Newborns with congestive heart failure in children often present with hundreds of specific symptoms such as lethargy, apathy, fatigue, refusal to milk or vomiting. Congestive heart faiture 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 the relevant parts of the body. The clinical signs and symptoms of the series 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.
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 degrees 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 of ventricular end-diastolic period and the pressure generated by it. According to Frank-Starling's law, within a certain limit, as the ventricular end-diastolic volume and pressure increase, cardiac output also increases. Ventricular end-diastolic volume is associated with circulating blood volume, venous return blood volume, and ventricular compliance. The preload can be expressed as ventricular end-diastolic pressure.
2) Afterload: Also known as pressure load, it refers to the load that the ventricle bears after it begins to contract. It can be expressed by systolic blood pressure or aortic pressure at the time of ventricular ejection. 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. According to 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 ability of ventricular contraction that is unrelated to the anterior and posterior load of the heart, and is related to the conversion of Ca++ ion concentration, contractile protein and energy in cardiomyocytes. Mainly affected by sympathetic regulation.
4) Heart rate: cardiac output (L/min) = stroke volume (L/time) × heart rate. Within a certain range, the heart rate is increased and the cardiac output is increased. However, the ventricular diastolic phase is shortened as the heart rate increases. When the heart rate exceeds 150 beats/min, the ventricular diastolic phase is too short, the filling volume is too low, the heart rate is decreased, and the cardiac output is decreased. The heart rate is significantly slower, and below 40 beats/min, although the heart rate increases, the cardiac output decreases.
5) Coordination of ventricular contraction: Coordination of wall motion during ventricular contraction is also one of the important factors in maintaining normal cardiac output. In myocardial ischemia and myocardial infarction, local myocardial motion may be weakened or disappeared, and the movement may be asynchronous or even form contradictory movements, which may cause the ventricular contraction to lose coordination, resulting in a decrease in cardiac output.
The regulation of the first three of these 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, which should be taken seriously.
(2) Changes in hemodynamic parameters during heart failure:
1) Heart Index: The cardiac output is calculated as the body surface area. The normal value of children is 3.5 ~ 5.5L / (min? m2), decreased 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). Reflects right ventricular end-diastolic pressure, more than 1.18 kPa in right heart failure.
4) Pulmonary capillary wedge pressure: normal value is 0.8 to 1.6 kPa (6 to 12 mmHg). Reflecting left ventricular end-diastolic pressure is the earliest hemodynamic change in left heart failure. When the temperature is 2.0 to 2.67 kPa (15 to 20 mmHg), the heart is in the best 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 Both the heart and the energy are consumed in the process of pulsation. The contraction and relaxation of the myocardium are caused by the interaction of the contractile proteins contained in the basal ganglia of the myocardium with the participation of calcium ions. The contraction proteins contained in the sarcomere are produced by the interaction of calcium ions. The sarcomere contains two contractile proteins, myocin and actin; there are two regulatory proteins, tropomycin and troponin, with a transverse bridge and ATP. Enzyme activity that catalyzes the decomposition of ATP. Myofibrillar protein is present in fine filaments, has no ability to contract by itself, has no ATPase activity, and has a receptor site that can react with Hengqiao. Myosin and myofibrillin are arranged in a cross. During myocardial relaxation, between the tropism of the tropism, the binding of the myosin cross-bridge to the receptor site of myofibrillar is blocked. When Ca++ reaches a certain concentration in the sarcoplasm, Ca++ is released from the sarcoplasm to the gonadotropin, and combines with the tropomin to form a Ca++-nein protein-pro-myosin complex, so the tropin contraction is tight and the muscle fiber is made. The receptor site of the protein is exposed to the transverse bridge of myosin to form a muscle fibrin complex, at which time the ATPase on the myosin is activated, causing ATP to decompose, providing energy and causing myocardial contraction. The more Ca++-gonimin-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, and the Ca++ content of mitochondria is more. Since the affinity of mitochondria combined with Ca++ is stronger than that of sarcoplasmic reticulum, the release rate of Ca++ is slowed and reduced when the cells are excited, and the Ca++ which supplies contractile protein during myocardial depolarization is significantly reduced, and myocardial contraction is inhibited.
In heart failure, the activity of ATPase in the myocardium is reduced, which affects the conversion of chemical energy, which limits the decomposition of ATP and energy production, and slows down the reaction rate, affecting myocardial contractility. The depletion of myocardial catecholamines, the conversion of ATP to cAMP is insufficient, cAMP can reduce AMP, 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 make cardiac output. It can maintain or approach normal levels in a large resting state. To some extent, it may be beneficial to heart failure hemodynamics, but excessive compensation is harmful. The main compensatory mechanism for 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, the greater the contractility of the heart muscle, the increase in stroke volume, thus maintaining a balance between cardiac output and blood flow. However, the role of this compensatory mechanism is limited, and when the end-diastolic volume is significantly increased, the stroke volume is reduced.
(2) Ventricular hypertrophy: increase the contractility of the myocardium by increasing the unit of myocardial contraction, thereby increasing the stroke volume. However, cardiac hypertrophy itself can be one of the factors of heart failure, because the hypertrophic myocardial blood supply can be reduced accordingly, and in some cases can cause obstruction of the outflow tract, which exacerbates cardiac dysfunction.
(3) Regulation of neurohumoral fluid: it is the main compensatory process of heart failure. Activation of the sympathetic nervous system, the renin-angiotensin-aldosterone system, tenena and vasopressin may occur.
1) Sympathetic nervous system: Sympathetic nervous system excitement can be caused reflexively due to a decrease in 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. The level of norepinephrine in urine is also significantly higher than that in normal people, and the concentration of norepinephrine in the blood is increased. Cardiac function, pulmonary capillary wedge pressure and cardiac index are directly related. Sympathetic excitation can increase heart rate, strengthen myocardial contractility and peripheral vasoconstriction, leading to increased cardiac output and maintenance of blood pressure, which can partially compensate for hemodynamic abnormalities in heart failure. However, sustained and excessive increase in sympathetic tone can cause cardiac 1 receptor-mediated adenylate cyclase activity to decrease, affect myocardial contractility; and activate the renin-angiotensin-aldosterone system to make renin, Angiotensin II levels are elevated.
2) Renin-angiotensin-aldosterone system: a major neurohumoral regulation process in heart failure. Decreased renal blood perfusion during heart failure and stimulation of 1 agonist in the juxtaglomerular apparatus is the main mechanism for activation of the renin-angiotensin-aldosterone system; however, low-salt diet and diuretics cause low sodium in heart failure , is also the reason to activate the system. Plasma renin activity, angiotensin II and aldosterol levels were elevated in patients with heart failure. Angiotensin II increased peripheral vasoconstriction 40 times more than norepinephrine; it can promote sympathetic excitation, strengthen norepinephrine release, and further allow peripheral vasoconstriction. In addition, angiotensin II also promotes the production and release of aldosterone from the adrenal gland, causing sodium retention. This system activates the inactivation of bradykinin by the action of a converting enzyme, and can lower the concentration of prostaglandin E and impede vasodilation. These changes can compensate for some of the heart failure hemodynamic processes, but excessive can further aggravate the anterior and posterior heart and body fluid disorders. In recent years, the application of transferase inhibitors can inhibit the above-mentioned excessive compensation and transform the pathophysiological changes of heart failure into a benign cycle. Therefore, it has been widely used in the treatment of 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, produces diuretic, discharges sodium, dilates blood vessels and inhibits renin and aldosterone. The level of atrial natriuretic peptide in healthy children was 129-356 pg/ml (average 227 pg/ml) 2 to 4 days after birth, which was significantly higher than that of other age groups of 2 to 109 pg/ml, with an average of 47 pg/ml. As a result of postnatal changes in circulation, decreased pulmonary vascular resistance, increased pulmonary blood flow, and increased vascular resistance, these changes may be associated with increased atrial pressure and volume, thereby stimulating atrial natriuretic release from the atrial wall. The atrial natriuretic peptide of patients with congenital heart and lung disease is 2 to 10 times higher than that of the control group. Factors that promote atrial natriuretic release include: 1 heart failure causes increased left and right atrial pressure; 2 heart failure increases extracellular fluid volume, resulting in increased atrial volume. Observations showed that the concentration of atrial natriuretic peptide in peripheral blood was positively correlated with the severity of heart failure, and the condition improved atrial natriuretic peptide. Therefore, the determination of atrial natriuretic peptide can determine the degree of heart failure and the therapeutic effect. However, in patients with a long-term heart failure, patients with longer course of disease have a lower atrial natriuretic peptide, which may be related to depletion due to long-term hypersecretion.
Increased atrial natriuretic peptide secretion during heart failure, resulting in dilated blood vessels, sodium excretion and diuresis, anti-reoxygenation of the renin-angiotensin-aldosterol system, has a national role, and is beneficial to curb the progression of the vicious circle of heart failure. However, the increase in endogenous atrial natriuretic peptide is relatively weak and is generally insufficient to counteract the potent role of the activated sympathetic nervous system and the renin-angiotensin-aldosterone system. Another reason is the decreased sensitivity of local atrial natriuretic receptors such as kidneys in heart failure. 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 failure, and heart rate, right atrial pressure, pulmonary capillary wedge pressure and peripheral vascular resistance have been significantly decreased, cardiac index, stroke index of work and blood, and blood Aldosterone and norepinephrine decreased. It is possible to evade a new way to treat heart failure.
4) Vasopressin: synthesized in the hypothalamus, stored in the posterior pituitary, often released in a small amount in the blood circulation. Vasopressin has anti-diuretic effect, which can increase the reabsorption of water, so it is also called anti-urea. The blood vasopressin in patients with heart failure can be 1 times higher than normal, and the mechanism of vasopressin elevation is still unclear. Increased secretion of vasopressin can cause extracellular fluid retention, reduced free water discharge, hyponatremia; and can cause external peripheral blood vessels to contract. The above effects can increase the symptoms of heart failure.
(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. Increased end-diastolic pressure associated with ventricular dilatation leads to an increase in atrial pressure and pulmonary congestion. Increased sympathetic tone has arteriovenous contractions, redistribution of blood flow, palpitation, and increased sweating. As the small arteries in most tissues and organs in the body contract, the peripheral vascular resistance increases, which aggravates the heart's afterload. Fluid retention can exacerbate edema. Ventricular hypertrophy increases the oxygen consumption of the myocardium, which is counteracted by the relative lack of blood supply.
In the 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. Therefore, the contractility of cardiomyocytes is inhibited. In addition, islet ischemia, insufficient insulin secretion, causes myocardial use of glucose as a source of energy, and myocardial function is further inhibited. The biochemical changes in children with heart failure are quite significant, most of them have respiratory and / or metabolic acidosis, blood sodium, blood chlorine is low.
ECG chest CT examination
The signs of heart failure are mainly due to cardiac compensatory dysfunction, sympathetic excitation, venous system congestion, increased blood volume, and sodium and water retention. Because of differences in age, etiology, and hemodynamic changes, clinical features vary in different age groups in children.
1. Infants and young children often present with symptoms such as lethargy, apathy, fatigue, refusal to milk or vomiting. The symptoms of heart failure in infants and young children are often atypical. Generally, the onset is more urgent, and the disease progresses rapidly. When acute myocarditis and cardiac periosteal fibroelastosis occur in heart failure, it is often a sudden onset. The child may suddenly have difficulty breathing within a few minutes or a few hours. When inhaling, the upper sternum and the ribs are sagged, and the breathing increases rapidly, often exceeding 60 times per minute, or even more than 100 times. At the same time, vomiting, irritability, excessive sweating, pale or bruising, cold limbs, rapid pulse and weakness, tachycardia, galloping, dry lungs, and acute congestive heart failure. Congenital cardiovascular malformations, such as septal defects, are mostly chronic congestive heart failure. The onset is slightly slower. The main symptoms are feeding difficulties. Children with small amounts of sputum have difficulty breathing, fatigue and refusal to eat, and weight does not increase. Irritated and sweaty, willing to pick up and rely on the shoulders of adults (this is the performance of the baby sitting breathing), breathing difficulties when quiet, common in cough, children crying weakly, sometimes hoarse, due to dilated pulmonary artery compression left Caused by recurrent laryngeal nerve. The pre-cardiac area is prominent, the apex beats and the heart expands. Hepatosplenomegaly, its edges are blunt and tender. The lungs often have no wet or only wheezing. Jugular vein engorgement and edema are not obvious, and the degree of edema can only be judged by observing the weight gain.
2. The symptoms of elderly children with heart failure are similar to those of adults, and the onset is slow. Left and right heart failures are as follows:
(1) Left heart failure: can be seen in rheumatic mitral valve disease and hypertensive heart disease, etc., the main symptoms are caused by acute or chronic pulmonary congestion. Clinical manifestations include: 1 Dyspnea: often the earliest symptoms, starting to be light, only after the activity, the child's activity is limited, easy to fatigue, and finally appear at rest, breathing fast and shallow. The main cause of dyspnea is the increased stimulation of the respiratory center caused by the lungs. Difficulty breathing is often aggravated when lying down, so the child likes to take a seat, showing a sitting breathing phenomenon. Because of the gravity, the blood accumulates in the lower limbs and the abdomen during the sitting position, so that the blood volume returned to the right ventricle is reduced, so it can be alleviated. The lungs are congested, and when the seat is lowered, the diaphragm is lowered and the chest cavity is easy to expand. Paroxysmal dyspnea at night is rare in children. 2 cough: due to pulmonary congestion, bronchial mucosal congestion caused by chronic dry cough. 3 hemoptysis: bleeds so that blood oxygenation through the pulmonary blood vessels is not complete. 4 cyanosis, generally heavier, due to lung congestion caused by blood oxygenation through the pulmonary vascular insufficiency. 5 The lungs may have wheezing or wet rales. 6 acute pulmonary edema: due to acute left heart failure, pulmonary congestion is aggravated, body fluids ooze out of the capillaries and accumulate in the alveoli. The child has extreme difficulty breathing, sitting breathing, pale skin or blemishes, cleft lip, and sudden drop in heart rate, so the limbs are cold, the pulse is fast and weak or can not be touched, occasionally alternating pulse, that is, the pulse is strong and weak The blood pressure drops, the tachycardia often runs galloping, the lungs have wheezing sounds and wet rales. The children have frequent cough and bloody sputum. In severe cases, a large amount of bloody liquid is poured out from the mouth and nostrils.
(2) right heart failure: due to left heart failure, due to left heart failure, pulmonary congestion, increased pulmonary pressure, increased right ventricular systolic load; congenital cardiovascular malformation with pulmonary hypertension often occur right heart failure. Symptoms of right heart failure are mainly caused by systemic hyperemia. The clinical manifestations are: 1 edema: beginning to appear in the body's pituitary body. There are two main causes of severe cases: one is the increase in sodium and no absorption of the kidney, so that the extracellular fluid Increased; one is the increase of systemic venous pressure, capillary water infiltration into the tissue more than the reflux of the capillaries and lymphatic vessels. 2 liver enlargement often accompanied by pain: acute heart failure, abdominal pain and liver tenderness, liver blunt edge, liver can appear before edema, it is one of the early symptoms of right heart failure. Chronic heart failure, long-term liver and blood stasis can occur jaundice. 3 jugular vein engorgement: jugular vein engorgement when sitting, more obvious when the liver is pressed by hand (hepatic neck reflux sign). 4 loss of appetite, nausea, vomiting, due to gastrointestinal bleeding. 5 less urine, and mild proteinuria and a small number of red blood cells, due to kidney blood stasis.
3. Evaluation of cardiac function status In general, the initial stage of heart failure can be left heart or right heart failure, and the development of the disease is characterized by whole heart failure. The clinical manifestation is more common in heart failure. Heart function status of heart patients is usually divided into four levels according to the patient's medical history, clinical manifestations and labor endurance:
Grade I: only signs of heart disease, asymptomatic, unrestricted activity, and cardiac function compensation.
Level II: Symptoms occur when activity is large, and activity is mildly restricted.
Level III: Symptoms appear when there is a little more activity, and activity is significantly limited.
Grade IV: Symptoms of rest and rest, complete loss of labor.
The above cardiac function classification is for adults and children and is not applicable to infants. Some authors believe that most of the heart failure of infants is caused by a large left-to-right shunt, which leads to an increase in blood volume in the pulmonary circulation, which is different from that in adults. Cardiac function grading should accurately describe the feeding history, respiratory rate, respiratory patterns such as nasal, tri-concave and sputum-like breathing, heart rate, peripheral perfusion, diastolic gallop and liver enlargement. The evaluation of infant heart function was graded as follows.
0 line: no heart failure performance.
Grade I: mild heart failure. The indication is that each breastfeeding amount is <90ml, or the breastfeeding time is more than 40 minutes, the breathing is >60 times/min, the breathing pattern is abnormal, the heart rate is >160 times/min, and the liver is under the ribs 2~3cm, there is galloping.
Grade II: severe heart failure. Indications <75ml per time, or more than 40 minutes of breastfeeding time, breathing >60 times / min, abnormal breathing pattern, heart rate >170 times / min, galloping, more than 3cm under the liver ribs, and peripheral perfusion bad. According to the above clinical manifestations of heart failure, the infant heart failure grading score is formulated, which can be used as a reference for the classification of heart failure in infants.
1. Infant heart failure should be different from the following:
(1) severe bronchitis and pneumonia and bronchiolitis: children with signs of difficulty breathing, breathing and pulse increase. Due to emphysema and lowering of the diaphragm, the liver can be reached 2 to 3 cm below the rib. The above signs are similar to heart failure, but the heart does not enlarge and the liver edge is not round.
(2) in the purple congenital heart disease: due to lack of oxygen in children, often increased breathing, irritability, aggravation of 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 following diseases:
(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 the pericardial disease has 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 the child has signs of jugular vein engorgement, ascites and liver enlargement, but the breathing difficulty is 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.