentrations, disorientation, psychiatric symptoms, stupor, and even convulsions may occur. Sodium nitroprusside degrades upon exposure to light, so it should be protected from light and used immediately after preparation.

(2) Phentolamine (benzamine, phentolamine, regitine): It is an α-adrenergic receptor blocker. It mainly dilates small arteries, reduces afterload, decreases peripheral vascular resistance, and increases peripheral blood volume, with a lesser effect on venous capacitance vessels. Additionally, it has positive inotropic and chronotropic effects, acts rapidly, and has a short duration of action. It is suitable for intravenous infusion, and its effects disappear 15 minutes after intravenous injection. Generally, 5-10 mg can be added to 100-200 ml of glucose solution for intravenous drip, starting at 10 drops per minute, or 0.1-0.3 mg/(kg·dose) dissolved in 20 ml of glucose solution, administered slowly intravenously over 10-15 minutes. The maximum single dose for older children should not exceed 10 mg, and it can be repeated every 0.5-1 hour if necessary, or administered at 1-2 μg/(kg·min) by intravenous drip. It is effective for severe left heart failure and pulmonary edema. The drawbacks of this drug include a tendency to cause tachycardia, sudden hypotension, and arrhythmias, so close monitoring is required during use.

(3) Prazosin: It is an α-adrenergic receptor blocker that dilates small arteries and veins, reducing cardiac load, primarily by reducing afterload. The effect lasts 4-6 hours after oral administration, with an initial dose of 5 μg/(kg·dose) every 6 hours. Side effects include dizziness, fatigue, weakness, flusteredness, and headache. Patients are prone to orthostatic hypotension when taking the first dose, but this reaction does not occur with subsequent doses. Some reports indicate that intravenous nitroprusside was used to treat 6 cases of severe congestive heart failure that did not respond to conventional digitalis and diuretics. The primary heart conditions were postoperative congenital heart disease and congestive cardiomyopathy. Symptoms improved in 4 cases after intravenous nitroprusside. After discontinuing nitroprusside, oral prazosin was continued along with daily digitalis and diuretics, resulting in varying degrees of improvement, control of heart failure, and reduction in the cardiothoracic ratio.

Other vasodilators include nitroglycerin, isosorbide dinitrate, hydralazine, and phenoxybenzamine, which are still in the experimental stage in pediatric clinical practice.

(4) Combination of vasodilators and catecholamine drugs: Some authors report that combining vasodilators with catecholamine drugs, such as nitroprusside with dopamine or nitroprusside with adrenaline, sometimes yields better results than using either drug alone. This is particularly suitable for heart failure accompanied by hypotension. Low-dose dopamine can increase stroke volume and prevent excessive blood pressure drop.

Reports indicate that the combination of nitroprusside at 1.5-10.8 μg/(kg·min) and adrenaline [0.15-0.45 μg/(kg·min)] was used to treat 13 children with low-output heart failure after open-heart surgery, achieving significant results. Although the cardiac index slightly increased with nitroprusside alone, it did not exceed 2 L/(min·m²). After adding adrenaline, the cardiac index increased in all cases, exceeding 2 L/(min·m²). In adult patients with chronic congestive heart failure, the combination of nitroprusside (40-100 μg/min) and dopamine [5-7 μg/(kg·min)] also improved left ventricular function more significantly than using nitroprusside or dopamine alone. Vasodilator therapy is mainly used for patients with refractory heart failure who do not respond well to cardiac and diuretic treatments.

7. Angiotensin-converting enzyme inhibitors (ACE inhibitors) The main mechanism of their treatment for heart failure is to inhibit the overcompensation effect of the renin-angiotensin-aldosterone system. By inhibiting the activity of angiotensin-converting enzyme, the production of angiotensin II is reduced, leading to the dilation of small stirred pulses, a decrease in peripheral resistance, and a reduction in afterload. Additionally, the production of aldosterone is reduced, alleviating water and sodium retention, decreasing preload, and improving cardiac function. Furthermore, ACE inhibitors have some non-angiotensin-dependent effects: ① They affect the kallikrein-kinin system, increasing the level of bradykinin. Bradykinin has a vasodilatory effect, particularly more pronounced in the kidneys. ② They increase the synthesis of prostaglandins, leading to vasodilation, improved renal function, enhanced diuresis, resulting in a decrease in preload and left ventricular filling pressure. ③ They reduce sympathetic nervous system excitability, inhibit the secretion of norepinephrine, and weaken vasoconstriction. ④ They inhibit the effect of vasopressin. ACE inhibitors have achieved significant results in the treatment of heart failure. Commonly used preparations include:

(1) Captopril: Also known as Capoten and Lopirin. 65-75% is absorbed through the gastrointestinal tract after oral administration, reaching peak blood concentration after 1 hour. The plasma half-life is 1.9±0.5 hours, and it is undetectable in the blood after 8 hours, excreted through the kidneys. It should be taken 3-4 times daily. The plasma half-life is prolonged in uremic patients. When used with digoxin, it can increase the blood concentration of digoxin by about 10%, but the toxic effects of digoxin are not increased. When used to treat heart failure, the total potassium content and serum potassium concentration increase, so potassium supplements should be reduced and potassium-sparing diuretics should be used with caution.

After the application of captopril, the short-term hemodynamic effects include a decrease in systemic and pulmonary vascular resistance, a decrease in pulmonary capillary wedge pressure, an increase in cardiac index and stroke index, a reduction in myocardial oxygen consumption, and an improvement in the oxygen supply-demand ratio. Symptoms such as shortness of breath and lack of strength are alleviated, heart function improves by I-II grades, exercise tolerance increases, urine output increases, and the incidence of arrhythmias in heart failure is reduced, possibly related to the correction of hypokalemia and the suppression of sympathetic nerve excitement. Long-term effects: The improvement in hemodynamics is maintained, heart function further improves, and the cardiothoracic ratio decreases.

The oral dosage for newborns starts at 0.1mg/kg per dose, 2-3 times daily, then gradually increases to 1mg/(kg·d). For infants and preschool children, 0.5-5mg/(kg·d), divided into 3 doses. For adolescents, 6.25-50mg per dose, 2-3 times daily. Start with a small dose and monitor blood pressure, then gradually increase the dose. Most patients can tolerate it, and side effects are rare. Side effects include hypotension, granulocytopenia, taste disturbances, oral ulcers, rash, fever, proteinuria, and renal function injury. Patients with pre-existing sick sinus syndrome are prone to severe bradycardia.

(2) Enalapril: Also known as Vasotec. Compared with captopril, it has the following differences: ① The onset of action is slower, reaching peak concentration 4 hours after oral administration, with a long half-life of about 33 hours, and can be taken 1-2 times daily. ② Blood pressure decreases more significantly after administration, so blood pressure should be monitored, but other side effects are less common.

The initial oral dose is 0.1mg/kg daily, divided into 2 doses, gradually increasing to 0.5mg/(kg·d). It has been reported that enalapril was used to treat 8 infants with severe heart failure, aged 4 days to 12 weeks, including one case each of myocarditis with left-to-right shunt. After 2 weeks of treatment, except for one case of osteomyelitis, the heart failure in the remaining 7 cases significantly improved, hyponatremia recovered, and hematuria decreased. Blood pressure decreased by less than 1.3kPa (10mmHg) after the first dose. The average dose was 0.26mg/(kg·d) [0.12-0.43mg/(kg·d)].

Angiotensin-converting enzyme inhibitors can be used in combinatio