Pediatric congestive heart failure

Introduction to Congestive Heart Failure in Children Congestive heart failure (congestive heartfaiture) is due to cardiac function impairment. Although the cardiac output can not meet the systemic metabolic needs of resting or active after exerting compensatory ability, blood accumulation occurs in related parts of the body, resulting in a series of Clinical signs and symptoms are common clinical syndromes. According to the rapid onset of congestive heart failure, it can be divided into acute congestive heart failure and chronic congestive heart failure; according to the order of left and right ventricle, it can be divided into left ventricular failure and right ventricular failure; hemodynamics according to heart failure The changes can be divided into low cardiac output and high cardiac output heart failure, the latter such as severe anemia or arteriovenous fistula, even if the heart function is not significantly reduced, the cardiac output is normal or correspondingly increased, dare not meet the needs, and Heart failure occurs. Clinically, chronic low cardiac output with congestive heart failure is more common. basic knowledge The proportion of the disease: the incidence rate is about 0.001% -0.002%, more common in children with severe pneumonia Susceptible people: young children Mode of infection: non-infectious Complications: arrhythmia premature beats

Causes of congestive heart failure in children

Cause:

pathology:

The weakening of cardiac function may cause the myocardium to bear normal load due to primary myocardial lesions such as myocarditis or cardiomyopathy, or other myocardial metabolic dystrophy. It may also be secondary to cardiac capacity or stress overload, such as congenital Sexual septal defect or aortic regurgitation, resulting in blood shunt or reflux, increased ventricular volume load; or pulmonary stenosis or aortic stenosis, high blood pressure, etc., excessive ventricular pressure overload; or both .

Congestive heart failure can occur in the fetal period, more common in infancy in childhood, the main cause of heart failure in infancy is congenital cardiovascular malformation, common ventricular septal defect, complete large blood vessel translocation, aortic coarctation And patent ductus arteriosus and endocardial pad defect, left ventricular dysplasia syndrome occurs after birth, complete in arterial transposition, the most common cause of heart failure is chronic congestive heart failure , myocarditis, severe pneumonia, endocardial fibroelastosis and paroxysmal supraventricular tachycardia in infants with acute congestive heart failure, the incidence of Kawasaki disease increased in recent years, is one of the causes of infant heart failure The cause of congestive heart failure in children after 4 years old is mainly rheumatic fever and cardiomyopathy: 1 acute myocarditis or carditis; 2 left chronic valvular disease, mainly in children before.

Myocarditis such as viral myocarditis, diphtheria myocarditis and acute streptococcal infection caused by infectious myocarditis often occur in acute congestive heart failure, severe anemia and vitamin B1 deficiency and other diseases, due to affecting myocardial function, can cause heart failure, Keshan The disease is endemic cardiomyopathy in China, which can occur in childhood. It is rare before 2 years old and is the main cause of heart failure in endemic areas.

Pediatric plateau heart disease is more common in high altitude areas of 3000m above sea level. It is preliminarily believed that pulmonary hypertension caused by chronic hypoxia in the plateau is the cause of this disease.

Other rare causes such as infective periostitis, pulmonary heart disease, vitamin B1 deficiency, cardiogenic glycogen accumulation disease and hypertension, etc., excessive intravenous fluids or speed, can cause acute heart failure Especially in malnourished babies.

Acute pericarditis, pericardial fluid and chronic constrictive pericarditis can cause venous return obstruction, venous stagnation, insufficient ventricular diastolic filling, decreased cardiac output, pericardial occlusion, symptoms similar to congestive heart failure However, its pathophysiological changes and treatment methods are different, so it does not belong to true congestive heart failure.

Acute heart disease can cause heart failure immediately, but chronic heart disease often causes congestive heart failure. Common causes are: 1 infection, especially respiratory infection, left-to-right shunt congenital cardiovascular malformation often induced by pneumonia Heart failure; rheumatic fever is the main cause of heart failure in rheumatic heart disease, 2 overwork and emotional agitation, 3 anemia and malnutrition can aggravate heart burden and damage myocardium, 4 arrhythmia, paroxysmal supraventricular tachycardia Speed and atrial fibrillation are common, 5 sodium intake is too much, 6 premature digitalis or digitalis overdose, chronic congestive heart failure patients, often can cause recurrence of heart failure due to stop taking digitalis, digitalis overdose The toxic reaction often causes refractory heart failure. 7 The application of inhibiting cardiac drugs such as propranolol can often attenuate the role of sympathetic nerves in strengthening myocardial contractile function and induce heart failure.

1. Changes in hemodynamics during congestive heart failure Under normal circumstances, the function of the ventricle changes greatly. The resting state cardiac output and ventricular work are at the basic level. Different levels of physical activity make the body need oxygen to increase. Different levels of blood supply needs.

(1) Regulation of cardiac function or cardiac output: mainly related to the following five basic factors:

1) Preload: Also known as volumetric load, it refers to the load that the heart is subjected to before contraction, which is equivalent to the blood volume of the returning heart or the end-diastolic blood volume and the pressure generated by it. According to Frank-Starling's law, within a certain limit, At the end of diastolic volume and pressure increase, cardiac output also increased, ventricular end-diastolic volume and circulating blood volume, venous return blood volume and ventricular compliance, preload can be expressed by ventricular end-diastolic pressure.

2) Afterload: also known as pressure load, refers to the load that the ventricle bears after contraction, which can be expressed by systolic blood pressure or aortic pressure when the ventricle is ejected. It is mainly determined by the resistance of the surrounding circulation, which is mainly determined by The degree of relaxation and contraction of the small arteries is based on the following formula.

Cardiac output (blood pressure / peripheral circulation resistance)

When the blood pressure is constant, the increase in peripheral resistance causes the cardiac output to decrease; conversely, under the action of the vasodilator, the peripheral circulation resistance is reduced, and the cardiac output is correspondingly increased.

3) Myocardial contractility: refers to the ventricular contraction ability unrelated to the anterior and posterior load of the heart. It is related to the Ca++ ion concentration in the cardiomyocytes, the contraction of protein and energy, and is mainly regulated by sympathetic nerves.

4) Heart rate: cardiac output (L/min) = stroke volume (L / time) × heart rate, within a certain range, heart rate increases, cardiac output increases, but ventricular diastolic period decreases with heart rate, when heart rate exceeds At 150 times/min, the ventricular diastolic phase is too short, the filling volume is too low, the heart rate is decreased, the cardiac output is decreased, and the heart rate is significantly slow. Below 40 beats/min, although the stroke volume is increased, The cardiac output is reduced.

5) Coordination of ventricular contraction: Coordination of wall motion during ventricular contraction is also one of the important factors for maintaining normal cardiac output. In myocardial ischemia and myocardial infarction, myocardial local motion may be weakened or disappeared, motion is not synchronized, and even contradictory movement is formed. , the ventricular contraction lost coordination, resulting in decreased cardiac output.

The regulation of the first three factors is more important. Although the reduction of ventricular contraction is the main cause of heart failure, it is not uncommon for diastolic dysfunction to cause heart failure.

(2) Changes in hemodynamic parameters during heart failure:

1) Heart index: The cardiac output is calculated according to the body surface area. The normal value of children is 3.5-5.5L/(min·m2), which is reduced in heart failure.

2) Blood pressure: The heart rate is reduced in heart failure, and the reflex sympathetic nerve increases the peripheral resistance and the blood pressure can maintain normal.

3) Central venous pressure: normal value 0.59 ~ 1.18kPa (6 ~ 12cmH2O), reflecting right ventricular end-diastolic pressure, more than 1.18kPa in right heart failure, systemic bleeds.

4) Pulmonary capillary wedge pressure: normal value of 0.8 ~ 1.6kPa (6 ~ 12mmHg), reflecting left ventricular end-diastolic pressure, is the earliest hemodynamic change of left heart failure, up to 2,0 ~ 2.67kPa (15 ~ 20mmHg At the time of the heart, the heart is in an optimal filling state, and the cardiac output is increased to the maximum; more than 2.67 kPa (20 mmHg), pulmonary blood stasis and left heart failure occur.

2. Biochemical changes in congestive heart failure The heart produces both force and energy in the process of pulsation. The contraction and relaxation of the myocardium are the involvement of calcium ions in the contractile proteins contained in the sarcolemma of the basic functional unit of the myocardium. The contraction protein contained in the sarcomere is produced by the interaction of calcium ions, and the sarcoma contains myocin and actin. Two regulatory proteins, tropomycin and troponin, with transverse bridges, have ATPase activity, can catalyze the decomposition of ATP, and muscle fibrin is present in thin filaments, without the ability to shrink by itself, no ATPase activity, which has a receptor site, can react with Hengqiao, and myosin and myofibin are cross-aligned. When myocardial relaxation, between tropism, blocking myosin cross-bridge and myofibrillar The binding site is combined. When Ca++ reaches a concentration in the sarcoplasm, Ca++ is released from the sarcoplasm to the gonadotropin, and combines with the tropomin to form a Ca++-gonimin-pro-myosin complex, thus the promyosin The contraction of the muscle fibrin is exposed to the transverse bridge of myosin to form a muscle fibrin protein complex. At this time, the ATPase on the myosin is activated, causing ATP to decompose, providing energy and causing myocardial damage. Contraction, the more Ca++-nein protein-pro-myosin complex, the greater the myocardial contractility.

In heart failure, calcium metabolism in myocardial fibers is abnormal. Although there is a lot of total calcium in the cells, a large amount of Ca++ is transferred to the mitochondria, Ca++ is reduced in the sarcoplasmic reticulum, and the heart failure is heavier. The more Ca++ content of mitochondria is due to mitochondria combined with Ca++. The affinity is stronger than that of the sarcoplasmic reticulum. When the cells are excited, the release rate of Ca++ is slowed down, and the Ca++, which supplies the contractile protein during myocardial depolarization, is significantly reduced, and the myocardial contraction is inhibited.

In heart failure, myocardial ATPase activity is reduced, affecting the conversion of chemical energy, limiting ATP decomposition and energy production, slowing down the reaction rate, affecting myocardial contractility, depletion of myocardial catecholamine, and converting ATP into cAMP. Insufficient effect, cAMP can release Ca++ from the calcium pool, reduce cAMP, inhibit the release of Ca++, and inhibit myocardial contraction.

3. Compensatory mechanism of congestive heart failure The various compensatory mechanisms of heart failure are to directly or indirectly change the anterior and posterior sodium and myocardial contractility of the heart to regulate cardiac output. The ultimate goal is to achieve cardiac output. It can maintain or approach normal levels in a large resting state, which may be beneficial to heart failure hemodynamics to a certain extent, but excessive compensation is harmful. The main compensatory mechanism of heart failure is:

(1) Ventricular enlargement: After myocardial involvement, in the case of increased pressure load, the ventricular expansion is to maintain the initial compensatory mechanism of stroke volume. According to the Frank-Starling principle, within a certain limit, the diastolic volume is more Large, myocardial contractility is also greater, the amount of stroke increases, thus maintaining a balance between cardiac output and returning blood volume, however, the role of this compensatory mechanism is limited, when the end-diastolic capacity is significantly increased, the heart The stroke volume is reduced.

(2) ventricular hypertrophy: increase myocardial contraction unit to increase the contractility of the myocardium, thereby increasing the stroke volume, but cardiac hypertrophy itself can become one of the factors of heart failure, because the hypertrophic myocardial blood supply can be correspondingly reduced, in a certain In some cases, the outflow tract can be blocked, which can exacerbate cardiac dysfunction.

(3) regulation of neurohumoral fluid: it is the main compensatory process of heart failure, and the activation of the sympathetic nervous system, renin-angiotensin-aldosterone system, tenorin and vasopressin may occur.

1) Sympathetic nervous system: The sympathetic nervous system can be reflexively caused by the decrease of cardiac output. The concentration of norepinephrine in the heart of patients with heart failure can be increased by 2 to 3 times compared with normal people. 24-hour urinary norepinephrine The content is also significantly higher than normal, and the increase of norepinephrine concentration in the blood is directly related to left heart function, pulmonary capillary wedge pressure and cardiac index. Sympathetic excitation can accelerate heart rate and strengthen myocardial contractility. Peripheral vasoconstriction, resulting in increased cardiac output and maintenance of blood pressure, can partially compensate for hemodynamic abnormalities in heart failure, but sustained and excessive increase in sympathetic tone can cause cardiac 1 receptor-mediated adenylate cyclase Reduced activity, affecting myocardial contractility; and activation of the renin-angiotensin-aldosterone system, elevated levels of renin and angiotensin II.

2) Renin-angiotensin-aldosterone system: a major neurohumoral regulation process in heart failure, reduced renal blood perfusion during heart failure, and stimulation of 1 sympathetic receptors in the juxtaglomerular apparatus to activate renin- The main mechanism of the angiotensin-aldosterone system; however, low-salt diet and diuretic-induced hyponatremia in heart failure are also responsible for the activation of the system. Plasma renin activity, angiotensin II and aldosterol levels in patients with heart failure Increased, angiotensin II increased peripheral vasoconstriction 40 times stronger than norepinephrine; can promote sympathetic nerve excitation, strengthen norepinephrine release, further peripheral vasoconstriction, in addition, angiotensin II It also promotes the production and release of aldosterone from the adrenal gland, causing sodium retention. The system activates the inactivation of bradykinin by converting the enzyme, and can reduce the concentration of prostaglandin E, which hinders vasodilation. Repay part of the hemodynamic process of heart failure, but excessive can further aggravate the pre- and post-load and body fluid disorders of the heart. In recent years, the application of transferase inhibitors can inhibit the above-mentioned excessive Compensating the pathophysiology of heart failure conversion to a virtuous cycle, therefore, it has been widely used to treat heart failure.

3) Atrial natriuretic peptide: also known as atrial peptide, is an important type of cardiac endocrine hormone discovered in recent years. It is synthesized by atrial myocytes and stored in special particles of atrial muscle. It acts on target organs such as kidney and vascular smooth muscle to produce diuretic. Sodium, dilated blood vessels and inhibits renin and aldosterone. The level of atrial natriuretic peptide in healthy children is 129-356pg/ml (average 227pg/ml) 2 to 4 days after birth, which is significantly higher than other age groups of 2109pg. /ml, an average of 47pg/ml, due to postnatal changes in circulation, decreased pulmonary vascular resistance, increased pulmonary blood flow and increased vascular resistance, these changes may be accompanied by increased atrial pressure and volume, thereby stimulating atrial natriuretic atrial natriuretic peptide, congenital The atrial natriuretic peptide in patients with cardiopulmonary disease is 2 to 10 times higher than that of the control group. The factors that promote the release of atrial natriuretic peptide include:

1 heart failure causes left and right atrial pressure to increase;

2 In the case of heart failure, the extracellular fluid capacity is enlarged, resulting in an increase in atrial volume. The observation shows that the concentration of atrial natriuretic peptide in the peripheral blood is positively correlated with the severity of heart failure, and the condition improves the atrial natriuretic peptide. Therefore, the determination of atrial natriuretic peptide can determine the degree of heart failure. And the effect of treatment, but in the late stage of heart failure, patients with longer course of disease, peripheral blood atrial natriuretic peptide decreased, may be due to long-term hypersecretion, leading to exhaustion.

Increased atrial natriuretic peptide secretion during heart failure, resulting in dilated blood vessels, sodium and diuretic effects, anti-reoxygenation of the renin-angiotensin-aldosteron system, has a national role, is beneficial to curb the progression of the vicious circle of heart failure, but The increase in endogenous atrial natriuretic peptide is relatively weak, usually insufficient to counteract the powerful role of the activated sympathetic nervous system and the renin-angiotensin-aldosterone system, and the other is the local atrial natriuretic peptide such as the kidney during heart failure. The sensitivity of the receptor is decreased. Therefore, although the level of atrial natriuretic peptide in peripheral blood of patients with heart failure is significantly increased, it usually does not appear to have sodium, diuretic, and vasodilator effects. In recent years, intravenous infusion of synthetic atrial natriuretic peptide has been used to treat heart. Decline, and observed heart rate, right atrial pressure, pulmonary capillary wedge pressure and peripheral vascular resistance have a significant decrease, heart index, increased stroke index, and decreased blood aldosterone and norepinephrine, possibly for treatment Heart failure avoids a new path.

4) vasopressin: synthesized in the hypothalamus, stored in the posterior pituitary, often released in a small amount of blood circulation, vasopressin has anti-diuretic effect, can increase water reabsorption, it is also known as anti-urea, heart failure patients The vasopressin in blood can be 1 times higher than the normal level, and the mechanism of vasopressin elevation is unclear. The secretion of vasopressin is increased, which can cause extracellular fluid retention, free water discharge, hyponatremia. And can cause contraction of the peripheral blood vessels, the above effects can make heart failure symptoms.

(4) Changes in red blood cells: In the red blood cells of children with heart failure, the concentration of 2,3-diphosphoglycerate increases, which helps the red blood cells release more oxygen into the tissue when they are organized.

The symptomatic part of congestive heart failure is related to the side effects caused by the above compensatory mechanism. The end-diastolic pressure associated with ventricular dilatation increases, resulting in increased atrial pressure and pulmonary congestion. Sympathetic tension increases with arteriovenous contraction and blood flow. Redistribution, palpitation, increased sweating, due to the contraction of small arteries in most tissues and organs in the body, the peripheral vascular resistance increases, and the heart's afterload is aggravated, fluid retention may aggravate edema, and ventricular hypertrophy increases myocardial oxygen consumption. Due to the lack of relative blood supply, it offsets its beneficial effects.

In heart failure, the perfusion of tissues and organs in the body is reduced, and the blood stasis of the lungs causes the tissue to be in anoxic state, and the clearance of metabolites is also affected, resulting in acidemia and hypoxemia, so the contractility of cardiomyocytes is inhibited. In addition, islet ischemia, insufficient insulin secretion, myocardial use of glucose as a source of energy disorders, myocardial function is further inhibited, biochemical changes in children with heart failure is quite significant, most have respiratory and / or metabolic acidosis , blood sodium, blood chlorine is low.

Pediatric congestive heart failure prevention

Treatment of chronic heart failure must rely on patient coordination, and patient education can help improve treatment compliance.

1. Understand the purpose and goals of treatment, return to the clinic regularly, and follow the doctor's advice.

2. Understand the basic knowledge of heart failure, promptly see the following situations: rapid weight gain, recurrence or aggravation of lower extremity edema, increased fatigue, decreased exercise tolerance, increased heart rate (rest increase 15-20 times/min) or slow ( 55 beats / min), blood pressure decreased or increased (> 130 / 80mmHg), arrhythmia and so on.

3. Master the use of essential drugs, including diuretics, and adjust the dosage according to the condition.

4. Daily weight measurement and record, limited salt, water limit (daily liquid <2L), alcohol restriction, smoking cessation. Cardiomyopathy should stop drinking. Avoid stress levels such as overwork and physical activity, emotional agitation, and stress. Appropriate to exercise, walk 30 minutes a day, adhere to 5 to 6 days a week, and gradually increase the amount. Avoid all kinds of infections. Drug abuse is prohibited, such as non-steroidal anti-inflammatory drugs, hormones, antiarrhythmic drugs, etc.

Complications of congestive heart failure in children Complications, arrhythmia, premature beats

The disease has some potential complications, drug side effects, and the use of digitalis preparations, vasodilators, diuretics and other drug treatment.

(1) Digitalis preparation: The most common manifestation of pediatric digitalis poisoning is arrhythmia. Arrhythmia is the most common complication of heart failure, especially the incidence of ventricular arrhythmia, mainly manifested as atrioventricular block. Early pulsation, rapid tachycardia, bradycardia; followed by gastrointestinal reactions, loss of appetite, nausea, vomiting; nervous system symptoms such as drowsiness, dizziness, color vision, etc. are rare, immature and newborn Newborns within 2 weeks, liver and kidney dysfunction, electrolyte imbalance, low potassium, low magnesium, high calcium, severe diffuse myocardial damage and a large number of diuretics are prone to digitalis poisoning, 5 patients should be closely observed after medication The improvement of symptoms and signs, the main indicators of the efficacy of digitalis preparation are: slow heart rate, liver shrinkage, improvement of shortness of breath, quiet, improved appetite, increased urine output, long-term use of digitalis preparations, to monitor serum height The concentration of sputum and the blood collection sample should be about 6 hours after taking the drug, and the maintenance time should be 24 hours. The effective blood concentration of the serum digoxin in children is 1 to 3 ng/ml.

(2) vasodilator: pay attention to the side effects of drugs, mainly blood pressure, followed by heart palpitations, headache, nausea, blood pressure, heart rate should be measured before medication, monitoring should be monitored during the course of medication, discretionary adjustment of drip rate, and found adverse reactions, The doctor should be promptly notified to handle the treatment. The dose should be strictly controlled when using sodium nitroprusside. The monitor should be used to monitor the blood pressure changes. At the same time, the infusion bottle and tube should be wrapped in black cloth to avoid light.

(3) diuretics: the use of alkaline diuretics can easily cause hypokalemia, be wary of the digitalis poisoning reaction when combined with digitalis preparations, long-term use of diuretics should pay attention to whether there is mental wilting, fatigue, bloating, heart sounds Low blunt, arrhythmia and other clinical manifestations of hypokalemia, if necessary, can check the electrocardiogram and blood potassium, in order to confirm the diagnosis, should be supplemented with potassium-rich foods, such as bananas, oranges, green leafy vegetables.

(4) Prevention of secondary infections Due to systemic circulation and pulmonary circulation, the body's resistance is low, and a reasonable living system should be established according to the condition, to assist in life care and body cleansing, long-term bed rest and edema, Regularly turn over and massage the compression site to prevent hemorrhoids, infect and non-infected children living in the compartment, avoid respiratory infections, pay attention to food hygiene, prevent intestinal infections.

Symptoms of congestive heart failure in children Common symptoms Breathing end sitting breathing pale pale fatigue diastolic galloping tachycardia drowsiness sleepy nausea weight gain

1. Sympathetic excitation and cardiac dysfunction

Tachycardia: The baby's heart rate is more than 160 beats per minute; the school-age children's heart rate is more than 100 beats per minute. It is an early phenomenon of compensation; irritability is often crying; appetite is falling; sweating; activity is reduced; The percussion of the heart is enlarged; the first heart sound of the auscultation is low and blunt and can be heard and galloped. The pulse of the child is weak, the blood pressure is low, the finger, the toe is cold and the skin is squirting.

2. Performance of pulmonary circulation congestion

Shortness of breath, agitation of the nose, three concave signs, difficulty breathing, coughing, perioral and finger and toe twitching. Auscultation of the lungs can be heard with wheezing and wet rales.

3. The performance of systemic venous congestion

Liver enlargement or progressive enlargement. Older children can complain of pain or tenderness in the liver area. Long-term liver congestion, mild jaundice may occur; jugular vein engorgement: this sign is obvious in older children, and infants and young children have short neck and many subcutaneous fats, which are difficult to display. The dorsal vein of the hand is full and full, and it is also a common sign of venous congestion. The edema of the elderly is an important sign of right heart failure. Infants are not obvious because of the relatively large volume of the vascular bed. However, the daily weight gain is an objective indicator of fluid retention.

Examination of congestive heart failure in children

1. X-ray chest radiograph is universally enlarged, heart beat is weakened, lung texture is increased, interlobular pleura is obvious, and a small amount of pleural effusion shows pulmonary sputum blood. According to the size of each heart chamber and pulmonary blood condition, it can assist in the diagnosis of the cause. Normal baby thymus heart shadow can be misdiagnosed as a heart enlargement, should be noted.

2, ECG examination can show the hypertrophy of the atrioventricular, repolarization and changes in heart rhythm, which is helpful for the diagnosis of the cause and the application of digitalis drugs.

3, echocardiography provides accurate information on the anatomy of the heart, large blood vessels, hemodynamic changes, cardiac function and condition, which is helpful for the diagnosis of pathogenesis and the pathophysiology, assessment of cardiac contraction and diastolic function.

4, blood gas analysis and pH determination of pulmonary edema, PaO2 decreased in left heart failure, PaCO2 increased, respiratory acidosis, severe heart failure, poor tissue perfusion, accumulation of acidic metabolites, can lead to metabolic acidosis.

5, blood biochemistry and blood glucose measurement to understand the serum sodium, potassium, chlorine levels, neonatal hypoglycemia can lead to heart failure, can still detect myocardial ischemia, renal function and anemia, etc., help to judge the cause and guide treatment.

Diagnosis and diagnosis of congestive heart failure in children

1, infant heart failure should be different from the following:

(1) severe bronchitis and pneumonia and bronchiolitis: the child has difficulty breathing, respiratory and pulse increase and other signs, due to emphysema and diaphragmatic muscle drop, the liver can be touched 2 to 3 cm below the rib, the above signs and Heart failure is similar, but the heart does not enlarge and the liver's edges are not rounded.

(2) in the purple congenital heart disease: due to hypoxia, children often have increased breathing, irritability, increased bruising and heart rate, but no other manifestations of heart failure such as liver enlargement.

2, elderly children with heart failure should be identified with the next disease:

(1) Acute pericarditis, pericardial effusion and chronic constrictive pericarditis: When these diseases occur with pericardial occlusion and venous congestion, the symptoms are similar to heart failure, but pericardial diseases have the following characteristics:

1 odd pulse is obvious;

2 The abdomen is not prominent, and is not proportional to edema in other parts;

3 pulmonary congestion is not obvious, so although the child has jugular vein engorgement, ascites and liver significantly increased and other signs, but the breathing difficulties are not significant, and can be supine;

4X-ray examination, echocardiography and isotope heart blood pool scanning can also assist in diagnosis.

(2) Liver and kidney disease caused by obvious ascites: should be differentiated from right heart failure.

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