Ventricular septal defect (VSD): causes, manifestations, treatment. VSD (ventricular septal defect) in newborns and adults

The health of the unborn baby is influenced by many factors. Improper intrauterine development can cause congenital defects of internal organs. One of the disorders is ventricular septal defect (VSD), which occurs in a third of cases.

Peculiarities

VSD is a congenital heart defect (CHD). As a result of the pathology, a hole is formed connecting the lower chambers of the heart: its ventricles. The level of pressure in them is different, which is why when the heart muscle contracts, some blood from the more powerful left side enters the right. As a result, its wall stretches and enlarges, and the blood flow of the pulmonary circle, for which the right ventricle is responsible, is disrupted. Due to increased pressure, the venous vessels are overloaded, spasms and compactions occur.

The left ventricle is responsible for blood flow in the systemic circle, so it is more powerful and has higher pressure. In case of pathological course arterial blood into the right ventricle the required level of pressure decreases. For supporting normal indicators the ventricle begins to work with greater force, which further increases the load on the right side of the heart and leads to its enlargement.

The amount of blood in the pulmonary circle increases and the right ventricle has to increase pressure to ensure normal flow through the vessels. This is how the reverse process occurs - the pressure in the pulmonary circle now becomes higher and blood flows from the right ventricle to the left. Oxygen-enriched blood is diluted with venous (depleted) blood, and a lack of oxygen occurs in organs and tissues.

This condition is observed with large holes and is accompanied by disturbances in breathing and heart rhythm. Often the diagnosis is made in the first few days of a baby's life, and doctors begin immediate treatment, prepare for surgery, and if it is possible to avoid surgery, carry out regular monitoring.

A small VSD may not immediately appear or may not be diagnosed due to mild symptoms. Therefore, it is important to know about possible signs of the presence of this type of CHD in order to take timely measures and treat the child.

Blood flow in newborns

Communication between the ventricles is not always a pathological abnormality. In the fetus when intrauterine development the lungs do not participate in enriching the blood with oxygen, so there is an open oval window (ooo) in the heart, through which blood flows from the right side of the heart to the left.

In newborns, the lungs begin to work and the lungs gradually become overgrown. The window closes completely at the age of about 3 months; for some, overgrowth is not considered a pathology by the age of 2 years. With some deviations, OOO can be observed in children 5–6 years of age and older.

Normally, in newborns, the ooo is no more than 5 mm, in the absence of signs cardiovascular diseases and other pathologies, this should not cause concern. Dr. Komarovsky recommends constantly monitoring the baby’s condition and regularly visiting a pediatric cardiologist.

If the hole size is 6-10 mm, this may be a sign of VSD and surgical treatment is required.

Types of defect

The cardiac septum may contain one or more pathological holes of different diameters (for example, 2 and 6 mm) - the more of them, the more difficult degree diseases. Their size varies from 0.5 to 30 mm. Wherein:

• A defect measuring up to 10 mm is considered small;
• Holes from 10 to 20 mm are medium;
• A defect over 20 mm is large.

According to the anatomical division of VSD in a newborn, there are three types and differ in location:

1. A hole occurs in the membranous (upper part of the heart septum) in more than 80% of cases. Defects in the shape of a circle or oval reach 3 cm; if they are small (about 2 mm), they can spontaneously close as the child grows up. In some cases, defects of 6 mm heal; whether surgery is needed is decided by the doctor, focusing on the general condition of the child and the specific course of the disease.
2. Muscular JMP in the middle part of the septum is less common (about 20%), in most cases it is round in shape, with a size of 2 - 3 mm and can close with the age of the child.
3. At the border of the ventricular efferent vessels, a supracrestal septal defect is formed - the rarest (approximately 2%) and almost never self-limiting.

IN in rare cases There is a combination of several types of JMP. The defect can be an independent disease, or accompany other severe abnormalities in the development of the heart: a defect interatrial septum(ASD), problems with arterial blood flow, coarctation of the aorta, stenosis of the aorta and pulmonary artery.

Reasons for development

The defect forms in the fetus from 3 weeks to 2.5 months of intrauterine development. If the course of pregnancy is unfavorable, pathologies may occur in the structure of internal organs. Factors that increase the risk of VSD:

1. Heredity. Predisposition to VSD can be transmitted genetically. If any of your close relatives had defects various organs, including the heart, there is a high probability of abnormalities occurring in the child;
2. Viral diseases of an infectious nature (influenza, rubella) that a woman suffered in the first 2.5 months of pregnancy. Herpes and measles are also dangerous;
3. Reception medicines– many of them can cause intoxication of the embryo and lead to the formation of various defects. Particularly dangerous are antibacterial, hormonal, anti-epileptic drugs and those affecting the central nervous system;
4. Bad habits of the mother - alcohol, smoking. This factor, especially at the beginning of pregnancy, increases the risk of abnormalities in the fetus several times;
5. The presence of chronic diseases in a pregnant woman - diabetes, problems of the nervous, cardiac system and the like can provoke pathologies in the baby;
6. Vitamin deficiency, deficiency of essential nutrients and microelements, strict diets during pregnancy increase the risk of birth defects;
7. Severe toxicosis on early stages pregnancy;
8. External factors - hazardous environmental conditions, harmful working conditions, increased fatigue, overexertion and stress.

The presence of these factors does not always cause the occurrence serious illnesses, but increases this probability. To reduce it, you need to limit their exposure as much as possible. Timely measures taken to prevent problems in the development of the fetus are a good prevention of congenital diseases in the unborn child.

Possible complications

Defects small size(up to 2 mm) at in good condition the baby is not a threat to his life. Regular examination and observation by a specialist are required and can spontaneously stop over time.

Large holes cause disruption of the heart, which manifests itself in the first days of the baby’s life. Children with VSD have a hard time suffering from colds and infectious diseases, often with lung complications and pneumonia. They may develop worse than their peers and have difficulty withstanding physical activity. With age, shortness of breath occurs even at rest, problems with internal organs due to oxygen starvation.

Interventricular defect can cause serious complications:

• Pulmonary hypertension - increased resistance in the pulmonary vessels, which causes right ventricular failure and the development of Eisenmenger syndrome;
• Acute cardiac dysfunction;
• Inflammation of the inner lining of the heart of an infectious nature (endocarditis);
• Thrombosis, threat of stroke;
• Malfunctions of the heart valves, the formation of valvular heart defects.

To minimize the consequences harmful to the baby’s health, timely qualified assistance is necessary.

Symptoms

The clinical manifestations of the disease are determined by the size and location of the pathological holes. Minor defects membranous part of the heart septum (up to 5 mm) occur in some cases without symptoms, sometimes the first signs appear in children from 1 to 2 years old.

In the first days after birth, the baby can hear heart murmurs caused by the flow of blood between the ventricles. Sometimes you can feel a slight vibration if you put your hand on your baby's chest. Subsequently, the noise may weaken when the child is in an upright position or has experienced physical exertion. This is caused by compression muscle tissue in the hole area.

Major defects can be detected in the fetus even before or immediately after birth. Due to the characteristics of blood flow during intrauterine development, newborns have normal weight. After birth, the system is rebuilt to normal and the deviation begins to manifest itself.

Small defects located in the lower region of the heart septum are especially dangerous. They may not show symptoms in the first few days of the child's life, but over time, breathing and heart problems develop. If you pay close attention to your child, you can notice the symptoms of the disease in time and contact a specialist.

Signs of possible pathology that should be reported to your pediatrician:

1. Pallor skin, blue lips, skin around the nose, arms, legs during exertion (crying, screaming, overexertion);
2. The baby loses appetite, gets tired, often drops the breast during feeding, and slowly gains weight;
3. During physical activity and crying, babies experience shortness of breath;
4. Increased sweating;
5. An infant older than 2 months is lethargic, drowsy, has decreased motor activity, and there is a delay in development;
6. Frequent colds that are difficult to treat and develop into pneumonia.

If such signs are detected, the baby is examined to identify the causes.

Diagnostics

The following research methods allow you to check the condition and functioning of the heart and identify the disease:

• Electrocardiogram (ECG). Allows you to determine congestion of the cardiac ventricles, identify the presence and degree of pulmonary hypertension;
• Phonocardiography (PCG). As a result of the study, it is possible to detect heart murmurs;
• Echocardiography (EchoCG). Able to detect blood flow disturbances and help to suspect VSD;
• Ultrasonography. Helps evaluate the work of the myocardium, the pressure level of the pulmonary artery, the amount of blood discharged;
• Radiography. Chest photographs can be used to determine changes in the pulmonary pattern and an increase in the size of the heart;
• Probing of the heart. Allows you to determine the level of pressure in the arteries of the lungs and the ventricle of the heart, increased content oxygen in venous blood;
• Pulse oximetry. Helps determine the level of oxygen in the blood - a deficiency indicates disorders in the cardiovascular system;
• Cardiac catheterization. Helps assess the condition of the heart structure and determine the level of pressure in the heart ventricles.

Treatment

VSD 4 mm, sometimes up to 6 mm - small in size - in the absence of disturbances in respiratory, cardiac rhythm and normal development child allows in some cases not to use surgical treatment.

If the general clinical picture worsens or complications arise, surgery may be prescribed in 2–3 years.

Surgery is performed with the patient connected to a heart-lung machine. If the defect is less than 5 mm, it is closed with U-shaped sutures. If the hole is larger than 5 mm, it is covered with patches made of artificial or specially prepared bio-material, which is subsequently overgrown with the body’s own cells.

If surgical treatment is necessary for a child in the first weeks of life, but it is impossible due to some indicators of the baby’s health and condition, a temporary cuff is placed on the pulmonary artery. It helps equalize the pressure in the ventricles of the heart and alleviates the patient's condition. After a few months, the cuff is removed and surgery is performed to close the defects.

After birth, children may be diagnosed with a serious heart pathology - a malformation of its development. These include ventricular septal defect - a diagnosis that requires confirmation and early treatment. But in many situations, the problem resolves itself, since there is a high probability of closing the defect without surgery. What the pathology threatens, how it manifests itself and when an urgent examination is needed - we will look at it in the article.

Features of the disease

The interventricular septum forms the inner wall of the ventricles of the heart and takes part in the contraction and relaxation of the organ. In the fetus, the septum is formed by the 4-5th week of development, but sometimes it is not completely tightened. VSD (ventricular septal defect) is a heart defect that a person has from birth, which is more common than other defects and often develops in combination with other diseases of the heart and blood vessels (coarctation of the aorta, mitral valve insufficiency, pulmonary stenosis, etc.).

With congenital heart disease (CHD) of this type, there is a defect between the right and left ventricles - an unclosed hole. Among all heart defects, pathology accounts for, according to various sources, 30-42%, while it is diagnosed with equal frequency in boys and girls.

There are several classifications of VSD. According to the type of localization, in accordance with the location on one or another part of the interventricular septum, VSD can be:

1. defect of the membranous part (high VSD);
2. muscle defect;
3. defect of the supra-ridge part.

The overwhelming majority of VSDs are perimembranous (they are located at the top of the interventricular septum, directly under the aortic valve and the septal cusp of the tricuspid cardiac valve), and muscular and supracrestal ones account for no more than 20%. Among the perimembral defects, subaortic and subtricuspid defects are distinguished.

Defects are also classified by size into medium, small, large, for which a comparison is made with the aortic diameter, indicating the size as ¼, ½ of the caliber of the aorta, etc. Typically the defects are 1mm. - 3 cm and more, their shape is round, oval, and occasionally slit-like. If the VSD in a newborn is small, it is called Tolochinov-Roger disease. When a minor defect does not cause any symptoms, there is a high chance that it will close on its own. On the contrary, if a child has several minor defects, he needs surgical treatment as early as possible due to the unfavorable independent prognosis of the disease.

If a child has a ventricular septal disorder, this may have a negative effect on hemodynamics due to changes in the pressure difference between the right and left ventricles (normally, the left ventricle has 5 times higher pressure than the right during systole). With VSD, there is a left-to-right shunt of blood, and the volume of blood will directly depend on the size of the defect.

Small defects, as already noted, have almost no effect on hemodynamics, so the patient’s condition remains normal. At significant volume blood that returns to the left side of the heart, ventricular overload occurs. With severe defect of the interventricular septum, pulmonary hypertension develops.

Causes of pathology

In some cases, there is a connection between the occurrence of pathology in a child when it has already occurred in close relatives. Therefore, some experts note the possibility of hereditary transmission of VSD, although such cases account for no more than 4% of total number. In addition, the causes of the disease may be due to gene mutations, and in such a situation, in addition to heart defects, other abnormalities are found in the baby - Down's disease, structural abnormalities of the kidneys, large vessels etc.

For the most part, VSD appears at the stage of embryogenesis, when during the formation of fetal organs, some factors have a teratogenic effect and lead to the appearance of a defect. Such consequences can be observed due to the influence of the following factors in the first trimester:

• infections suffered during pregnancy, for example, influenza, rubella, herpes;
• taking certain medications, alcohol, drugs;
• the mother’s adherence to a strict diet lacking the necessary vitamins;
• late pregnancy (after 40 years);
• early toxicosis and frequent threats of miscarriage;
• the presence of severe somatic diseases in the mother - diabetes, heart failure, endocrine pathologies etc.;
• undergoing an x-ray examination.

Occasionally, acquired VSD appears in adults. An incomplete septum in the ventricle of the heart may remain after a myocardial infarction.

Symptoms of the disease

The symptom complex of the disease, as well as the age of onset of the first clinical manifestations directly depends on the size of the defect. Symptoms of small and large defects vary greatly, since the volume of pathological blood discharge is not the same. Small VSDs (up to 1 cm in diameter) may not have any effect on the well-being of a child who grows and develops on par with his peers. However, when listening to the heart, the doctor determines heart murmurs - low, rough, scraping during systole (heart contraction).

When the child is standing, the noise becomes somewhat quieter due to compression of the defect by the heart muscle, sometimes it is supplemented by a slight tremor and vibration of the left edge of the sternum at the time of heart contraction. There may be no other clinical signs or objective data at all. Medium defects can be expressed by the following symptoms:

• shortness of breath on exertion;
• slightly increased fatigue of the child;
• slight protrusion of the chest in the form of a dome (the so-called “heart hump”);
• marbling of the skin of the arms, legs, chest, which does not go away with age;
• a rough systolic murmur already from the first week of a child’s life, which is clearly heard in the region of the heart.

Large defects of the perimembranous type (other types of defects are usually small in size) usually make themselves felt immediately after birth, or within several weeks or months. Symptoms may be as follows:

• difficulty feeding due to shortness of breath;
• anxiety, frequent moodiness of the baby;
• hyperhidrosis in combination with pallor, cyanosis of the skin;
• marble pattern on the skin; Also read about marbled skin color in adults
• coldness of hands and feet;
• lag in physical development due to a decrease in the amount of circulating blood in big circle blood circulation;
• low body weight up to severe underweight and dystrophy;
• often - increased breathing;
• shortness of breath when lying down;
• marbled skin color in adults; coughing in fits and starts, especially when changing body position;
• chest deformation;
• systolic vibration at the left edge of the sternum in the 3-4 intercostal space;
• rough systolic murmurs in the same area;
• moist rales at the bottom of the lungs;
• enlarged liver, spleen.

In children with large defects of the interventricular septum, clinical improvement is still possible if subpulmonary (infundibular) stenosis develops by 1-2 years, but such an improvement is only temporary and masks the development of complications. For the most part, symptoms increase with age. Hypertrophy of the upper basal part of the interventricular septum or its other parts often develops rapidly. In the lungs, recurrent pneumonia is observed, which is difficult to cure. Older children (3-4 years old) often notice chest pain on the left and increased heart rate. Possible nosebleeds, fainting, cyanosis of the fingers, widening and flattening of the phalanges. Up to ¼ of children must be urgently operated on early age because of high risk lethal outcome.

As for adults who have acquired VSD after myocardial infarction, signs of heart failure come to the fore. These include heart pain during exercise and at rest, shortness of breath, heaviness and pressure in the chest, cough, arrhythmia. Angina attacks often occur, during which dyskinesia of the interventricular septum develops with a displacement of the right ventricle towards the sternum. The disease requires emergency treatment, since without surgery only 7% of patients remain alive within a year. Unfortunately, during surgery to eliminate post-infarction VSD, about 15-30% of patients die.

Possible complications

Small defects can close with age and, as a rule, do not lead to the development of any complications. However, if there is communication between the ventricles of the heart during life, there is a risk of developing infective endocarditis - bacterial damage to the inner lining of the heart and heart valves. This risk is up to 0.2% annually and may increase over time. Endocarditis usually develops in older children or adults. The disease is associated with injury to the endocardium against the background of pathological discharge of blood, and its immediate causes caused by any previous bacterial disease and even dental procedures.

An untreated large VSD is much more dangerous. Even if the child survives, and the severity of the clinic decreases, this does not mean recovery. A decrease in the intensity of symptoms is observed due to the development of obstructive lesions of large pulmonary vessels. If the operation is delayed, irreversible, constantly progressive pulmonary hypertension may occur - an increase in pressure in the pulmonary circulation. Against the background of pulmonary hypertension, the walls of the arteries and arterioles thicken, which sometimes cannot be corrected even through surgery.

By the age of 5-7 years, pulmonary hypertension manifests itself in the form of Eisenmenger syndrome (subaortic VSD, complemented by vascular sclerosis in the lungs).

The patient has an enlarged trunk of the pulmonary artery, and the right (rarely the left) ventricle of the heart is hypertrophied. Both diseases, as a rule, entail severe ventricular failure and death at the age of no more than 20 years, and sometimes even before one year old.

Other severe complications of VSD without timely surgery, which can lead to disability and death:

• aortic regurgitation - a combination of blood reflux with aortic valve insufficiency, which seriously increases the load on the left ventricle;
• infundibular stenosis - trauma to the supraventricular crest, its hypertrophy and scarring, as a result of which the infundibular section of the right ventricle narrows and pulmonary artery stenosis develops;
• thromboembolism - blockage of blood vessels by a detached blood clot, which forms in the heart and enters the circulating bloodstream. Read more about postoperative thromboembolic complications

Carrying out diagnostics

After birth, children are always carefully examined by a special specialist - a neonatologist. He must have extensive experience in searching for congenital diseases based on external signs and objective examination data. At the age of 1 month, all infants should be examined by a number of specialists, and also undergo instrumental studies and perform blood tests. If there are suspicions of heart defects, various examinations of the child are carried out, which will confirm, exclude or clarify the diagnosis. Often minor defects are found at an older age, however, the diagnostic program will be approximately the same:

1. Frontal chest x-ray. Cardiomegaly and enlargement of the heart chambers, increased vascular pattern of the lung tissue are detected. In the presence of complications in the lungs, changes may appear such as an increase in the size of the trunk, as well as the branches of the pulmonary artery.
2. ECG. Shows overload of the right atrium and one ventricle, disturbances of heart rhythm and conduction.
3. Ultrasound of the heart with Doppler sonography. Reflects pathological discharge of blood through an existing defect, enlargement of the cavities of the heart, increased thickness heart muscle, etc.
4. Phonocardiography. Helps to record heart murmurs.
5. General blood test, blood gas composition. As a rule, these tests are normal.
6. Angiocardiography with cardiac catheterization. Necessary for measuring pressure in the chambers of the heart and pulmonary artery, as well as the level of oxygen saturation. This method allows you to determine the severity of tissue hypoxia, as well as identify pulmonary artery hypertension.

The disease should be differentiated from the common arterial trunk, stenosis of the pulmonary artery or aorta, open artrioventricular canal, aortopulmonary septal defect, thromboembolism, mitral valve insufficiency. Treatment methods

Conservative therapy is necessary for any size and type of heart defects if there are signs of heart failure. It may include the following drugs:

• cardiac glycosides;
• diuretics;
• cardiotrophics;
• ACE inhibitors;
• sympathomimetics;
• thrombolytics;
• B vitamins;
• potassium and magnesium preparations;
• antioxidants.

All medications should be prescribed only by a doctor, as well as the selection of their dosage and duration of use. If the course of the disease is asymptomatic and the defect is small, this will allow us to limit ourselves to supportive therapy and regular examinations and examinations of the child’s heart. Spontaneous closure of the defect often occurs by 4-5 years of age. However, for larger defects, the child usually requires surgery around age 3.

In some cases, palliative operations are performed on an infant, which will improve the quality of life, reduce the volume of pathological blood discharge and help him wait for radical intervention to eliminate the defect before irreversible changes develop. During palliative surgery, an artificial stenosis of the pulmonary artery is created using a cuff (pulmonary artery narrowing operation according to Müller).

At older ages, radical operations are performed, but sometimes this type of intervention is forced to be performed in children under one year of age. Indications for surgery:

• rapid progression of pulmonary hypertension;
• intense symptoms of heart failure;
• recurrent pneumonia;
• serious delay in the child’s body weight and development.

Currently, all types of operations to eliminate VSD are well developed and provide 100% effectiveness with a mortality rate of no more than 1-3%. Depending on the type of defect and its size, the operation may be as follows:

1. Plastic surgery of the defect with a special patch made from a pericardial sheet. The operation is performed under conditions of hypothermia, cardioplegia, and artificial circulation. Patches made of synthetic materials are also used - Teflon, Dacron, etc. Typically, such operations are prescribed for large VSDs.
2. Suturing the defect with a U-shaped suture. Recommended for defects less than 5 mm. size.
3. Occlusion with an Amplatzer device. Small defects can be easily removed in a minimally invasive way, such as inserting an Amplatzer occluder into the heart, which opens into the opening of the interventricular septum like an umbrella. Thus, the defect is completely closed.

In the postoperative period, a child or adult needs regular examination by a cardiologist at least once every six months, then once a year.

Complications of surgery, including AV block, are most often observed in late-operated patients. In such patients, among other things, pulmonary hypertension may persist against the background of irreversible vascular damage.

Pregnancy and childbirth during illness

Many women with a ventricular septal defect can carry and give birth to a child, but only if the hole is small. The situation is much more complicated if the defect is significant and the woman has symptoms of heart failure or other complications of the disease. The risk for the fetus and the pregnant woman herself is especially high in the presence of arrhythmia and pulmonary hypertension. If Eisenmenger syndrome is diagnosed, the pregnancy is terminated at any stage, since this threatens the death of the mother.

Women with heart disease need to plan their pregnancy in advance, and also take into account that there is a risk of having a child with the same disease or with other congenital heart defects. Before conception, you should take a course of special medications to support cardiac activity, and during pregnancy you will have to stop taking most medications. Management of pregnancy in women with VSD requires close attention from doctors, as well as the participation of a cardiologist. Childbirth with small defects is independent, in the presence of complications - by caesarean section.

What not to do with VSD

1. Do not miss visits to the pediatrician or cardiologist for dynamic monitoring of the patient.
2. Remember to report any changes in behavior or symptoms to your doctor.
3. Avoid excessive physical activity of the child, but, nevertheless, do not force him to lead a passive life.
4. Do not take part in competitions or do heavy physical work.
5. Don't ignore exercise therapy.
6. Do not hold your breath (for example, do not dive).
7. Avoid sudden changes in ambient temperature.
8. Do not go to the bathhouse, sauna, or sunbathe for a long time.
9. Avoid ARVI, flu, and colds due to hypothermia.
10. Cure all foci of chronic infection.
11. Eliminate stress and anxiety in the patient.

Prognosis for ventricular septal defect

A favorable prognosis for the natural course of VSD is not common, of course, if the defect does not close spontaneously (this happens in 25-40% of cases). Life expectancy without surgery is 20-30 years, and with large defects, up to 50-80% of children die before the age of one due to complications (thromboembolism, pulmonary hypertension, heart failure). 15% of them develop Eisenmenger syndrome, and therefore babies can die within the first six months of life.

For small defects that do not lead to the development of a clinical picture, but, nevertheless, do not close on their own, life expectancy is on average 60 years. That's why surgery It is better to carry out even in adulthood to prevent the gradual wear and tear of the heart. In pregnant women with untreated VSD, the mortality rate reaches 50%, and the woman and child die especially often in the second half of gestation.

A ventricular septal defect is a congenital defect that results in communication between the right and left ventricles. With an isolated ventricular septal defect, the remaining parts of the heart are developed normally, and all segments are connected concordantly.

Ventricular septal defect (VSD) is the most common congenital anomaly heart, relatively easily diagnosed using traditional methods research. However, the true frequency of its occurrence, oddly enough, is unknown. Thus, a significant increase in the diagnosis of VSD among live births (from 1.35-4.0 per 1000 to 3.6-6.5 per 1000) was noted after the introduction of extensive practice echocardiographic technique. A further increase in the detection rate of VSD among “healthy” newborns was associated with the advent of color Doppler scanning, which made it possible to detect small defects.

It is likely that widespread adoption of prenatal echocardiography will also affect these indicators. Among all congenital heart defects, ventricular septal defect occurs on average in 20-41% of cases (depending on the criteria for its “isolation”). The incidence of critical illness is about 21%.

The defect can be located in any area of ​​the interventricular septum. The septum itself consists of two main components: a small membranous and the rest muscular. The latter, in turn, has three parts: inflow, trabecular, outflow (infundibular).

The direction of blood discharge and its magnitude are determined by the size of the ventricular septal defect and the pressure difference between the left and right ventricles. The latter depends on the ratio of the total pulmonary and total peripheral resistance, the distensibility of the ventricles, and the venous return to them. In this regard, other things being equal, different phases of the development of the disease can be distinguished.

1. Immediately after birth, due to a high TLC and a “hard” right ventricle, blood discharge from left to right may be absent or may be crossed. The volume load on the left ventricle is slightly increased. Heart sizes vary with age.

2. After the usual evolutionary decrease in the OPS, it becomes several times lower than the OPS. This leads to an increase in left-right shunt and volumetric blood flow through the pulmonary circulation (hypervolemia of the pulmonary circulation). In this case, the blood flowing through the lungs is divided into ineffective and effective parts. The effective part of the pulmonary blood flow is the blood entering from the lungs into the left parts of the heart and further into systemic vessels. Blood recirculating through the lungs is an inefficient fraction of the blood flow. Due to the increased return of blood to the left sections, volume overload of the left atrium and left ventricle develops. The size of the heart increases. In cases of a large shunt, moderate systolic overload of the right ventricle also appears. If the redistribution of blood flow in favor of the ineffective pulmonary flow increases and it becomes impossible to meet the needs of peripheral organs and tissues, heart failure occurs. The pressure in the pulmonary vessels during this period depends on the volume of the shunt and is usually determined by one or another level of their compensatory spasm (“reset” hypertension).

With large defects of the interventricular septum, leading to early hypertrophy of the left ventricle, an increase in the speed and volume of blood flow in the left ventricle is noted already in the neonatal period. coronary artery, which reflects the increased myocardial oxygen demand.

Fetal echocardiography. Due to the absence of changes in the four-chamber projection of the heart and clear signs of blood discharge, identifying the defect is difficult; it is diagnosed prenatally in only 7% of cases. The diagnosis is made when an echo-negative area of ​​the septum with clear edges is detected in at least two projections. Trabecular defects less than 4 mm in diameter are the most difficult to diagnose. Among the identified defects, some may close by the time of birth.

Natural history of ventricular septal defect.

In the prenatal period, a ventricular septal defect does not affect hemodynamics and fetal development due to the fact that the pressure in the ventricles is equal and a large discharge of blood does not occur.

Since early deterioration of the condition after the birth of the child is unlikely, delivery in a specialized institution is not necessary. The defect belongs to the 2nd category of severity.

In the postnatal period, with small defects, the course is favorable, compatible with a long active life. Large ventricular septal defects can lead to the death of a child in the first months of life. Critical conditions in this group develop in 18-21% of patients, but currently the mortality rate in the first year of life does not exceed 9%.

Spontaneous closure of a ventricular septal defect is quite common (45-78% of cases), but the exact probability of this event is unknown. This is due to the different characteristics of the defects included in the study. It is known that large defects associated with Down syndrome or manifested by significant heart failure rarely close on their own. Small and muscular VSDs disappear spontaneously more often. More than 40% of the holes close in the first year of life, but this process can continue up to 10 years. Unfortunately, it is impossible to predict the course of the defect in each specific case. It is only known that in periods up to 6 years, perimembranous defects have a worse prognosis, closing spontaneously only in 29% of cases, and in 39% they require surgery. The corresponding figures for muscular ventricular septal defects are 69% and 3%.

During dynamic observation of large defects, accompanied by severe pulmonary hypervolemia, even an increase in their diameter was noted as the child grew.

During the first weeks of life, the noise may be completely absent due to the high resistance of the pulmonary vessels and the absence of blood discharge through the defect. A characteristic auscultatory sign of the defect is the gradual appearance and increase of holosystolic or early systolic murmur at the left lower edge of the sternum. As a large discharge develops, the second sound on the pulmonary artery becomes intensified and split.

Generally clinical picture determined by the magnitude and direction of blood discharge through the defect. With small defects (Tolochinov-Roget disease), patients have practically no symptoms except for noise, develop and grow normally. Defects with a large left-to-right shunt usually manifest clinically from 4-8 weeks, accompanied by delayed growth and development, repeated respiratory infections, decreased exercise tolerance, heart failure with all the classic symptoms - sweating, rapid breathing (including with the participation of the abdominal muscles ), tachycardia, congestive wheezing in the lungs, hepatomegaly, edematous syndrome.

It should be noted that the reason serious condition Infants with ventricular septal defect almost always have cardiac volume overload rather than high pulmonary hypertension.

Electrocardiography for ventricular septal defect. ECG changes reflect the degree of load on the left or right ventricle. In newborns, right ventricular dominance remains. As the discharge through the defect increases, signs of overload of the left ventricle and left atrium appear.

Chest X-ray. The degree of cardiomegaly and severity of the pulmonary pattern directly depends on the size of the shunt. An increase in the cardiac shadow is associated mainly with the left ventricle and left atrium, and to a lesser extent with the right ventricle. Noticeable changes in the pulmonary pattern occur when the ratio of pulmonary and systemic blood flow is 2:1 or more.

Characteristic for children in the first 1.5-3 months of life with large defects is an increase in the dynamics of the degree of pulmonary hypervolemia. This is due to a physiological decrease in TLC and an increase in left-to-right shunt.

Echocardiography. Two-dimensional echocardiography is the leading method for diagnosing ventricular septal defect. Main diagnostic sign is direct visualization of the defect. To study various parts of the septum, it is necessary to use heart scanning in several sections along the longitudinal and short axes. At the same time, the size, location and number of defects are determined. The discharge and its direction can be established using spectral and color Doppler mapping. The latter technique is extremely useful for visualizing small defects, including those in the muscular part of the septum.

After identifying the defect, the degree of dilatation and hypertrophy of various parts of the heart is analyzed, and the pressure in the right ventricle and pulmonary artery is determined.

If there are defects of type 1 or 2 (subarterial or membranous), it is also necessary to evaluate the condition of the aortic valve, since its prolapse or insufficiency is likely.

Treatment of ventricular septal defect.

Treatment tactics are determined by the hemodynamic significance of the defect and its known prognosis. Given the high probability of spontaneous closure of defects (40% in the first year of life) or their reduction in size, in patients with heart failure it is advisable to first resort to therapy with diuretics and digoxin. It is also possible to use ACE synthesis inhibitors, which facilitate antegrade blood flow from the left ventricle and thereby reduce discharge through the VSD. Additionally, it is necessary to provide treatment for concomitant diseases (anemia, infectious processes), energetically adequate nutrition.

For children who respond to therapy, delayed surgery is possible. Children with small ventricular septal defects who have reached six months of age without signs of heart failure, pulmonary hypertension, or developmental delay are usually not candidates for surgery. Correction of the defect is usually not indicated when the Qp/Qs ratio is less than 1.5:1.0.

Indications for surgical intervention are heart failure and delayed physical development in children who are not amenable to therapy. In these cases, surgery is resorted to starting from the first six months of life. In children over one year of age, surgery is indicated when the ratio of pulmonary to systemic blood flow (Qp/Qs) is more than 2:1. A ratio of pulmonary and systemic resistances of 0.5 or the presence of reverse blood discharge casts doubt on the possibility of surgery and requires an in-depth analysis of the causes of this condition.

Surgical interventions are divided into palliative and radical. Currently, palliative narrowing of the pulmonary artery to limit pulmonary blood flow is used only in the presence of concomitant defects and anomalies that complicate the primary correction of VSD. The operation of choice is to close the defect under artificial circulation. Hospital mortality does not exceed 2-5%. The risk of surgery increases in children under 3 months of age, in the presence of multiple VSDs or concomitant serious developmental anomalies (damage to the central nervous system, lungs, kidneys, genetic diseases, prematurity, etc.).

Attestattau makalalary

Figure 1. Diagram healthy heart Figure 1 shows a diagram of the blood circulation. Venous blood (blue in the figure) enters the right atrium (RA) through the vena cava. It then enters the right ventricle (RV) and through the pulmonary artery (PA) to the lungs. In the lungs, the blood is saturated with oxygen and returned to left atrium(LP). Next - to the left ventricle (LV) and the aorta (Ao), through which it is distributed throughout the body. Having saturated the tissues with oxygen and taken away carbon dioxide, the blood is collected in the vena cava, right atrium, etc. Naturally, the left ventricle does much more work than the right, and therefore its pressure is higher (4-5 times higher than in the right). What happens if there is a defect in the septum between the ventricles? During systole (contraction) of the heart, blood flows from the left ventricle not only into the aorta, as it should be, but also into the right ventricle, in which the pressure is lower, and in the right ventricle there is not only venous, but also arterial (oxygenated) blood. blood.

Figure 2. Hemodynamics of VSD Let's trace the blood flow with a ventricular septal defect (Fig. 2): blood flows from the vena cava into the right atrium, then the right ventricle, pulmonary artery, lungs, left atrium, left ventricle, and then part of it is shunted into the right ventricle, and it again enters the pulmonary artery, lungs, etc. Thus, an additional volume of blood is constantly moving through the pulmonary circulation (right ventricle - lungs - left atrium). In this case, an additional load occurs first on the left ventricle (it still must provide the body with oxygen, i.e. the necessary volume of blood that carries this oxygen), and then on the right ventricle, which leads to their hypertrophy, i.e. . increase. But the most important thing is that a large volume of blood, passing through the vessels of the lungs, the bed of which is not designed for this, causes pathological changes in their walls, the vessels become sclerotic over time, their internal lumen decreases, and intravascular resistance increases. After all, the right ventricle can only “pump” blood through narrowed vessels: by increasing pressure. A condition called pulmonary hypertension occurs. The pressure in the pulmonary artery (and, accordingly, in the right ventricle) increases to prohibitive numbers, over time it becomes higher than in the left ventricle, and the blood changes the direction of shunting: it begins to be discharged from the right ventricle to the left. This severe condition is called Eisenmenger syndrome. In this case, the patient can only be helped by a heart and lung transplant.

The course of the disease depends on many factors: one of the main ones is the size of the defect and the volume of shunted blood. It often happens that children are already inoperable by the age of one year. Sufficient for diagnosis ultrasound examination heart, sometimes in doubtful cases they resort to catheterization (probing) of the heart.

There is only one method of treating the defect: surgery. The operation is performed under conditions of artificial circulation, with cardiac arrest. To close a VSD, it is usually enough to stop the heart for 20-30 minutes, which is quite safe for the patient. Small defects are sutured, large ones are closed with patches made of various synthetics. The treatment results are good. Sometimes children are given digoxin and other heart medications to treat heart failure before surgery.

There are interventricular defects that do not require surgical treatment, so-called Tolochinov-Roger disease. These are muscle defects with a diameter of 1-2 mm, with minimal blood discharge. This diagnosis must be confirmed by a qualified cardiologist at a cardiac surgery hospital. Recently, it has become possible to close some VSDs endocardially with special occluders without opening the chest.

Ventricular septal defect

In a child, a small defect located in the interventricular septum may not appear at all. With a significant size of the defect, the mixing of the two types of blood becomes more pronounced and is revealed by bluishness of the skin, especially on the fingertips and lips.

But ventricular septal defect, fortunately, is easy to treat. Small VSDs may not cause complications or heal on their own. With a significant size of the VSD, surgery is necessary, which is sometimes required only when the first symptoms of this type of heart defect appear.

Signs of VSD

Manifestations of VSD in most cases occur in the very first days, months or weeks after the birth of a child.

Main signs of VSD:

Cyanosis (blueness) of the skin, most severe on the lips and fingertips; Bad general development, lack of appetite; Fast fatiguability; Shortness of breath; Swelling of the abdomen, legs and feet; Cardiopalmus.

These signs can be observed in other conditions, but they can be combined with congenital heart disease, in particular with a ventricular septal defect.

There are cases when at the birth of a child there are no signs of VSD. And if the defect is small enough in size, then the symptoms of VSD may appear in late childhood.

Symptoms of this heart defect can be different, it all depends on the size of the defect in the septum. The doctor may first suspect the presence of a VSD when auscultating the heart or listening to a heart murmur.

Also, manifestations of VSD can be observed in adulthood, with signs of heart failure, for example, shortness of breath.

When to see a doctor

You should consult a doctor if you have the following symptoms:

Lack of weight gain; Fatigue during games and eating; Crying or shortness of breath while eating; Blueness of the skin, especially in the nail area and around the lips;

A doctor should be called if:

Irregular or fast heartbeat; Shortness of breath when exerting yourself; Weakness or fatigue; Swelling in the legs, feet and ankles.

Causes defect

The cause of the formation of defects, like VSD, is a violation of the development of the heart on initial stages fetal formation. In this case, the main role is played by genetic factors and externally environmental factors.

With a defective VSD, there is an opening between the ventricles, right and left.

The muscles of the left ventricle are somewhat “stronger” than the muscles of the right ventricle, so oxygen-rich blood passes from the left ventricle to the right, and there merges with oxygen-poor blood.

As a result, a small volume of oxygenated blood reaches the organs and tissues, which causes chronic hypoxia. And the congestion of the right ventricle with excess blood volume causes its expansion, hypertrophy of its myocardium with the further formation of right ventricular heart failure.

Main risk factors for VSD

The true causes of the formation of VSD, like many other congenital heart defects. does not exist, but researchers have identified a number of main risk factors leading to the appearance of VSD in a child.

For example, these may be genetic factors, therefore, if someone in your family has a congenital heart defect, then you should resort to genetic counseling to find out the risk of a defect in your unborn baby.

Among the risk factors that play a role in the formation of VSD during pregnancy, the following are determined:

Rubella - viral disease. Rubella during pregnancy increases the risk of congenital heart defects in the newborn, including VSD, and many other anomalies. Drinking alcohol and certain drugs during pregnancy. Alcohol and certain drugs that are taken especially in early pregnancy, during the formation of the main organs of the fetus, can increase the risk of developmental abnormalities, including VSD. Wrong treatment diabetes mellitus. High blood sugar levels in the expectant mother lead to hyperglycemia in the fetus, which also creates a risk of various developmental anomalies, including VSD.

Complications with the most common congenital heart defect

With a small ventricular septal defect, a person may not feel any problems. Small-sized VSDs in infancy can close on their own.

But life-threatening complications can arise if this defect is large:

Eisenmenger syndrome.

Pulmonary hypertension can in some cases cause irreversible changes in the lungs. This complication is called Eisenmenger syndrome, which most often develops in a small number of patients with VSD after a long period of time.

This complication may appear at older ages and in early childhood. With this complication, most of the blood flows through the defect from the right ventricle to the left ventricle, this is due to the fact that the right ventricle becomes “stronger” than the left. Therefore oxygen poor blood is flowing to tissues and organs, after which chronic hypoxia occurs (lack of oxygen in tissues). This is manifested by cyanosis of the skin, most of all in the area of ​​the lips and nail phalanges, as well as irreversible changes in the lungs.

Heart failure

Heart failure can also be caused by increased blood flow to the heart in the presence of a defect in the interventricular septum, since in this condition, the heart is unable to pump blood properly.

Endocarditis

The risk of endocardium (an infection of the inner layer of the heart) is quite high in patients with VSD.

Stroke

In patients with a large defect in the interventricular septum, the risk of stroke is increased, since blood passing through this defect can form blood clots that can close the vessels of the brain.

Many other heart diseases.

Also, VSD can lead to pathology of the riveted apparatus and cardiac arrhythmia.

Ventricular septal defect during pregnancy

Many women with VSD without large size defect, they can endure pregnancy without problems.

But, with a sufficiently large size of the ventricular septal defect, or if a woman has complications of this defect, in the form of heart failure, pulmonary hypertension or arrhythmia, the risk of complications during pregnancy increases.

Women with heart defects, including a VSD, are at high risk of having a baby with a congenital heart defect.

Women without a heart defect can very rarely give birth to a child with this pathology. A patient with a heart defect should consult a doctor before deciding to become pregnant. She should also stop taking certain medications that contribute to VSD, so a visit to the doctor is necessary.

Diagnosis of VSD

With regular examination, a ventricular septal defect may be suspected.

In some cases, the doctor, through auscultation, learns about the possibility of a VSD when heart murmurs are heard.

Also, VSD can be detected by ultrasound of the heart, which is performed for any reason.

When auscultation by a doctor reveals a heart murmur, special research methods become necessary to determine the type of heart defect:

Ultrasound of the heart (Echocardiography).

This method is a safe research method that allows you to assess the condition of the heart muscle, its work and cardiac conduction.

Chest X-ray.

This type of test can detect enlargement of the heart and the presence of additional fluid in the lungs, which can be a sign of heart failure.

Pulse oximetry.

This test procedure helps detect oxygen saturation in the blood. A special sensor is installed on the tip of the finger to record the level of oxygen in the blood. Low oxygen saturation in the blood indicates heart problems.

Cardiac catheterization.

The method is radiological. Through femur A catheter is inserted, with its help a special contrast agent is injected into the bloodstream, after which a series of x-rays are taken. This helps the doctor determine the condition of the heart structures. This method also helps to identify the pressure in the chambers of the heart, which makes it possible to indirectly judge the pathology of the heart.

Magnetic resonance imaging.

This method, without x-ray radiation allows you to obtain a layer-by-layer structure of tissues and organs. Being an expensive diagnostic method, MRI is used when echocardiography does not give a clear answer.

Treatment defect between the left and right ventricles of the heart

VSD does not require urgent surgical treatment if its complications do not threaten the patient’s life. If a VSD has been detected in a child, then the doctor may first observe his general condition, since the defect may heal on its own over time.

But when the VSD does not close on its own, but the hole is small, it may not in any way interfere with the person’s normal lifestyle, so surgical correction is also not required here.

In most cases, VSD cannot be treated without surgical intervention.

The time required for surgical correction for a given heart defect is directly dependent on general condition the health of the child and the presence of other congenital heart defects.

Methods of drug treatment of VSD

It should be noted right away that not a single drug leads to healing of the atrial septal defect. But still, conservative treatment helps to reduce the manifestation of VSD and reduces the risk of complications after surgery.

Here are some of the medications that may be used by patients with VSD:

Drugs that regulate heart rhythm: digoxin and beta blockers such as inderal and anaprilin; Drugs that reduce blood clotting: Anticoagulants (aspirin and warfarin), which reduce blood clotting, reduce the risk of a complication of VSD - stroke.

Surgical treatment of VSD

Surgical treatment of VSD in infancy is recommended by many cardiac surgeons in order to prevent possible complications in adulthood.

Surgical treatment, both in adults and in children, consists of closing the defect by applying a “patch” that prevents blood from passing from the left side of the heart to the right. For which one of the following methods can be performed:

— Cardiac catheterization

It is a minimally invasive treatment method in which, under X-ray control, a thin probe is inserted through the femoral vein, and its end is brought to the site of the defect. After which, a mesh patch is inserted through it to cover the defect in the septum.

After some time, this mesh grows into tissue, which leads to complete closure of the defect.

This intervention has significant advantages - a shorter postoperative period and a minimal incidence of complications. Since this treatment method is less traumatic, it is easier for the patient to tolerate.

Possible complications with this treatment method:

Infectious complications on the side of the insertion crater, pain or bleeding. Allergic reaction to a substance used during catheterization. Damage to a blood vessel.

— Open surgery

This method of surgical treatment of heart defects is performed under general anesthesia. It consists of making an incision in the chest and connecting the patient to a heart-lung machine. An incision is made into the heart, after which a patch of synthetic material is sewn into the interventricular septum. The disadvantage of this method is that it has a longer postoperative period and a much greater risk of complications.

The human heart has a complex four-chamber structure, which begins to form from the first days after conception.

But there are cases when this process is disrupted, which causes large and small defects in the structure of the organ that affect the functioning of the entire organism. One of them is called a ventricular septal defect, or VSD for short.

Ventricular septal defect is a congenital (sometimes acquired) heart defect (CHD), which is characterized by the presence of a pathogenic opening between the cavities of the left and right ventricles. For this reason, blood from one ventricle (usually the left) flows into the other, thereby disrupting the function of the heart and the entire circulatory system.

Its prevalence is approximately 3-6 cases per 1000 full-term newborns, not counting children who are born with minor septal defects, which self-limit during the first years of life.

Among congenital defects, VSD is the second most common among children over 3 years of age.

Causes and risk factors

Usually, a ventricular septal defect in a fetus develops in the early stages of pregnancy, from about 3 to 10 weeks. The main reason for this is considered to be a combination of external and internal negative factors, including:

• genetic predisposition;
• viral infections suffered during pregnancy (rubella, measles, influenza);
• alcohol abuse and smoking;
• taking antibiotics that have a teratogenic effect ( psychotropic drugs, antibiotics, etc.);
• exposure to toxins, heavy metals and radiation;
• severe stress.

Classification

Ventricular septal defect in newborns and older children can be diagnosed as an independent problem (isolated defect), or as a component of other cardiovascular diseases, for example, Cantrell's pentad (to read about it).

The size of the defect is estimated based on its size in relation to the diameter of the aortic opening:

• a defect up to 1 cm in size is classified as small (Tolochinov-Roger disease);
• Large defects are considered to be defects from 1 cm or those that in size exceed half of the aortic mouth.

Finally, by hole location in the septum, VSD is divided into three types:

• Muscular ventricular septal defect in a newborn. The hole is located in the muscular part, away from the conduction system of the heart and valves, and if small in size, can close on its own.
• Membranous. The defect is localized in the upper segment of the septum below the aortic valve. Usually it has a small diameter and stops on its own as the child grows.
• Supracrest. It is considered the most complex type of defect, since the hole in this case is located on the border of the efferent vessels of the left and right ventricles, and very rarely closes spontaneously.

Danger and complications

If the hole size is small and the child is in normal condition VSD does not pose a particular danger to the child’s health, and only requires regular monitoring by a specialist.

Large defects are a completely different matter. They are the reason heart failure, which can develop immediately after the baby is born.

Such children are susceptible colds with a tendency to pneumonia, may be delayed in development, have difficulty with the sucking reflex, suffer from shortness of breath even after a short physical activity. Over time, breathing difficulties also arise at rest, which disrupts the functioning of the lungs, liver and other organs.

Besides, VSD can cause the following serious complications:

• as a consequence;
• formation of acute heart failure;
• endocarditis, or infectious inflammation intracardiac membrane;
• strokes and;
• disruption of the valve apparatus, which leads to the formation of valvular heart defects.

Symptoms

Large ventricular septal defects appear already in the first days of life, and are characterized by the following symptoms:

• blue discoloration of the skin (mainly the limbs and face), which intensifies when crying;
• appetite disturbances and feeding problems;
• slow pace of development, impaired weight gain and growth;
• constant drowsiness and fatigue;
• swelling localized in the extremities and abdomen;
• heart rhythm disturbances and shortness of breath.

Small defects often do not have pronounced manifestations and are determined by listening(a rough systolic murmur is heard in the patient’s chest) or other studies. In some cases, children experience the so-called, that is, protrusion of the chest in the area of ​​the heart.

If the disease was not diagnosed in infancy, then with the development of heart failure in the child Complaints appear at 3-4 years of age to strong heartbeat and chest pain, a tendency to nosebleeds and loss of consciousness develops.

Patients often suffer from pulmonary congestion, shortness of breath and cough, and become very tired even after minor physical exertion.

When to see a doctor

VSD, like any other heart defect (even if it is compensated and does not cause inconvenience to the patient), necessarily requires constant monitoring by a cardiologist, since the situation can worsen at any time.

So as not to miss alarming symptoms and the time when the situation can be corrected with minimal losses, parents are very It is important to observe the child’s behavior from the very first days. If he sleeps too much and for a long time, is often capricious for no reason and does not gain weight well, this is serious reason for consultation with a pediatrician and pediatric cardiologist.

Symptoms are similar for different congenital heart diseases. Find out more about , so you don't miss any complaints.

Diagnostics

The main methods for diagnosing VSD include:

• Electrocardiogram. The study determines the degree of ventricular overload, as well as the presence and severity of pulmonary hypertension. In addition, in older patients, signs of arrhythmia and cardiac conduction disturbances may be detected.
• Phonocardiography. Using FCG, you can record high-frequency systolic murmur in the 3rd-4th intercostal space to the left of the sternum.
• Echocardiography. EchoCG allows you to identify a hole in the interventricular septum or suspect its presence based on circulatory disorders in the vessels.
• Ultrasonography. Ultrasound evaluates the work of the myocardium, its structure, condition and patency, as well as two very important indicators - pressure in the pulmonary artery and the amount of blood discharge.
• Radiography. On a chest x-ray, you can see an increase in the pulmonary pattern and pulsation of the roots of the lungs, a significant increase in the size of the heart.
• Probing of the right heart cavities. The study makes it possible to detect increased pressure in the pulmonary artery and ventricle, as well as increased oxygenation of venous blood.
• Pulse oximetry. The method determines the degree of oxygen saturation of the blood - low performance are a sign serious problems with the cardiovascular system.
• Catheterization of the heart muscle. With its help, the doctor assesses the condition of the heart structures and determines the pressure in its chambers.

Treatment

Small septal defects that do not give bright severe symptoms, usually do not require any special treatment, since heal independently by 1-4 years of age or later.

In difficult cases, when the hole does not heal for a long time, the presence of a defect affects the child’s well-being or it is too large, the question of surgical intervention is raised.

In preparation for surgery, conservative treatment is used to help regulate heartbeat, normalize blood pressure and support myocardial function.

Surgical correction of VSD can be palliative or radical: palliative operations are performed on infants with severe malnutrition and multiple complications in order to prepare for radical intervention. In this case, the doctor creates an artificial pulmonary artery stenosis, which significantly alleviates the patient’s condition.

TO radical operations that are used to treat VSD include:

• suturing pathogenic holes with U-shaped sutures;
• plastic defects using patches made of synthetic or biological tissue performed under ultrasound control;
• Open heart surgery is effective for combined defects(such as tetralogy of Fallot) or large holes that cannot be closed with a single patch.

Gives the best results surgical interventions, carried out at the age of 2-2.5 years, when patients usually show the first signs of heart failure.

This video talks about one of the most effective operations against VSD:

Predictions and prevention

Small ventricular septal defects (1-2 mm) usually have a favorable prognosis– children with this disease do not suffer from unpleasant symptoms and do not lag behind their peers in development. With more significant defects accompanied by heart failure, the prognosis is significantly worse, since without appropriate treatment they can lead to serious complications and even death.

Preventive measures to prevent VSD should be taken even at the stage of planning pregnancy and bearing a child: they consist in maintaining healthy image life, timely attendance at antenatal clinics, refusal bad habits and self-medication.

Despite serious complications and not always favorable forecasts, the diagnosis of “ventricular septal defect” cannot be considered a death sentence little patient. Modern treatment methods and advances in cardiac surgery can significantly improve the child’s quality of life and prolong it as long as possible.