Ventricular septal defect in adults. Ventricular septal defect

One of the common congenital heart defects that is diagnosed in children under three years of age is a ventricular septal defect. This disease is the second most common disease among heart muscle defects. It is a hole in the wall between the left and right ventricles. Because of this, blood from the left half of the heart enters the right and overflows the pulmonary circulation. It occurs both as an independent defect and in combination with other defects.

Features of the disease

With a ventricular septal defect (VSD), the condition of patients can vary greatly - this directly depends on the size of the pathology. It comes to the point that patients with a hole size of two to five millimeters do not feel the defect at all, and the disease proceeds without visible signs. If the diameter of the defect is large (ten to fifteen millimeters), urgent surgical intervention is necessary. There are cases when the septum is completely absent, but such a pathology is fatal and is not operated on.

With a ventricular septal defect, during the period of muscle contraction, the pressure in the right side of the heart is much lower than in the left. Mixing of blood occurs and the load on the vessels of the lungs increases. The pulmonary circulation receives an excess of oxygen-enriched blood, while the large circulation receives less of it. This can lead to sclerotic changes in the pulmonary vessels, right ventricular failure and pulmonary hypertension.

VSD is formed in the fetus during intrauterine development. In rare cases, such a defect develops already during life. If the size of the defect is small, it can only be detected in children by chance, based on the results of echocardiography. It usually closes on its own by the age of one, and sometimes a little later. But in this case, the child needs to be constantly monitored by a pediatrician to prevent the development of the disease and its transition to the active phase. If the child’s defect has not disappeared by the age of three, then treatment is only possible through surgery.

Forms and types

Cardiologists distinguish several forms of ventricular septal defect depending on its location:

• lower part of the septum - trabecular pathologies (supracrestal);
• middle part - muscular defects of the interventricular septum (Tolochinov-Roget disease);
• upper part, the most common defects are pyremembranous pathologies.

In the first form of the defect, independent closure is impossible. In the case of pathology in the middle part of the heart muscle, the defect closes itself with a small hole diameter. pyremembranous pathology almost always heals on its own.

The differences in VSD size are classified as follows:

• small. Almost invisible, asymptomatic;
• average. Symptoms of the disease begin to appear in the first months of a child’s life;
• big. They are extremely severe and often lead to death.

Reasons for appearance

Ventricular septal defects occur under the influence of two factors:

• genetic. In a large number of cases, VSD is inherited from parents to children. If a similar pathology was observed in a family among close relatives, then it is possible that it will appear in descendants. This occurs due to changes in chromosomes or genes. Heart defects are essentially caused by gene mutations;
• environmental. When the fetus in the womb is exposed to unfavorable environmental factors, gene mutations may develop. When a expectant mother uses potent drugs, alcohol, tobacco and drugs, as well as suffers from severe viral infections, the risk of pathology increases significantly.

Diagram of a ventricular septal defect

Symptoms of ventricular septal defect

• With small ventricular septal defects, symptoms do not appear.
• With moderate VSD, symptoms uncharacteristic of heart defects may occur. Weakness, increased fatigue, retarded physical development, susceptibility to pneumonia and pulmonary infections.
• Large defects manifest themselves in the form of pale skin, swelling of the legs, chest pain, severe shortness of breath during physical exertion. Such symptoms are more typical of heart defects.

Ultrasound examination (echocardiography) of the heart muscle allows the most accurate diagnosis of VSD.

Diagnostics

Doctors can determine a ventricular septal defect based on this type of diagnosis:

• a thorough analysis of complaints from the patient or his parents (fatigue during physical activity, pale skin, pain in the heart, shortness of breath, weakness);
• a detailed examination of the life history and heredity (condition at birth, previous operations and diseases, the presence of heart muscle defects in relatives);
• examination by a doctor, percussion and examination of heart murmurs;
• study of blood and urine test data;
• analysis of electrocardiogram and echocardiography data;
• viewing the results of radiographic examination;
• cardiac examinations using catheterization, ventriculography and angiography. Special procedures by which a catheter or contrast agents are introduced into the body, allowing pathology to be seen using various methods;
• analysis of magnetic resonance therapy data.

Treatment

Therapeutic and medicinal methods

Conservative treatment for ventricular septal defect is used mainly as preparation for surgery or if the hole has a small diameter and there is hope that it will close on its own. The patient is prescribed diuretics, cardiotrophics and inotropic support drugs. But non-surgical treatment, as a rule, only prevents complications from developing and does not eliminate the defect itself.

Remember to avoid strenuous exercise in your child. Try to make him cry and strain less. After all, such actions are also a type of stress in the body. Be sure to ensure that your baby does not lift heavy objects.

Operation

The main treatment for VSD is surgery. Operations can be emergency or planned. In an emergency, surgical intervention in the patient’s body is performed to prevent death without prior preparation.

In the case when a planned operation is prescribed (as a rule, it is performed in childhood), the patient is first prepared for it. Cardiologists monitor his condition and conduct a course of conservative treatment. Surgery to close a ventricular septal defect is performed in two different ways:

• radical. A method in which a patch made from the lining of the heart or an artificial material is applied to the hole in the septum. In this case, the patient must be connected to an artificial blood pumping machine;
• palliative. With this operation, the heart muscle defect is not eliminated, but the pulmonary artery is only narrowed. The method makes life easier for the patient and prevents the development of complications. Used for patients intolerant of radical intervention.

The following video will tell you more about what the technology of minimally invasive elimination of ventricular septal defect is:

Disease prevention

There are no preventative measures to prevent the development of VSD. There are only recommendations for expectant mothers that will help avoid the development of a defect in the fetus or detect it at an early stage:

• timely registration at the antenatal clinic (for up to twelve weeks);
• maintaining a daily routine and proper nutrition;
• regular visits to an obstetrician-gynecologist;
• exclude

Ventricular septal defect (VSD): causes, manifestations, treatment

Ventricular septal defect (VSD) is a fairly common pathology, which is an intracardiac anomaly with a hole in the wall separating the ventricles of the heart.

picture: ventricular septal defect (VSD)

Small defects practically do not cause complaints from patients and heal on their own with age. If there is a large hole in the myocardium, surgical correction is performed. Patients complain of frequent pneumonia, colds, severe.

Classification

VSD can be considered as:

• Independent congenital heart disease (congenital),
• An integral part of the combined congenital heart disease,
• Complication.

Based on the location of the hole, 3 types of pathology are distinguished:

1. Perimembranous defect
2. muscle defect,
3. Subarterial defect.

By hole size:

• Large VSD - larger than the aortic lumen,
• Middle VSD - half of the aortic lumen,
• Small VSD - less than a third of the lumen of the aorta.

Causes

At the stage of early intrauterine development of the fetus, a hole appears in the muscular septum separating the left and right chambers of the heart. In the first trimester of pregnancy, its main parts develop, compare and connect correctly with each other. If this process is disrupted by endogenous and exogenous factors, a defect will remain in the septum.

The main causes of VSD:

1. Heredity - the risk of having a sick child is increased in those families where there are persons with congenital heart abnormalities.
2. Infectious diseases of a pregnant woman - ARVI, mumps, chicken pox, rubella.
3. A pregnant woman taking antibiotics or other medications with embryotoxic effects - antiepileptic drugs, hormones.
4. Unfavorable environmental conditions.
5. Alcohol and drug intoxication.
6. Ionizing radiation.
7. Early toxicosis of a pregnant woman.
8. Lack of vitamins and microelements in a pregnant woman’s diet, starvation diets.
9. Age-related changes in the body of a pregnant woman after 40 years.
10. Endocrine diseases in a pregnant woman - hyperglycemia, thyrotoxicosis.
11. Frequent stress and overwork.

Symptoms

- a symptom characteristic of all “blue” heart defects

A VSD does not cause problems to the fetus and does not interfere with its development. The first symptoms of pathology appear after the birth of a child: acrocyanosis, lack of appetite, shortness of breath, weakness, swelling of the abdomen and limbs, delayed psychophysical development.

Children with signs of VSD often develop severe forms of pneumonia that are difficult to treat. A doctor, examining and examining a sick child, discovers an enlarged heart, systolic murmur, and hepatosplenomegaly.

• If there is a small VSD, the development of children does not change significantly. There are no complaints, shortness of breath and slight fatigue occur only after physical activity. The main symptoms of the pathology are systolic murmur, which is found in newborns, spreads in both directions and is clearly audible on the back. For a long time it remains the only symptom of the pathology. In more rare cases, you may feel a slight vibration or trembling when you place your palm on your chest. In this case, there are no symptoms of heart failure.
• A pronounced defect manifests itself acutely in children from the first days of life.. Children are born with malnutrition. They eat poorly, become restless, pale, develop hyperhidrosis, cyanosis, and shortness of breath, first while eating and then at rest. Over time, breathing becomes rapid and difficult, a paroxysmal cough appears, and a heart hump forms. Moist wheezing appears in the lungs, the liver enlarges. Older children complain of palpitations and cardialgia, shortness of breath, frequent nosebleeds and fainting. They are significantly behind their peers in development.

If a child gets tired quickly, cries often, eats poorly, refuses to breastfeed, does not gain weight, has shortness of breath and cyanosis, you should consult a doctor as soon as possible. If shortness of breath and swelling of the extremities occur suddenly, and the heartbeat becomes fast and irregular, an ambulance should be called.

Stages of disease development:

1. The first stage of pathology also manifests itself in the pulmonary vessels. In the absence of adequate and timely therapy, pulmonary edema or pneumonia may develop.
2. The second stage of the disease is characterized by spasm of the pulmonary and coronary vessels in response to their overstretching.
3. In the absence of timely treatment for congenital heart disease, irreversible sclerosis develops in the pulmonary vessels. At this stage of the disease, the main pathological signs appear, and cardiac surgeons refuse to perform the operation.

disorders with VSD

Downstream, there are 2 types of VSD:

• Asymptomatic disease is detected by noise. It is characterized by an increase in the size of the heart and an increase in the pulmonary component of the 2nd tone. These signs indicate the presence of a small VSD. Medical supervision is required for 1 year. If the noise disappears and there are no other symptoms, spontaneous closure of the defect occurs. If the noise remains, long-term observation and consultation with a cardiologist are required, and surgery is possible. Small defects occur in 5% of newborns and close on their own by 12 months.
• Large VSD is symptomatic and manifests itself by signs. Echocardiography data indicate the presence or absence of associated defects. Conservative treatment in some cases gives satisfactory results. If drug therapy is ineffective, surgery is indicated.

Complications

A significant size of the hole in the interventricular septum or the lack of adequate therapy are the main reasons for the development of severe complications.

Diagnostics

Diagnosis of the disease includes a general examination and examination of the patient. During auscultation specialists discover what allows one to suspect the presence of a VSD in a patient. To make a final diagnosis and prescribe adequate treatment, special diagnostic procedures are performed.

• carried out to detect a defect, determine its size and location, and the direction of blood flow. This method provides comprehensive data about the defect and condition of the heart. This is a safe, highly informative study of the heart cavities and hemodynamic parameters.
• Only if there is a large defect on pathological changes appear. The electrical axis of the heart usually deviates to the right, and signs of left ventricular hypertrophy appear. In adults, arrhythmia and conduction disturbances are recorded. This is an indispensable research method that allows you to identify dangerous heart rhythm disturbances.
• allows you to detect pathological noises and altered heart sounds, which are not always determined by auscultation. This is an objective qualitative and quantitative analysis that does not depend on the doctor’s hearing characteristics. A phonocardiograph consists of a microphone, which converts sound waves into electrical impulses, and a recording device, which records them.
• Dopplerography- a primary technique for diagnosing and identifying the consequences of valve disorders. It evaluates the parameters of pathological blood flow caused by congenital heart disease.
• On X-ray the heart with VSD is significantly enlarged, there is no narrowing in the middle, spasm and congestion of the vessels of the lungs, flattening and low standing of the diaphragm, horizontal arrangement of the ribs, fluid in the lungs in the form of darkening over the entire surface are detected. This is a classic study that allows you to detect an increase in the shadow of the heart and a change in its contours.
• Angiocardiography carried out by injecting a contrast agent into the cavity of the heart. It allows us to judge the location of the birth defect, its volume and exclude concomitant diseases.
• - a method for determining the amount of oxyhemoglobin in the blood.
• Magnetic resonance imaging- an expensive diagnostic procedure, which is a real alternative to echocardiography and Dopplerography and allows you to visualize the existing defect.
• Cardiac catheterization- visual examination of the cavities of the heart, allowing to establish the exact nature of the lesion and the features of the morphological structure of the heart.

Treatment

If the hole has not closed before one year, but it has significantly decreased in size, conservative treatment is carried out and the child’s condition is monitored for 3 years. Minor defects in the muscle part usually heal on their own and do not require medical intervention.

Conservative treatment

Drug therapy does not lead to healing of the defect, but only reduces the manifestations of the disease and the risk of developing severe complications.

Surgery

Indications for the operation:

• The presence of concomitant congenital heart defects,
• Lack of positive results from conservative treatment,
• Recurrent heart failure,
• Frequent pneumonia
• Down syndrome,
• Social indications,
• Slow increase in head circumference,
• Pulmonary hypertension,
• Large VSD.

endovascular installation of a “patch” is a modern method of treating the defect

Radical surgery - plastic surgery of a birth defect. It is performed using a heart-lung machine. Small defects are sutured with U-shaped sutures, and large holes are closed with a patch. The wall of the right atrium is incised and the VSD is detected through the tricuspid valve. If such access is not possible, the right ventricle is opened. Radical surgery usually gives good results.

Endovascular correction The defect is carried out by piercing the femoral vein and inserting a mesh through a thin catheter into the heart, which closes the hole. This is a low-traumatic operation that does not require long-term rehabilitation and the patient’s stay in intensive care.

Palliative surgery- narrowing of the lumen of the pulmonary artery with a cuff, which allows to reduce the penetration of blood through the defect and normalize the pressure in the pulmonary artery. This is an intermediate operation that relieves the symptoms of the pathology and gives the child a chance for normal development. The operation is performed on children in the first days of life for whom conservative treatment has proven ineffective, as well as on those who have multiple defects or concomitant intracardiac anomalies.

The prognosis of the disease is favorable in most cases. Proper management of pregnancy and childbirth, adequate treatment in the postpartum period give 80% of sick children a chance to survive.

Video: report on surgery for VSD

Video: lecture on VSD

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. With pathological flow of arterial blood into the right ventricle, the required pressure level decreases. To maintain 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 the baby’s life, and doctors begin immediate treatment, prepare for surgery, and, if it is possible to avoid surgery, conduct 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 during intrauterine development, the lungs do not participate in enriching the blood with oxygen, so the heart has an open oval window (ooo), 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 of 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 there are, the more complex the degree of the disease. 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 rare cases, a combination of several types of JMP occurs. The defect can be an independent disease, or accompany other severe abnormalities in the development of the heart: atrial septal defect (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 one of your close relatives has had defects of 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. Taking medications - 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 in early pregnancy;
8. External factors - hazardous environmental conditions, harmful working conditions, increased fatigue, overexertion and stress.

The presence of these factors does not always cause severe illness, but it increases the likelihood. 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

Small defects (up to 2 mm) in the normal condition of the baby are 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, and problems with internal organs appear 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. Small defects of the membranous part of the cardiac septum (up to 5 mm) occur in some cases without symptoms; sometimes the first signs appear in children from 1 to 2 years of age.

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 of the muscle tissue in the area of ​​the hole.

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. Paleness of the 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, the increased oxygen content 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 respiratory or heart rhythm disturbances and the normal development of the child, in some cases it allows 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.

A ventricular septal defect in children is a congenital abnormal connection between the two ventricles of the heart, which occurs due to underdevelopment at different levels. This type of anomaly is one of the most common congenital heart defects in children - it occurs, according to various authors, in 11-48% of cases.

Depending on the location of the ventricular septal defect in the fetus, the following types are distinguished:

• Defects of the membranous part of the septum. Their sizes range from 2 to 60 mm, their shape is different, they are observed in 90% of cases,
• Defects of the muscular part of the septum. Their sizes are small (5-20 mm), and with contraction of the heart muscle, the lumen of the defect decreases even more; they appear in 2-8% of cases.
• The absence of the interventricular septum occurs in 1-2% of cases.

How does ventricular septal defect manifest in children?

Ventricular septal defect in children is accompanied by the development of compensatory hypertrophy of the ventricular myocardium and pulmonary circulation, the severity of which depends on the age of the child and the size of the defect.

Difficulty in the movement of blood through the pulmonary and systemic circulation with a ventricular septal defect in children gives the main clinical picture. Hemodynamic disturbances depend on the magnitude and direction of blood flow through the defect, which, in turn, is determined by the size and location of the defect, the vessels of the pulmonary circulation, the gradient of vascular resistance of the pulmonary and systemic circulation, the state of the myocardium and ventricles of the heart. Hemodynamic disorders are not static, but change as the child grows and develops, which leads to changes in the clinical picture of the defects and their transformation into other clinical forms.

With a small ventricular septal defect in the fetus (up to 5 mm in size), the discharge of blood through it from the left ventricle to the right is small and does not cause pronounced hemodynamic disturbances. Due to the large capacity of the vessels of the pulmonary circulation, the pressure in the right ventricle does not increase; additional load falls only on the left ventricle, which often hypertrophies.

In case of a ventricular septal defect in children with a size range of 10-20 mm, the discharge through it reaches 70% of the blood that is discharged by the left ventricle. This causes significant volume overload of the pulmonary circulation, which leads to low overload of the right ventricle and then to its hypertrophy. First, under the influence of high blood pressure, the arteries of the pulmonary circulation expand, thereby facilitating the work of the right ventricle. The pressure in the vessels of the pulmonary circulation remains normal, however, severe large blood volume syndrome can lead to the development of increased pressure in the pulmonary artery; with a large defect, the amount of blood discharge through it depends mainly on the ratio of vascular resistance of the pulmonary and systemic circulation.

Systolic pressure in the pulmonary artery with a large ventricular septal defect remains at a high level. This is due to the fact that pressure is transferred to the pulmonary artery from the left ventricle (hydrodynamic factor). High pressure in the pulmonary artery leads to overload and enlargement of the right ventricle. This provokes a large volume of blood discharged through the defect, which ultimately leads to overflow of the venous bed of the pulmonary circulation and causes volume overload of the left atrium, resulting in an increase in systolic and diastolic pressure in the left ventricle, left atrium, and pulmonary veins. With prolonged similar overloads, this leads to hypertrophy (increase in size) of the left ventricle and left atrium. Increased pressure in the pulmonary veins and left atrium, due to the neurohumoral mechanism of load compensation, leads to spasm, and then to sclerosis of the pulmonary arterioles. Children in the first year of life develop heart failure, and more than 50% of children die before the age of one year.

Ventricular septal defect in the fetus and its types

An isolated ventricular septal defect in the fetus, depending on its size and the amount of blood discharge, is clinically divided into 2 forms.

1. first includes small defects of the interventricular septum in the pload, located mainly in the muscular septum, which are not accompanied by severe hemodynamic disturbances (Tolochishov-Roger disease);
2. to the second group These include defects of the interventricular septum in the fetus of sufficiently large size, located in the membranous part of the septum, leading to severe hemodynamic disturbances.

Clinic of Topochinov-Roger disease. The first, and sometimes the only manifestation of the defect is a systolic murmur in the heart region, which appears, as a rule, from the first days of the child’s life. The children are growing well and have no complaints. The boundaries of the heart are within the age norm. In the III-IV intercostal space to the left of the sternum, systolic trembling is heard in most patients. A characteristic symptom of the defects is a rough, very loud systolic murmur that occurs when blood passes through a narrow hole in the septum under high pressure from the left ventricle to the right. The murmur, as a rule, occupies the entire systole and often merges with the second sound. Its maximum sound is in the III-IV intercostal space from the sternum, it is well conducted throughout the entire region of the heart, to the right behind the sternum, is heard on the back near the interscapular space, is well conducted along the bones, transmitted through the air and can be heard even if the stethoscope is raised above the heart (remote noise ).

In some children, a very gentle systolic murmur is heard, which is better detected in the supine position and significantly decreases or even completely disappears with physical activity. This change in noise can be explained by the fact that during exercise, due to the powerful contraction of the heart muscles, the hole in the interventricular septum in children closes completely, and the blood flow through it ends. There are no signs of heart failure in Tolochinov-Roger disease.

Signs of a severe ventricular septal defect

Severe ventricular septal defect in children manifests itself acutely from the first days after birth. Children are born at term, but in 37-45% moderate congenital malnutrition is observed, the cause of which is not clear.

The first symptom of defects is systolic murmur, which is heard from the neonatal period. In some children, already in the first weeks of life, signs of circulatory failure appear in the form of shortness of breath, which occurs first with anxiety, sucking, and then in a calm state.

During this period, children often suffer from acute respiratory diseases and pneumonia. More than 2/3 of children are lagging behind in physical and psychomotor development, 30% develop grade II malnutrition.

The skin is pale. The pulse is rhythmic, tachycardia is often observed. Blood pressure is not changed. In most children, a central “heart hump” begins to form early, and a pathological pulsation appears over the upper region of the stomach. Systolic tremor is detected in the III-IV intercostal space to the left of the sternum. The borders of the heart are slightly expanded across and upward. Pathological accent of the 2nd tone in the 2nd intercostal space on the left at the sternum, which is often combined with its splitting. All children hear a typical murmur of an interventricular defect - a systolic, rough murmur that occupies the entire systole, with a maximum sound in the 3rd intercostal space to the left of the sternum, well transmitted to the right behind the sternum in the 3rd-4th intercostal space, to the left auscular zone and to the back, it is often "encircling" the chest. In 2/3 of children, from the first months of life, pronounced signs of circulatory failure appear, manifesting first in the form of anxiety, difficulty sucking, shortness of breath, tachycardia, which is not always interpreted as a manifestation of heart failure, but is often regarded as concomitant diseases (acute, pneumonia).

Ventricular septal defect of the heart in children after one year

A ventricular septal defect in children over one year of age enters the stage of attenuation of clinical signs due to the intensive growth and anatomical development of the baby’s body. At the age of 1-2 years, a phase of relative compensation begins, which is characterized by the absence of shortness of breath and tachycardia. Children become more active, begin to gain weight better, grow better, and many of them catch up with their peers in their development; much less suffer from concomitant diseases compared to the first year of life. During an objective examination, 2/3 of children have a centrally located “heart hump”; systolic tremors are detected in the III-IV intercostal space to the left of the sternum.

The borders of the heart are slightly expanded across and upward. The apical impulse is of medium strength and strengthened. On auscultation, there is a splitting of the second tone in the second intercostal space on the left at the sternum and there may be its accentuation. A rough systolic murmur is heard along the left edge of the sternum with a maximum sound in the third intercostal space on the left and a large distribution area.

In some children, diastolic murmurs of relative pulmonary valve insufficiency are also heard, arising as a result of increased pulmonary circulation in the pulmonary artery and an increase in pulmonary hypertension (Graham-Still murmur) or relative mitral stenosis, which occurs with a large cavity of the left atrium due to large arteriovenous discharge of blood through the defect (Flint noise). The Graham-Still murmur is heard in the 2-3 intercostal space to the left of the sternum and is well carried up to the base of the heart. Flint's murmur is better identified at Botkin's point and is carried to the apex of the heart.

Depending on the degree of hemodynamic disturbance, there is a very large variability in the clinical course of ventricular septal defect in children, which requires a different therapeutic and surgical approach to such children.

The diagnosis of ventricular septal defect in children is made based on the results of ECG, Echo-CG, and catheterization of cavities.

Differential diagnosis is carried out with congenital heart defects, which occur with overload of the pulmonary circulation, as well as with acquired problems - mitral valve insufficiency. Diagnosis is difficult when a ventricular septal defect is combined with other congenital heart defects, especially in early childhood.

Complications and prognosis for ventricular septal defect in children

In children of the first year of life, frequent complications are malnutrition, circulatory failure, and recurrent congestive bacterial pneumonia. In older children - bacterial endocarditis. Embolisms of the vessels of the pulmonary circulation often occur, leading to the development of heart attacks and lung abscesses. In 80-90% of children, the defect is complicated by the development of pulmonary hypertension with age.

Ventricular septal defect (VSD) is a congenital heart defect characterized by a defect in the muscular septum between the right and left ventricles of the heart. VSD is the most common congenital heart defect in newborns, its incidence is approximately 30-40% of all cases of congenital heart defects. This defect was first described in 1874 by P. F. Tolochinov and in 1879 by H. L. Roger.

According to the anatomical division of the interventricular septum into 3 parts (upper - membranous, or membranous, middle - muscular, lower - trabecular), they also give names to defects of the interventricular septum. In approximately 85% of cases, the VSD is located in the so-called membranous part, that is, immediately under the right coronary and non-coronary cusps of the aortic valve (when viewed from the left ventricle of the heart) and at the junction of the anterior cusp of the tricuspid valve into its septal cusp (when viewed from side of the right ventricle). In 2% of cases, the defect is located in the muscular part of the septum, and there may be several pathological holes. A combination of muscle and other localizations of VSD is quite rare.

The size of ventricular septal defects can range from 1 mm to 3.0 cm or even more. Depending on the size, large defects are distinguished, the size of which is similar to or greater than the diameter of the aorta, medium defects, having a diameter of ¼ to ½ the diameter of the aorta, and small defects. Defects of the membranous part, as a rule, have a round or oval shape and reach 3 cm; defects of the muscular part of the interventricular septum are most often round and small.

Quite often, in approximately 2/3 of cases, VSD can be combined with another concomitant anomaly: atrial septal defect (20%), patent ductus arteriosus (20%), coarctation of the aorta (12%), congenital mitral valve insufficiency (2%), stanosis of the aorta (5%) and pulmonary artery.

Schematic representation of a ventricular septal defect.

Causes of VSD

Disturbances in the formation of the interventricular septum have been found to occur during the first three months of pregnancy. The interventricular septum of the fetus is formed from three components, which during this period must be compared and adequately connected to each other. Violation of this process leads to the fact that a defect remains in the interventricular septum.

The mechanism of development of hemodynamic disturbances (blood movement)

In the fetus located in the mother's uterus, blood circulation is carried out along the so-called placental circle (placental circulation) and has its own characteristics. However, soon after birth, the newborn establishes normal blood flow through the systemic and pulmonary circulation, which is accompanied by the emergence of a significant difference between the blood pressure in the left (more pressure) and right (less pressure) ventricles. In this case, the existing VSD leads to the fact that blood from the left ventricle is pumped not only into the aorta (where it should flow normally), but also through the VSD into the right ventricle, which should not normally be the case. Thus, with each heartbeat (systole), a pathological discharge of blood occurs from the left ventricle of the heart to the right. This leads to an increase in the load on the right ventricle of the heart, as it does extra work to pump an additional volume of blood back to the lungs and left chambers of the heart.

The volume of this pathological discharge depends on the size and location of the VSD: in the case of a small defect, the latter has virtually no effect on the functioning of the heart. On the opposite side of the defect in the wall of the right ventricle, and in some cases on the tricuspid valve, a scar thickening may develop, resulting from a reaction to injury from the pathological release of blood gushing through the defect.

In addition, due to pathological discharge, the additional volume of blood entering the vessels of the lungs (pulmonary circulation) leads to the formation of pulmonary hypertension (increased blood pressure in the vessels of the pulmonary circulation). Over time, compensatory mechanisms are activated in the body: the muscle mass of the ventricles of the heart increases, the vessels of the lungs gradually adapt, which first accept the incoming excess volume of blood, and then change pathologically - thickening of the walls of the arteries and arterioles is formed, which makes them less elastic and more dense . An increase in blood pressure in the right ventricle and pulmonary arteries occurs until, finally, the pressure in the right and left ventricles is equalized in all phases of the cardiac cycle, after which the pathological discharge from the left ventricle of the heart to the right stops. If, over time, the blood pressure in the right ventricle is higher than in the left, a so-called “reverse shunt” occurs, in which venous blood from the right ventricle of the heart flows through the same VSD into the left ventricle.

Symptoms of VSD

The timing of the appearance of the first signs of VSD depends on the size of the defect itself, as well as the size and direction of the pathological discharge of blood.

Minor defects in the lower parts of the interventricular septum in the vast majority of cases do not have a significant effect on the development of children. Such children feel satisfactory. Already in the first few days after birth, a heart murmur of medium intensity, with a rough, scraping timbre, appears, which the doctor listens to in systole (during heart contraction). This noise is better heard in the fourth-fifth intercostal space and is not carried to other places; its intensity may decrease in a standing position. Since this noise is often the only manifestation of a small VSD, which does not have a significant impact on the well-being and development of the child, this situation in the medical literature has received the figurative name “much ado about nothing.”

In some cases, in the third or fourth intercostal space along the left edge of the sternum, you can feel a tremor at the moment of heart contraction - systolic tremor, or systolic “cat purr”.

At large defects membranous area of ​​the interventricular septum, the symptoms of this congenital heart defect, as a rule, do not appear immediately after the birth of the child, but after 12 months. Parents begin to notice difficulties when feeding the child: he begins to feel short of breath, he is forced to pause and take breaths, which is why he may remain hungry, and anxiety appears.

Born with a normal weight, such children begin to lag behind in their physical development, which is explained by malnutrition and a decrease in the volume of blood circulating in the systemic circulation (due to pathological discharge into the right ventricle of the heart). Severe sweating, pallor, marbling of the skin, and slight cyanosis of the final parts of the arms and legs (peripheral cyanosis) appear.

Characterized by rapid breathing with the involvement of auxiliary respiratory muscles, paroxysmal cough that occurs when changing body position. Recurrent pneumonia (pneumonia) develops, which is difficult to treat. To the left of the sternum, deformation of the chest occurs - a cardiac hump is formed. The apical impulse shifts to the left and down. Systolic trembling is palpable in the third or fourth intercostal space at the left edge of the sternum. Upon auscultation (listening) of the heart, a rough systolic murmur is detected in the third or fourth intercostal spaces. In children of an older age group, the main clinical signs of the defect remain; they have complaints of pain in the heart area and rapid heartbeat, and children continue to lag behind in their physical development. With age, the health and condition of many children improves.

Complications of VSD:

Aortic regurgitation observed among patients with VSD in approximately 5% of cases. It develops if the defect is located in such a way that it also causes sagging of one of the aortic valve leaflets, which leads to a combination of this defect with aortic valve insufficiency, the addition of which significantly complicates the course of the disease due to a significant increase in the load on the left ventricle of the heart. Among the clinical manifestations, severe shortness of breath predominates, and sometimes acute left ventricular failure develops. When auscultating the heart, not only the above-described systolic murmur is heard, but also a diastolic (during the phase of cardiac relaxation) murmur at the left edge of the sternum.

Infundibular stenosis observed among patients with VSD also in approximately 5% of cases. It develops if the defect is located in the posterior part of the interventricular septum under the so-called septal cusp of the tricuspid (three-leaf) valve below the supraventricular crest, which causes a large amount of blood to pass through the defect and traumatize the supraventricular crest, which consequently increases in size and becomes scarred. As a consequence, narrowing of the infundibular section of the right ventricle occurs and the formation of subvalvular stenosis of the pulmonary artery. This leads to a decrease in pathological discharge through the VSD from the left ventricle of the heart to the right and unloading of the pulmonary circulation, but there is also a sharp increase in the load on the right ventricle. The blood pressure in the right ventricle begins to increase significantly, which gradually leads to a pathological discharge of blood from the right ventricle to the left. With severe infundibular stenosis, the patient develops cyanosis (blueness of the skin).

Infectious (bacterial) endocarditis– damage to the endocardium (the inner lining of the heart) and heart valves caused by infection (most often bacterial). In patients with a VSD, the risk of developing infective endocarditis is approximately 0.2% per year. It usually occurs in older children and adults; more often with small VSDs, which is caused by endocardial injury due to the high speed of the pathological discharge of blood. Endocarditis can be provoked by dental procedures or purulent skin lesions. Inflammation first occurs in the wall of the right ventricle, located on the opposite side of the defect or along the edges of the defect itself, and then spreads to the aortic and tricuspid valves.

Pulmonary hypertension– increased blood pressure in the vessels of the pulmonary circulation. In the case of this congenital heart defect, it develops due to the entry of an additional volume of blood into the vessels of the lungs, caused by its pathological discharge through the VSD from the left ventricle of the heart to the right. Over time, pulmonary hypertension worsens due to the development of compensatory mechanisms - the formation of thickening of the walls of arteries and arterioles.

Eisenmenger syndrome– subaortic location of the ventricular septal defect in combination with sclerotic changes in the pulmonary vessels, dilation of the pulmonary artery trunk and an increase in muscle mass and size (hypertrophy) mainly of the right ventricle of the heart.

Recurrent pneumonia– caused by stagnation of blood in the pulmonary circulation.
Heart rhythm disturbances.

Heart failure.

Thromboembolism– acute blockage of a blood vessel by a thrombus that has broken away from its place of formation on the wall of the heart and entered the circulating blood.

Instrumental diagnosis of VSD

1. Electrocardiography (ECG): In the case of a small VSD, significant changes in the electrocardiogram may not be detected. As a rule, the electrical axis of the heart is in a normal position, but in some cases it may deviate to the left or right. If the defect is large, this is more significantly reflected in electrocardiography. With a pronounced pathological discharge of blood through a defect from the left ventricle of the heart to the right without pulmonary hypertension, the electrocardiogram reveals signs of overload and an increase in the muscle mass of the left ventricle. If significant pulmonary hypertension develops, symptoms of overload of the right ventricle of the heart and right atrium appear. Heart rhythm disturbances occur infrequently, usually in adult patients in the form of extrasystole and atrial fibrillation.

2. Phonocardiography(recording of vibrations and sound signals emitted during the activity of the heart and blood vessels) allows instrumental recording of pathological noises and altered heart sounds caused by the presence of a VSD.

3. Echocardiography(ultrasound examination of the heart) allows not only to detect a direct sign of a congenital defect - a break in the echo signal in the interventricular septum, but also to accurately determine the location, number and size of defects, as well as determine the presence of indirect signs of this defect (increase in the size of the ventricles of the heart and left atrium, increase in the thickness walls of the right ventricle and others). Doppler echocardiography allows us to identify another direct sign of a defect - pathological blood flow through the VSD into systole. In addition, it is possible to assess blood pressure in the pulmonary artery, the magnitude and direction of pathological blood discharge.

4.X-ray of the chest organs(heart and lungs). With small VSDs, no pathological changes are detected. With a significant size of the defect with a pronounced discharge of blood from the left ventricle of the heart to the right, an increase in the size of the left ventricle and left atrium, and then the right ventricle, and an increase in the vascular pattern of the lungs are determined. As pulmonary hypertension develops, expansion of the roots of the lungs and bulging of the pulmonary artery arch are determined.

5. Catheterization of the heart cavities carried out to measure pressure in the pulmonary artery and right ventricle, as well as determine the level of oxygen saturation in the blood. Characterized by a higher degree of blood saturation with oxygen (oxygenation) in the right ventricle than in the right atrium.

6. Angiocardiography– introduction of a contrast agent into the cavities of the heart through special catheters. When contrast is introduced into the right ventricle or pulmonary artery, repeated contrasting is observed, which is explained by the return of contrast to the right ventricle with pathological discharge of blood from the left ventricle through the VSD after passing through the pulmonary circulation. When water-soluble contrast is introduced into the left ventricle, the flow of contrast from the left ventricle of the heart to the right through the VSD is determined.

Treatment of VSD

If the VSD is small in size, there are no signs of pulmonary hypertension and heart failure, and normal physical development, in the hope of spontaneous closure of the defect, it is possible to refrain from surgical intervention.

In children of early preschool age, indications for surgical intervention are early progression of pulmonary hypertension, persistent heart failure, recurrent pneumonia, severe retardation in physical development and body weight deficiency.

Indications for surgical treatment in adults and children over the age of 3 years are: increased fatigue, frequent acute respiratory viral infections leading to the development of pneumonia, heart failure and a typical clinical picture of the defect with a pathological discharge of more than 40%.

Surgical intervention is reduced to plastic surgery of the VSD. The operation is performed using a heart-lung machine. If the defect diameter is up to 5 mm, it is closed by suturing with U-shaped sutures. If the diameter of the defect is more than 5 mm, it is closed with a patch made of synthetic or specially treated biological material, which is covered with its own tissues within a short time.

In cases where open radical surgery is not immediately possible due to the high risk of surgical intervention using artificial circulation in children in the first months of life with large VSDs, low weight, and severe heart failure that cannot be corrected with medication, surgical treatment is carried out in two stages . First, a special cuff is placed on the pulmonary artery above its valves, which increases the resistance to ejection from the right ventricle, thereby leading to equalization of blood pressure in the right and left ventricles of the heart, which helps reduce the volume of pathological discharge through the VSD. After a few months, the second stage is carried out: removal of the previously applied cuff from the pulmonary artery and closure of the VSD.

Prognosis for VSD

The duration and quality of life with a ventricular septal defect depend on the size of the defect, the condition of the vessels of the pulmonary circulation, and the severity of developing heart failure.

Small ventricular septal defects do not have a significant impact on the life expectancy of patients, but they increase the risk of developing infective endocarditis by up to 1-2%. If a small defect is located in the muscular area of ​​the interventricular septum, it can close on its own before the age of 4 years in 30-50% of such patients.

In the case of a medium-sized defect, heart failure develops already in early childhood. Over time, the condition may improve due to some reduction in the size of the defect, and in 14% of such patients, spontaneous closure of the defect is observed. At older ages, pulmonary hypertension develops.

In the case of a large VSD, the prognosis is serious. Such children develop severe heart failure at an early age, and pneumonia often occurs and recurs. Approximately 10-15% of such patients develop Eisenmenger syndrome. Most patients with large ventricular septal defects without surgical intervention die in childhood or adolescence from progressive heart failure, often in combination with pneumonia or infective endocarditis, thrombosis of the pulmonary artery or rupture of its aneurysm, paradoxical embolism in the vessels of the brain.

The average life expectancy of patients without surgical intervention in the natural course of VSD (without treatment) is approximately 23-27 years, and in patients with small defects - up to 60 years.

Surgeon M.E. Kletkin