Ventricular septal defect in adults. Ventricular septal defect

One of the most common congenital heart defects diagnosed in children under three years of age is a ventricular septal defect. A similar ailment is the second most common disease found among defects in the heart muscle. It is an opening 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 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 in any way, and the disease proceeds without visible signs. With a large diameter defect (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 muscle contraction, the pressure in the right side of the heart is much lower than in the left. There is a mixture of blood and an increase in the load on the vessels of the lungs. An excess of oxygen-enriched blood enters the pulmonary circulation, while the large one does not receive it. This can lead to pulmonary vascular sclerosis, right ventricular failure, and pulmonary hypertension.

VSD is formed in the fetus during fetal development. In rare cases, such a defect develops in the process of life. With a small defect, it can be detected in children only randomly, according to the results of echocardiography. It usually closes itself 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 baby has not lost the defect before the age of three, then treatment is possible only surgically.

Forms and types

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

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

In the first form of the defect, self-closing 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 overgrows on its own.

VSD differences in size are classified as follows:

• small. Virtually invisible, asymptomatic;
• medium. Symptoms of the disease begin to appear in the first months of a child's life;
• large. They are extremely severe, often leading to death.

Reasons for the 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 close relatives in the family had a similar pathology, then its appearance in descendants is not excluded. This happens due to changes in chromosomes or genes. In essence, heart defects are caused by gene mutations;
• ecological. When the fetus, which is in the womb, is exposed to adverse environmental factors, the development of gene mutations is possible. When a future mother uses potent drugs, alcohol, tobacco and drugs, as well as severe viral infections, the risk of pathology increases significantly.

Diagram of a ventricular septal defect

Symptoms of a ventricular septal defect

• Small ventricular septal defects do not cause symptoms.
• With moderate VSD, symptoms uncharacteristic of heart defects may occur. Weakness, fatigue, lag in physical development, a tendency to pneumonia and lung infections.
• Large defects are manifested in the form of pale skin, swelling of the legs, chest pain, severe shortness of breath during exercise. Such symptoms are more characteristic of heart defects.

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

Diagnostics

Doctors can establish a ventricular septal defect based on this kind of diagnosis:

• a thorough analysis of the complaints of the patient or his parents (the appearance of fatigue during physical exertion, pallor of the skin, pain in the heart, shortness of breath, weakness);
• a detailed consideration of the anamnesis of life 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 data from blood and urine tests;
• analysis of electrocardiogram and echocardiography data;
• viewing the results of X-ray examination;
• cardiac studies using catheterization, ventriculography and angiography. Special procedures, with the help of which a catheter or contrast agents are introduced into the body, allowing various methods to see the pathology;
• analysis of magnetic resonance therapy data.

Treatment

Therapeutic and medicinal methods

Conservative treatment for a ventricular septal defect is mainly used 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 diuretic drugs, cardiotrophics and inotropic support drugs. But non-surgical treatment, as a rule, only prevents complications from developing, and the defect itself does not eliminate.

Remember to avoid physical activity in your child. Try to make him cry and push less. After all, such actions are also a kind of tension in the body. Be sure to make sure that the baby does not lift heavy objects.

Operation

The main treatment for VSD is surgery. Operations are emergency and 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 preliminarily prepared for it. Cardiologists monitor his condition and conduct a course of conservative treatment. The operation to close a ventricular septal defect is performed in two different ways:

• radical. A method in which a patch of heart shell or artificial material is applied to a hole in the septum. In this case, the patient must be connected to an artificial blood pump;
• palliative. With such an operation, the defect of the heart muscle is not eliminated, but only the pulmonary artery narrows. The method makes life easier for the patient and prevents the development of complications. It is used for patients with intolerance to radical intervention.

In more detail about what the technology of minimally invasive elimination of a ventricular septal defect is, the following video will tell you:

Disease prevention

There are no preventive 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 in the antenatal clinic (for up to twelve weeks);
• observance of the daily regimen and good 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.

figure: ventricular septal defect (VSD)

Small defects practically do not cause complaints in patients and grow 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 viewed as:

• Independent CHD (congenital),
• An integral part of the combined UPU,
• Complication.

According to the localization of the hole, 3 types of pathology are distinguished:

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

Hole size:

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

The reasons

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, juxtapose and properly connect with each other. If this process is disturbed under the influence of 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 anomalies.
2. Infectious diseases of a pregnant woman - SARS, parotitis, chicken pox, rubella.
3. Reception by a pregnant woman of antibiotics or other medicines with an embryotoxic effect - 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 the diet of a pregnant woman, 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

VSD does not cause problems for 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 extremities, delayed psychophysical development.

Children with signs of VSD often develop severe forms of pneumonia that are difficult to treat. The doctor, examining and examining a sick child, detects an enlarged heart, systolic murmur, 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 exertion. The main symptoms of the pathology are systolic murmur, which is found in newborns, spreads in both directions and is well heard on the back. It remains the only symptom of pathology for a long time. In more rare cases, when placing the palm on the chest, you can feel a slight vibration or trembling. 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, they develop hyperhidrosis, cyanosis, shortness of breath, first during meals, and then at rest. Over time, breathing becomes rapid and difficult, a paroxysmal cough appears, and a heart hump forms. Wet rales appear in the lungs, the liver enlarges. Older children complain of palpitations and cardialgia, shortness of breath, frequent nosebleeds and fainting. They are significantly behind in development from their peers.

If the child gets tired quickly, cries often, eats poorly, refuses to breastfeed, has no weight gain, shortness of breath and cyanosis appears, you should consult a doctor as soon as possible. If shortness of breath and swelling of the limbs occur suddenly, the heartbeat becomes fast and irregular, an ambulance should be called.

Stages of development of the disease:

1. The first stage of the pathology is also manifested 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 of CHD, 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 in VSD

Downstream, 2 types of VSD are distinguished:

• Asymptomatic course 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. Requires medical supervision 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 is required, and surgery is possible. Small defects occur in 5% of newborns and close spontaneously by 12 months.
• A large VSD has a symptomatic course and is manifested by signs. Echocardiography data indicate the presence or absence of concomitant 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 experts discover that allows you to suspect the presence of a VSD in a patient. To make a final diagnosis and prescribe adequate treatment, special diagnostic procedures are carried out.

• is carried out in order to detect a defect, determine its size and localization, the direction of blood flow. This method provides comprehensive data on 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, there are signs of left ventricular hypertrophy. In adults, arrhythmia, 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 characteristics of the doctor's hearing. The phonocardiograph consists of a microphone that converts sound waves into electrical impulses and a recording device that records them.
• dopplerography- the primary method for diagnosing and identifying the consequences of valvular disorders. It evaluates the parameters of pathological blood flow caused by CHD.
• On the radiograph the heart with VSD is significantly enlarged, there is no narrowing in the middle, spasm and overflow 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 performed by injecting a contrast agent into the cavity of the heart. It allows you to judge the localization of a congenital 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, which allows 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 up to a 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 fusion 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 testimony,
• Slow increase in head circumference
• pulmonary hypertension,
• Big DMZHP.

endovascular “patch” installation is a modern method of defect treatment

Radical surgery - birth defect plasty. It is carried out 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 cut and a VSD is detected through the tricuspid valve. If such access is impossible, open the right ventricle. Radical surgery usually gives good results.

Endovascular correction The defect is performed by piercing the femoral vein and introducing 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 pathology and gives the child a chance for normal development. The operation is performed for children of the first days of life for whom conservative treatment has proved ineffective, as well as for those who have multiple defects or concomitant intracardiac anomalies.

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

Video: report on surgery for VSD

Video: lecture on VSD

Many factors influence the health of the unborn baby. Improper intrauterine development can cause congenital malformation of internal organs. One of the disorders is a ventricular septal defect (VSD), which occurs in a third of cases.

Peculiarities

Dmzhp is a congenital heart disease (CHD). As a result of pathology, a hole is formed connecting the lower chambers of the heart: its ventricles. The pressure level in them is different, because of which, when the heart muscle contracts, a little blood from the more powerful left part enters the right. As a result, its wall is stretched and enlarged, the blood flow of the small circle, for which the right ventricle is responsible, is disturbed. Due to the increase in pressure, the venous vessels are overloaded, spasms and seals occur.

The left ventricle is responsible for blood flow in a large circle, so it is more powerful and has a higher pressure. With the pathological flow of arterial blood into the right ventricle, the required level of pressure decreases. To maintain normal performance, the ventricle begins to work with greater force, which further adds to the load on the right side of the heart and leads to its increase.

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

This condition is observed with large holes and is accompanied by a violation of 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.

Small VSD may not immediately appear, or is not diagnosed due to mild symptoms. Therefore, it is important to be aware of the 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 the enrichment of blood with oxygen, therefore, 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 ooo gradually overgrows. The window completely closes at the age of about 3 months; in some cases, overgrowth is not considered a pathology by 2 years. With some deviations, ooo can be observed in children aged 5-6 years and older.

Normally, in newborns, ooo is not 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, regularly visiting a pediatric cardiologist.

If the size of the hole is 6-10 mm, this may be a sign of vmjp, 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 difficult the degree of the disease. Their size varies from 0.5 to 30 mm. Wherein:

• A defect up to 10 mm in size is considered small;
• Holes from 10 to 20 mm - medium;
• A defect larger than 20 mm is considered large.

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

1. In the membranous (upper part of the heart septum), a hole occurs in more than 80% of cases. Defects in the form of a circle or oval reach 3 cm, if they are small (about 2 mm), they are able to spontaneously close in the process of growing up a child. In some cases, defects of 6 mm are overgrown, whether an operation is needed, the doctor decides, focusing on the general condition of the child, the features of the course of the disease.
2. Muscle jump in the middle part of the septum is less common (about 20%), in most cases round in shape, with a size of 2–3 mm, it can close with the age of the child.
3. At the border of the excretory vessels of the ventricles, a supracrestal septal defect is formed - the rarest (about 2%), and almost does not stop on its own.

In rare cases, there is a combination of several types of jmp. The defect can be an independent disease, or be accompanied by other severe abnormalities in the development of the heart: atrial septal defect (ASD), problems with arterial blood flow, aortic coarctation, stenosis of the aorta and pulmonary artery.

Reasons for development

The defect is formed in the fetus from 3 weeks to 2.5 months of intrauterine development. With an unfavorable course of pregnancy, pathologies in the structure of internal organs can occur. Factors that increase the risk of VSD include:

1. Heredity. A predisposition to VSD can be genetically transmitted. If any of the close relatives had defects in various organs, including the heart, there is a high probability of abnormalities in the child;
2. Viral diseases of an infectious nature (flu, rubella), which a woman suffered in the first 2.5 months of pregnancy. Herpes, 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-epilepsy and CNS drugs;
4. Bad habits in 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 mellitus, problems of the nervous, cardiac system, and the like can provoke pathologies in the baby;
6. Avitaminosis, deficiency of essential nutrients and trace elements, strict diets during pregnancy increase the risk of birth defects;
7. Severe toxicosis in early pregnancy;
8. External factors - dangerous environmental conditions, harmful working conditions, increased fatigue, overstrain and stress.

The presence of these factors does not always cause the occurrence of severe diseases, but increases this likelihood. To reduce it, you need to limit their impact 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 state of the baby are not a threat to his life. Regular examination, supervision by a specialist is necessary and are able to stop spontaneously over time.

Large holes cause disruption of the heart, which manifests itself in the first days of a baby's life. Children with VSD have a hard time with colds and infectious diseases, often with complications in the lungs, pneumonia. They can develop worse than their peers, they are hard to tolerate physical exertion. With age, shortness of breath occurs even at rest, problems with internal organs appear due to oxygen starvation.

An interventricular defect can cause serious complications:

• Pulmonary hypertension - an increase in resistance in the vessels of the lungs, which causes right ventricular failure and the development of Eisenmenger's syndrome;
• Violation of the heart in an acute form;
• Inflammation of the inner heart membrane of an infectious nature (endocarditis);
• Thrombosis, the threat of a stroke;
• Malfunctions of the heart valves, the formation of valvular heart defects.

To minimize the consequences detrimental to the health of the baby, timely qualified assistance is needed.

Symptoms

Clinical manifestations of the disease are due to the size and location of the pathological openings. Small defects in the membranous part of the cardiac septum (up to 5 mm) occur in some cases without symptoms, sometimes the first signs occur in children from 1 to 2 years old.

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

Large defects can be found in the fetus even before or in the first time after birth. Due to the peculiarities of blood flow during intrauterine development, newborns have a normal weight. After birth, the system is rebuilt to the usual one and the deviation begins to manifest itself.

Especially dangerous are small defects located in the lower region of the cardiac septum. They may not show symptoms in the first few days of a child's life, but for some time breathing and heart problems develop. With careful attention to the child, you can notice the symptoms of the disease in time and consult a specialist.

Signs of a possible pathology, which must be reported to the pediatrician:

1. Paleness of the skin, blue lips, skin around the nose, arms, legs during exercise (crying, screaming, overexertion);
2. The baby loses appetite, gets tired, often throws the breast during feeding, slowly gains weight;
3. During physical exertion, crying, shortness of breath appears in babies;
4. increased sweating;
5. A baby older than 2 months is lethargic, drowsy, it has reduced motor activity, there is a developmental delay;
6. Frequent colds that are difficult to treat and flow into pneumonia.

If such signs are identified, an examination of the baby is carried out to identify the causes.

Diagnostics

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

• Electrocardiogram (ECG). Allows you to determine the congestion of the heart ventricles, to identify the presence and degree of pulmonary hypertension;
• Phonocardiography (FCG). As a result of the study, it is possible to identify heart murmurs;
• Echocardiography (EchoCG). Able to detect blood flow disorders and helps to suspect VSD;
• Ultrasound procedure. Helps to assess the work of the myocardium, the pressure level of the artery of the lung, the amount of blood discharged;
• Radiography. According to the pictures of the chest, it is possible to determine changes in the pulmonary pattern, 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 the venous blood;
• Pulse oximetry. Helps to find out the level of oxygen in the blood - a lack indicates disorders in the cardiovascular system;
• Cardiac catheterization. It helps to assess the state of the structure of the heart, to determine the level of pressure in the heart ventricles.

Treatment

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

With the deterioration of the overall clinical picture, the appearance of complications, it is possible to prescribe an operation in 2-3 years.

Surgical intervention is performed with the patient connected to a heart-lung machine. If the defect is less than 5 mm, it is tightened with P-shaped sutures. If the hole is larger than 5 mm, it is covered with patches made of artificial or specially prepared bio-material, which subsequently overgrows with the body's own cells.

If surgical treatment is necessary for a child in the first weeks of life, but it is impossible for some indicators of the health and condition of the baby, a temporary cuff is placed on the pulmonary artery. It helps to equalize the pressure in the ventricles of the heart and alleviates the patient's condition. A few months later, the cuff is removed and an operation 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 as a result of underdevelopment at its 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 in the membranous part of the septum. Their sizes are from 2 to 60 mm, the shape is different, they are observed in 90% of cases,
• Defects in the muscular part of the septum. Their sizes are small (5-20 mm), and with the contraction of the heart muscle, the lumen of the defect decreases even more, they appear in 2-8% of cases.
• The absence of an interventricular septum occurs in 1-2% of cases.

How does a 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 small and large circles of blood circulation with a ventricular septal defect in children gives the main clinical picture. Violation of hemodynamics depends on the size 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 as the child grows and develops, it changes, which leads to changes in the clinical picture of defects, 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, the additional load falls only on the left ventricle, which is often hypertrophied.

With a ventricular septal defect in children in the redistribution of sizes of 10-20 mm, the discharge through it reaches 70% of the blood that is discharged by the left ventricle. This causes significant volume overloads of the pulmonary circulation, which leads to low overloads 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, a pronounced syndrome of a large volume of blood 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 is kept at a high level. This is due to the fact that pressure is transmitted to the pulmonary artery from the left ventricle (hydrodynamic factor). High pressure in the pulmonary artery leads to congestion 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 a volume overload of the left atrium, resulting in increased 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.

Ventricular septal defect in the fetus and its types

An isolated ventricular septal defect in a fetus, depending on its size, the amount of blood shunting, 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 include defects of the interventricular septum in the fetus of a 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 region of the heart, which appears, as a rule, from the first days of a child's life. Children are growing well, there are no complaints in them. 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 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. Noise occupies, as a rule, the entire systole, often merges with the second tone. Its maximum sound is in the III-IV intercostal space from the sternum, it is well conducted over the entire region of the heart, to the right behind the sternum, auscultated on the back near the interscapular space, well conducted through the bones, transmitted through the air and audible, even if you raise the stethoscope above the heart (remote noise ).

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

Signs of severe ventricular septal defect

A pronounced ventricular septal defect in children manifests itself acutely from the first days after birth. Children are born on time, but in 37-45% there is a moderately pronounced congenital malnutrition, the cause of which is not clear.

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

During the children often get sick with acute respiratory diseases, pneumonia. More than 2/3 of children lag behind in physical and psychomotor development, 30% develop hypotrophy of the II degree.

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

Ventricular septal defect in children after a year

The defect of the interventricular septum of the heart in children older than a year passes into 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, the phase of relative compensation begins, which is characterized by the absence of shortness of breath, tachycardia. Children become more active, begin to put on weight better, grow better, and many of them catch up with their peers in their development, they suffer from concomitant diseases much less compared to the first year of life. An objective examination in 2/3 of children shows a centrally located "heart hump", systolic trembling is determined in the III-IV intercostal space to the left of the sternum.

The borders of the heart are slightly expanded in diameter and upwards. Apical push of medium strength and reinforced. On auscultation, there is a splitting of the II tone in the II intercostal space on the left side of 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 area of ​​distribution.

In some children, diastolic murmurs of relative pulmonary valve insufficiency are also heard, arising from 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 a large arteriovenous shunt of blood through the defect (Flint noise). Graham-Still's murmur is heard in the 2-3rd intercostal space to the left of the sternum and is well conducted upward to the base of the heart. Flint's murmur is better defined at the Botkin point and conducted 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 based on the results of ECG, Echo-KG, catheterization of cavities.

The differential diagnosis is carried out with congenital heart defects that occur with an 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 at an early age.

Complications and prognosis of ventricular septal defect in children

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

Ventricular septal defect (VSD) is a congenital heart disease characterized by a defect in the muscular septum between the right and left ventricles of the heart. VSD is the most common congenital heart disease in newborns, accounting for approximately 30-40% of all 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 in the interventricular septum. In about 85% of cases, the VSD is located in the so-called membranous part of it, 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 point of transition 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 muscular and other VSD localizations 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 of the aorta diameter, and small defects. Defects of the membranous part, as a rule, have a round or oval shape and reach 3 cm, defects in the muscular part of the interventricular septum are most often round and small.

Quite often, in about 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

Ventricular septal defects 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 disorders (blood movement)

In a fetus located in the mother's uterus, blood circulation is carried out in the so-called placental circle (placental circulation) and has its own characteristics. However, soon after birth, the newborn establishes normal blood flow in the systemic and pulmonary circulation, which is accompanied by a significant difference between the blood pressure in the left (higher pressure) and right (lower pressure) ventricles. At the same time, the existing VSD leads to the fact that blood from the left ventricle is pumped not only into the aorta (where it should normally flow), but also through the VSD into the right ventricle, which should not be normal. Thus, with each heartbeat (systole) there is a pathological discharge of blood 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 the extra work of pumping additional blood volume back to the lungs and left 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 practically does not affect the work 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 cicatricial thickening may develop, which is the result of a reaction to injury from an abnormal ejection of blood spurting through the defect.

In addition, due to pathological discharge, an 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: there is an increase in the muscle mass of the ventricles of the heart, a gradual adaptation of the vessels of the lungs, which first take in the incoming excess volume of blood, and then pathologically change - a 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, pressure equalization occurs in the right and left ventricles 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 ventricle, the so-called "reverse reset" occurs, in which venous blood from the right ventricle of the heart through the same VSD enters the left ventricle.

VSD symptoms

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

Small defects in the lower parts of the interventricular septum in the vast majority of cases do not have a significant impact on the development of children. These children are doing well. Already in the first few days after birth, a heart murmur of 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 conducted to other places, its intensity in the standing position may decrease. Since this noise is often the only manifestation of a small VSD that does not have a significant impact on the well-being and development of the child, this situation in the medical literature has been figuratively called “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 trembling at the moment of heart contraction - systolic trembling, or systolic "cat's purr".

At large defects membranous (membranous) section of the interventricular septum, the symptoms of this congenital heart disease, as a rule, do not appear immediately after the birth of the child, but after 12 months. Parents begin to notice difficulties in feeding the child: he has shortness of breath, he is forced to pause and breathe, because of which he can remain hungry, 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, slight cyanosis of the final parts of the arms and legs (peripheral cyanosis) appear.

Characterized by rapid breathing with the involvement of the auxiliary respiratory muscles, paroxysmal cough that occurs when changing body position. Recurrent pneumonias (pneumonia) develop and are difficult to treat. To the left of the sternum there is a deformation of the chest - a heart hump is formed. The apex beat shifts to the left side and down. Systolic trembling is felt in the third or fourth intercostal space at the left edge of the sternum. Auscultation (listening) of the heart is determined by a rough systolic murmur in the third or fourth intercostal space. In children of an older age group, the main clinical signs of the defect persist, they complain of pain in the region of the heart and palpitations, children continue to lag behind in their physical development. With age, the well-being and condition of many children improves.

Complications of VSD:

Aortic regurgitation observed among patients with VSD in about 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 cusps, 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, sometimes acute left ventricular failure develops. During auscultation of the heart, not only the above-described systolic murmur is heard, but also diastolic (in the phase of cardiac relaxation) murmur at the left edge of the sternum.

Infundibular stenosis observed among patients with VSD also in about 5% of cases. It develops if the defect is located in the posterior part of the interventricular septum under the so-called septal leaflet of the tricuspid (tricuspid) valve below the supraventricular ridge, which causes a large amount of blood to pass through the defect and traumatize the supraventricular ridge, which consequently increases in size and scars. As a result, there is a narrowing of the infundibular section of the right ventricle and the formation of subvalvular pulmonary stenosis. This leads to a decrease in pathological discharge through the VSD from the left ventricle of the heart to the right one and unloading of the pulmonary circulation, however, 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 (cyanosis 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 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 sizes of VSD, which is caused by endocardial injury at a high jet velocity of pathological blood shunt. Endocarditis can be provoked by dental procedures, 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 the aortic and tricuspid valves spread.

Pulmonary hypertension- increased blood pressure in the vessels of the pulmonary circulation. In the case of this congenital heart disease, it develops as a result of an additional volume of blood entering the vessels of the lungs, due to its pathological discharge through the VSD from the left ventricle of the heart to the right. Over time, there is an aggravation of pulmonary hypertension 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, expansion of the pulmonary artery trunk and an increase in muscle mass and size (hypertrophy) of the predominantly right ventricle of the heart.

Recurring pneumonia- due to stagnation of blood in the pulmonary circulation.
Heart rhythm disturbances.

Heart failure.

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

Instrumental diagnosis of VSD

1. Electrocardiography (ECG): In the case of small VSD, significant changes in the electrocardiogram may not be detected. As a rule, the normal position of the electrical axis of the heart is characteristic, but in some cases it may deviate to the left or right. If the defect is large, this is reflected more significantly 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. In the case of the development of significant pulmonary hypertension, symptoms of overload of the right ventricle of the heart and the right atrium appear. Heart rhythm disturbances are rare, as a rule, in adult patients in the form of extrasystole, atrial fibrillation.

2. Phonocardiography(recording of vibrations and sound signals emitted during the activity of the heart and blood vessels) allows you to instrumentally fix pathological noises and altered heart sounds caused by the presence of 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 (an increase in the size of the ventricles of the heart and left atrium, an increase in the thickness walls of the right ventricle, etc.). Doppler echocardiography reveals another direct sign of malformation - abnormal blood flow through the VSD into systole. In addition, it is possible to assess the blood pressure in the pulmonary artery, the magnitude and direction of the pathological discharge of blood.

4.Chest X-ray(heart and lungs). With small sizes of VSD, pathological changes are not determined. 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, the expansion of the roots of the lungs and the bulging of the arch of the pulmonary artery are determined.

5. Cardiac catheterization is performed to measure the pressure in the pulmonary artery and in the right ventricle, as well as to determine the level of blood oxygen saturation. A higher degree of blood oxygen saturation (oxygenation) in the right ventricle is characteristic than in the right atrium.

6. Angiocardiography- the introduction of a contrast agent into the cavity of the heart through special catheters. With the introduction of contrast into the right ventricle or pulmonary artery, their 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. With the introduction of water-soluble contrast into the left ventricle, the flow of contrast from the left ventricle of the heart to the right through the VSD is determined.

VSD treatment

With a small VSD, no signs of pulmonary hypertension and heart failure, 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, marked lag in physical development, and underweight.

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 VSD. The operation is performed using a heart-lung machine. With a defect diameter of up to 5 mm, it is closed by suturing with U-shaped sutures. With a defect diameter of more than 5 mm, it is closed with a patch of synthetic or specially processed biological material, which is covered with its own tissues for a short time.

In cases where open radical surgery is not immediately possible due to the high risk of surgical intervention using cardiopulmonary bypass in children in the first months of life with large VSDs, underweight, severe heart failure that cannot be corrected with medication, surgical treatment is performed in two stages . First, a special cuff is applied to 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 to reduce the volume of pathological discharge through the VSD. A few months later, 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 significantly affect the life expectancy of patients, but up to 1-2% increase the risk of developing infective endocarditis. 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 decrease in the size of the defect, and in 14% of such patients, an independent closure of the defect is observed. At an older age, pulmonary hypertension develops.

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

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

Surgeon Kletkin M.E.