Symptoms of CVD in children. Diseases of the cardiovascular system. Methods for studying the cardiovascular system in children

Heart disease in children - pretty common problem. They develop in both adolescents and infants. Heart disease reduces life expectancy and is one of the leading causes of sudden death.

Parents should carefully monitor their lives and the lives of their children, because the development of many pathologies can be prevented.

Heart disease in children

Heart diseases are congenital and acquired. Most congenital pathologies are diagnosed at the prenatal stage of a baby's development. Many of them can be eliminated only with the help of surgeons.

Acquired may occur regardless of age. The reasons for this can be different: from an infection in childhood to a mother’s illness during the period of bearing a baby.

Common diseases of the cardiovascular system (CVS):

1. Arrhythmia. Pathological condition of the heart, in which there is a violation of the rhythm, contraction and sequence of excitation of the heart muscle. The disease can manifest itself regardless of age, often after serious disorders of the nervous system. There is arrhythmia in healthy children. It is noted against the background of physical exertion, under the influence of heat or strong emotional upheavals.
2. Syndrome of vegetative-vascular dystonia (VVD). Diagnosed due to a pronounced whole complex various symptoms. It manifests itself in children in the form of cardiac, respiratory, neurotic syndromes, vegetative-vascular crises, a syndrome of thermoregulation disorders. For VSD treatment in children, medical, physiotherapeutic, psychological methods are used.
3. Malformations and anomalies in the development of the cardiovascular system. Such problems manifest themselves even at the intrauterine stage of development. Negative external factors that affected a woman at 4-8 weeks of pregnancy (past viral diseases such as influenza, rubella, chronic diseases, work in hazardous industries, drug treatment, hereditary factor, bad habits).

The number of children suffering from heart disease is increasing every year. Stressful conditions, poor nutrition, poor environmental situation - all this negatively affects preschool children. Many of them become disabled. Everything is aggravated by the fact that the child cannot clearly express his complaints, so most diseases are diagnosed only on examination by a doctor.

Don't miss your pediatrician appointments.

"White" and "blue" vices

In addition to the congenital and acquired classification of diseases, there are:

1. Defects at the location of the defect (in the mitral, aortic, tricuspid valve or foramen ovale).
2. Also on anatomical changes in the heart muscle (stenosis, coarctation, atresia, hypoplasia, as well as a defect in cardiac structures).
3. According to the degree of pathology, based on hemodynamic data (1, 2, 3 and 4 degrees).

According to hemodynamic parameters, the defects are divided into:

1. "white",
2. "blue".

In the first type of defects, there is a discharge of blood from left to right. Mixing of arterial and venous is not noted. In the second form, there is a reflux of venous blood into the arterial one, characterized by cyanosis.

These include:

1. Fallot disease.
2. Transposition of the great vessels.
3. Common arterial trunk.
4. Atresia of the tricuspid valve.

Until recently, most of these pathologies took the lives of children, often even at the prenatal stage of development. Now such children are being helped, undergoing complex operations, and not only do they survive, some of them have a chance for a full recovery.

Heart disease in adolescents

Parents should pay special attention to the health of the child in adolescence. During this period, it grows rapidly, and the heart muscle also increases.

Such changes can provoke the development of various CCC diseases:

1. Bicuspid valve prolapse. A pathology in which there is a malfunction of the valve located between the left atrium and the ventricle.
2. Neurocirculatory dystonia is a multifactorial disease that can occur against the background of stressful situations. It is characterized by primary functional disorders of the activity of the cardiovascular system, which are based on an imperfection or disorder in the regulation of autonomic functions that is not associated with neurosis or organic pathology of the nervous and endocrine systems.
3. VVD is a complex of common problems that often arise at this age due to the restructuring of the body. The body of a teenager is growing rapidly, and the CCC does not keep up with it. Therefore, such a diagnosis can be made to almost every second person at the age of 13-16 years. The internal organs receive less oxygen, tachycardia and headaches are observed.

Important! With VVD, there may be pain in the region of the heart, tachycardia, or vice versa - bradycardia, bad mood, a feeling of depression, tearfulness. The child becomes suspicious, there are sharp mood swings, unfounded fears appear, which can lead to a state of depression.

When to sound the alarm:

1. the appearance of shortness of breath,
2. cyanosis or excessive pallor of individual areas,
3. swelling,
4. dry cough,
5. pain in the region of the heart,
6. heart murmurs or tachycardia.

In any case, without the advice of a specialist can not do. It is necessary to conduct a thorough examination and monitor the state of the disease. Many of them are treated in the early stages and do not make themselves felt in adulthood.

Heart hump: what is it, the reasons for the formation

This is the formation of a rounded bulge at the level of the sternum. It occurs due to congenital cardiac pathologies. In the 6th and 7th intercostal spaces, shocks of the heart muscle are visible. There is also cyanosis of the lips and face of the child. Pain in the region of the heart, cough, hoarse voice, bouts of hiccups are noted. To get rid of a heart hump, you need to eliminate the root cause - a congenital pathology of the heart. After the examination, the cardiac surgeon will tell you what to do and prescribe an operation. Self-medication in such cases can be deadly.

Features of the CCC of a teenager

The mass of the heart of a child, relative to his body, is much larger than that of an adult. Accordingly, the heart rate is higher. With age, it decreases, but in the pubertal period, a jump is again noted.

As the body grows, so do the internal organs. Sometimes there is such a picture that the CCC cavities increase faster than the lumen of the valve openings of the main veins. In this regard, the syndrome of "youthful" heart is revealed.

There are three forms:

1. mitral,
2. teenage drip heart syndrome
3. organ hypertrophy.

As the child grows, so does the number of blood vessels.

Risk factors

Each person has their own predisposition to certain diseases. If you follow the advice of specialists, then the risk of developing these diseases or worsening the condition is minimized.

What do you need to know in order to properly prepare?

Factors in the development of congenital heart pathologies:

1. Inherited from close relatives.
2. Bad habits of the mother of the child during pregnancy and before conception.
3. Infection at the stage of intrauterine development.
4. The mother has diabetes and hypertension.
5. Injuries received during childbirth.

Acquired CVD diseases occur due to:

1. The use of products with great content cholesterol.
2. Presence of arterial hypertension.
3. Overweight.
4. Sedentary and inactive lifestyle.

If parents are planning a pregnancy, they must pay due attention to their lifestyle. After all, many diseases of the cardiovascular system could not have been in a child if the parents behaved correctly.

Prevention

In order for not only an individual child to be healthy, but future generations in general, society must understand the importance of preventive measures.

So, the basic rules:

1. Balanced diet. The child should eat according to his age. It is necessary to provide him with fresh vegetables, fruits, a sufficient amount of meat and dairy products.
2. Physical exercise. The child can attend sports clubs or dance clubs, or just walk in the fresh air every day.
3. Child weight control. AT last years children and adolescents have significantly “recovered”. Do not ignore the problem, you need to contact a specialist at the first sign.
4. Completely give up bad habits.
5. Monitor the health of the child and, in case of rapid growth, be sure to visit a doctor.

These rules do not restrict the child in any way. On the contrary, they will help to live fully and not depend on CCC diseases. Heart disease in both adolescents and children is treated comprehensively. The main thing is to consult a doctor in time. Any CCC disease is very dangerous and, in case of untimely treatment, can have irreparable consequences.

Heart disease in children is a fairly common problem. They develop in both adolescents and infants. Heart disease reduces life expectancy and is one of the leading causes of sudden death. Parents should carefully monitor their lives and the lives of their children, because the development of many pathologies can be prevented.

Heart disease in children

Heart diseases are congenital and acquired. Most congenital pathologies are diagnosed at the prenatal stage of a baby's development. Many of them can be eliminated only with the help of surgeons.

Acquired may occur regardless of age. The reasons for this can be different: from an infection in childhood to a mother’s illness during the period of bearing a baby.

Common diseases of the cardiovascular system (CVS):

1. Arrhythmia. Pathological condition of the heart, in which there is a violation of the rhythm, contraction and sequence of excitation of the heart muscle. The disease can manifest itself regardless of age, often after serious disorders of the nervous system. There is arrhythmia in healthy children. It is noted against the background of physical exertion, under the influence of heat or strong emotional upheavals.
2. Syndrome of vegetative-vascular dystonia (VVD). It is diagnosed due to a pronounced whole complex of various symptoms. It manifests itself in children in the form of cardiac, respiratory, neurotic syndromes, vegetative-vascular crises, a syndrome of thermoregulation disorders. For the treatment of VVD in children, medication, physiotherapy, and psychological methods are used.
3. Malformations and anomalies in the development of CCC. Such problems manifest themselves even at the intrauterine stage of development. Negative external factors that affected a woman at 4-8 weeks of pregnancy (past viral diseases such as influenza, rubella, chronic diseases, work in hazardous industries, drug treatment, hereditary factors, bad habits) have a great influence.

The number of children suffering from heart disease is increasing every year. Stressful conditions, poor nutrition, poor environmental situation - all this negatively affects preschool children. Many of them become disabled. Everything is aggravated by the fact that the child cannot clearly express his complaints, so most diseases are diagnosed only on examination by a doctor.

Don't miss your pediatrician appointments.

"White" and "blue" vices

In addition to the congenital and acquired classification of diseases, there are:

1. Defects at the location of the defect (in the mitral, aortic, tricuspid valve or foramen ovale).
2. Also on anatomical changes in the heart muscle (stenosis, coarctation, atresia, hypoplasia, as well as a defect in cardiac structures).
3. According to the degree of pathology, based on hemodynamic data (1, 2, 3 and 4 degrees).

According to hemodynamic parameters, the defects are divided into:

• "white";
• "blue".

In the first type of defects, there is a discharge of blood from left to right. Mixing of arterial and venous is not noted. In the second form, there is a reflux of venous blood into the arterial one, characterized by cyanosis.

These include:

• Fallot disease.
• Transposition of the great vessels.
• Common arterial trunk.
• Atresia of the tricuspid valve.

Until recently, most of these pathologies took the lives of children, often even at the prenatal stage of development. Now such children are being helped, undergoing complex operations, and not only do they survive, some of them have a chance for a full recovery.

Heart disease in adolescents

Parents should pay special attention to the health of the child in adolescence. During this period, it grows rapidly, and the heart muscle also increases. Such changes can provoke the development of various CCC diseases:

1. Bicuspid valve prolapse. A pathology in which there is a malfunction of the valve located between the left atrium and the ventricle.
2. Neurocirculatory dystonia is a multifactorial disease that can occur against the background of stressful situations. It is characterized by primary functional disorders of the activity of the cardiovascular system, which are based on an imperfection or disorder in the regulation of autonomic functions that is not associated with neurosis or organic pathology of the nervous and endocrine systems.
3. VVD is a complex of common problems that often arise at this age due to the restructuring of the body. The body of a teenager is growing rapidly, and the CCC does not keep up with it. Therefore, such a diagnosis can be made to almost every second person at the age of 13-16 years. The internal organs receive less oxygen, tachycardia and headaches are observed.

Important! With VVD, there may be pain in the region of the heart, tachycardia, or vice versa - bradycardia, bad mood, a feeling of depression, tearfulness. The child becomes suspicious, there are sharp mood swings, unfounded fears appear, which can lead to a state of depression.

When to sound the alarm:

• the appearance of shortness of breath;
• cyanosis or excessive pallor of individual areas;
• puffiness;
• dry cough;
• pain in the region of the heart;
• heart murmurs or tachycardia.

In any case, without the advice of a specialist can not do. It is necessary to conduct a thorough examination and monitor the state of the disease. Many of them are treated in the early stages and do not make themselves felt in adulthood.

Heart hump: what is it, the reasons for the formation

This is the formation of a rounded bulge at the level of the sternum. It occurs due to congenital cardiac pathologies. In the 6th and 7th intercostal spaces, shocks of the heart muscle are visible. There is also cyanosis of the lips and face of the child. Pain in the region of the heart, cough, hoarse voice, bouts of hiccups are noted. To get rid of a heart hump, you need to eliminate the root cause - a congenital pathology of the heart. After the examination, the cardiac surgeon will tell you what to do and prescribe an operation. Self-medication in such cases can be deadly.

Features of the CCC of a teenager

The mass of the heart of a child, relative to his body, is much larger than that of an adult. Accordingly, the heart rate is higher. With age, it decreases, but in the pubertal period, a jump is again noted.

As the body grows, so do the internal organs. Sometimes there is such a picture that the CCC cavities increase faster than the lumen of the valve openings of the main veins. In this regard, the syndrome of "youthful" heart is revealed.

There are three forms:

• mitral;
• syndrome of teenage "drip" heart;
• organ hypertrophy.

As the child grows, so does the number of blood vessels.

Risk factors

Each person has their own predisposition to certain diseases. If you follow the advice of specialists, then the risk of developing these diseases or worsening the condition is minimized. What do you need to know in order to properly prepare?

Factors in the development of congenital heart pathologies:

• Inherited from close relatives.
• Bad habits of the mother of the child during pregnancy and before conception.
• Infection at the stage of intrauterine development.
• The mother has diabetes and hypertension.
• Injuries received during childbirth.

Acquired CVD diseases occur due to:

• Eating foods high in cholesterol.
• Presence of arterial hypertension.
• Overweight.
• Sedentary and inactive lifestyle.

If parents are planning a pregnancy, they must pay due attention to their lifestyle. After all, many diseases of the cardiovascular system could not have been in a child if the parents behaved correctly.

Prevention

In order for not only an individual child to be healthy, but future generations in general, society must understand the importance of preventive measures. So, the basic rules:

1. Balanced diet. The child should eat according to his age. It is necessary to provide him with fresh vegetables, fruits, a sufficient amount of meat and dairy products.
2. Physical exercise. The child can attend sports clubs or dance clubs, or just walk in the fresh air every day.
3. Child weight control. In recent years, children and adolescents have significantly “recovered”. Do not ignore the problem, you need to contact a specialist at the first sign.
4. Completely give up bad habits.
5. Monitor the health of the child and, in case of rapid growth, be sure to visit a doctor.

These rules do not restrict the child in any way. On the contrary, they will help to live fully and not depend on CCC diseases. Heart disease in both adolescents and children is treated comprehensively. The main thing is to consult a doctor in time. Any CCC disease is very dangerous and, in case of untimely treatment, can have irreparable consequences.

What heart conditions are more common in children? Most often, doctors are faced with such conditions as arterial hypertension in adolescents, disorders heart rate, congenital heart defects.

ARTERIAL HYPERTENSION (HYPERTENSION) IN CHILDREN

About 20-30 years ago, arterial hypertension was considered a problem of the elderly. But large-scale studies, including those with the participation of our department, have shown high percent detection of arterial hypertension in children, namely in adolescents. Employees of the Department of Children's Diseases, cardiology department, which is the main clinical base, algorithms for identifying the diagnosis and management of children with arterial hypertension were developed. These algorithms have been implemented and are actively used in the daily practice of cardiologists and pediatricians in our region.

Most common causes arterial hypertension in children depending on age

More rare (not related to age) causes of secondary arterial hypertension - systemic vasculitis, diffuse diseases connective tissue, as well as endocrine diseases (pheochromocytoma, neuroblastoma, hyperparathyroidism, congenital adrenal hyperplasia, primary hyperaldosteronism, endogenous or exogenous Cushing's syndrome). An increase in systemic arterial pressure may be accompanied by hypertension-hydrocephalic syndrome and the abuse of adrenomimetics [ephedrine, salbutamol, naphazoline (for example, naphthyzinum), etc.].

HEART RHYTHM IN CHILDREN

second large group cardiovascular diseases in children are various cardiac arrhythmias. Here, the main goal of doctors is to identify such disorders that are fraught with the development of life-threatening conditions.

Arrhythmias are widespread: they are observed in 20-30% of children with diseases of the cardiovascular system, but are often detected in healthy children. A heart rhythm disturbance can occur in a child of any age, even in a newborn.

As is known, there are a number of rhythm and conduction disturbances, which are asymptomatic until a certain time, i.e. without disturbing the well-being of the child. And the first manifestation of such a disease may be the development of a life-threatening condition. Pediatric cardiologists literally "sift" patients with even minimal changes in electrocardiography, paying special attention to children with syncope. In federal or regional centers of cardiovascular surgery, surgical treatment such children, allowing once and for all to eliminate the threat of sudden cardiac death. After operations, patients return to us under dynamic observation.

Most arrhythmias childhood are reversible and do not pose a threat to the life of the child. Some types of arrhythmias ( sinus tachycardia/bradycardia) are observed in healthy children. In newborns and young children, arrhythmias can lead to the development of cardiomyopathy, or heart failure, contributing to early disability. There are dangerous types of arrhythmias (for example, paroxysmal tachycardia, atrial fibrillation, atrioventricular block, sick sinus syndrome, prolonged Q-T interval), which adversely affect hemodynamics, cause a decrease cardiac output and blood supply to the heart muscle, resulting in a poor outcome, and some of them, in rare cases, to sudden death.

Sinus tachycardia (an increase in the normal rhythm) may be accompanied by a sensation of palpitations. In healthy children, it occurs during physical exertion and emotional arousal.

With sinus bradycardia (decreased normal rhythm), most children do not complain, but some experience weakness, fatigue, dizziness. This type of arrhythmia also occurs in healthy children (more often at rest, in sleep) who play sports.

Paroxysmal tachycardia is manifested by a sudden sharp increase in heart rate, often sweating, weakness, fainting, discomfort in the region of the heart.

Extrasystole is associated with the appearance in the heart muscle of additional foci of excitation, impulses from which cause premature contractions of the heart (extrasystoles). Patients either do not feel them, or perceive them as an increased push in the region of the heart or its fading.

Sick sinus syndrome is characterized by a combination of pronounced sinus bradycardia (or bradyarrhythmia) with episodes of tachycardia. Many patients have no discomfort. But some children show signs of insufficient blood supply to the brain, possibly developing heart failure.

Heart blocks occur when the conduction of an impulse from the atria to the ventricles is disrupted. Non-severe violations do not manifest themselves in any way; with severe disorders in children, weakness, dizziness, fainting appear.

CONGENITAL HEART DEFECT (CHD)

And another significant group of cardiovascular diseases in children is congenital heart disease.

There are more than 100 types of congenital heart defects in children. There are also a large number of classifications, including ICD-10. Some researchers divide the UPU into blue and white. With blue, the child has a blue tint to the skin, and with white, the skin is pale. Blue-type malformations include transposition of the great vessels, tetralogy of Fallot, pulmonary atresia, etc. White type defects: defect interventricular septum, atrial septal defect, etc.

multiple damage to organs and systems, which is caused by abnormalities of chromosomes or mutation of any genes. This form requires examination of the child and his relatives in the genetic center.

The structure of congenital heart defects in newborns

Most often, cardiologists encounter children after surgical correction heart defect. Thanks to the introduction of perinatal screening, as well as the mandatory examination of all children in the first year of life (ECHOCG screening), heart defects are generally detected early. This allows timely conduct of adequate surgical treatment. Most children receive this type of care in a federal or regional cardiology center. After operations, it is often necessary to continue nursing the child in a hospital, including the cardiology department. The selection and correction of therapy for heart failure is carried out, as well as dynamic monitoring in the early and long-term after the operation. If a heart disease is detected for the first time in an adult child (over three years old), a cardiologist conducts a full examination, preparation for surgery and transfer to a federal or regional cardio center. Close contact and cooperation with cardiologists and cardiac surgeons of the Cardiology Center allows us to provide the necessary highly specialized assistance to a sick child as quickly as possible, without delay.

Where are cardiovascular diseases treated in children

Krasnoyarsk children are being treated at the cardio-rehabilitation and nephrology department of the Krasnoyarsk Regional Clinical Center for Maternal and Child Health, which has 56 beds. Of these, 15 are cardiac beds, 18 are rheumatological, and 23 are nephrological. internal organs, duplex scanning of the vessels of the brain and kidneys, computed tomography and magnetic resonance imaging. Full laboratory examination, biopsy of the kidneys, skin. The department has tested and uses progressive methods of treatment: modern antihypertensive drugs, intra-articular punctures, pulse therapy, genetically engineered drugs for connective tissue diseases, hyperbaric oxygenation.

To the department planned hospitalization children is carried out in the direction of a cardiologist or a local pediatrician. In case of emergency hospitalization during an exacerbation of the disease, or to assess the effectiveness of the prescribed therapy, or its correction by transferring from the local district medical institution through the emergency room.

Every year the number of children with congenital pathologies. Among childhood diseases, one of the first places is occupied by diseases associated with the cardiovascular system. Among heart diseases in children, congenital malformations are distinguished, arterial hypertension and hypotension, rheumatism, inflammatory diseases and acquired vices.

All these diseases are dangerous and can lead not only to disability, but also to premature death of the child.

Children's heart compared with adults has a number of physiological features that change with age.

The heart of newborns is larger than that of adults when compared to the total body weight. Both ventricles are approximately equal, and the thickness of their walls is about 5 mm. The mass of the heart increases in parallel with the growing up of the child: by the age of 8 months, the heart doubles, by the third year of life - the mass of the heart triples, and by the age of six, the mass increases 11 times. In newborns, the heart is located higher and lowers with age. In children, the pulse is normal more often than in adults. This phenomenon is caused by a higher contractility of the heart muscle, which is increased due to intensive metabolism and less influence of the vagus nerve on the work of the heart. For newborns normal pulse- 120-140 beats per minute. With age, the heart rate gradually decreases. A normal children's pulse is unusual compared to an adult (respiratory arrhythmia is observed): on inspiration, the pulse rate quickens, on exhalation it becomes less frequent. In addition, in the heart of a newborn child there are anatomical prerequisites for unnatural blood flow - an oval window through which the right and left atrium can communicate, and an arterial duct connecting the pulmonary trunk with the descending aorta. These formations function during the intrauterine period and can remain active in a healthy child for quite a long time. The ductus arteriosus may remain open for the first two months of life, and the foramen ovale may remain open for 8 days to 4 years or more.

An increase in cardiac output in children is associated with increased needs of organs and tissues of a growing organism. Children's blood pressure is lower than in adults and increases gradually with the age of the child. For newborns, normal systolic blood pressure is approximately 70 mm Hg. Art., by the 1st year of life it averages about 90 mm Hg. Art. In the future, the increase in pressure occurs intensively in the first two or three years of life and during puberty. In the future, the pressure increases in parallel with an increase in the speed of propagation of the pulse wave through the muscle vessels and depends on their tone.

Summarizing all that has been said, it can be seen that in childhood there are a number of factors that facilitate the circulation of blood through the vessels and chambers of the heart. Namely, a large mass of the heart relative to body weight and rather wide openings between its departments and the main vessels. In young children, a small systolic blood volume is compensated by a high frequency of cardiac messages, as a result, the minute volume of blood relative to body weight is greater than in adults. Also, children have structures that are uncharacteristic for an adult, through which communication of the large and small circles of blood circulation is possible. All these factors, in addition to their adaptive function, are fraught with some danger. Namely, they significantly limit the reserve capacity of the heart at an early age due to stiffness (weak elasticity) of the heart muscle, a high heart rate and, consequently, a shorter diastole.

The main heart diseases that occur in children are:

congenital heart defects

Congenital heart disease (CHD) called an anatomical defect in the structure of the heart or great vessels, which is present from the moment of birth. Congenital malformations arise as a result of a violation of the embryonic development of the cardiovascular system, or are formed as a result of the negative impact of adverse factors on the body of a newborn, for example, respiratory disorders. The latter is especially important for premature babies.
All vices can be divided into three large groups.

1. Congenital heart disease of the pale type - with an arteriovenous shunt: atrial septal defect, ventricular septal defect, patent ductus arteriosus.
2. Congenital heart disease of the blue type - with a veno-arterial shunt: tetralogy of Fallot, transposition of the great vessels, etc.
3. Congenital heart disease without a shunt, but with obstruction of blood flow: stenosis of the aorta and pulmonary artery.

Unfortunately, in recent years, the number of cases of birth of children with heart defects has increased.

Causes of the disease

There are several groups among the causes leading to congenital heart defects.

1. Chromosomal disorders - 5%. In this case, CHD is part of the syndrome of polysystemic malformation. For example, in Down syndrome, atrial and ventricular septal defects are very often observed. Down syndrome is a variant of chromosomal pathology that often occurs in perfectly healthy parents.
2. Mutations of individual genes - 2-3%. As in the first case, congenital prophets of the heart with gene mutations are combined with anomalies in the development of other organs. Gene mutations are inherited.
3. Environmental factors - 1-2%. Of the most important factors This group can be divided into somatic diseases of a pregnant woman (for example, diabetes mellitus), the effect of X-ray radiation on the mother's body in the first trimester of pregnancy, certain medications, viruses, alcohol, etc.
4. Polygenic multifactorial inheritance - 90%. In most cases, a predisposition to a defect is inherited, which is provoked by environmental factors acting on the embryo (fetus) or newborn.

Congenital heart defects are detected with a fairly high accuracy during planned ultrasound scans during pregnancy. This procedure allows you to identify up to 90% of CHD.

Clinical picture

A variety of anatomical and functional disorders determines the originality of the clinical picture for each of the defects. However, there are several common symptoms that are characteristic of all congenital heart defects:

• discoloration of the skin - pallor or cyanosis - depending on the type of defect;
• shortness of breath that appears or worsens with physical exertion;
• fatigue, lag in physical and mental development;
• children with congenital heart disease often fall into the category of CHD - often suffering from respiratory infections for a long time.

Treatment

The main method of treatment of congenital heart defects today remains surgical method. Moreover, it is very important that surgical correction is made as early as possible.

Congenital heart defects of the pale type

This group includes defects of the interatrial and interventricular septa, open ductus arteriosus. With each of these defects, there is an anastomosis between the left and right parts of the heart or the main vessels. Since the pressure in the left parts of the heart and the aorta is much greater than in the right, the blood is discharged from left to right. That is, part of the arterial blood mixes with the venous blood and again goes to the pulmonary circulation. This leads to an overload of the small (pulmonary) circulation. Therefore, the main clinical manifestation of these defects will be shortness of breath during physical exertion. Paleness appears only with a significant amount of shunting. With age, symptoms of heart failure appear in both circles.

Diagnosis is based on echocardiography data, or, more simply, ultrasound of the heart.
With an open ductus arteriosus, only surgery.

With a ventricular septal defect in its lower (muscular) part, spontaneous closure of the defect or a significant decrease in its size is possible. If the hole is located in the upper, membranous, part, only surgical correction is possible.
Treatment of an atrial septal defect is also surgical. In some cases, when the atrial septal defect is an open oval window, this defect may not manifest itself as heart failure. Therefore, unclosed foramen ovale are classified as minor developmental anomalies.

Congenital heart defects of the blue type

This group got its name because of the cyanotic color of the skin of children suffering from such defects. The bluish color of the skin is due to the ingress of venous blood from the right sections into the systemic circulation.

Tetralogy of Fallot

Tetralogy of Fallot is a complex congenital heart disease. At classic version four signs are found: ventricular septal defect, right ventricular outflow stenosis, aortic dextroposition (malposition) and right ventricular myocardial hypertrophy. Since the dextroposition of the aorta is secondary, associated with a high location of the ventricular septal defect, it is often said that the aorta originates from the left and right ventricles.

Symptoms of Fallot's tetrad.
The main symptom is cyanosis, which reaches its maximum by the age of one. One of permanent signs is shortness of breath, which in Fallot's tetrad is characterized by arrhythmic deep breathing with a normal frequency. Quite quickly formed Drumsticks"and" watch glasses "- thickening of the nail phalanges of the fingers, along with an increase in size and the nail plate. The most severe manifestation of Fallot's tetrad is shortness of breath and cyanotic attacks. The mechanism of their occurrence is associated with a spasm of the efferent section of the right ventricle, as a result of which almost all the blood depleted of oxygen from the right ventricle enters the aorta. The consequence of this is the strongest hypoxia of the brain, manifested by anxiety, fear, loss of consciousness and convulsions. The lack of blood flow to the lungs is manifested by a sharp attack of shortness of breath. Possible death.

Treatment. All children with Fallot's tetrad are shown surgical treatment, which is carried out in two stages. AT preoperative period prevention is being carried out bacterial complications antibiotics.

Complete transposition of the great vessels

With this congenital heart disease, blood from the right ventricle enters the aorta, and from the left - into the pulmonary artery. Severe shortness of breath and cyanosis appear immediately after birth. Without surgical treatment, the life expectancy of patients usually does not exceed two years.

Birth defects with obstruction of blood flow

Stenosis (narrowing) of the aorta

Narrowing of the aortic orifice creates an obstruction to blood flow from the left ventricle to the aorta. Narrowing may be at the level aortic valve, above or below it. The small circle of blood circulation in this case, the UPU suffers from congestion, and the large one - from a lack of blood.
Symptoms of the disease are pale skin, tachycardia, shortness of breath, palpitations, pain in the heart area, headache and dizziness, fainting
These symptoms increase dramatically with physical activity, so children should not play sports and perform heavy physical activity, as they can lead not only to an exacerbation of symptoms, but also to the death of a child.
Treatment. Aortic stenosis is treated surgically. Treatment is prescribed for the severity of symptoms.

Coarctation of the aorta

Aortic coarctation is a segmental narrowing of the aortic lumen. The length of the stenosis site can be different, but usually begins above the place where the left subclavian artery. Thus, in the upper half of the body there is an increased arterial pressure, lower - reduced blood pressure and signs of tissue ischemia. With severe arterial hypertension in the upper half of the body, headache, nausea, vomiting, vision changes, frequent nosebleeds. Lack of blood supply to the lower half causes numbness of the lower extremities, a feeling of crawling, weakness when walking, pain in the legs, constantly cold feet. When measuring blood pressure in the legs, its decrease is detected. These symptoms sharply increase with physical exertion.

Diagnostics. Diagnosis of coarctation of the aorta is usually not difficult and is based on the clinical picture and instrumental methods- ECG, echocardiography (EchoCG). However, sometimes this congenital heart disease remains unrecognized, since the first months - a year of life, children can grow and develop normally.

Treatment. The only treatment for coarctation is surgery. Without such treatment, children usually do not live past 2-3 years of age.

Isolated pulmonary stenosis

Pulmonary stenosis is characterized by obstruction of blood flow from the right ventricle to the pulmonary circulation.
With a small stenosis, the growth and development of the child is not disturbed, and clinical symptoms may appear in adulthood. With severe stenosis, the child develops early shortness of breath, pain in the heart, palpitations, and later - swelling in the legs, fluid accumulation in the cavities. This course of the defect requires surgical treatment.

Arterial hypertension and hypotension in children

Arterial hypertension and hypotension are most often signs of neurocirculatory (vegetative-vascular) dystonia, which, in addition to pressure changes, is manifested by shortness of breath, weakness, pain in the heart, weakness, fatigue, and neurotic disorders. All these violations are functional in nature and are not dangerous to the life and health of the child. But still, it is better that such children are registered with a pediatrician, since with age functional disorders can be transformed into organic changes.

Rheumatism

It is extremely important in childhood not to miss acute rheumatic fever. It is caused by β - hemolytic streptococcus group A. Acute rheumatic fever occurs 1-5 weeks after suffering a sore throat. During acute rheumatic fever, antibodies are formed against the body's own tissues, but the heart suffers the most.
Clinical manifestations. The fever itself is manifested by temporary inflammation of large joints, carditis - inflammation of the myocardium and endocardium. Small painless subcutaneous nodules appear on the legs and arms, a rash in the form of annular erythema is possible on the skin. Damage to the nervous system is noticeable by a change in the emotional sphere and convulsive syndrome in the form of irregular twitches - chorea. All manifestations of acute rheumatic fever are temporary, except for carditis. Even myocarditis can pass without a trace. Rheumatic endocarditis is extremely dangerous, since inflammation of the endocardium also spreads to the valves of the heart, leading to the formation of various acquired defects. The mitral valve is most commonly affected. Deficiency is forming mitral valve, its stenosis, or a combination of these defects.
If acute rheumatic fever is not recognized in time, then the acquired heart disease remains undiagnosed for a long time and progresses. In 20-30 years, signs of heart failure begin to appear. First, there is stagnation of blood in the pulmonary circulation, which is manifested by shortness of breath and nocturnal attacks of suffocation. With decompensation of mitral defect, stagnation occurs in a large circle in the form of edema, accumulation of fluid in the cavities and damage to internal organs.

For the prevention of acquired mitral valve disease, it is necessary:

1. Prevention of purulent tonsillitis, and if they occur, adequate treatment and only in a hospital.
2. After suffering a purulent tonsillitis, observation by a district pediatrician is necessary for at least a year. Timely listening to the systolic murmur at the apex of the heart allows the pediatrician to take timely measures to prevent the occurrence of mitral valve disease.

Inflammatory heart disease

Myocarditis is an inflammation of the heart muscle due to various reasons. An important etiological factor in the development of myocarditis is rheumatism. Myocarditis can also be the result of bacterial and viral infections, sometimes an allergic process, and other less significant causes.

clinical picture. Myocarditis is manifested by weakness, fatigue, shortness of breath, palpitations, shortness of breath, a feeling of heaviness in the chest. If myocarditis is combined with endocarditis, then signs of an emerging heart disease are found, and when combined with pericarditis, a pronounced pain syndrome is detected.
Diagnosis of myocarditis is based on ECG, EchoCG, X-ray data, results of physical (external examination of the child) and laboratory examination.
Treatment is aimed at eliminating the causes of myocarditis and preventing complications.

The nuances of pediatric cardiology

Pediatric cardiology has its own characteristics. Unlike an adult, children rarely complain of symptoms characteristic of diseases of the cardiovascular system, so it is necessary to more carefully interview the child and focus on physical and instrumental examination. It should also be remembered that with a slight severity of the defect, the child can grow and develop normally for a long time, play and run with healthy children. However, late diagnosis of heart disease can lead to severe heart failure in a person and early death. The use of CardioVisor can come to the rescue. Thanks to the services, the child's heart will always be under reliable control, since the cardiovisor can be used even at home.

Risk of childhood heart disease

Such defects as tetralogy of Fallot, transposition of the great vessels, etc. pose a direct threat to the life of the child immediately after birth. Sick children are either operated on or they soon die. Postoperative mortality in these cases is also high.

But many congenital heart defects are fraught with hidden danger. If these defects are identified, children are recommended surgical treatment of the defect, but parents refuse the operation, since the child does not look sick. When symptoms of heart failure appear at the age of 20-25, it is already too late to do the operation due to the very high operational risk. Thus, a person lives for the last few years as a severely disabled person and dies at a young age.

Parents whose children have heart disease need to carefully monitor the general state of health, the child's nutrition, daily routine, as well as physical and emotional stress.
Firstly, for such a child it is necessary to draw up a strict regime of work and rest, which does not allow long and heavy physical exertion. However, physical activity should not be completely excluded, as this will lead to a sharp weakening of the heart muscle.

You also need to limit psycho-emotional stress.

Equally important is a diet rich in complete proteins (meat, eggs, fish, cottage cheese), fresh fruits and vegetables, which contain potassium and magnesium (dried fruits, decoctions of them).
For the prevention of heart disease in children, the most important measure is the timely detection and treatment of bacterial and viral infections. This is especially true for purulent tonsillitis. Do not forget about hardening and physical education.

You also need to remember to undergo regular check-ups with pediatrician and pediatric cardiologist. Today there is a unique opportunity to monitor a child's heart. There has always been a difficulty in analyzing the ECG of babies due to the peculiarities of the work of the children's cardiovascular system. Thanks to the site service, today it is possible to monitor children's health, namely at the work of a small heart, with the help of CardioVisor. Using the services, parents will always be aware of the health status of their beloved child. The service site can provide invaluable assistance in monitoring the heart of operated children, since after a major heart operation, the likelihood of complications is high. At this stage of a child's life, the CardioVisor can always be nearby and provide assistance in detecting an impending pathological condition.

Take care of the child's heart!

Rostislav Zhadeiko, especially for the project .

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Diseases of the cardiovascular system occupy one of the leading places in the structure of morbidity of the population, determining the level of loss of the able-bodied population and mortality. Currently, mortality from diseases of the circulatory system in Russia is 900:100,000 among men and 600:100,000 among women.

The origins of many diseases of the circulatory system, usually slowly developing, lie in childhood, especially since over the past decade the prevalence of cardiovascular diseases in children has increased 3 times. Apparently, earlier there were more children with this pathology than expected, since during the same time the diagnostic capabilities have improved significantly. Also noteworthy is the increase in the number of children with chronic diseases of the cardiovascular system, including children with disabilities. The structure of cardiovascular pathology in childhood has also changed: the frequency of rheumatic heart disease and infective endocarditis has decreased, but the proportion of rhythm disturbances, arterial hypertension, cardiomyopathies, SVD, and functional disorders has increased. The number of children with congenital malformations and metabolic disorders of the myocardium increases annually. The development of these diseases is often due to dysplasia of the connective tissue of the heart, hereditary predisposition or genetic defects.

In childhood, subjective symptoms of pathology of the circulatory organs are often absent or minimally expressed. In the future, as the child grows and is exposed to many different factors (emotional and physical overload, bad habits, unfavorable environmental conditions, etc.), this pathology manifests itself, in some cases leading to death.

It follows from the above that not only a pediatrician, but also a general practitioner needs to have an idea about the entire spectrum of pathology of the circulatory organs in children. Attention should be paid

for weakness, shortness of breath, complaints that are not characteristic of children (pain in the heart, palpitations, etc.), coloration of the skin, deformities of the chest and fingers, lag in physical development and timely conduct the necessary examination of the child. Prevention of diseases of the cardiovascular system and adverse outcomes associated with the pathology of the heart and blood vessels in adults must begin in childhood. Dispensary monitoring of the state of the cardiovascular system should be carried out in all children without exception, starting from the neonatal period, with the obligatory measurement of blood pressure in the arms and legs, ECG, EchoCG.

Congenital malformations of the heart and great vessels

Congenital heart defects (CHD) are abnormalities in the morphological development of the heart and large vessels. UPUs are usually formed at the 2-8th week of intrauterine development as a result of a violation of the processes of embryogenesis.

CHD is observed with an average frequency of 5-8 per 1000 live births. When stillbirths and late miscarriages are taken into account, the frequency increases to 9-12:1000, exceeding the prevalence of all other developmental anomalies. At an older age, CHD is observed much less frequently, since up to 70% of children with this pathology (in the absence of proper, including surgical, treatment) die in the first year of life.

Etiology

The specific causes of CHD are unknown. They are often associated with chromosomal abnormalities detected by karyotyping in more than 1/3 of patients with congenital heart disease. Most often, trisomy is detected on chromosomes 21, 18 and 13. In addition to Down's disease, there are about twenty hereditary syndromes, often accompanied by CHD. In total, syndromal pathology is found in 6-36% of patients. The monogenic nature of CHD has been proven in 8% of cases; about 90% are inherited multifactorially, i.e. is the result of a combination of genetic predisposition and exposure to environmental factors. The latter act as provoking, revealing a hereditary predisposition when the "threshold" of their joint action is exceeded.

Defects in the genetic code and violations of embryogenesis can also be acquired when the fetus and mother's body are exposed to certain adverse factors [radiation; alcoholism, drug addiction, maternal endocrine diseases (DM, thyrotoxicosis); viral

and other infections suffered by a woman in the first trimester of pregnancy (rubella, influenza, hepatitis B); intake of certain drugs by a pregnant woman (lithium preparations, warfarin, antimetabolites, anticonvulsants)]. Of great importance in the occurrence of pathology of the heart and blood vessels are mixed viral-viral and enterovirus infections transferred by the child in utero.

Pathogenesis

The factors listed above, affecting the fetus at critical moments of embryogenesis, disrupt the formation of heart structures, cause dysplastic changes in its framework. Incomplete, incorrect or untimely closure of the septa between the atria and ventricles occurs, defective formation of valves, insufficient rotation of the primary heart tube with the formation of aplastic ventricles and improperly located great vessels, openings characteristic of embryonic circulation are preserved. Fetal hemodynamics usually do not suffer, and the child is born well developed. Compensation may persist for some time after birth. In this case, CHD appears only after a few weeks or months, and sometimes even in the second or third year of life.

Depending on the characteristics of blood circulation in the large and small circles, the UPU is divided into three groups (Table 12-1).

Table 12-1.Classification of congenital heart defects

Malformations with overflow of the pulmonary circulation account for up to 80% of all CHD. They are united by the presence of a pathological communication between the large and small circles of blood circulation and (initially) the discharge of blood from the arterial bed into the venous. The overflow of the right parts of the heart leads to their gradual hypertrophy, as a result of which the direction of the discharge can change to the opposite. As a result, a total

heart failure and circulatory failure. The overflow of the small circle contributes to the emergence of acute, and then chronic pathology of the respiratory system.

The basis of defects with depletion of the pulmonary circulation is most often the narrowing of the pulmonary artery. Insufficient saturation of venous blood with oxygen leads to constant hypoxemia and cyanosis, developmental delay, the formation of fingers in the form of "drumsticks".

With defects with depletion of the systemic circulation, hypertension develops above the narrowing site, spreading to the vessels of the head, shoulder girdle, and upper limbs. The vessels of the lower half of the body receive little blood. Chronic left ventricular failure develops, often with impaired cerebral circulation or with coronary insufficiency.

Clinical picture

It depends on the size and location of the septal defect, the degree of vasoconstriction, the direction of blood flow and changes in this direction, the degree of pressure drop in the pulmonary artery system, etc. For small defects (eg, atrial septum, ventricular septal muscle, minor pulmonary stenosis) clinical manifestations may be missing.

Congenital heart disease should be suspected if a child is lagging behind in physical development, shortness of breath occurs during movement, pallor (aortic defects) or cyanotic coloration of the skin, severe acrocyanosis (pulmonary artery stenosis, tetralogy of Fallot). When examining the chest, a "heart hump" can be detected, with palpation of the heart area - systolic (with high VSD) or systolic-diastolic (with open ductus arteriosus) trembling. Percussion reveals an increase in size and / or a change in the configuration of the heart. During auscultation, attention is paid to the splitting of tones, the accent of the II tone on the aorta or pulmonary artery. With most defects, you can hear a systolic rough, sometimes scraping noise. It is often carried out on the back and usually does not change with a change in body position and load.

The features of the "blue" defects, combined with narrowing of the pulmonary artery (primarily tetralogy of Fallot), in addition to total cyanosis, include the favorite resting position "squatting" and shortness of breath-cyanotic (hypoxemic) attacks associated with spastic narrowing of the outflow tract of the right ventricle and acute hypoxia of the brain. A hypoxemic attack occurs suddenly: anxiety, agitation appear, shortness of breath and cyanosis increase,

possible loss of consciousness (fainting, convulsions, apnea). Attacks last from several minutes to 10-12 hours, and they are more often observed in young children (up to 2 years) with iron deficiency anemia and perinatal encephalopathy.

Narrowing of the aorta at any level leads to systolic and diastolic overload of the left ventricle and changes in blood pressure: with stenosis in the area of ​​the aortic valve, blood pressure is lowered, with coarctation of the aorta, it is increased on the arms and lowered on the legs. Aortic malformations are characterized by a lag in the development of the lower half of the body and the appearance (at 8-12 years) of complaints that are unusual for children and associated with circulatory disorders in a large circle (headache, weakness, shortness of breath, dizziness, pain in the heart, abdomen and legs).

The course of the IPN has a certain periodicity, which makes it possible to distinguish three phases.

1. Phase of primary adaptation. After birth, the child's body adapts to the hemodynamic disturbances caused by CHD. Insufficient compensation opportunities, the unstable state of the child at an early age sometimes lead to a severe course of the defect and even death.

2. The phase of relative compensation begins in the 2nd or 3rd year of life and may last for several years. The condition of the child and his development are improved due to hypertrophy and hyperfunction of the myocardium. different departments hearts.

3. The terminal (irreversible) phase is associated with gradually developing myocardial dystrophy, cardiosclerosis, and a decrease in coronary blood flow.

Complications.CHD can be complicated by cerebral hemorrhages, myocardial infarction, and the addition of infective endocarditis.

Laboratory and instrumental research

In blood tests with "blue" defects, a decrease in p a O 2 and an increase in p a CO 2, an increase in the content of erythrocytes, hematocrit and Hb concentration are detected. The ECG reveals signs of hypertrophy and overload of individual chambers of the heart: the right sections - with "blue" defects, the left - with "pale". On PCG, systolic and diastolic murmurs, typical for each defect in form, amplitude, frequency, location and duration. Echocardiography allows visualization of septal defects (Fig. 12-1 on the insert), the caliber of large vessels, and the distribution of blood flows.

X-ray reveals cardiomegaly, defiguration of the heart shadow [mitral, with a smoothed "waist of the heart", with

covered ductus arteriosus, aortic ("slipper") with tetralogy of Fallot, fig. 12-2 on the insert], narrowing of the vascular bundle in the frontal plane and its expansion in the sagittal plane (with transposition of the great vessels). With defects accompanied by overflow of the small circle (pulmonary hypertension), the vascular pattern of the lungs increases (Fig. 12-3 on the insert).

The diagnosis of congenital heart disease is based on the early (from the moment of birth or during the first 2-3 years of life) the appearance of fatigue, shortness of breath, cyanosis, "heart hump", trembling over the region of the heart, cardiomegaly, constant intense noise, conducted on the back. Measure blood pressure in the arms and legs. The diagnosis is confirmed by the detection of ECG signs of hypertrophy and overload of the heart chambers, fixation of typical murmurs on FCG, visualization of the defect on EchoCG, and detection of arterial blood gas disorders. A change in the configuration of the heart is detected on a chest x-ray.

Differential diagnosis in the neonatal period and in early childhood is carried out with congenital early and late carditis. After 3 years, CHD is differentiated from non-rheumatic carditis, rheumatism, bacterial endocarditis, cardiomyopathies, and functional disorders of the cardiovascular system. The latter are often based on dysplasia of the connective tissue structures of the heart and its congenital minor anomalies (additional chords, PMC, structural features of the septa, papillary muscles, etc.). It is also necessary to differentiate the IPU among themselves.

Treatment

Treatment for most CHD is surgical. The term of surgical intervention depends on the degree of compensation of hemodynamic disorders. Recently, in connection with the success of cardiac surgery, there has been a tendency towards earlier correction of defects. At the same time, with defects such as a small ASD or low-lying VSD (Tolochinov-Roger disease), there is no need for surgical correction, and the patent ductus arteriosus and some septal defects close with age.

The operation is carried out in the phase of relative compensation in a specialized hospital more often in one stage. They perform not only interventions on the open heart under conditions of hypothermia, but also sparing operations - X-ray endovascular closure of septal

defects, balloon angioplasty, endoprosthetics (aorta), stenting, vascular embolization. Sparing techniques for some defects can be an alternative to major cardiological operations.

Conservative treatment is carried out in preparation for surgery and after it (rehabilitation). It includes the following components.

Sparing (with heart failure - bed) rest.

Wholesome fractional nutrition.

Aerotherapy and oxygen treatment for severe symptoms of oxygen deficiency.

Medicines that affect metabolic processes in the myocardium (potassium and magnesium aspartate, inosine, cocarboxylase, vitamins C and group B), in age doses.

Means that improve the rheological properties of blood and microcirculation, for example, xanthinol nicotinate 0.15 mg / kg / day, vitamin E.

β-blockers (propranolol 0.5-2.0 mg / kg / day in 3-4 doses) to prevent hypoxic crises and as membrane stabilizers in arrhythmias.

Cardiac glycosides and diuretics are prescribed for acute or subacute heart failure.

Treatment for a hypoxic crisis is carried out according to the scheme proposed by V.I. Burakovsky and B.A. Konstantinov (Table 12-2).

Table 12-2.Treatment for hypoxic crisis

Prevention

Prevention is aimed at protecting the health of a pregnant woman, especially in the early stages of gestation: preventing viral and other infectious diseases, eliminating bad habits and adverse environmental impacts; compliance with a gentle work regime, proper nutrition, etc. In families with hereditary diseases medical genetic counseling is required. If a complex heart defect is detected by ultrasound of the fetus, termination of pregnancy is indicated.

Children before and after surgery should be observed by a cardiorheumatologist and a cardiac surgeon. All foci of chronic infection must be sanitized. Surgical interventions (tonsillectomy, adenotomy, tooth extraction) are carried out under the cover of antibiotics.

Forecast

The prognosis for most patients is favorable for life, provided that the diagnosis is established in a timely manner and a qualified surgical intervention is performed at the optimum time. Mortality in such cases is 1-2%. With complex combined defects (and they are not more than 5% of the total number of CHD), mortality reaches 25%. CHD is the third leading cause of childhood disability.

Mitral valve prolapse

Mitral valve prolapse (MVP) - bending of one or both leaflets of the mitral valve into the cavity of the left atrium during left ventricular systole. This is one of the most common and clinically significant anomalies of the valvular apparatus of the heart. PMK may be accompanied by prolapse of other valves or be combined with other minor anomalies in the development of the heart.

MVP is detected in 2-18% of children and adolescents, i.e. significantly more frequently than in adults. In heart diseases, MVP is recorded much more often: up to 37% in CHD, up to 30-47% in patients with rheumatism, and up to 60-100% in patients with hereditary connective tissue diseases. MVP can be detected at any age, including the neonatal period, but it is more often observed in children older than 7 years. Up to 10 years, MVP is found with the same frequency in boys and girls. In the older age group, MVP is detected 2 times more often in girls.

Etiology and pathogenesis

By origin, primary (idiopathic) and secondary MVP are distinguished.

Primary MVP is associated with connective tissue dysplasia with an autosomal dominant type of inheritance, which is also manifested by other microanomalies in the structure of the valvular apparatus (changes in the structure of the valve and papillary muscles, impaired distribution, improper attachment, shortening or lengthening of the chords, the appearance of additional chords, etc.). In the development of connective tissue dysplasia, an important role is played by metabolic disorders, deficiency of trace elements, in particular magnesium and zinc.

Secondary MVP accompanies or complicates various diseases. With secondary MVP, as with primary,

of great importance is the initial inferiority of the connective tissue. Thus, it often accompanies some hereditary syndromes (Marfan syndrome, Ehlers-Danlos syndrome, congenital contracture arachnodactyly, osteogenesis imperfecta, pseudoxanthoma elastic), as well as CHD, rheumatism and other rheumatic diseases, non-rheumatic carditis, cardiomyopathies, some forms of arrhythmia, SVD , endocrine pathology (hyperthyroidism), etc.

Dysfunction of the autonomic nervous system undoubtedly takes part in the formation of the clinical picture of MVP. In addition, metabolic disorders and micronutrient deficiencies, in particular magnesium ions, are important.

Structural and functional inferiority of the valvular apparatus of the heart leads to the fact that during the period of left ventricular systole there is a deflection of the leaflets of the mitral valve into the cavity of the left atrium. With prolapse of the free part of the valves, accompanied by their incomplete closure in systole, auscultatory recording of isolated mesosystolic clicks associated with excessive tension of the chords. Loose contact of the valve leaflets or their divergence in systole determines the appearance of systolic murmur of varying intensity, indicating the development of mitral regurgitation. Changes in the subvalvular apparatus (elongation of the chords, a decrease in the contractile ability of the papillary muscles) also create conditions for the onset or intensification of mitral regurgitation.

Classification

There is no generally accepted classification of PMC. In addition to distinguishing between MVP by origin (primary or secondary), it is customary to distinguish auscultatory and “silent” forms, indicate the localization of prolapse (anterior, posterior, both valves), the degree of its

intensity (I degree - from 3 to 6 mm, II degree - from 6 to 9 mm, III degree- more than 9 mm), the time of occurrence in relation to systole (early, late, holosystolic), the presence and severity of mitral regurgitation. The state of the autonomic nervous system is also assessed, the type of MVP flow is determined, and possible complications and outcomes.

Clinical picture

MVP is characterized by a variety of symptoms, depending primarily on the severity of connective tissue dysplasia and autonomic disorders.

Complaints in children with MVP are very diverse: increased fatigue, headaches, dizziness, fainting, shortness of breath, pain in the left side of the chest, which are in the nature of cardialgia, palpitations, a feeling of interruptions in the work of the heart. Characterized by reduced physical performance, psycho-emotional lability, increased excitability, irritability, anxiety, depressive and hypochondriacal reactions.

In most cases, with MVP, various manifestations of connective tissue dysplasia are found: asthenic physique, tall stature, reduced body weight, increased skin elasticity, poor muscle development, joint hypermobility, posture disorder, scoliosis, chest deformity, pterygoid scapulae, flat feet, myopia. You can find hypertelorism of the eyes and nipples, the peculiar structure of the auricles, the gothic palate, the sandal-like gap and other minor developmental anomalies. Visceral manifestations of connective tissue dysplasia include nephroptosis, anomalies in the structure of the gallbladder, etc.

Often, with MVP, a change in heart rate and blood pressure is observed, mainly due to hypersympathicotonia. The borders of the heart are usually not expanded. Auscultatory data are the most informative: isolated clicks or their combination with late systolic murmur are more often heard, less often - isolated late systolic or holosystolic murmur. Clicks are recorded in the middle or at the end of systole, usually at the apex or at the fifth point of auscultation of the heart. They are not carried out outside the region of the heart and do not exceed the second tone in volume, can be transient or permanent, appear or increase in intensity in a vertical position and during physical activity. In some cases (with the "silent" variant of MVP), auscultatory symptoms are absent.

The symptomatology of secondary MVP is similar to the primary one and is combined with manifestations characteristic of a concomitant disease (Marfan's syndrome, congenital heart disease, rheumatic heart disease, etc.).

Instrumental Research

On the radiograph, as a rule, determine the normal or reduced size of the heart. Often, a moderate bulging of the pulmonary artery arch is found, associated with inferiority of the connective tissue. On the ECG, transient or persistent changes in the terminal part of the ventricular complex (decrease in the amplitude of the T wave, shift of the ST segment), various arrhythmias (tachyarrhythmia, extrasystole, slowing of atrioventricular conduction), more often detected with Holter monitoring, are recorded on the ECG. Possible prolongation of the Q-T interval. Echocardiography is the most informative, revealing displacement of one (mainly posterior) or both leaflets of the mitral valve, changes in the excursion of the mitral ring, interventricular septum and other parts of the heart, thickening and uneven contours of the leaflets (signs of myxomatous degeneration), microanomalies in the structure of the valvular apparatus, as well as signs of mitral regurgitation . Sometimes, echocardiography reveals dilatation of the aorta, pulmonary artery trunk, open foramen ovale, prolapse of other valves, which indicates widespread connective tissue dysplasia.

Diagnosis and differential diagnosis

Clinical and instrumental criteria are used to diagnose MVP. The main criteria are characteristic auscultatory and echocardiographic signs, which is of decisive importance. Anamnesis data, complaints, manifestations of connective tissue dysplasia, ECG and X-ray results contribute to the diagnosis, but are of auxiliary importance.

MVP must be differentiated primarily from congenital or acquired mitral valve insufficiency, from systolic murmurs caused by other variants of minor anomalies in the development of the heart or dysfunction of the valvular apparatus. Echocardiography is the most informative, contributing to the correct assessment of the detected cardiac changes.

Treatment

Treatment for MVP depends on its form, the severity of clinical symptoms, including the nature of cardiovascular and autonomic changes, as well as the characteristics of the underlying disease.

With a "silent" form, treatment is limited to general measures aimed at normalizing the vegetative and psycho-emotional status of children, without reducing physical activity.

In the auscultatory variant, children who satisfactorily tolerate physical activity and who do not have noticeable ECG abnormalities, can engage in physical education in general group. Exclude only exercises associated with sudden movements, running, jumping. In some cases, exemption from participation in competitions is necessary.

When mitral regurgitation, pronounced violations of repolarization processes on the ECG, distinct arrhythmias are detected, a significant limitation of physical activity with an individual selection of the exercise therapy complex is necessary.

In the treatment of children with MVP, the correction of autonomic disorders, both non-drug and drug, is of great importance. In case of violations of ventricular repolarization (according to ECG data), agents that improve myocardial metabolism (potassium orotate, inosine, vitamins B 5, B 15, levocarnitine, etc.) are used. Effective drugs that correct magnesium metabolism, in particular orotic acid, magnesium salt. In some cases (with persistent tachycardia, frequent ventricular extrasystoles, the presence of an elongated interval Q-T, persistent disorders of repolarization processes), the appointment of β-blockers (propranolol) is justified, if necessary, antiarrhythmic drugs of other classes. With pronounced changes in the valvular apparatus, prophylactic courses of antibiotic therapy are indicated (especially in connection with surgical intervention) in order to prevent the development of infective endocarditis. Necessarily conservative or surgical treatment of foci of chronic infection.

In case of mitral insufficiency, accompanied by severe, treatment-resistant cardiac decompensation, as well as with the addition of infective endocarditis and other serious complications (pronounced arrhythmias), it is possible to perform surgical correction of MVP (restorative operations or mitral valve replacement).

Prevention

Prevention is aimed mainly at preventing the progression of existing valvular disease and the occurrence of complications. For this purpose, an individual selection of physical activity and the necessary medical and recreational activities, adequate treatment of other existing pathologies (with secondary MVP) are carried out. Children with MVP are subject to dispensary observation with regular examinations (ECG, echocardiography, etc.).

Forecast

The prognosis for MVP in children depends on its origin, the severity of morphological changes in the mitral valve, the degree of regurgitation, the presence or absence of complications. In childhood, MVP, as a rule, proceeds favorably. Complications of MVP in children are rare. It is possible to develop acute (due to detachment of chords, with pulmonary venous hypertension) or chronic mitral insufficiency, infective endocarditis, severe forms of arrhythmias, thromboembolism, sudden death syndrome, most often of an arrhythmogenic nature.

The development of complications, the progression of valvular disorders and mitral regurgitation adversely affect the prognosis. MVP that occurs in a child can lead to difficult-to-correct disorders at a more mature age. In this regard, timely diagnosis, accurate conduct of the necessary therapeutic and preventive measures just in childhood.

Non-rheumatic carditis

Non-rheumatic carditis - inflammatory lesions of the heart of various etiologies, not associated with rheumatism or other systemic diseases. The expediency of using the term "carditis" in pediatric practice is justified by the possibility of simultaneous damage to two or three membranes of the heart.

The prevalence of non-rheumatic carditis in the population is not precisely known. This is due to the lack of a unified approach and the great difficulties in diagnosing this pathology. Non-rheumatic carditis is detected in all age groups, but more often in children of the first years of life with a predominance in boys. According to autopsy, non-rheumatic carditis is found in 3-9% of children who died from various causes.

ETIOLOGY

Non-rheumatic carditis develops under the influence of various factors, mainly infectious. Among the latter, viruses have a leading role, especially Coxsackie A and B, ECHO. In some patients (up to 10%), it is not possible to establish the cause that caused the carditis.

PATHOGENESIS

Non-rheumatic carditis can develop due to the direct cardiotoxic effect of an infectious agent with the formation of inflammatory and destructive changes.

in the membranes of the heart (mainly myocardium). An important role is assigned to immune disorders, often genetically determined.

CLASSIFICATION

The classification of non-rheumatic carditis used in pediatric practice (N.A. Belokon, 1987) provides for the allocation of the period of occurrence [congenital (early, late) and acquired], etiological affiliation, the nature of the course (acute, subacute, chronic), severity, severity heart failure, possible outcomes and complications of the disease.

CLINICAL PICTURE

The clinical picture of non-rheumatic carditis depends on the period of their occurrence, the nature of the course and the age of the child.

congenital carditis

Congenital carditis can manifest immediately after birth or in the first 6 months of life, less often in the 2-3rd year.

Early congenital carditis develops, as a rule, under the action of an infectious agent on the fetus at 16-28 weeks of gestation. Manifested by low body weight at birth or its poor increase in the future, rapid fatigue during feeding, unreasonable anxiety, sweating, pallor. Characterized by cardiomegaly (Fig. 12-4 on the insert), "heart hump", muffled heart sounds on auscultation, progressive heart failure (often total with a predominance of the left ventricular), refractory to treatment. Often there is shortness of breath at rest, cough, aphonia, moderate cyanosis (sometimes with a raspberry tint), various wet and wheezing rales in the lungs, liver enlargement, edema or pastosity of tissues. Arrhythmias (with the exception of tachycardia) are rare. The appearance of systolic murmur may be associated with relative or organic insufficiency of the mitral valve, but more often there is no murmur.

On the radiograph, the heart is spherical or ovoid, and with fibroelastosis, it is trapezoidal. The ECG reveals a rigid rhythm, signs of left ventricular hypertrophy due to an increase in myocardial thickness due to infiltration, damage to its subendocardial sections. With echocardiography, in addition to cardiomegaly and dilatation of the heart cavities, a decrease in the contractile and especially relaxation function of the left ventricular myocardium, valve damage, more often mitral, and pulmonary hypertension are detected.

Late congenital carditis characterized by moderate cardiomegaly, various arrhythmias and conduction disorders up to complete transverse heart block and atrial flutter, loud heart sounds, less pronounced (compared to early congenital carditis) heart failure. Often there are signs of damage to two or three membranes of the heart. Some patients experience attacks of sudden anxiety, shortness of breath, tachycardia with increased cyanosis, seizures, which reflects the combined damage to the heart and central nervous system due to a previous infection, especially caused by Coxsackie viruses.

Acquired carditis

Acquired carditis can occur at any age, but more often in children of the first 3 years of life. Acute carditis

Against the background of the current or shortly after the infection, lethargy, irritability, pallor, an obsessive cough that increases with a change in body position appear; possible bouts of cyanosis, nausea, vomiting, abdominal pain, encephalitic reactions. Gradually or rather acutely develop symptoms of left ventricular failure (shortness of breath, tachycardia, congestive rales in the lungs). Objectively determine the pulse of weak filling, weakening of the apex beat, an increase in the size of the heart, mainly to the left, weakening of the first tone, gallop rhythm, various arrhythmias. There is no systolic murmur, but it is possible with the development of insufficiency (relative or organic) of the mitral valve.

X-ray reveals an increase in the size of the heart of various severity, venous congestion in the lungs, a decrease in the amplitude of systolic-diastolic fluctuations, and sometimes an increase in the thymus gland. On the ECG, a decrease in the voltage of the QRS complex, signs of overload of the left or both ventricles, various rhythm and conduction disturbances (sinus tachya or bradyarrhythmia, extrasystole, atrioventricular and intraventricular blockade; Fig. 12-5), shift of the ST segment, smoothed or negative T wave. Possible infarction-like changes and ECG signs of concomitant pericarditis. On echocardiography, dilatation of the right ventricle and left atrium, hypokinesia of the interventricular septum and rear wall left ventricle, decreased ejection fraction, an increase in the end-systolic and end-diastolic diameters of the left ventricle, signs of mitral valve insufficiency, effusion in the pericardial cavity.

In young children, the disease is severe, with severe clinical manifestations and progression of cardiac

Rice. 12-5.Complete atrioventricular block (ECG in three standard leads).

insufficiency. In older children, carditis usually occurs in a mild or moderate form, with less pronounced symptoms of the disease, rare and less pronounced decompensation, but often accompanied by a variety of rhythm and conduction disturbances, which often determine the clinical picture.

During the treatment of acute carditis, clinical symptoms gradually disappear. Changes on the ECG persist for a longer time. The reverse development of the process occurs after 3 months from its beginning; in addition, carditis can take subacute or chronic course.

Subacute carditis

Subacute carditis is more common in children aged 2 to 5 years. It can develop either after acute carditis, or on its own (primarily subacute carditis) after a long time after SARS, manifesting as pallor, increased fatigue, irritability, loss of appetite, dystrophy. Gradually (sometimes suddenly) heart failure develops or arrhythmias, an increase in the size of the heart, and systolic murmur are accidentally detected.

Symptoms of subacute carditis are similar to those of its acute variant. The formation of a heart hump is possible, the heart tones are loud, the accent of the II tone over the pulmonary artery is pronounced. On the ECG - signs of overload not only the ventricles, but also the atria, persistent arrhythmias and conduction. Heart failure is difficult to treat. These changes are associated with the duration of the process, the development of compensatory hypertrophy of the left ventricular myocardium, a simultaneous decrease in its contractile function, initial manifestations pulmonary hypertension. reverse development

process occurs after 12-18 months, or it acquires a chronic course.

Chronic carditis

Chronic carditis develops more often in children older than 7 years, either in the primary chronic form, or as an outcome of acute or subacute carditis. The clinical picture of chronic carditis is diverse, which is associated, in particular, with the long duration of the disease and the varied ratio of inflammatory, sclerotic and hypertrophic changes in the heart.

Primary chronic variant non-rheumatic carditis a long, asymptomatic course with a predominance of extracardiac manifestations (lagging behind in physical development, weakness, increased fatigue, loss of appetite, sweating, pallor, recurrent pneumonia) is characteristic. Children often lead a normal life, they can play sports. Periodically there are dizziness, shortness of breath, pain in the heart, palpitations, obsessive cough, nausea, vomiting, pain in the right hypochondrium due to heart failure. Perhaps the acute development of bouts of blanching, anxiety, loss of consciousness, convulsions associated with cardiac decompensation or inflammatory changes in the central nervous system associated with carditis. Often, the assumption of cardiac pathology arises only with the manifestation of cardiac decompensation or with the detection of cardiomegaly, persistent arrhythmias, systolic murmur, hepatomegaly during a routine examination, or in connection with an intercurrent disease. Depending on the predominance of cardiosclerosis or myocardial hypertrophy, the following variants of chronic carditis are distinguished: with an enlarged left ventricular cavity - a congestive variant (cardiosclerosis predominates), with a normal left ventricular cavity - a hypertrophic variant, with a reduced left ventricular cavity - a restrictive variant (with or without hypertrophy ).

DIAGNOSTICS

Diagnosis of non-rheumatic carditis is often difficult. It is based on the identification of clinical and instrumental signs of heart damage, mainly myocardium, anamnestic data (establishing a connection between the development of the process and a previous infection, especially a viral one), exclusion of diseases similar in symptoms, dynamic monitoring and evaluation of the effectiveness of therapy. It is also necessary to take into account the level of physical development of the child and the presence of various unmotivated persistent disorders of well-being.

Even more difficulties arise in the diagnosis of rarely developing congenital carditis. There is a need for convincing evidence of the impact on the fetus of an infectious agent, the identification of a generalized infection with reliable laboratory confirmation of it, and the use of all available diagnostic methods including endomyocardial biopsy.

DIFFERENTIAL DIAGNOSIS

The list of diseases with which differential diagnosis of non-rheumatic carditis is carried out depends on the age of the child and the form of carditis.

In newborns and young children, non-rheumatic carditis, especially congenital ones, must be differentiated from congenital heart disease, in particular, with an incomplete form of atrioventricular communication, Ebstein anomaly, and abnormal origin of the left coronary artery from the pulmonary artery.

In newborns, changes in the heart, resembling non-rheumatic carditis, may occur due to perinatal hypoxia (cardiovascular maladaptation syndrome). In this case, cardiomegaly, muffled heart tones, rhythm and conduction disturbances, sometimes heart murmurs and symptoms of circulatory failure are possible. The study of anamnesis, the presence of neurological symptoms, the transient nature of cardiac changes make it possible to exclude the diagnosis of congenital carditis.

In older children, non-rheumatic carditis must be differentiated from rheumatism, arrhythmias of extracardiac origin, myocardial dystrophy, etc.

TREATMENT

Treatment for non-rheumatic carditis depends on its etiology, variant, period of the disease, the presence or absence of circulatory failure. Treatment is carried out in two stages.

At the first stage (hospital) limit motor activity, prescribe a diet enriched with vitamins and potassium salts, establish a drinking regimen. Bed rest for 2-4 weeks is prescribed for acute or subacute carditis, as well as for exacerbation of a chronic one. The expansion of the motor regime should be carried out gradually, under the control of the functional state of the cardiovascular system and ECG dynamics. Mandatory exercise therapy. Drug therapy includes the following drugs.

Non-steroidal anti-inflammatory drugs (NSAIDs) - indomethacin, diclofenac and others for 1-1.5 months.

At severe course, a common process, a high degree of activity, a predominant lesion of the conduction system of the heart - glucocorticoids (prednisolone at a dose of 0.5-0.75 mg / kg / day).

With a protracted and chronic course of carditis - aminoquinoline derivatives (hydroxychloroquine, chloroquine).

In heart failure - cardiac glycosides, ACE inhibitors, diuretics, vasodilators, etc.

Mandatory correction of metabolic disorders in the myocardium, microcirculatory disorders is carried out, according to indications, anticoagulants, antiaggregants, antiarrhythmic drugs are prescribed.

When installed etiological factor(viruses, bacterial flora) - antiviral (Ig, interferon) and antibacterial drugs, immunostimulants.

At the second stage (after discharge from the hospital), the child needs to continue treatment and carry out rehabilitation measures in a local cardio-rheumatological sanatorium. Subsequently, children with carditis are observed by a cardiorheumatologist at the place of residence. Medical examination of patients who have undergone acute and subacute carditis is carried out until complete recovery (on average 2-3 years), and with congenital and chronic variants - constantly. The regularity of control, the scope of studies (X-ray, ECG, EchoCG) is determined individually. During the observation period in the clinic, if necessary, the treatment is corrected, drugs that stimulate metabolic processes are prescribed, and foci of chronic infection are sanitized. Preventive vaccinations can be carried out after suffering acute or subacute carditis no earlier than 3 years later; in the presence of chronic process vaccination is contraindicated.

PREVENTION

Primary prevention includes the prevention of infection of the fetus during pregnancy, hardening of the child, treatment of acute and chronic focal infections, dispensary monitoring of children at risk for cardiovascular diseases. Secondary prevention is aimed at preventing complications and recurrence of the process, achieved by strict adherence to the principles of dispensary observation of patients.

FORECAST

The prognosis of non-rheumatic carditis depends on its variant.

Early congenital carditis is usually severe and often leads to death in the first years and even months of life.

Late congenital carditis with adequate and timely prescribed therapy, the process can acquire a chronic course without progression of cardiac changes; recovery is possible.

The acute variant of carditis in 44.1% of children ends in recovery, in about 50% of patients it acquires a subacute or chronic course and rarely (in 2.2% of cases) leads to death with a slowly, gradually developing process, persistent arrhythmias.

Subacute carditis proceeds less favorably with a higher mortality (up to 16.6%), is resistant to therapy and often transitions to a chronic variant.

In chronic carditis, the prognosis is also often unfavorable, especially with the development of cardiosclerosis, progressive heart failure, pulmonary hypertension, persistent rhythm and conduction disturbances that can lead to the formation of arrhythmogenic cardiomyopathy. The presence of arrhythmias can cause sudden death of children not only with chronic carditis, but also with its other variants.

Infective endocarditis

Infective endocarditis is an acute or subacute inflammation of the valvular and / or parietal endocardium caused by various infectious agents.

Infectious (including abacterial) endocarditis is one of the major causes of death in children and adolescents. The variability and non-specificity of its clinical picture cause objective diagnostic difficulties. Insufficient familiarity of pediatricians, dentists and parents with the principles of prevention of infective endocarditis, as well as an increase in the number of persons at risk (drug addicts, patients after surgical interventions on the heart, patients on immunosuppressive therapy, with long-term central venous catheterization, etc.), lead to an increase in the number of cases.

Infective endocarditis can develop on intact valves (5-6%), but more often complicates congenital (90%) and rheumatic (3%) heart defects, especially after surgical interventions for them.

The frequency of infective endocarditis in children is unknown, but the number of sick children is gradually increasing and is 0.55 per 1000 hospitalized. Boys get sick 2-3 times more often than girls.

Etiology

The most common causative agents of infective endocarditis at present are viridescent streptococcus and Staphylococcus aureus (up to 80% of cases). The former often causes disease on intact valves, the latter on damaged valves. Less often, infective endocarditis is caused by other microorganisms: enterococci, meningo-, pneumo- and gonococci, epidermal staphylococcus, chlamydia, salmonella, brucella, HACEK group (a combination of several gram-negative rods), as well as viruses and fungi; the last two agents mentioned cause the "abacterial" form of infective endocarditis (about 10% of cases). With cardiac catheterization and prolonged standing of the catheter in the central veins, Pseudomonas aeruginosa is often detected, during heart operations and prolonged antibiotic therapy - fungi (Candida, histoplasma).

Infective endocarditis can be congenital or acquired.

Congenital endocarditis develops with acute or exacerbation of chronic viral and bacterial infections in the mother and is one of the manifestations of septicemia.

Acquired infective endocarditis in children of the first 2 years of life occurs more often on intact valves; in older children, the disease usually develops in the presence of heart disease (as in adults). Cardiac surgery is a predisposing factor for the development of infective endocarditis. Predisposing factors are found in approximately 30%

sick. Surgical interventions, primarily on the heart, urinary tract and oral cavity, precede the development of infective endocarditis in 65% of cases.

Pathogenesis

The pathogenesis of infective endocarditis is complex and associated with several factors: an altered immune response of the body, dysplasia of the connective tissue of the heart, damage to the collagen structures of the valvular and parietal endocardium by hemodynamic and infectious effects, a violation of the rheological properties and blood coagulation system, the characteristics of the pathogen itself, etc.

Most often, infective endocarditis develops in patients with morphological defects in the structures of the heart, in which turbulent, slow or increased blood flow leads to changes in the valvular or atrial endocardium (tetralogy of Fallot, small VSD, open ductus ductus arteriosus, coarctation of the aorta, mitral valve defects). The infectious agent circulating in the blood stream settles on the damaged or intact endocardium of the heart and large vessels, causing an inflammatory reaction, delamination of the collagen-rich edges of the valves, deposition of fibrin on them and the formation of thrombotic masses (vegetations). It is also possible that primary thrombosis associated with hemodynamic and rheological disorders(abacterial endocarditis). In this case, the sedimentation of microorganisms on already modified valves occurs later.

In the future, growing vegetations can come off and cause embolism of small and large vessels of the large and small circles of blood circulation.

There are three phases of pathogenesis: infectious-toxic, immuno-inflammatory and dystrophic.

The infectious-toxic phase is formed as a response acute inflammatory reaction of the macroorganism. In this phase, bacteremia is more often detected, while the actual cardiac changes are moderately expressed, the disease proceeds as acute infection with fever, intoxication, inflammatory changes in peripheral blood.

The immunoinflammatory phase is associated with the formation of antibodies both to the antigen of the pathogen and to its own tissues and cryoglobulins. This process proceeds with the participation of complement and the formation of the CEC. This phase is accompanied by a generalization of the process, damage to other internal organs and more distinct changes in the heart. It is considered as an immunocomplex disease.

The dystrophic phase is manifested by chronic inflammation of the endocardium and internal organs, the formation of defects, the deposition of calcium salts in valvular structures, and hemodynamic heart failure. It is possible to identify heart disease a few years after recovery and re-disease with infective endocarditis.

Classification

The classification of infective endocarditis was proposed by A.A. Demin in 1978. A simplified and modified version of it is presented in Table. 12-3.

Table 12-3.Clinical classification of infective endocarditis"

* According to Demin A.A., 1978, modified.

Clinical picture

Three main syndromes play a leading role in the clinical picture: infectious-toxic, cardiac (current endocarditis) and thromboembolic.

Infective endocarditis, especially streptococcal etiology, can begin gradually - with repeated episodes of fever in the evening, malaise, arthralgia, myalgia, sweating, unmotivated weight loss. An acute onset is also possible - with hectic fever, a sharp violation of the general condition, stunning chills and profuse sweats (more often with staphylococcus infection).

In the infectious-toxic phase, endocarditis may not have distinct clinical manifestations, although a proto-diastolic murmur of aortic valve insufficiency can be heard a few days after the onset of the disease. In secondary endocarditis, the number and nature of noises in the area of ​​the already changed valve change. During this period, manifestations of thromboembolism are possible: hemorrhagic rash, periodic hematuria, heart attacks of internal organs. Lukin-Libman spots on the conjunctiva, Janeway spots on the palms and feet, banded hemorrhages under the nails, indicating vasculitis, rarely occur with timely treatment.

In the immunoinflammatory phase, a generalization of the immunopathological process occurs and the addition of myocarditis, and sometimes pericarditis, diffuse glomerulonephritis, anemia, damage to the lymph nodes, liver, and spleen. The color of the skin becomes grayish-icteric ("coffee with milk"), sometimes jaundice develops. The current process in the heart is manifested by moderate pain syndrome, tachycardia, cardiomegaly and deafness of tones (with concomitant myocarditis). There are noises accompanying the defect or destruction of the valvular apparatus (separation of chords or valve leaflets, its perforation). Embolism and heart attacks in this phase of the disease are observed less frequently.

In the dystrophic phase, insufficiency comes to the fore: cardiac, renal, sometimes hepatic, as a result of severe damage to internal organs in a generalized immunopathological process.

In some cases, the features of the clinical picture of infective endocarditis suggest which infectious agent caused its development. The features of streptococcal and staphylococcal endocarditis have already been mentioned above.

Pneumococcal endocarditis develops during the period of convalescence with pneumonia, is localized on the tricuspid and aortic valves, proceeds with high fever, severe toxicosis, and peripheral bacterial embolisms.

Brucella endocarditis has the same localization as pneumococcal. Sometimes it causes the formation of bacterial aneurysms of the sinus of Valsalva with the passage of infection through the aortic wall to the atria, ventricles and other membranes of the heart with the development of intra-atrial and intra-ventricular blocks.

Salmonella endocarditis leads to destruction of the aortic and mitral valves with the formation of blood clots, damage to the vascular endothelium and the development of endarteritis and vascular aneurysms.

Fungal endocarditis is accompanied by the development of pulmonary infarctions, pneumonia, uveitis, and endophthalmitis.

Complicationsinfective endocarditis include heart and kidney failure, the consequences of thromboembolism in the form of cerebral and myocardial infarctions, abscesses of the brain and other organs. These complications can also be regarded as manifestations of the terminal phase of the disease. Perhaps the development of pericarditis, meningitis, arthritis, osteomyelitis and other purulent processes.

Diagnostics

Data from laboratory studies depend on the activity of the process and its phase.

In the initial phase, signs of acute inflammation are found in the peripheral blood: leukocytosis, neutrophilia with a shift leukocyte formula to the left, high levels of ESR, C-reactive protein and a 2 -globulin fraction. An exception is congenital endocarditis, in which such changes may be absent. Subsequently, anemia appears, an increase in γ-globulins, leukocytosis can be replaced by leukopenia, the level of antibodies (including autoantibodies) and the CEC increase.

Urinalysis reveals first transient, then permanent hematuria, proteinuria.

A bacteriological blood test (it is advisable to take the material for the study at the height of the fever and before the start of antibiotic therapy) allows you to identify the pathogen.

With the help of an ECG, the state of the myocardium and pericardium is clarified.

When conducting an echocardiogram, especially a Doppler study, visualize changes in the endocardium: reveal vegetations on the valves (if they are more than 2 mm), specify their size, mobility, ruptures of chords and cusps, signs and degree of aortic and mitral insufficiency.

The diagnosis of infective endocarditis in the initial phase is usually presumptive, since the clinical and laboratory manifestations of the disease are nonspecific.

The main criterion for making a diagnosis is re-inoculation of the pathogen from the blood of a patient with a history of such specific predisposing factors as CHD, recent surgical interventions (especially on the heart), treatment and extraction of teeth, central vein catheterization, intravenous infusions, purulent diseases.

The second, very important criterion for making a diagnosis is typical changes in echocardiography.

Differential Diagnosis

Differential diagnosis in the initial phase is carried out with generalized infectious diseases, salmonellosis, meningococcemia, hemorrhagic vasculitis (in the presence of a hemorrhagic rash); with JRA and polyarteritis nodosa (with severe fever, arthralgia and changes in peripheral blood). It is especially difficult to differentiate infective endocarditis from acute rheumatic fever and SLE, occurring with endocarditis, arthralgia, and multiple organ changes. In this case, take into account:

Previous history (streptococcal infection in rheumatic fever; excessive sun exposure, stress, vaccination in SLE; congenital heart disease and surgical procedures and interventions in infective endocarditis);

Features of the articular and weak severity of the infectious-toxic syndrome in rheumatism (see the section "Rheumatism" in the chapter "Rheumatic diseases");

The presence of thromboembolic syndrome, not characteristic of rheumatism and SLE;

Laboratory data (antistreptococcal antibodies in acute rheumatic fever, LE cells in SLE);

The results of repeated blood cultures (sterile in rheumatism and

SLE).

Treatment

Necessary good nutrition. In the acute period, bed rest is prescribed. The main method of treatment is massive and prolonged antibiotic therapy, taking into account the sensitivity of the isolated microorganism. Antibiotics, their doses, course duration are presented in Table. 12-4.

Table 12-4.The main antibiotics used in children with infective endocarditis of various etiologies

In the absence of positive dynamics within 5-7 days, the therapy is corrected - the antibiotic is changed or its combination with another antibiotic (most often with a short course of gentamicin). With severe immune disorders, prednisolone is added at the rate of 0.5-0.75 mg / kg / day for 2-3 weeks with gradual withdrawal. Spend conventional symptomatic therapy: detoxification, treatment of anemia. With the ineffectiveness of drug therapy resort to surgical intervention. The main indications for surgical treatment of infective endocarditis:

An infectious process not controlled by antibiotics;

Repeated thromboembolism;

Fungal endocarditis;

Uncorrected congestive insufficiency blood circulation;

Abscesses of the myocardium, aneurysms of the sinuses or aorta;

Early (up to 2 months after the operation) endocarditis of the operated heart.

Prevention

Prevention is carried out mainly in risk groups.

preventive antibiotic therapy with any surgical interventions and long-term intravenous, as well as dental manipulations.

Compliance with oral hygiene, regular monitoring by the dentist.

Timely rehabilitation of all foci of chronic infection. Forecast

The prognosis is unfavorable. Mortality is 20-25%, rising to 30-40% with repeated diseases. In half of the patients, the disease leads to the formation of a defect in the aortic or mitral valve. Toxic myocarditis and myocardial abscesses lead to treatment-resistant congestive heart failure. Possible embolism of large vessels, rupture of aneurysms.

Pericarditis

Pericarditis - acute or chronic inflammation sheets of the epicardium and pericardium. Pericarditis may be clinically asymptomatic or develop acutely, leading to cardiac tamponade and sudden death.

The population frequency of pericarditis is unknown. They are diagnosed in approximately 1% of children, and are found at autopsy in 4-5% of cases.

ETIOLOGY

Pericarditis can be infectious and aseptic, accompanying allergic reactions, systemic or metabolic diseases. Sometimes their cause cannot be established. These are the so-called idiopathic pericarditis. It is assumed that a viral infection plays a role in their occurrence. The causative agents of the infectious process in the pericardium can be viruses (Coxsackie B, Epstein-Barr, influenza, adenovirus) and rickettsia; bacteria (strepto-, staphylo-, meningococci, mycoplasmas), tubercle bacillus, actinomycetes; protozoa (amoeba, malarial plasmodium, toxoplasma) and helminths (echinococcus); fungi (histoplasma, candida). In addition, pericarditis can accompany infections such as typhus, cholera, brucellosis, syphilis. Aseptic pericarditis occurs when allergic reactions to the introduction of vaccines, sera, antibiotics. They can be a manifestation of polyserositis that develops with acute rheumatic fever, diffuse connective tissue diseases, JRA, sarcoidosis, periodic illness, hematological and oncological diseases, as well as trauma, heart surgery, hypoparathyroidism, uremia.

PATHOGENESIS

With infectious pericarditis, the pathogen can penetrate into the pericardial cavity by the hematogenous, lymphogenous route, as well as by direct spread from adjacent organs (Koch's stick - from the pleura, coccal flora - with a breakthrough of an abscess of the myocardium, lungs).

Aseptic inflammatory reactions in the pericardium may occur with increased permeability vascular wall, under the influence of protein breakdown products, toxic substances (with uremia, gout), radiation (for example, in the treatment of tumors), and also due to a systemic immunopathological process.

In the initial phase of the development of pericarditis, fluid exudation increases in choroid plexus visceral layer of the pericardium in the region of the great vessels at the base of the heart. The effusion spreads along the posterior surface of the heart from top to bottom. With a small effusion, its rapid reverse absorption occurs, and fibrin overlays (dry pericarditis) may remain on the surface of the epicardium. With a more widespread and intense involvement of the visceral and parietal layers in the process, a more massive effusion is formed. The possibilities of its reabsorption decrease, the fluid accumulates in the pericardial cavity, first in the lower part, pushing the heart forward and upward. In the future, the effusion occupies the entire space between the sheets of the pericardium (effusion pericarditis).

It should be noted that this process can stop (spontaneously or under the influence of treatment) at any stage and end with the patient's recovery, which, apparently, is observed in most cases of this disease (benign pericarditis).

CLASSIFICATION

Classification of diseases of the pericardium is built according to the clinical and morphological principle (Table 12-5)

Table 12-5.Classification of pericardial diseases*

* According to Gogin E.E., 1979, modified.

CLINICAL PICTURE

The clinical picture depends on the form of pericarditis, as well as on its etiology (Table 12-6). However, it should be borne in mind that both acute dry and long-term chronic adhesive pericarditis may not have any clinical manifestations. The main clinical symptoms of pericarditis are associated with the deposition of fibrin or fluid accumulation in the pericardial cavity and with compression of the heart cavities by a large effusion and impaired diastolic function of the heart.

Table 12-6.Some clinical features of acute pericarditis associated with their etiology

Acute dry pericarditis

Acute dry pericarditis usually begins with fever, tachycardia, and almost constant pain. In young children, pain syndrome is manifested by intermittent anxiety, screaming. Pain is often localized in the navel. Palpation of the abdomen is painful, especially in the epigastric region. Older children complain of pain in the chest, behind the sternum, aggravated by deep breathing and a change in body position, radiating to left shoulder. In half of the patients at the onset of the disease, it is possible to hear a pericardial friction rub (ranging from gentle crepitus to a coarse systolic-diastolic murmur - “crunching of snow”) in the region of the base of the heart along the left edge of the sternum. Noise is best heard in the patient's sitting position. Friction noise is often heard for a very short time.

Acute effusion pericarditis

Acute effusion pericarditis, especially with a rapid increase in the volume of exudate, causes a sharp deterioration in the patient's condition. Shortness of breath, dull pains in the region of the heart appear, the child takes a forced semi-sitting position with the head tilted forward. Some patients develop hoarseness, cough, hiccups (irritation of the phrenic nerve), nausea, vomiting, and abdominal pain. Objectively detect smoothness of the intercostal space and swelling subcutaneous tissue on the left, weakening or upward displacement of the apical impulse, expansion of the boundaries of the heart, first due to absolute, and then relative dullness. Heart sounds at first can be even more sonorous (above the top of the heart shifted forward and upward), and then - significantly weakened, as if coming from afar. Blood pressure decreases (by approximately 10-20 mm Hg), a paradoxical pulse appears (decrease in the filling of the pulse on inspiration). The liver enlarges and becomes painful, ascites appears, edema is possible.

The syndrome of compression of the cavities of the heart develops. In infants, this syndrome has nonspecific manifestations. An increase in pressure in the superior vena cava causes an increase in intracranial pressure, which is accompanied by meningism (vomiting, bulging of the large fontanel, stiff neck). Become well visible and palpable veins of the hand, cervical and ulnar veins, usually invisible at this age.

An increase in the volume of fluid in the pericardial cavity can cause cardiac tamponade. At the same time, the child's condition deteriorates sharply, he becomes very restless, feels fear, shortness of breath increases,

acrocyanosis and cold sweat appear. In the absence of emergency care (puncture or paracentesis of the pericardium), syncope and sudden death are possible.

Chronic pericarditis

Chronic pericarditis can be exudative (usually tuberculous etiology), adhesive (constrictive) and mixed; with or without compression of the cavities of the heart. Both the primary chronic course and the outcome of acute pericarditis of any etiology are possible.

In chronic exudative pericarditis, children are worried about fatigue, shortness of breath, discomfort in the heart, especially with excessive physical exertion. With long-term, from early childhood, exudative pericarditis, a "heart hump" can form. Significant cardiomegaly, muffled heart tones, hepatomegaly occur.

Adhesive pericarditis without cardiac compression is asymptomatic. Attention is drawn only to the preservation of the dimensions of absolute cardiac dullness on inspiration and the late systolic flapping pleuropericardial tone or click.

Constrictive pericarditis is manifested by general weakness, a feeling of heaviness in the right hypochondrium. On examination, attention is drawn to puffiness of the face, swelling and pulsation of the jugular veins, cyanosis, increasing in a horizontal position, ascites. Leg swelling is rare. The cardiac impulse is weakened or not determined, sometimes it can be negative. The borders of the heart are not changed or somewhat expanded. Tachycardia is noted, the accent of the II tone over the pulmonary artery is noted with a general moderate muting of the tones. Often they listen to an enhanced pathological III tone (“pericardial knock”, “click”), sometimes a pericardial friction rub.

Complications.With acute exudative pericarditis, cardiac tamponade is possible, with constrictive - circulatory failure.

DIAGNOSTICS

Diagnosis of pericarditis is often difficult due to the slight severity clinical symptoms and (often) insufficiently complete examination of the patient.

Changes in the peripheral blood are nonspecific and indicate only a current inflammatory or purulent process.

Biochemical, immunological and bacteriological studies are usually carried out to clarify the etiology and form of pericarditis.

Dynamic ECG is informative in acute fibrinous pericarditis, in the initial stage of effusion pericarditis, as well as in the adhesive process (syndrome of compression of the heart cavities). With exudative and chronic pericarditis, a decrease in the electrical activity of the myocardium is found.

On FCG, systole-diastolic murmur not associated with the cardiac cycle and periodic high-frequency oscillations (“clicks”) are recorded.

Radiography is of great importance in the diagnosis of the exudative process, in which the size and configuration of the heart shadow change (acquires a spherical, trapezoidal shape); atelectasis of the lower lobe of the left lung is also possible due to compression of the bronchus. With constrictive pericarditis, radiographs show an enlarged shadow of the superior vena cava, note the fuzziness of the contour of the heart due to pleuropericardial adhesions. When conducting X-ray kymography, a decrease in the amplitude of the pulsation along the contours of the heart is revealed. To clarify the etiology of pericarditis in severe and unclear cases, puncture and biopsy of the pericardium allow.

The main diagnostic method is EchoCG, which makes it possible to judge the presence and amount of fluid in the pericardial cavity (Fig. 12-6 on the insert), changes in the kinetics of the heart, the presence of intrapericardial and pleuropericardial adhesions, and residual phenomena of the process in the form of thickening of the epicardial and pericardial layers. Clinical and laboratory-instrumental diagnostic

criteria for pericarditis are presented in Table. 12-7.

Table 12-7.Diagnostic criteria various forms pericarditis

DIFFERENTIAL DIAGNOSIS

At acute development both dry and effusion pericarditis, it is differentiated primarily with myocarditis. In rheumatic diseases, the membranes of the heart are usually affected simultaneously, so myopericarditis is most often diagnosed. ECG has a certain diagnostic value, which makes it possible to identify rhythm disturbances, intraatrial and intraventricular conduction, characteristic of myocarditis.

Chronically current, especially asymptomatic effusion pericarditis is differentiated from non-rheumatic carditis and cardiomyopathies. Unlike the latter, the well-being of children, despite severe cardiomegaly, is not disturbed, there is no "heart hump", heart sounds are distinct, although weakened. On the ECG, there are no signs of overload of the heart chambers, arrhythmias, blockades, but a decrease in the electrical activity of the myocardium persists for a long time. The final diagnosis is made after echocardiography.

With constrictive pericarditis, differential diagnosis is carried out with portal hypertension, cirrhosis of the liver, chronic carditis, type Ia glycogenosis (von Gierke's disease). The appearance of patients, the presence of dilated veins of the esophagus, signs of hypersplenism according to peripheral blood tests, the level of glucose-6-phosphatase, and splenoportography data are taken into account. In difficult cases, a puncture biopsy of the liver and pericardium is performed. In most cases, diagnosis is based on echocardiography.

TREATMENT

In acute pericarditis, bed rest is necessary for the entire duration of the activity of the process. In chronic pericarditis, the regimen depends on the condition of the patient. Limit physical activity. The diet should be complete, food should be taken fractionally, in small portions. Limit the intake of table salt.

Treatment for acute dry or with a small pericarditis effusion is predominantly symptomatic (anti-inflammatory drugs, analgesics for severe pain, agents that improve metabolic processes in the myocardium, potassium preparations, vitamins). When establishing the pathogen, etiotropic therapy is carried out.

Antibiotics for bacterial pericarditis are prescribed according to the same principles as for infective endocarditis (see section "Infective endocarditis"), taking into account the sensitivity of the pathogen.

For pericardial tuberculosis, two (or three) drugs (isoniazid, rifampicin, pyrazinamide) are prescribed for 6-8 months.

With effusion pericarditis with rapidly increasing or recurrent fluid accumulation, an urgent puncture (paracentesis) of the pericardium may be necessary. With purulent pericarditis, it is sometimes necessary to drain the pericardial cavity and inject antibiotics into it.

In case of constrictive pericarditis with compression of the heart cavities, surgical intervention is necessary (pericardotomy with maximum removal of adhesions and scar-changed pericardial sheets).

Treatment for secondary pericarditis is included in the treatment program for the underlying disease (acute rheumatic fever, SLE, JRA, etc.; see the chapter "Rheumatic diseases") and includes the appointment of NSAIDs, prednisolone, cardiac glycosides, agents that improve metabolic processes in the myocardium (potassium and magnesium aspartate, inosine, etc.).

PREVENTION

Prevention is possible only secondary: dispensary observation in a cardio-rheumatological office, regular ECG and echocardiography, elimination of foci of chronic infection, health-improving measures, dosed physical activity.

FORECAST

In most cases of acute pericarditis, the prognosis is favorable. In secondary pericarditis, it depends on the course of the underlying disease. The outcome of any variant of pericarditis can be a transition to a chronic course, the organization of effusion with the formation of adhesions and adhesions of the sheets, the formation of a "armored" heart (constrictive, adhesive, adhesive pericarditis). Danger to life is acutely developed cardiac tamponade. Chronic pericarditis, especially with compression of the cavities of the heart, can lead to disability of the patient.

Rhythm and conduction disorders

Heart rhythm and conduction disorders - changes in the normal sequence of heart contractions due to a disorder in the functions of automatism, excitability, conduction and contractility. Rhythm disturbances are one of the most common manifestations of heart disease and other pathological conditions. In children, the same rhythm disturbances are observed as in adults, but the causes of their occurrence, course, approaches to treatment and prognosis have a number of features.

There are no reliable data on the prevalence of arrhythmias in children. In the structure of cardiovascular diseases in childhood, arrhythmias account for (by negotiability) from 2.3 to 27%, but they are often detected in healthy children. Heart rhythm and conduction disorders are found in children of all ages, including newborns, they are detected even in the fetus. The frequency increases during puberty.

Etiology and pathogenesis

Rhythm disturbances can be congenital or acquired and are due to cardiac, extracardiac and combined causes. In childhood, arrhythmias are more often extracardiac in origin. At the same time, perinatal pathology plays an important role (unfavorable course of pregnancy and childbirth, prematurity, intrauterine malnutrition, infection), leading to impaired morphogenesis and functional immaturity of the cardiac conduction system. Perinatal damage to the CNS can lead to disruption of the neurovegetative regulation of the rhythm with a change in the relationship between the sympathetic and parasympathetic divisions autonomic nervous system, resulting in electrical instability of the myocardium and the conduction system of the heart, as well as a decrease in the functional reserves of adaptation of the sympathoadrenal link in the regulation of heart rhythm.

Classification

1. Violations of automatism (nomotopic - sinus arrhythmia, tachycardia and bradycardia, heterotopic - extrasystole, paroxysmal and non-paroxysmal tachycardia, flutter and flicker of the atria and ventricles).

2. Conduction disorders (sinoauricular, intraatrial, atrioventricular, intraventricular block).

3. Combined arrhythmias (sinus node weakness syndrome, atrioventricular dissociation, ventricular premature excitation syndrome).

Clinical picture

In anamnesis, children with rhythm disturbances often reveal an unfavorable course of the perinatal period, a family history of cardiovascular pathology, repeated acute infectious diseases and foci of chronic infection. On examination, hypertensive-hydrocephalic syndrome, residual neurological symptoms, various psychovegetative disorders, manifestations of connective tissue dysplasia, and sometimes delayed motor development and puberty are often found.

Rhythm disturbances in children are often asymptomatic, which makes it impossible to accurately determine the time of their appearance. In approximately 40% of cases, arrhythmias are detected by chance (on an ECG) or they are detected during examination in connection with an acute respiratory viral infection. Children are much less likely than adults to complain of palpitations, a feeling of interruptions in the activity of the heart, its fading, even with severe forms of arrhythmia. Along with this, in prepubertal and pubertal age, rhythm disturbances can have a bright emotional coloring due to psycho-vegetative disorders, and are accompanied by other cardiac and extracardiac complaints: pain in the heart, increased excitability, sleep disturbances, meteosensitivity. With arrhythmias, weakness, dizziness and fainting are possible (with sinus bradycardia, atrioventricular blockade, sick sinus syndrome, paroxysmal tachycardia).

At objective examination in children with rhythm disturbances, it is possible to detect an increase or decrease in the pulse, a change in its character (irregular with periodic drops, alternating periods of acceleration and decrease, temporary or permanent weakening of the pulse wave, the presence of a compensatory pause). Evaluation of other basic characteristics of the cardiovascular system (BP, heart size, sonority of tones, heart murmurs) allows you to establish or exclude cardiac pathology as the cause of arrhythmia.

Diagnostics

The main method for detecting and evaluating arrhythmias is the ECG. With its help, it is possible to detect such asymptomatic rhythm disturbances as single extrasystoles (Fig. 12-7), Wolff-Parkinson-White syndrome, slowing of atrioventricular conduction, pacemaker migration. Often, when conducting an ECG in children, sinus arrhythmia and an isolated incomplete blockade of the right leg of the His bundle are detected, which are a variant of the age norm.

Rice. 12-7.Ventricular extrasystole (ECG in three standard leads).

Clinical and electrocardiographic examination allows you to establish the type of rhythm disturbances (functional or organic), especially extrasystoles. Extrasystoles of functional origin are most often detected in the pre- and puberty period, they are unstable, usually disappear or significantly decrease with changes in body position and physical activity. Most often they are of supraventricular origin.

In order to clarify the origin of rhythm disturbances, cardiointervalography, daily Holter ECG monitoring, functional tests are performed: stress (test with dosed physical activity, bicycle ergometry, treadmill test) and drug (atropine, with propranolol, isoprenaline, aymaline, etc.). If organic heart disease is suspected, x-ray examination and echocardiography. It is also necessary to assess the autonomic and psychological status of the child, neurophysiological examination [EEG, echoencephalography (EchoEG), REG], consultations of a neurologist, otolaryngologist, endocrinologist, ophthalmologist.

In difficult cases, electrography of the atrionodal conduction system, surface ECG mapping (for topical diagnosis of rhythm disturbances) and other special studies are performed in a specialized hospital.

Flow

A number of arrhythmias (isolated tachycardia and bradycardia, rare non-permanent monotopic extrasystoles, mild degrees of pro-

conduction, pacemaker migration) are usually not accompanied by organic cardiac pathology and distinct subjective manifestations and proceed quite favorably. Some forms of arrhythmia, especially persistent ones, can worsen the patient's condition, adversely affect hemodynamics, cause a decrease in cardiac output and coronary circulation disorders, and as a result lead to an unfavorable outcome. This is possible with ventricular and supraventricular tachycardia, frequent polytopic extrasystoles, significant slowing of the heart rate, atrioventricular blockade, syndrome extended interval Q-T (Romano-Ward syndrome).

In newborns and young children, rhythm disturbances can be asymptomatic or severe, with complications. In older children, the prognosis of rhythm disturbances is usually favorable, but persistent arrhythmias, especially severe forms may also lead to poor outcomes.

Treatment

Treatment of rhythm disturbances, especially life threatening, are carried out strictly individually, depending on their origin, form, duration, impact on the well-being of the child and the state of his hemodynamics. It is necessary to stop the arrhythmia and carry out maintenance therapy to prevent its recurrence. For all types of arrhythmias, cardiac and extracardiac causes should be treated simultaneously. Basic therapy includes a course (at least 2-3 months) use of nootropics (piracetam, pyritinol, gamma-aminobutyric acid, glutamic acid, hopantenic acid, nicotinoyl gamma-aminobutyric acid, etc.) to correct neurovegetative disorders and normalize trophic processes in the nervous system. The use of cell membrane stabilizers and antioxidants (vitamins E and A, cytochrome C, polyvitamin, etidronic acid), agents that correct metabolic processes in the myocardium (vitamins C, B1, B2, B15, benfotiamine, potassium orotate, inosine, levocarnitine) are shown. , orotic acid, magnesium salt), as well as electrolyte imbalance (potassium and magnesium aspartate, potassium chloride, calcium glycerophosphate). In complex treatment, vasodilators (vinpocetine, vincamine, pentoxifylline), angioprotectors (pyricarbate), belladonna alkaloids + phenobarbital + ergotamine, biogenic stimulants (tinctures of aralia, magnolia vine, ginseng, zamaniha) are used. Consistent use of these remedies is often

helps to normalize the well-being of patients, eliminate arrhythmias or improve their tolerance. Fainting, palpitations require a special therapeutic approach, since they can be the result of not only severe violations rhythm, but also associated hemodynamic and other disorders.

Antiarrhythmic drugs (procainamide, amiodarone, lidocaine, verapamil, etc.) are used in children with certain restrictions due to the fact that they are not always effective enough and can cause adverse reactions(decrease in blood pressure and myocardial contractility, deterioration in the course of arrhythmias, slow conduction). Their use is justified in severe subjective intolerance to arrhythmias, significant hemodynamic changes, as well as in conditions with an unfavorable prognosis (with paroxysmal tachycardia, frequent ventricular and supraventricular extrasystoles, atrial fibrillation). Attacks of paroxysmal tachycardia can be stopped by the introduction of propranolol or verapamil. Determination of indications for the use of antiarrhythmic drugs, their individual selection is carried out in a hospital.

With conduction disorders (isolated or accompanying other forms of arrhythmias), it is possible to use adrenomimetics (isoprenaline, orciprenaline, norepinephrine), atropine, and glucocorticoids (with high-degree atrioventricular blockade). With long QT syndrome, long-term administration of β-blockers is necessary.

In some persistent, unfavorable prognostic, life-threatening arrhythmias (paroxysmal supraventricular and ventricular tachycardia, atrial fibrillation), cardiac defibrillation is indicated to restore sinus rhythm. With atrioventricular blockade of a high degree, and in some cases with a syndrome of weakness of the sinus node, a pacemaker is implanted. Patients with treatment-resistant chronic non-paroxysmal and paroxysmal supraventricular tachycardia, atrial fibrillation may be indicated for cardiac surgery.

Dispensary observation

Dispensary observation should be regular, its frequency is determined depending on the underlying disease (rheumatism, non-rheumatic carditis, congenital heart disease, SVD, etc.), the form of arrhythmia and the characteristics of its course. Mandatory dynamic control of the ECG, according to indications, daily Holter monitoring and other studies are prescribed. They also control the implementation of medical appointments.

ny and efficiency of therapy. Dispensary observation of children with arrhythmias has no time limits, and it is often continued until the patient is transferred to the supervision of an adolescent therapist. Children treated in a hospital are monitored monthly in the first quarter, up to 1 year - at least 1 time in 3 months, then 1 time in six months.

Prevention

Prevention of rhythm and conduction disorders is aimed at eliminating predisposing risk factors. In order to timely detect arrhythmias, it is advisable to conduct regular ECG monitoring, especially during periods of the greatest risk of their development (in newborns, at 4-5, 7-8 and 12-13 years old). Secondary prevention involves maintaining normal rhythmic activity of the heart and preventing the progression of arrhythmias and includes a complex of non-drug effects (psychological correction, restorative measures, exercise therapy) and drug treatment (courses of nootropic, membrane stabilizing drugs, antioxidants, etc.) depending on the characteristics of a particular case.

Forecast

Most arrhythmias in childhood are benign, reversible, and do not aggravate life prognosis. However, in newborns and young children, they can cause the development of arrhythmogenic cardiomyopathy or heart failure, which can lead to early disability and even death. Chronic non-paroxysmal and paroxysmal tachycardia, atrial fibrillation, acquired complete transverse heart block have an unfavorable prognosis. For diseases associated with high risk the development of sudden death (more often due to asystole or ventricular fibrillation), include long QT syndrome, pronounced violations sinus node function, some tachyarrhythmias, especially ventricular, accompanied by syncope, myocardial ischemia, acute heart failure, arterial hypertension.

Syndrome of vegetative dystonia

Autonomic dystonia syndrome (VDS) is a symptom complex of diverse clinical manifestations affecting various organs and systems and developing as a result of deviations in the structure and function of the central and / or peripheral parts of the autonomic nervous system.

SVD is not an independent nosological form, but in combination with other pathogenic factors, it can contribute to the development of many diseases and pathological conditions, most often having a psychosomatic component (arterial hypertension, coronary heart disease, bronchial asthma, peptic ulcer, etc.). Vegetative shifts determine the development and course of many childhood diseases. In turn, somatic and any other diseases can exacerbate autonomic disorders.

Signs of SVD are detected in 25-80% of children, mainly among urban residents. They can be found in any age period, but are more often observed in children 7-8 years old and adolescents. More often this syndrome observed in girls.

ETIOLOGY AND PATHOGENESIS

Reasons for the formation autonomic disorders numerous. Primary, hereditary deviations in the structure and function of various parts of the autonomic nervous system, more often traced along the maternal line, are of primary importance. Other factors, as a rule, play the role of triggers that cause the manifestation of an already existing latent autonomic dysfunction. Often there is a combination of several causes.

The formation of SVD is largely facilitated by perinatal lesions of the central nervous system, leading to cerebral vascular disorders, impaired liquorodynamics, hydrocephalus, damage to the hypothalamus and other parts of the limbic-reticular complex. Damage to the central parts of the autonomic nervous system leads to emotional imbalance, neurotic and psychotic disorders in children, inadequate reactions to stressful situations, which also affects the formation and course of SVD.

In the development of SVD, the role of various psycho-traumatic influences (conflict situations in the family, school, family alcoholism, single-parent families, isolation of the child or excessive guardianship of his parents) plays a very large role, leading to mental maladjustment of children, contributing to the implementation and strengthening of vegetative disorders. Of no less importance are often recurring acute emotional overload, chronic stress, mental and physical overstrain.

Provoking factors include a variety of infectious, somatic, endocrine and neurological diseases, anomalies of the constitution, allergic conditions, unfavorable or rapidly changing meteorological conditions, climate features, environmental problems, micronutrient imbalances, physical inactivity or excessive physical activity,

hormonal changes puberty, non-compliance with the diet, etc.

Undoubtedly, age-related features of the sympathetic and parasympathetic parts of the autonomic nervous system, instability of brain metabolism, as well as the ability of the child's body to develop generalized reactions in response to local irritation, which determines the greater polymorphism and severity of the syndrome in children compared to adults, are of undoubted importance.

Disorders that have arisen in the autonomic nervous system lead to various changes in the functions of the sympathetic and parasympathetic systems with a violation of the release of mediators (norepinephrine, acetylcholine), hormones of the adrenal cortex and other endocrine glands, a number of biologically active substances [polypeptides, prostaglandins (Pg )], as well as to impaired sensitivity of vascular α- and β-adrenergic receptors.

CLASSIFICATION

To date, there is no generally accepted classification of SVD. When formulating a diagnosis, consider:

Etiological factors;

Variant of vegetative disorders (vagotonic, sympathicotonic, mixed);

The prevalence of vegetative disorders (generalized, systemic or local form);

Organ systems most involved in the pathological process;

Functional state of the autonomic nervous system;

Severity (mild, moderate, severe);

The nature of the course (latent, permanent, paroxysmal).

CLINICAL PICTURE

SVD is characterized by diverse, often vivid subjective symptoms of the disease that do not correspond to much less pronounced objective manifestations of a particular organ pathology. The clinical picture of SVD largely depends on the direction of autonomic disorders (the predominance of vago or sympathicotonia).

Vagotonia

Children with vagotonia are characterized by many hypochondriacal complaints, increased fatigue, decreased performance, memory impairment, sleep disorders (difficulty falling asleep, drowsiness), apathy, indecision, fearfulness, and a tendency to depression.

Characterized by a decrease in appetite in combination with overweight, poor cold tolerance, intolerance to stuffy rooms, a feeling of chilliness, a feeling of lack of air, periodic deep sighs, a feeling of a "lump" in the throat, as well as vestibular disorders, dizziness, pain in the legs (more often at night). time), nausea, unmotivated abdominal pain, marbling of the skin, acrocyanosis, pronounced red dermographism, increased sweating, sebum secretion, tendency to fluid retention, transient swelling under the eyes, frequent urination, hypersalivation, spastic constipation, allergic reactions. Cardiovascular disorders are manifested by pain in the region of the heart, bradyarrhythmia, a tendency to decrease in blood pressure, an increase in the size of the heart due to a decrease in the tone of the heart muscle, and muffled heart tones. On the ECG, sinus bradycardia (bradyarrhythmia) is detected, extrasystoles, prolongation of the P-Q interval (up to atrioventricular blockade of I-II degree), as well as ST segment displacement above the isoline and an increase in the amplitude of the T wave are possible.

Sympathicotonia

Children with sympathicotonia are characterized by temperament, irascibility, mood variability, increased sensitivity to pain, quick distractibility, absent-mindedness, and various neurotic states. They often complain of a feeling of heat, a feeling of palpitations. With sympathicotonia, asthenic physique is often observed against the background of increased appetite, pallor and dryness of the skin, pronounced white dermographism, cold extremities, numbness and paresthesia in them in the morning, unmotivated fever, poor heat tolerance, polyuria, atonic constipation. Respiratory disorders are absent, vestibular disorders are uncharacteristic. Cardiovascular disorders are manifested by a tendency to tachycardia and increased blood pressure with normal heart size and loud tones. ECG often reveals sinus tachycardia, shortening of the P-Q interval, shift of the ST segment below the isoline, flattened T wave.

Cardiopsychoneurosis

With the predominance of cardiovascular disorders in the complex of existing vegetative disorders, it is permissible to use the term "neurocirculatory dystonia". However, it should be borne in mind that neurocirculatory dystonia is an integral part of the broader concept of SVD. There are three types of neurocirculatory dystonia: cardiac, vascular and mixed.

Flow

SVD in children can occur latently, being realized under the influence of adverse factors, or permanently. Perhaps the development of vegetative crises (paroxysms, vegetative storms, panic attacks). Crisis states occur during emotional overload, mental and physical overstrain, acute infectious diseases, a sharp change in weather conditions and reflect a breakdown in the autonomic regulation system. They can be short-term, lasting several minutes or hours, or long-term (several days) and occur in the form of vagoinsular, sympathoadrenal or mixed crises.

SVD has some characteristics in children different ages. In preschoolers, autonomic disorders are usually moderate, subclinical, with a predominance of signs of vagotonia (increased tone of the parasympathetic division of the autonomic nervous system). In adolescents, SVD is more severe, with diverse and pronounced complaints and the frequent development of paroxysms. An increase in vagal influence in them is accompanied by a significant decrease in sympathetic activity.

DIAGNOSTICS

Already when collecting an anamnesis, a family burden for vegetative disorders and psychosomatic pathology is revealed. In families of patients with vagotonia, bronchial asthma is more often detected, peptic ulcer stomach, neurodermatitis, and with sympathicotonia - hypertension, coronary heart disease, hyperthyroidism, diabetes. In anamnesis, children with SVD often reveal an unfavorable course of the perinatal period, recurrent acute and chronic focal infections, an indication of connective tissue dysplasia.

The state of the autonomic nervous system is determined by the initial autonomic tone, autonomic reactivity and autonomic activity. The initial autonomic tone, which characterizes the direction of the functioning of the autonomic nervous system at rest, is assessed by analyzing subjective complaints and objective parameters, ECG data and cardiointervalography. Indicators of vegetative reactivity and vegetative support of activity (results of various tests - clinoorthostatic, pharmacological, etc.) make it possible to more accurately assess the characteristics of vegetative reactions in each specific case.

In the diagnosis of SVD, an important role is played by EEG, EchoEG, REG, rheovasography, which allows assessing the functional state of the central nervous system, identifying changes in cerebral and peripheral vessels.

If rhythm and conduction disturbances are detected, ST segment changes on the ECG are detected, the necessary pharmacological tests, ECG Holter monitoring, etc. are carried out. With SVD, consultations of a neurologist, ENT doctor, ophthalmologist, endocrinologist, and in some cases, a psychiatrist are necessary.

DIFFERENTIAL DIAGNOSIS

Differential diagnosis allows to exclude diseases that have symptoms similar to SVD.

In the presence of cardiac complaints, accompanied by objective changes in the heart, in particular - systolic murmur, it is necessary to exclude rheumatism, which has sufficiently characteristic diagnostic criteria (see the section "Rheumatism" in the chapter "Rheumatic diseases"). Consideration should be given to the frequent combination of autonomic disorders with signs of connective tissue dysplasia, the clinical manifestations of which together resemble not only rheumatic heart disease, but also congenital heart disease, non-rheumatic carditis.

With elevated blood pressure, it is necessary to conduct a diagnostic search aimed at excluding primary and symptomatic arterial hypertension (see the section "Juvenile arterial hypertension").

Respiratory disorders (shortness of breath and especially asthma attacks) that occur during crisis reactions in children with SVD are in some cases differentiated from bronchial asthma (see the section "Bronchial asthma" in the chapter "Allergic diseases").

In the presence of febrile reactions, it is necessary to exclude an acute infectious disease, sepsis, infective endocarditis, as well as oncological pathology.

In the presence of severe psychovegetative symptoms, it is necessary to exclude mental disorders.

TREATMENT

Treatment for SVD should be comprehensive, long-term, individual, taking into account the characteristics of autonomic disorders and their etiology. Preference is given to non-drug methods. These include normalization of the daily routine, elimination of physical inactivity, dosed physical activity, limitation of emotional influences (TV shows, computer games), individual and family psychological correction and a regular and balanced diet. Have a positive effect massotherapy, acupuncture, water procedures. Features of physiotherapeutic effects depend on the form of vegetative disorders

(for example, with vagotonia, electrophoresis with calcium, caffeine, phenylephrine is prescribed, with sympathicotonia - with aminofillin, papaverine, magnesium, bromine).

With insufficient effectiveness of non-drug treatment, individually selected drug therapy is prescribed with a limited number of drugs in minimal doses with a gradual increase to effective ones. Great importance in the complex therapy of SVD is given to the treatment of chronic focal infection, as well as concomitant somatic, endocrine or other pathology.

Sedatives are widely used (preparations of valerian, motherwort, St. John's wort, hawthorn, etc.), as well as tranquilizers, antidepressants, nootropics (for example, carbamazepine, diazepam, amitriptyline, piracetam, pyritinol).

Often, the use of glycine, hopantenic acid, glutamic acid, complex vitamin and microelement preparations has a beneficial effect.

Vinpocetine, cinnarizine, nicotinic acid, pentoxifylline are used to improve cerebral and peripheral circulation, restore microcirculation.

With sympathicotonia, it is possible to use β-blockers (propranolol), in the presence of vagotonic reactions - psychostimulants of plant origin (drugs of eleutherococcus, magnolia vine, zamanihi, etc.).

In children with intracranial hypertension, dehydration therapy is performed (acetazolamide with potassium preparations, glycerol). Great importance in the complex therapy of SVD is given to the treatment of chronic focal infection, as well as concomitant somatic, endocrine or other pathology.

With the development of vegetative paroxysms in severe cases along with the use of non-drug methods and drug oral therapy, parenteral administration of tranquilizers, neuroleptics, β-blockers, atropine is necessary, depending on the nature of the crisis.

Dispensary observation of children with SVD should be regular (once every 3-6 months or more often depending on the form, severity and type of the syndrome), especially in the transitional seasons (spring, autumn), when it is necessary to repeat the examination and, according to indications, prescribe a set of therapeutic measures.

PREVENTION

Prevention is a complex preventive measures aimed at preventing the action of possible risk factors,

prevention of the progression of existing vegetative changes and the development of paroxysms.

FORECAST

With the timely detection and treatment of vegetative disorders, the consistent implementation of preventive measures, the prognosis is favorable. The progressive course of SVD can contribute to the formation of a variety of psychosomatic pathologies, and also leads to physical and psychological maladjustment of the child, adversely affects the quality of his life not only in childhood, but also in the future.

Juvenile arterial hypertension

Arterial hypertension is a persistent increase in blood pressure above the 95th centile of the blood pressure distribution scale for a specific age, sex, weight and length of the child's body. Normal blood pressure is considered to be the values ​​of systolic and diastolic blood pressure that do not go beyond the 10th and 90th centiles. High normal blood pressure, or borderline hypertension, is defined as a blood pressure between the 90th and 95th centiles. Children with such AD constitute a risk group and require dispensary observation.

Arterial hypertension in adults is one of the most common cardiovascular diseases. Arterial hypertension affects up to 1/3 of the population of Russia, while up to 40% of them do not know about it and, therefore, do not receive treatment. Therefore, such serious complications of arterial hypertension as myocardial infarction or stroke occur quite suddenly.

Population studies of blood pressure in children in our country have not been conducted. The prevalence of arterial hypertension in children, according to different authors, ranges from 1% to 14%, among schoolchildren - 12-18%. In children of the first year of life, as well as early and preschool age, arterial hypertension develops extremely rarely and in most cases has a secondary symptomatic character. The most predisposed to the development of arterial hypertension are children of prepubertal and pubertal age, which is largely determined by autonomic dysfunctions characteristic of these periods of childhood.

Etiology

In most cases, persistent arterial hypertension in children is secondary. The structure of the causes of arterial hypertension has

There are no distinct age-related features, while kidney pathology predominates (Table 12-8).

Table 12-8.The most common causes of arterial hypertension in children, depending on their age*

According to Tsygin A.N., 1998.

More rare (not age-related) causes of secondary arterial hypertension are systemic vasculitis, diffuse connective tissue diseases, and endocrine diseases (pheochromocytoma, neuroblastoma, hyperparathyroidism, congenital adrenal hyperplasia, primary hyperaldosteronism, endogenous or exogenous Cushing's syndrome). An increase in systemic blood pressure may be accompanied by hypertensive-hydrocephalic syndrome and the abuse of adrenomimetics (ephedrine, salbutamol, naphazoline, etc.).

The diagnosis is primary, i.e. essential arterial hypertension is put after exclusion of all diseases that can cause an increase in blood pressure (secondary symptomatic arterial hypertension). The etiology of essential arterial hypertension is associated with many factors, primarily with heredity. Risk factors for developing hypertension include:

Constant psycho-emotional stress, conflict situations in the family and school;

Personal characteristics of the child (anxiety, suspiciousness, tendency to depression, fear, etc.) and his reaction to stress;

Excess body weight;

Features of metabolism (hyperuricemia, low glucose tolerance, violation of the ratio of cholesterol fractions);

Excessive intake of table salt.

Risk groups also include children with hereditary burden of arterial hypertension, adolescents with "high normal blood pressure" (90-95th centile).

Pathogenesis

Arterial hypertension develops against the background of the presence of genetic abnormalities (some of them are reliably established, for example, mutations in the angiotensin gene, mutations leading to the expression of the aldosterone synthase enzyme). Exposure to provoking factors contributes to the disruption of autoregulation mechanisms that normally maintain a balance between cardiac output and peripheral vascular resistance.

It is believed that the role of the trigger mechanism for the development of hypertension in children is played by multiple negative psycho-emotional effects, which, against the background of such personality traits characteristic of adolescents as anxiety, suspiciousness, etc., cause a constant overstrain of the sympathoadrenal system, accompanied by a spasm of the smooth muscles of the arterioles. Later, circulating (angiotensin II, ADH) and local (endothelin) vasoconstrictor hormones are involved in the process, the action of which is opposed by antihypertensive systems (natriuretic peptides, PgE 2 and PgE 12, kallikrein-kinin system, nitric oxide, etc.). Blood pressure begins to rise with an excessive increase in the activity of vasoconstrictors or with the depletion of vasodepressive systems.

The remaining overstrain of the sympathoadrenal system is accompanied by activation of the sympathetic innervation of the kidneys and spasm of the renal vessels, which contributes to the inclusion in the pathogenesis of the renin-angiotensin-aldosterone system - the leading pathogenetic mechanism for the development of secondary renal hypertension (Fig. 12-8).

Initially, transient and then permanent spasm of arterioles leads to hypertrophy of smooth muscle cells, which is supported by an increase in the intracellular concentration of free ionized calcium.

In the pathogenesis of hypertension, other metabolic disorders are also important, allowing us to speak about the beginning of the formation of a "metabolic syndrome" in children, characteristic of adults. Thus, in adolescents with persistent hypertension and overweight, hyperuricemia, an increase in the concentration of low-density lipoprotein cholesterol and a decrease in the concentration of high-density lipoprotein, hypertriglyceridemia, impaired glucose tolerance are often found.

Rice. 12-8.The pathogenesis of arterial hypertension.

Classification

There is no generally accepted classification of arterial hypertension in children. In adults, the classification is based on the level of blood pressure and the degree of target organ damage, while distinguishing three stages of the disease. In children, arterial hypertension is subdivided (Second working group on the control of blood pressure in children; USA, 1987) according to the level of systolic blood pressure in different age groups (Table 12-9.)

Along the course, arterial hypertension at any age is usually divided into benign and malignant forms.

Table 12-9.Criteria for arterial hypertension in children depending on age*

* According to Tsygin A.N., 1998.

Clinical picture

With moderate arterial hypertension, clinical manifestations may be absent, the child and his parents may not be aware of its presence. Complaints of headache, fatigue, irritability are possible. An objective examination often reveals excessive body weight and length, manifestations of autonomic dysfunction, undifferentiated mesenchymal dysplasia (asthenic physique, microanomalies in the structure of the heart and kidneys, etc.).

With severe arterial hypertension (stage II in adults), the well-being of children is always disturbed. In addition to more pronounced and persistent headaches, children note dizziness, memory loss, palpitations, and pain in the heart area. An objective examination reveals tachycardia, expansion of the boundaries of the heart to the left, increased heart sounds with an accent of the second tone above the aorta, ECG and EchoCG reveal signs of left ventricular hypertrophy, and examination of the fundus reveals narrowing of the retinal vessels.

Malignant arterial hypertension (most often occurs with secondary renal hypertension) is characterized by a persistent increase in blood pressure to high values ​​​​and the low effectiveness of ongoing therapeutic measures. This type of hypertension is characterized by high mortality.

Hypertensive crisis is characterized by the development of complications:

Acute hypertensive encephalopathy with severe headache, nausea, vomiting, visual disturbances, impaired consciousness, convulsions;

Acute left ventricular failure with pulmonary edema, shortness of breath, pain in the heart;

AKI with oliguria, hematuria, proteinuria.

Diagnostics

The diagnosis of arterial hypertension is made only after a threefold detection of the level of systolic and / or diastolic pressure exceeding the 95th centile of the blood pressure distribution scale for a given sex, age and height. When diagnosing, it is also possible to use uniform criteria (WHO recommendations) for arterial hypertension in children (Tables 12-10).

Table 12-10.Uniform Criteria for Arterial Hypertension in Children*

* According to Leontyeva I.V., 2000.

The diagnosis of arterial hypertension is confirmed by daily monitoring of blood pressure and tests with physical (bicycle ergometry) and informational psycho-emotional (TV game) load.

Differential Diagnosis

Essential arterial hypertension is differentiated from SVD according to hypertonic type and symptomatic hypertension.

SVD is characterized by the lability of all hemodynamic parameters, including blood pressure, and insufficient vegetative support in the study of the autonomic nervous system.

The distinction between primary and symptomatic hypertension is possible only after a thorough and comprehensive examination of the patient using all modern diagnostic methods. Especially carefully it is necessary to examine the central nervous system, cardiovascular, endocrine and urinary systems. Psychological testing is also required.

Treatment

With moderate arterial hypertension, treatment begins with non-drug effects.

Exclusion of negative psycho-emotional stressful situations.

Limitation (or complete exclusion) of the time spent at the computer and watching TV.

Compliance with the daily routine, sufficient sleep.

Diet correction (reduction of excess body weight).

Limiting salt intake.

Exercise therapy, dosed physical activity.

In teenagers - complete failure from bad habits, especially from smoking.

With severe stable arterial hypertension or the failure of non-drug therapy, the same medicines as in adults. It is recommended to start treatment with the use of small doses of drugs and reduce blood pressure gradually: at first by no more than 30%, with a further focus on indicators that are normal for a given age.

In addition to the actual antihypertensive therapy (see below), basic therapy is carried out, including agents that improve cerebral hemodynamics and metabolism (Tables 12-11).

Table 12-11.Basic drugs used in arterial hypertension*

* According to Leontyeva I.V., 2000.

The drugs are prescribed in courses of 1 month, their alternation is possible. Courses are held 2 times a year. The combination of vascular and metabolic agents is most effective.

With stable arterial hypertension, basic and antihypertensive drugs are combined with diuretics. Treatment begins with low-dose thiazide diuretics (Tables 12-12) or β-blockers

(Table 12-13) (I stage). In the absence of positive changes within 6 weeks-3 months, their combination is used (stage II); then a vasodilator (stage III) is added, usually ACE inhibitors, which, in addition to vasodilation, reduce pre- and afterload on the heart, improve the diastolic function of the left ventricle, reduce its hypertrophy, and do not cause withdrawal syndrome (Table 12-14).

Table 12-12.Main diuretics used in the treatment of arterial hypertension in children*

* According to Leontyeva I.V., 2000.

Table 12-13.Main β-blockers used in children*

* According to Leontyeva I.V., 2000.

Table 12-14.Major angiotensin-converting enzyme inhibitors*

* According to Leontyeva I.V., 2000.

Treatment is carried out in courses lasting at least 1 month with a gradual decrease in dose. There are usually two courses per year.

Prevention

Prevention of arterial hypertension should be carried out at the population and family levels, as well as in risk groups. First of all, prevention consists in organizing a healthy lifestyle for children and adolescents and correcting the identified risk factors. The main preventive measures must be organized in the family: the creation of a favorable psychological atmosphere, the correct mode of work and rest, nutrition that helps maintain normal body weight, adequate physical (dynamic) exercise.

Measurement of blood pressure (using age-sized cuffs) should be carried out at each medical examination of the child. This is important both for timely diagnosis and to reduce the possibility of overdiagnosis (“white coat reaction”).

Forecast

The prognosis of arterial hypertension depends on the etiology. Secondary arterial hypertension can be very difficult and end unfavorably. Essential arterial hypertension in a child can transform into essential arterial hypertension in adults. However, this transition does not always occur, and juvenile arterial hypertension, with timely treatment started, often ends in recovery.