Ventricular septal defect hemodynamics. What is VSD (ventricular septal defect)

The human heart consists of 4 chambers, the formation of which, and then the unification into one whole, begins almost immediately after conception. Under adverse conditions, the process goes with violations, small and more impressive flaws appear in the structure of the main organ. One of them is quite common - ventricular septal defect (VSD). It is proposed to get acquainted in detail with its origin, symptoms, diagnosis and methods of correction.

Violation of the integrity of the septum between the left and right ventricles is a congenital anomaly of the heart, it is formed in the first 2-3 months of intrauterine development of the fetus. For every 1000 newborns in the world, there are 8-9 children with a similar pathology. In percentage terms, the amount of JMP corresponds to 18-24% of all CHD (congenital heart defects). The defect manifests itself in the form of a hole ranging in size from 1 to 30 mm, located anywhere in the septum. Usually it is characterized by a small size and a round contour, however, when localized in the membranous zone, it resembles a rather large oval window.

At the moment of contraction of the ventricles through the gap in the septum between them, blood is discharged from left to right, this creates an overload of the right ventricle and the small (pulmonary) circulation. With a systematic incorrect reset, the pathology is aggravated, completely changing the functioning of the cardiovascular system.

1. The heart experiences increased stress pumping blood - as a result, its insufficiency is formed.
2. There is an increase in the capacities of the right ventricle, and later its walls grow (hypertrophy). The end result is the expansion of the pulmonary aorta, due to which venous blood rushes along its channel to the lungs.
3. In the circulatory system of the lungs, pressure increases, causing chronic hypertension in this organ, and then spasmodic phenomena in the arteries - this is how the respiratory organ is protected from excess blood.

When the left ventricle relaxes, part of the venous blood from the right gets into it, which leads to left ventricular hypertrophy and hypoxia of the internal organs.

Reference: A congenital heart disease characterized by a ventricular septal defect has been assigned a code Q21.0 according to ICD-10(international classifier of diseases).

JMP classification

Pathological perforation in the septum separating the ventricles is classified according to several criteria.

Taking into account the origin and nuances of the course, defects are divided into 3 groups:

• congenital heart disease - CHD VSD;
• one of the elements of the combined heart disease - corrected transposition of the great vessels or tetralogy of Fallot;
• complication after myocardial infarction.

When evaluating the dimensional parameters of the window, it is usually compared with the diameter of the patient's largest artery:

• Small (MJP) - less than one third of the aortic diameter. Such a gap allows 25% more blood to pass from the left ventricle to the right ventricle than is normal.
• Medium (SDJP) - is half the lumen of the aorta. When blood moves through such an injury, pressure readings in the two ventricles differ by 50%.
• Large (BDZHP) - the same diameter as the aorta or exceeds it. The pressure in the ventricles equalizes.

According to the place of localization, these types of septal defects of the heart are distinguished.

Single defects are more often recorded, but there are also group (especially muscular) ones.

Causes of the abnormal structure of the septum

The pathology of the intergastric septum is laid in the prenatal period due to improper formation of the heart in the fetus. This happens due to illness, non-compliance with diet and hygiene during pregnancy. Risk factors for congenital heart defects are:

Symptoms of IVS defects

Ventricular septal defects in both children and adults manifest themselves depending on the area of ​​damage. If it is minimal, the patient does not notice deviations. A large interventricular window provokes many unpleasant and life-threatening symptoms. They are grouped according to age categories.

Signs of VSD in newborns

In the fetus, under adverse conditions, one of two types of defects appears: a small size in the muscular sector (Tolchinov-Roger disease) or more voluminous and pronounced in the membrane area. Each option has characteristic manifestations.

Tolchinov-Roger disease

With a minor defect, the child is born at the expected time, without deviations in intellectual and physical development. Sometimes muscular VSD in a newborn is manifested only in the form of a systolic murmur, caught in the region of the heart. It sounds maximally to the left of the sternum, in the 3rd-4th intercostal space, and radiates to the area between the shoulder blades. With auscultation (listening with a stethoscope), the sound is felt even at a short distance from the body. In some babies, the systolic murmur is inexpressive, audible only in the supine position, disappearing during physical exertion. For Tolchinov-Roger disease, heart failure is unusual.

Severe IVS defect in newborns

Basically, the fetus develops normally, although in about 40% of cases malnutrition is noted: in pediatrics, this term refers to a lag in intrauterine development. Acute manifestations of VSD occur from the first days of a child's life:

In many children with a large window in the IVS, already in infancy, a heart hump grows (the chest protrudes), and an abnormal pulsation over the stomach is heard. Due to the increased volume of blood in the pulmonary vessels, pressure rises, so their walls are often damaged.

Symptoms of IVS pathology in children older than a year

Immediately after birth, the baby grows and develops at an accelerated pace. At about 1.5 years, due to relative compensation, shortness of breath and tachycardia disappear, and activity increases. The child noticeably gains weight, he is less worried about concomitant diseases. However, a deeper examination shows the presence of the following negative signs of VSD in children 2-3 years old:

In a number of young patients, the auscultatory method of listening also registers diastolic murmurs, indicating a relative insufficiency of the pulmonary aortic valve (loose closure of its valves). These noises are of two types:

• Graham-Still - due to excessive blood flow in the pulmonary artery and the growth of hypertension in it, is heard between the 2nd and 3rd ribs on the left side, gives up - to the base of the heart muscle;
• Flint - it is caused by mitral stenosis, which occurs due to an increase in the volume of the left atrium, due to the passage of a large amount of blood through a hole in the septum, the noise is most heard at the Botkin point, radiating to the top of the heart.

Signs of a defect in adults

In adults, the clinical picture of VSD is typical for this disease:

The disease in adults proceeds in the same way as in childhood. With a small size, the defect does not cause much damage to the body if the person has undergone full therapy. If the extent of the pathology is extensive, it is treated surgically in early childhood, therefore, by the onset of maturity, human health returns to a relative norm.

Diagnostics

Noticing the external signs of a defect in the heart septum, you should contact a pediatrician, therapist or cardiologist. After auscultation, the doctor directs the patient to hardware diagnostics in order to make a final conclusion about his condition and make a prognosis for the future. Here are the main types of diagnosis of VSD.

In addition, using a special catheter, the doctor checks the structure of the heart and measures the pressure in its chambers.

Tactics and methods of treatment of IVS defect

The choice in favor of a therapeutic or surgical method depends on where the defect is localized, how hemodynamically impaired, what is the clinical course of the disease and further prognosis. An individual approach is important: an experienced doctor must monitor the patient's response to medications and procedures.

Conservative treatment

The use of medications for a defect in the interchamber septum of the heart in newborns and older children aims to establish an outflow of blood from the lungs, reduce the accumulation of fluid in the pulmonary alveoli (avoiding edema), and generally reduce the volume of circulating blood. To achieve these goals, the following groups of drugs are prescribed.

Conservative treatment alleviates the patient's condition, relieves symptoms and creates a margin of time to wait for spontaneous, non-surgical closure of the VSD.

Surgical intervention

One of the factors determining the need and choice of the type of operation is the age of the child. In the first trimester of life, the indication for a surgical procedure is a large window size, symptoms of heart failure. When the baby is six months old, the doctor analyzes the level of pulmonary hypertension and decides on the appropriateness of the operation, choosing one of the following tactics.

Important: Upon reaching one year of age, there is a chance of spontaneous closing of the window. If at that time the pulmonary hypertension in the child is low, and the physical condition is satisfactory, the operation should be postponed until the age of 5 years.

Complications and prognosis

If the hole in the intergastric wall does not exceed 3-10 mm, the heart works practically without disturbance, without causing discomfort to a person. According to the well-known pediatrician Komarovsky, a small single defect of the interventricular septum in a newborn with a high degree of probability (25-40%) will grow together by itself by 4-5 years.

Larger windows or multiple lesions require immediate treatment, otherwise the signs of the defect become complications. The main one is Eisenheimer's syndrome - due to systematic pulmonary hypertension, vascular sclerosis, constant shortness of breath and cyanosis are noted, with further death from heart and respiratory failure. Other complications are possible:

In the complete absence of medical care, a child with large defects in the septum may die before reaching 6 months of age. If the therapy or operation is carried out correctly and in a timely manner, the patient lives for a long time, constantly being monitored by a cardiologist. Undertreated disease with the development of complications reduces life expectancy to 25-27 years.

For the first time this disease was diagnosed and described by a Russian physician in 1874, and later foreign doctors became interested in it. The patient's condition can deteriorate sharply, provoking the development of severe complications. Modern medicine can reduce the risk of consequences, but it all depends on the type of defect and the stage at which it was discovered.

A ventricular septal defect (VSD) is a congenital type of abnormal heart disease that develops in an organ. Pathology begins to form in children in the womb at an early stage, approximately during the first 8-9 weeks of pregnancy. According to the frequency of occurrence of such a defect, doctors distinguish figures of 18% -42% of all cases of congenital heart disease.

The problem is that the newborn needs urgent treatment, and it is not always possible to help him. The child is prone to this disease, regardless of his gender. The classification refers this disease to anomalies leading to the release of blood into the right heart from the left. A ventricular septal defect is diagnosed in case of violations in the septum of the heart muscle located between the left and right ventricles of the organ.

To understand what this pathology is, you need to know the structure of the heart, namely, the department where the anomaly developed. The interventricular section of the organ (septum) is divided into three parts, the lower zone is trabecular, the middle is muscular, and the upper is membranous (membranous). Depending on where the defect is localized, doctors give the name of the disease. Statistics show that most cases (about 85%-86%) occur in the membranous region of the septum.

The size of the VSD can be quite small - about 1 millimeter, or serious - in the range of 1-3 centimeters or more. The classification of the ventricular septal defect in newborns implies a division into sizes that characterize the window formed in this zone.

Table of values

A muscular ventricular septal defect is usually round and small in size, and such a violation in the membranous part appears as an oval defect, which can be large. Often there are cases when VSD is accompanied by other abnormalities in the heart, which worsens the clinical indicator and prognosis of the disease.

Features of the course and causes

With the formation of a small defect in the septum between the ventricles of the organ, the course of the disease directly depends on the size of such damage. The communication between the chambers of the heart may not always be closed, and if there is a constant discharge of blood from the left areas of the organ to the right, then the pathology develops, leading to a change in the entire functioning of this system.

1. It becomes increasingly difficult for the heart to pump blood, resulting in organ failure.
2. The cavities of the ventricle and atrium on the left side expand significantly, leading to a thickening of the wall of the ventricle itself.
3. The blood pressure in the circulatory system of the lungs increases, gradually developing hypertension in this area of ​​the body.

An infant with a similar disease is at risk of serious complications, since it is during the first months of life that such hemodynamics are observed. If the heart disease is small, then it can spontaneously overgrow, not accompanied by severe disruption of the organ. The survival rate for such a pathology is quite high, subject to all the recommendations of the doctor and timely treatment. When the defect is significantly open and large, such a condition often leads to the death of a child at any age before adulthood.

In adults, the course of the disease does not differ from children, the defect can be observed throughout life and not cause serious harm - if its size is small, and the therapy is carried out in full. If the disease is extensive, then the child undergoes an operation in the first years of life, therefore, by adulthood, this person is already relatively healthy.

VSD adversely affects the functioning of the heart. When the organ contracts, blood flows into the formed passage from left to right, which occurs due to increased pressure in the left section. When the window is quite large, a high volume of blood enters the right ventricle, which provokes the development of hypertrophy of the wall of this part of the organ. After that, the pulmonary artery expands, and venous blood rushes through it into the lung tissue. Pressure is built up in this area, causing the arteries of the lungs to spasm to protect the respiratory organ from excessive blood infusion.

When the heart relaxes, the pressure in the left ventricle decreases much more than in the right, since the left ventricle is better emptied. Blood begins to flow in the opposite direction, from the right side to the left. As a result of this process, the left ventricle is filled with blood from the left atrium, and additionally from the area of ​​the right ventricle. Such an excess creates conditions for the expansion of the cavity, and later hypertrophy of the wall of the left heart or ventricle.

Regular pathological discharge from the left ventricle, as well as dilution of venous, practically devoid of oxygen, blood threatens a person with hypoxia of all organs and tissues of the body. The clinical manifestations of the disease are completely dependent on several factors: the magnitude of the resulting defect, the rate of increase in changes in hemodynamics, the total duration of the disease and compensatory opportunities. The pathology code according to the ICD classification (international classification of the disease) is Q21.0, there are also classes that denote other concomitant heart diseases.

The etiology of the disease is quite studied and suggests that it begins to form only at the level of fetal development in the womb, in adults such destructive processes do not occur. Whatever the cause of the appearance of VSD, it is associated with violations in the bearing of a child.

Provoking factors:

1. Early and severe toxicosis during pregnancy.
2. Diets that the expectant mother observes during the period of bearing a child. A severe dietary restriction, when even the minimum set of nutrients a woman needs daily is missing, leads to the development of many anomalies in the fetus, including a violation of the structure of the IVS (interventricular septum).
3. Diseases of an infectious nature, such as rubella, viral pathologies, mumps or chicken pox.
4. Serious lack of vitamins in the body of the expectant mother.
5. The manifestation of side effects when taking various medications.
6. Failures of a genetic nature. Often, such a pathology accompanies other anomalies, Down syndrome in a baby, kidney disorders, or problems with the formation of limbs.
7. Chronic diseases present in a pregnant woman. It could be heart failure or diabetes.
8. If the age of a woman expecting a child already exceeds 40 years, then changes in the body of the expectant mother can provoke pathological processes in the development of the fetus.
9. Exposure to radiation.
10. Smoking, alcoholism or drug use while pregnant.

All women should be observed by a gynecologist during the period of bearing a baby. Constant intake of vitamins, proper nutrition and a healthy lifestyle will partly protect the child from such a pathology.

Varieties of the disease

Doctors divide the disease into several classifications. Depending on the localization of the destructive process occurring in any part of the heart, VSD can be:

• membranous ventricular septal defect;
• violation in the muscular zone of the organ;
• trabecular pathologies or supracrestial (secondary).

The vast majority of cases of such a disease are defined as a premembranous defect that occurs in the interventricular septum, and it, in turn, is divided into subtricuspid and subaortic. Such pathologies account for about 80% of all recorded diseases and are localized in the upper part of the interventricular septum, located under the aortic valve and septal leaflet. The septum is located between the ventricles of the organ, it consists of a special muscle tissue for more than half, and its upper zone is a membrane. The place of joining of such parts of the septum is called the premembranous opening, where pathology is most often found. Accordingly, the localization of disorders is called the types of the disease.

A muscular defect of the interventricular septum in newborns, as well as a supracrestal variety of the disease, are rare, about 20% of all cases of this disease. The trabecular type of the disease develops in the area located slightly above the supraventricular crest, and the muscular type is localized in the muscular section of the septum of the same name. This part of the heart is remote from the conducting and valvular system.

Symptoms

The manifestations of this disease depend entirely on the size of the damage. A small atrial defect may not be accompanied by symptoms at all, and a large window in the septum will cause a lot of unpleasant and severe symptoms. The pediatrician, Dr. Komarovsky, warns that one small hole is not dangerous for the life of the baby, does not manifest itself in any way and does not require treatment, but if there are many injuries, the situation needs immediate medical attention.

An adult with similar heart disorders will experience the same symptoms as a 2-3 year old child.

Breast symptoms:

• lack of weight gain or poor weight gain;
• breathing problems, shortness of breath;
• constant anxiety, the baby cries all the time;

• pneumonia that occurs at an early age and is difficult to treat;
• sleep disorder;
• at the birth of a child, his skin has a bluish tint;
• babies tire quickly, even when suckling.

There are several diagnostics that allow you to identify the pathology in infancy and immediately take all actions to eliminate it. If we talk about adult patients, then severe symptoms rarely accompany VSD at this age.

Signs in adults:

1. moist cough;
2. pain in the area of ​​the heart;
3. violation of the rhythm of the organ (arrhythmia);
4. shortness of breath, which is observed even at rest.

If the size of the defect is considered large, then surgical treatment is performed, the window disappears, and the person no longer experiences any deviations in well-being. When the hole is small, then the manifestations of this disease are practically absent.

Signs objective:

In the event of such conditions, the child is urgently hospitalized, deciding on his surgical treatment.

Diagnostics

Today, after birth, all infants are examined by a neonatologist, whose specialization is to detect abnormalities in the development of the child. The main reason for suspecting a ventricular septal defect is the violations detected when listening to the heart area.

Diagnostic methods:

Sometimes a doctor needs to prescribe a few more additional diagnostic procedures to a patient. Any kind of disease - premembranous, membranous or muscular will be detected during the examination. It is important to start therapy on time so that the prognosis of the disease is favorable.

Treatment and prognosis

When the course of the disease is asymptomatic, and the size of the defect is small, then doctors advise to refrain from surgery. The attending physician regularly monitors the little patient. Sometimes such violations pass on their own, by the onset of 1-4 years of age and later. The resulting hole in the septum between the ventricles can overgrow, without the use of therapeutic and other methods of treatment. If there is a development of heart failure, the doctor will prescribe a number of medications.

Preparations:

1. diuretics;
2. ACE inhibitors;
3. antioxidants;
4. cardiac glycosides;
5. cardiotrophy.

There is a surgical treatment for this pathology, which can be palliative or radical.

The doctor can determine the method of treatment only after a series of necessary diagnostic manipulations, evaluating the clinical picture.

The prognosis of the disease with a ventricular septal defect of the heart depends on how timely medical care is provided to such a patient. If we talk about the natural course of the disease, without the intervention of doctors, then the child may die before the onset of 6 months of age, when the damage is large. If therapy or surgery is carried out on time, then the person will live a long time. However, even after proper treatment, some complications may develop, so such patients are always under the supervision of a cardiologist.

Dangerous consequences:

• bacterial endocarditis;
• congestive pneumonia;
• thromboembolic disorders.

The approximate life expectancy of such patients is 25-27 years. Large or medium defects are more serious, with their development, a person's condition can become severe, which provokes heart failure.

VSD of the heart is a dangerous pathology. Organ damage caused by this disease is repaired today, which prolongs the lives of sick children. It is important to regularly undergo examinations by pediatricians and other specialists in order to diagnose the disease in time, before it causes significant harm.

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 develops 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 sections 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 the position of the body. 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 artery stenosis. This leads to a decrease in the 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 a 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, it 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 instrumental recording of pathological murmurs 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.

Ventricular septal defect (VSD) is a congenital pathological condition. In this case, there is a hole in the connecting septum between the ventricles. Small violations disappear on their own in the process of maturation of the body.

The disease in the initial stages gives shortness of breath, palpitations, weakness, fatigue, developmental disorders, both physical and emotional.

To detect pathology, there are many methods: ECG, Echo KG, radiography, MRI, ventriculography, aortography, catheterization of the heart chambers. In severe situations, surgery is recommended to close the hole or narrow the pulmonary artery.

General information about pathology

VSD refers more to childhood congenital pathologies. It makes up 10-24% of all congenital defects. In severe condition, no more than 20% of defects are diagnosed, while gender practically does not play a role.

In the pathology of the septum, blood under pressure from the left sections is transferred to the right, the so-called left-right shunt occurs. It is formed even in the prenatal period in the fetus, between 4 and 18 weeks.

Pathology can develop as an independent disease, or in conjunction with a number of other ailments of the arterial trunk, atresia of the tricuspid valve, transposition of the great vessels, tetralogy of Fallot. The only ventricle is diagnosed extremely rarely, in this case there is no septum at all.

Classification

Depending on the cause:

• Independent or congenital defect.
• As a component of a number of CHD pathologies.
• Complication after a heart attack.

Size classification:

• Big defect. It exceeds the size of the aortic lumen.
• Average. Occupies half the diameter of the aorta.
• Small, where less than a third of the diameter of the aortic lumen.

By location, there are:

• perimembranous defect. It is located at the exit of the left ventricle, in the area above the aortic valve. It is most common in patients, occurs in 80% of the total.

• Muscular VSD. It is diagnosed less frequently, in 10-20% of cases. Located along the muscular part of the septum.
• Subaortic, infundibular defect. Occurs only in 5% of cases. Affects the area under the aortic and pulmonary valve.

Kinds

Downstream pathology can be of two types:

• with signs of heart failure. characteristic of a large defect. An accurate diagnosis is established after echocardiography. Conservative therapy usually improves the patient's condition, but sometimes surgical correction is required.
• Asymptomatic. Typical for minor defects. The heart at the same time increases, the pulmonary component increases by 2 tones. The patient is followed up for about a year. If during this time the symptoms do not increase and the noise disappears, this indicates that the hole has closed on its own. When the condition worsens, special treatment or surgery may be required.

stages

There are 3 stages in the development of pathology:

1. The heart increases in size, there is stagnation of blood in the vessels of the lungs. If untreated, edema, pneumonia is possible.
2. There is a spasm of the coronary and pulmonary vessels with their excessive tension.
3. There is sclerosis of the pulmonary vessels, which are already taking an irreversible form. The patient begins to feel the presence of the disease, but surgery is already ineffective.

Causes of pathology in children and adults

In the first trimester of intrauterine development, the baby's heart is laid.

The appearance of a hole at this stage refers to the physiological norm, since all components are still being formed and compared with each other. If at this moment a failure occurs due to the influence of factors of an exogenous and endogenous nature, then this hole is not tightened, but is converted into a birth defect.

The most common causes of the development of pathology:

• hereditary predisposition.
• The presence of bad habits that a woman did not get rid of, even when she was pregnant.
• Side effects of taking certain drugs during the gestation period.
• The onset of conception after 40 years.
• Improper nutrition during pregnancy, when there was a deficiency of vitamins and trace elements.
• Bad ecology.
• Severe toxicity.
• The transfer of various viral diseases during the gestation period.
• Chronic pathologies of a pregnant woman, as well as lack of proper rest and overwork.

Since the pathology is considered congenital, the defect in adults can only be the result of a non-protracted opening of the septum since childhood.

Childbearing and VSD

If a woman has a septal defect, then before planning a pregnancy, it must be corrected surgically.

If this is not done, then at any time the doctor may recommend interruption of gestation when there is a threat to the life of the expectant mother. In addition, there is a high risk of detecting this pathology in infants..

If the diagnosis was not established before conception, then if an ailment is detected, it is imperative to follow all the recommendations of the doctor and, if necessary, hospitalization, do not refuse it.

Effect of VSD on blood flow

The size of the hole can reach from 0.5 to 3-4 cm. The shape can be both in the form of a circle and like a slit. With a small defect, the blood flow is not disturbed, if the hole is large, then the magnitude of the pathological complication is directly proportional to the diameter of the window.

When there is a gap in the left ventricular systole, blood under pressure enters the right ventricle, which causes pathological changes and wall hypertrophy in this area.

In addition, the pulmonary vessel expands, where venous blood enters. In this zone, pressure increases, which is transmitted to the arterial bed of the organ. To prevent the lung from being overloaded with blood, the body responds by spasming the arteries, which is fraught with pulmonary insufficiency.

The left-sided organ can receive blood again from the same atrium or right-sided ventricle by leaking through a septal defect.

Such circulatory disorders can lead to thrombosis with subsequent movement of clots and blockage of blood vessels. Also dangerous is the state of oxygen starvation of the brain and, as a result, cell hypoxia.

Symptoms of pathology in children

In newborns up to a month old from the moment of birth, symptoms appear only with a significant window size or if there are other deviations in the structure and functionality of the organ.

In the future, with a small defect in the baby, the pathology does not manifest itself in any way. The baby is active, eats well and gains weight depending on age.

If an average hole size is observed, then when the infection enters the respiratory tract, the signs of the disease become aggravated, as the blood pressure in the lung structures increases and their springiness decreases.

You can notice the disease by the following symptoms:

• Excessive sweating under normal temperature conditions.
• Lethargy in the process of sucking, the child quickly becomes tired, he often takes breaks.
• The baby does not reach the monthly norm by weight, at the same time, growth is within the required limits.
• The appearance of tachypnea. A child performs 40 or more respiratory movements in one minute, and the shoulder zone also takes part in this process.

A defect of significant size is accompanied by vivid symptoms and is an indication for an urgent call to a doctor. Signs can accompany both permanently and appear spontaneously. This includes all the characteristic symptoms of an average defect, but in an acute form.

In addition, the child may be disturbed by:

• The appearance of cyanosis. The neck and facial part turns blue, especially during exercise.
• The cyanotic color of all skin integuments may indicate the presence of a combined defect.
• Swelling of limbs and abdomen.
• Loss of appetite.
• Difficulties with breathing, moodiness of the baby. With any load, the pressure in the pulmonary circulation system increases and it becomes difficult for the child to breathe, a restrictive symptom of shortness of breath appears, pain in the chest area.

At an older age, children feel severe dizziness up to loss of consciousness.

If the child squats down, it becomes a little easier for him. As the pathology develops, breathing becomes rapid and a cough of a paroxysmal nature appears, then a heart hump may form.

In sick children, the liver is significantly enlarged and wet rales are heard, cardialgia is observed.. Nosebleeds can become constant companions of adolescents, and against the background of the overall picture, the latter lag behind their peers in mental and physiological development.

Symptoms of pathology in adults

In men and women, the signs are similar to those of children. During physical exertion, the patient does not have enough air, he has severe shortness of breath. At rest, breathing may become smoother, but there is still a slight shortness of breath.

Chest pain is accompanied by a wet cough, nosebleeds often occur. The heart rate is unstable, the patient is diagnosed with arrhythmia.

In children, swelling mainly affects the upper limbs, in adults this process can also spread to the legs.

Diagnosis in the fetus

Usually, defects can be detected on a planned ultrasound as early as 20 weeks or in the third trimester. Small holes are sometimes not visible until the baby is born. It happens that they are tightened even in the womb. A consultation with a neonatologist or fetal ECHO may be prescribed.

Diagnostics

The initial visit to the doctor includes an auscultatory examination, where a systolic heart murmur is detected.

After that, to confirm the diagnosis, the patient is sent for additional examination, which includes:

• Echocardiography. Ultrasound can detect the location and size of the defect.
• ECG. But it is informative only with a significant window diameter.
• Phonocardiography. Helps to listen to the pathology of the tones and noises of the organ.
• Dopplerography. It is aimed at detecting blood flow disorders and valve pathologies.
• Radiography. If there is a heart disease, the organ will be enlarged, the vessels of the lungs are spasmodic and full, there is no narrowing in the middle. Fluid in the lungs usually darkens their structure.
• Angiography. It is carried out by contrast in the cavities of the heart.
• Pulse oximetry. Detects the level of oxyhemoglobin in the blood.
• MRI. Can replace echocardiography and dopplerography.
• Cardiac catheterization. Helps to recognize the organ morphology.

Treatment

If there is no urgent indication for surgery, doctors seek to improve the condition in a conservative way.

If the defect has not yet healed after reaching one year after the birth of the child, then it is recommended to take drugs and follow up for 3 years, followed by a review of the question of surgical intervention. Medications at this stage play the role of support so that serious complications do not develop.

Usually prescribed:

• Cardiac glycosides: Strofantin, Digitoxin, Korglikon. They improve the functioning of the myocardium, cause antiarrhythmic and cardiotonic effects.
• Diuretics: Indapamide, Furosemide, Spironolactone. Needed to eliminate puffiness, normalize blood circulation, reduce the load on the heart.
• Cardioprotectors: Riboxin, Panangin, Mildronate. Improve nutrition and metabolism of the heart.
• Anticoagulants: Phenylin, Warfarin. Reduce the risk of blood clots, thin the blood.
• Beta blockers: Bisoprolol, Metoprolol.
• ACE inhibitors: Captopril, Enalapril.

Surgery

With small and medium-sized windows, doctors are in no hurry to carry out the operation, but sometimes there are certain circumstances when surgical treatment is inevitable:

• The presence of other defects.
• Pulmonary hypertension.
• Deceleration of the growth of the head circumference.
• Down Syndrome.
• Frequent colds, especially aggravated by pneumonia.
• Heart failure with severe course.
• Inefficiency of conservative methods.
• Big DMZHP.

The anomaly can be eliminated in several ways:

• Endovascular repair. Allows you to block the hole with a special mesh. Refers to minimally invasive treatment.
• palliative method. The pulmonary artery is pulled down by the cuff, which reduces the flow of blood through the window. Stabilizes for a while. It is indicated in severe cases in the first days of life or with multiple holes.
• radical intervention. During the operation, a heart-lung machine is used. Small defects are sewn together, patches are placed on large ones. There is a need to open the right atrium and penetrate to the VSD through the tricuspid valve. In the absence of such an opportunity, the right ventricle becomes the access route.

Consequences and complications of VSD

If the window is too large, or even with moderate severity, no measures are taken to stabilize the condition, then the patient is threatened with the development of serious pathologies, and in the worst case, even death.

The most common consequences are:

• Heart failure leading to tissue hypoxia.
• Hypotrophy of muscle structures. The trophism is disturbed, which causes weight loss, a slowdown in the development of all systems and organs of the child.
• Eisenmenger syndrome. Occurs as a complication of pulmonary hypertension supported by VSD. This complication can only be treated surgically.
• Endocarditis of a bacterial nature occurs with a staphylococcal infection.
• Pulmonary hypertension. At the same time, the pressure of the pulmonary artery and all vessels in the pulmonary circulation is increased.
• aortic insufficiency. Valve flaps do not close completely.
• Arrhythmia.
• Stroke.
• Sudden death.
• Pneumonia with frequent relapses.
• Heart block, pulmonary or coronary embolism.

Disability

Disability assignment is a mandatory procedure after heart surgery. Even if the correction has not yet been carried out, but in addition to the defect, the baby is diagnosed with the Tetra Fallot defect or other complex pathologies, the group can be given earlier.

The duration until the next review can be six months, 2, 5 or 16 years.

Adolescents, upon reaching the age of 16, must pass the commission again and receive a disability, depending on the adult classification.

Forecast

Life expectancy and prognosis entirely depend on the diameter of the hole and the quality of the functioning of the vascular bed in the pulmonary circulation.

With a minor defect, the quality indicator of life does not change, only 2% have a chance of developing viral endocarditis. About 40-50% of small holes themselves are tightened up to 4-5 years.

With an average window size, heart failure occurs early. Gradually, only 14% can close on their own, others can decrease in size. As the remaining patients grow older, pulmonary hypertension often develops.

With a large hole, heart failure is an integral companion of the patient.

Pneumonia often occurs. Eisenmenger's syndrome affects 10-15% of these children. There is a high risk of death in childhood or adolescence.

If surgery is not performed, then with medium holes, the patient can live for about 30 years, and with a minor defect, almost 60 years.

Muscle defects are most prone to self-closing, while infundibular ones require surgical correction.

When visiting dentistry, all patients with defects should undergo antibacterial prophylaxis. Physical activity is limited for all patients. If the operation is performed and the problem is eliminated, then in a year the children can perform any load.

Mortality from a septal defect is no more than 10%, including postoperative mortality.

A septal defect appears even in fetal development, which can be detected by ultrasound diagnostics during a routine examination. A small window does not bring significant inconvenience to the patient and even sometimes overgrows before birth, medium and large spaces are dangerous.

Most often, a perimembranous defect occurs, the probability of self-tightening of which is many times greater than that of other types. The overall mortality of patients with this defect does not exceed 10%.