Heart defect: ventricular septal defect. Congenital ventricular septal defect

Ventricular septal defects (VSD) are the most common congenital heart defects, accounting for 30 to 60% of all birth defects hearts in full-term babies; the prevalence is 3-6 per 1,000 births. This does not include the 3-5% of newborns with small muscular ventricular septal defects, which usually close on their own within the first year.

Ventricular septal defects are usually isolated, but can also be combined with other heart defects. Because ventricular septal defects reduce blood flow across the aortic isthmus, aortic coarctation should always be ruled out in severe heart failure in infants with this defect. Ventricular septal defects often occur with other heart defects. So, they occur with corrected transposition main arteries, and are often accompanied by other disorders (see below).

Ventricular septal defects are always present with a common truncus arteriosus and double origin of the great arteries from the right ventricle; in the latter case (if there is no pulmonary valve stenosis) clinical manifestations will be the same as when isolated defect interventricular septum.

Ventricular septal defects can occur in any part of the ventricular septum. At birth, about 90% of defects are localized in the muscular part of the septum, but since most of them close spontaneously within 6-12 months, perimembranous defects subsequently predominate. VSDs can vary in size from tiny holes to complete absence the entire interventricular septum (single ventricle). Most trabecular (with the exception of multiple “Swiss cheese” type defects) and perimembranous ventricular septal defects close on their own, which cannot be said about large defects of the afferent part of the interventricular septum and infundibular defects (subaortic, as in tetralogy of Fallot, subpulmonary or located under both semilunar valves) . Infundibular defects, especially subpulmonary and located under both semilunar valves, are often covered by prolapse of the septal cusp of the aortic valve in them, which leads to aortic insufficiency; the latter develops only in 5% of whites, but in 35% of Japanese and Chinese with this defect. When perimembranous ventricular septal defects spontaneously close, a pseudoaneurysm of the ventricular septum often forms; its identification indicates high probability spontaneous closure of the defect.

Clinical manifestations

When blood is shunted from left to right through a ventricular septal defect, both ventricles are subject to volume overload, since the excess volume of blood pumped by the left ventricle and dumped into the pulmonary vessels enters them through the right ventricle.

The systolic murmur from a ventricular septal defect is usually rough and ribbon-like. With a small discharge, the noise can be heard only at the beginning of systole, but as the discharge increases, it begins to occupy the entire systole and ends simultaneously with the aortic component of the second sound. The volume of the murmur may be disproportionate to the magnitude of the shunt, and sometimes a loud murmur can be heard with a hemodynamically insignificant shunt (Roger's disease). Loud noise often accompanied by systolic tremor. The murmur is usually best heard inferiorly at the left edge of the sternum and is heard in all directions, but is strongest in the direction xiphoid process. However, with a high subpulmonary ventricular septal defect, the murmur may be best heard mid- or superiorly at the left sternal border and carried to the right of the sternum. In rare cases, with very small defects, the murmur may be spindle-shaped and high-pitched, resembling a functional systolic murmur. With a large discharge of blood from left to right, when the ratio of pulmonary to systemic blood flow exceeds 2:1, a rumbling mesodiastolic noise, as well as a third sound, may appear at the apex or medial to it. In proportion to the magnitude of the discharge, the pulsation in the heart area increases.

With small defects of the interventricular septum, there is no pronounced pulmonary hypertension and the pulmonary component of the second tone remains normal or only slightly increases. With pulmonary hypertension, an accent of the second tone appears above the pulmonary trunk. On a chest x-ray, the size of the left ventricle and left atrium increases, and the pulmonary pattern also increases, but with a small discharge these changes may be very slight or absent altogether; with a large amount of discharge, signs of venous stagnation appear in the vessels of the pulmonary circle. Because blood is shunted at the level of the ventricles, the ascending aorta is not dilated. The ECG remains normal with small defects, but with a large discharge it shows signs of left ventricular hypertrophy, and with pulmonary hypertension, right ventricular hypertrophy. The size and location of the ventricular septal defect are determined using echocardiography.

Figure: Muscular defect of the posterior part of the interventricular septum with echocardiography in the four-chamber position from the apical approach. The diameter of the defect is about 1 cm. LA - left atrium; LV - left ventricle; RA - right atrium; RV - right ventricle.

Doppler study allows localization by disturbance of blood flow in the right ventricle, and with color Doppler study You can even see multiple ventricular septal defects. In the most severe form of ventricular septal defect - a single ventricle - an MRI can be used to get an idea of ​​the anatomy of the heart.

With a large left-to-right shunt, signs of volume overload and heart failure appear. In full-term infants this usually occurs between 2 and 6 months, but in preterm infants it may occur earlier. Although left-to-right shunting should reach a maximum by 2-3 months, when pulmonary vascular resistance reaches its minimum, sometimes heart failure in full-term infants develops already in the first month of life. This usually occurs when a ventricular septal defect is combined with anemia, large left-to-right shunt at the level of the atria or through a patent ductus arteriosus, or coarctation of the aorta. In addition, heart failure may develop earlier than expected with ventricular septal defects in combination with double origin of the great arteries from the right ventricle. This may be because before birth the fetal lungs receive blood from increased content oxygen and, as a result, pulmonary vascular resistance is lower after birth.

Treatment

Isolated ventricular septal defects are the most common congenital heart defects, so all pediatricians should know what to do when they are detected. The table shows the decision-making algorithm, and the numbers in brackets are explained below.

1. Small ventricular septal defects occur in 3-5% of newborns; in most cases they close on their own by 6-12 months. It is not necessary to perform an echocardiogram only to confirm such defects. It is important to note that with large ventricular septal defects in newborns, no noise is heard in the maternity hospital, since due to the high pulmonary vascular resistance, the discharge of blood through such a defect is very insignificant and does not form a turbulent blood flow. Therefore, murmurs indicating a ventricular septal defect detected in the maternity hospital are almost always caused by small defects.

2. Since perimembranous and trabecular defects very often close on their own, up to 1 year of age such children can be managed conservatively in the hope that surgery will not be necessary. Spontaneous closure of ventricular septal defects can occur in several ways: due to growth and hypertrophy of the muscular part of the defect, closure of the defect due to endocardial proliferation, integration of the tricuspid valve into the septal cusp defect and prolapse into the aortic valve cusp defect (in the latter case, aortic insufficiency occurs). As the defect decreases, the systolic murmur may initially intensify, but as the defect decreases further, it subsides, shortens, becomes fusiform, high-frequency and whistling, which usually portends its complete closure. Spontaneous closure of the defect occurs in 70% of cases, usually in the first three years. In 25%, the defect decreases, but does not close completely; hemodynamically, it can be almost insignificant. Therefore, if the defect decreases, surgical treatment should be postponed in the hope of spontaneous closure of the defect. The table lists situations in which surgical treatment should be considered without waiting for spontaneous closure of the defect.

3. With Down syndrome (trisomy of chromosome 21), the vessels of the lungs are affected very early, therefore, if the defect remains large, the operation is not delayed.

4. In rare cases, surgery is performed for social reasons. These include the impossibility of permanent medical supervision due to living in remote areas or parental negligence. In addition, some of these children are very difficult to care for. They need to be fed every two hours and require so much attention that other children often suffer; sometimes this even leads to family breakdown.

5. With large ventricular septal defects, growth is always delayed, weight is usually below the 5th percentile, and height is below the 10th percentile. However, after spontaneous or surgical closure of the defect, sudden jump growth. Most children have a normal head circumference, but sometimes its increase slows down sharply by 3-4 months. When the defect is closed at this age, the head circumference reaches normal values, but if the operation is postponed for 1-2 years, this does not happen.

6. In the absence of the above reasons requiring early surgical treatment, surgery can be delayed for up to 1 year in the hope that the defect will close or become smaller.

7. If by the age of 1 year there remains a large discharge of blood from left to right, surgical correction is not carried out only in special circumstances, since the risk of irreversible damage to the blood vessels of the lungs increases significantly in the future. By age 2, irreversible damage to the lung vessels occurs in one third of children.

8. With a decrease in blood discharge, the condition improves; pulsation in the heart region weakens, the size of the heart decreases, mesodiastolic murmur weakens or disappears, systolic murmur weakens or changes, tachypnea decreases and disappears, appetite improves, growth accelerates, and the need for drug treatment decreases. However, it should be remembered that improvement can be caused not only by a decrease in the ventricular septal defect, but also by damage to the pulmonary vessels and, less commonly, by obstruction of the outflow tract of the right ventricle. For determining further tactics at this stage it is necessary to carry out echocardiography and sometimes cardiac catheterization.

9. Severe damage to the pulmonary vessels with a ventricular septal defect rarely develops before the age of 1 year. However, sometimes this is possible, so if blood flow from left to right decreases, it is necessary to conduct an examination. When the vessels of the lungs are damaged, there is no or very little left-to-right shunting, and for several years there may be no right-to-left shunting. However, usually by the age of 5-6 years, cyanosis increases, especially during physical activity(Eisenmenger syndrome). With the development of severe pulmonary hypertension, the pulmonary trunk noticeably expands, and the pulmonary vascular pattern formed peripheral vessels, is getting poorer. In some cases, pulmonary vascular damage can progress very quickly, causing irreversible pulmonary hypertension by 12-18 months; This cannot be allowed under any circumstances. For any unclear change clinical picture perform echocardiography and, if necessary, cardiac catheterization; for large defects, catheterization can be performed routinely at the ages of 9 and 12 months to identify asymptomatic pulmonary vascular lesions.

10. Hypertrophy and obstruction of the outflow tract of the right ventricle usually develops quite quickly, so the discharge of blood from left to right can be observed very a short time. Then cyanosis appears, first during physical activity, and then at rest; The clinical picture may resemble tetralogy of Fallot. With obstruction of the right ventricular outflow tract, the likelihood of spontaneous closure of the ventricular septal defect is low. The discharge of blood from right to left can be complicated by thrombosis and embolism of cerebral vessels and brain abscesses, and hypertrophy of the outflow tract complicates the operation; therefore, closure of the defect, and, if necessary, resection of fibrous and muscle tissue outflow tract of the right ventricle is performed as early as possible.

The mortality rate for primary surgical closure of ventricular septal defects is very low. If primary closure is not possible due to multiple muscle defects or other complicating circumstances, surgical narrowing of the pulmonary trunk is performed, which reduces left-to-right shunt, reduces pulmonary blood flow and pulmonary artery pressure, and eliminates heart failure. When the pulmonary trunk is narrowed, there are complications; in addition, eliminating the narrowing of the pulmonary trunk with subsequent closure of the ventricular septal defect increases the mortality of this operation.

Consequences and complications

In some children, when the ventricular septal defect spontaneously closes, clicks may appear in the middle or end of systole. These clicks occur due to the protrusion into the right ventricle of the aneurysmally dilated membranous part of the interventricular septum or the tricuspid valve cusp embedded in the defect. Through a small hole remaining at the top of this pseudoaneurysm, a slight discharge of blood from left to right is maintained. Usually the defect is completely closed and the pseudoaneurysm gradually disappears, but occasionally it can increase. Pseudoaneurysm can be seen on echocardiography.

With ventricular septal defects, especially infundibular ones, aortic insufficiency often develops. The aortic valve leaflet prolapses into the defect, and the sinus of Valsalva dilates aneurysmically; As a result, the aneurysm of the sinus of Valsalva or the valve leaflet may rupture. It is believed that aortic insufficiency develops as a result of pressure on the valve, which is not supported by the interventricular septum, as well as the suction effect of the blood stream flowing through the defect. Even with a small or almost closed ventricular septal defect, the presence of aortic insufficiency requires surgical closure of the defect, since otherwise prolapse of the aortic valve leaflet may increase. In case of infundibular defects, early correction of the defect may be justified, before signs of aortic insufficiency appear.

Another complication of ventricular septal defect is infective endocarditis. It can occur even after spontaneous closure of the defect. If infective endocarditis occurs on the tricuspid valve leaflet covering the defect, its rupture may lead to direct message between the left ventricle and the right atrium. In this regard, prevention infective endocarditis should be continued even with very small defects; When the defect is completely spontaneously closed, the prevention of infective endocarditis is stopped.

Literature:

"Pediatric Cardiology" ed. J. Hoffman, Moscow 2006

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

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

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

How does ventricular septal defect manifest in children?

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

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

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

In case of a ventricular septal defect in children with a size range of 10-20 mm, the discharge through it reaches 70% of the blood that is discharged by the left ventricle. This causes significant volume overload of the pulmonary circulation, which leads to low overload of the right ventricle and then to its hypertrophy. First, under the influence of high blood pressure, the arteries of the pulmonary circulation expand, thereby facilitating the work of the right ventricle. The pressure in the vessels of the pulmonary circulation remains normal, however pronounced syndrome 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 remains at high level. This is due to the fact that pressure is transferred to the pulmonary artery from the left ventricle (hydrodynamic factor). High pressure in the pulmonary artery leads to overload and enlargement of the right ventricle. This provokes a large volume of blood discharged through the defect, which ultimately leads to overflow of the venous bed of the pulmonary circulation and causes volume overload of the left atrium, resulting in an increase in systolic and diastolic pressure in the left ventricle, left atrium, and pulmonary veins. With prolonged similar overloads, this leads to hypertrophy (increase in size) of the left ventricle and left atrium. High blood pressure in the pulmonary veins and left atrium, due to the neurohumoral mechanism of load compensation, leads to spasm, and then to sclerosis of the pulmonary arterioles. Children in the first year of life develop heart failure, and more than 50% of children die before the age of one year.

Ventricular septal defect in the fetus and its types

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

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

Clinic of Topochinov-Roger disease. The first, and sometimes the only manifestation of the defect is a systolic murmur in the heart region, which appears, as a rule, from the first days of the child’s life. The children are growing well and have no complaints. The boundaries of the heart within 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. The murmur, as a rule, occupies the entire systole and often merges with the second sound. Its maximum sound is in the III-IV intercostal space from the sternum, it is well conducted throughout the entire region of the heart, to the right behind the sternum, is heard on the back near the interscapular space, is well conducted along the bones, transmitted through the air and can be heard even if the stethoscope is raised above the heart (remote noise ).

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

Signs of a severe ventricular septal defect

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

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

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

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

Ventricular septal defect of the heart in children after one year

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

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

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

There is very large variability depending on the degree of hemodynamic impairment clinical course 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 ECG results, Echo-CG, catheterization of cavities.

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

Complications and prognosis for ventricular septal defect in children

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

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

Features of the disease

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

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

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

Forms and types

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

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

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

The differences in VSD size are classified as follows:

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

Reasons for appearance

Ventricular septal defects occur under the influence of two factors:

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

Diagram of a ventricular septal defect

Symptoms of ventricular septal defect

• With small ventricular septal defects, symptoms do not appear.
• With moderate VSD, symptoms uncharacteristic of heart defects may occur. Weakness, increased fatigue, lag in physical development, prone to pneumonia and lung infections.
• Large defects appear as pale skin, swelling of the legs, pain in chest, severe shortness of breath during physical activity. Such symptoms are more typical of heart defects.

The most accurate diagnosis of VSD allows ultrasonography(echocardiography) of the heart muscle.

Diagnostics

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

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

Treatment

Therapeutic and medicinal methods

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

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

Operation

The main treatment for VSD is surgery. Operations can be emergency or planned. IN emergency surgical intervention in the patient's body is carried out to prevent fatal outcome without prior preparation.

In the case when it is appointed elective surgery(usually it is carried out in childhood), the patient is previously prepared for it. Cardiologists monitor his condition and conduct a course of conservative treatment. Surgery to close a ventricular septal defect is performed in two different ways:

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

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

Disease prevention

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

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

Such a developmental anomaly as a ventricular septal defect occurs quite often in newborns. Modern statistics confirms that up to 40% of children with congenital heart changes suffer from a ventricular septal defect (VSD). This is a structural disorder (unclosed hole) that forms in the fetal heart in the first eight weeks. The size of the hole diameter can be different - from insignificant to not having much serious consequences(1 mm) to a large anomaly - more than 30 mm. The presence of such a pathology may have the consequence of pumping blood into the right side.

The anomaly can be localized in various parts of the interventricular septum. There are three parts: membranous, muscular (middle) and lower.

The most common option is the location of the disorder in the middle part, the membranous part (large pathologies can occur here). A defect in the muscle part is much less common (here the defects are small in size). The situation may be complicated by the fact that there may be several holes, and pathology can be observed in different parts partitions. In addition, the anomaly very often accompanies various other defects in heart development.

The interventricular septum of the heart is formed very early, in the first three months. It consists of three components, which before this period are formed and connected to each other. If this process is disrupted, then one or more holes may remain in the septum.

Modern medicine names the following main reasons for the development of the defect:

• transfer by mother infectious diseases on early stages pregnancy (can be affected by ARVI, chickenpox, rubella);
• Taking strong medications by a pregnant woman in the early stages;
• malnutrition, starvation, unbalanced diets, lack of vitamins;
• genetic mutations, poor environment, radiation;
• age (over 40 years);
• presence of serious chronic diseases;
• alcohol intoxication.

NOTE! Among the causes of the defect, doctors name infections suffered in the early stages, as well as poor nutrition, alcohol consumption and the presence of serious chronic diseases.

Main symptoms in newborns

NOTE! The main symptoms of a defect of any size include a heart murmur, marbling of the skin, and low weight. Possible complaints of a child with a significant defect

At 3-4 years old, the baby may report the following health problems:

• feel pain in the heart area;
• feel shortness of breath when lying down;
• complain of cough;
• complain of nosebleeds.

ATTENTION! Parents may observe fainting, flat phalanges of fingers, blue tint skin of the face and limbs, thinness, swelling. The doctor notes rough noise, wheezing, and enlarged liver.

Mechanism of violation

Peculiarity human heart- the difference between blood pressure in the left and right ventricles. If there is a hole in the septum, this causes the heart to malfunction. Normally, blood should enter the aorta, but due to a developmental abnormality, it is pumped into the right ventricle, causing it to overstrain. The size of the hole and its location influence the volume entering the other compartment. A small volume may not distort the functioning of the heart at all. But if the anomaly is significant, then a scar appears on the wall. Another result of the process is an increase in pressure in the pulmonary circulation.

The body tries to adapt to existing conditions: there is an increase in the mass of the ventricles, the walls of the vessels thicken. This pathological process because it leads to loss of elasticity.

NOTE! A child's blue skin tone, restlessness, and problems with shortness of breath may indicate a VSD.

Complications

The problem is compounded by the fact that if an abnormality is present, various additional diagnoses are possible.

NOTE! Children with VSD often suffer from pneumonia - this is due to a problem such as blood stasis .

Thromboembolism is of particular concern because it is associated with possible blockage of a vessel. This can lead to a stroke.

Diagnostics

1. Electrocardiography (ECG) – detects serious abnormalities.
2. Phonocardiography (recording of heart vibrations).
3. Echocardiography (ultrasound of the heart) – reliable way diagnostics
4. X-ray of the heart. Able to identify medium and large defects.
5. Catheterization of the heart cavities.
6. Angiocardiography (use of contrast agent).

Treatment

The main treatment for VSD is surgery. There are subtleties here: if the size of the pathology is small, then there is a very high probability of its independent restoration and closing of the holes. The essence of the operation is suturing the hole (if possible, up to 5 mm in diameter) or using a patch made of modern material. The origin of the material can be different - based on synthetic or biological matter.

What can serve as an indication for surgery?

In children under three years of age:

• lack of weight;
• problems with general development child;
• progression of pulmonary hypertension;
• insufficient blood supply to internal organs;
• constant cases of pneumonia.

For adults and children over 3 years of age:

• lack of energy, strength;
• prolonged acute respiratory viral infections and pneumonia;
• heart failure;
• reset more than 40%.

Very often there is a situation where surgery is too risky. For example, in the age group of infants in the first months of life, having serious problems Due to the large diameter anomaly, specialized treatment is carried out in two stages. First stage: surgery to apply pulmonary artery above a special cuff to equalize pressure. A few months later, after the situation has improved and weight has been gained, the child undergoes a second operation - a standard one: the previously applied device is removed and the anomaly is closed.

Video - Ventricular septal defect

Manifestations in adulthood

• persistent cough;
• arrhythmia;
• heartache;
• swelling;
• shortness of breath at rest.

Medicines used

It is worth immediately noting that the defect closes either itself or with the help of surgery. Medications, used in in this case, are not aimed at closing the hole, but at removing dangerous symptoms associated with the development of the anomaly.

The main purpose of the drugs is to support the heart muscle, providing more energy to weakened tissues (for example, Anaprilin, Digoxin).

Attention! Used to combat the formation of blood clots Aspirin, which quite successfully copes with the task of thinning the blood. Also appointed vitamin preparations, medicines containing trace elements (for example, selenium, potassium).

Life expectancy forecast

The general health and life expectancy of the patient are directly dependent on the size of the anomaly. Other factors also have an influence: for example, general state vessels.