Ventricular septal defect of the heart - Causes, Symptoms and Treatment .MF .
Ventricular septal defect (VSD) - a congenital heart defect characterized by the presence of a defect in the muscular septum between the right and left ventricles of the heart.VSD is the most frequent congenital heart disease in newborns, its frequency is approximately 30-40% of all cases of congenital heart defects.This defect was first described in 1874 by PF Tolochinovym and in 1879 H. L. Roger.
According to the anatomical division of the interventricular septum into 3 parts (upper - membranous or membranous, middle - muscle, lower - trabecular), give the names and ventricular septal defect.Approximately 85% of the VSD is located in the so-called preponchatoy part of it, that is immediately below the right coronary and non-coronary aortic valve (when viewed from the left ventricle of the heart) and at the junction of the anterior leaflet of tricuspid valve in its septal flap (when viewed fromside of the right ventricle).The 2% defect located in the muscular portion of the partition, with the possibl
ventricular septal defects can be from 3.0 mm to 1 cm or more.Depending on the size secrete large defects, the value of which is similar to or greater than the diameter of the aorta, medium defects having a diameter of from ¼ to ½ the diameter of the aorta, and small defects.Defects membranous portion usually have a circular or oval shape and reach 3 cm, muscular part of the interventricular septum defects usually are round and small.
Quite often, about 2/3 of the cases, the VSD can be combined with other related anomaly: atrial septal defect (20%), patent ductus arteriosus (20%), coarctation of the aorta (12%), congenital mitral valve failure (2%) stanozami aorta (5%) and pulmonary artery.
Schematic representation of the ventricular septal defect.
Violations of formation of the interventricular septum was found to occur during the first three months of pregnancy.Interventricular septum of the fetus is formed of three components, which in this period must be adequately compare and connect with each other.Violation of this process leads to the fact remains that the defect in the interventricular septum.
mechanism of violation of hemodynamics (blood flow)
the fetus, being in the mother's womb, blood circulation is carried out by the so-called circle of placental (placental circulation), and has its own characteristics.However, soon after the birth of a newborn is set to normal blood flow in the large and small circles of blood circulation, which is accompanied by the emergence of a significant difference between the blood pressure in the left (higher pressure) and the right (less pressure) ventricles.Thus existing VSD causes the blood pumped from the left ventricle into the aorta not only (and which must enter the normal), but also through the VSD - in the right ventricle, which normally should not be.Thus, for each cardiac contraction (systole) occurs abnormal discharge of blood from the left ventricle to the right.This increases the load on the right ventricle of the heart, as it produces extra work for pumping extra blood volume again to the lungs and the left side of the heart.
volume of abnormal discharge depends on the size and location of the VSD: in the case of the small size of the defect last practically no effect on the heart.On the opposite side from a defect in the wall of the right ventricle, and in some cases and on the tricuspid valve may develop scar thickening, which result from the reaction to the pathological injury of blood ejection, spurting through the defect.
In addition, due to abnormal discharge of an additional amount of blood entering the pulmonary vessels (pulmonary circulation), leads to the formation of pulmonary hypertension (increased blood pressure in the vessels of the pulmonary circulation).Over time, the body includes compensatory mechanisms: an increase in muscle mass of the heart ventricles, progressive vascular adaptation of the lungs, which first take an incoming excessive amount of blood, and then pathologically altered - shaped thickening of the walls of arteries and arterioles, which makes them less elastic and more dense.Increased blood pressure in the right ventricle and pulmonary arteries to occur until, finally, pressure compensation does not occur in the right and left ventricle in all phases of the cardiac cycle, then abnormal discharge from the left to the right ventricle of the heart ceases.If over time the blood pressure in the right ventricle is higher than the left, there is a so-called "reverse discharge", in which the venous blood from the right ventricle through the same VSD enters the left ventricle.
Timing the first signs of VSD depends on the size of the defect, as well as the magnitude and direction of the pathological blood discharge.
Small defects in the lower regions of the interventricular septum in the overwhelming number of cases did not have a significant impact on children's development.Such children feel satisfactory.Already in the first few days after birth, there is moderate-intensity murmur rough, scrubbing the tone that the doctor listens during systole (during a heart contraction).This noise can be heard better in the fourth or fifth intercostal space, and is not carried out in other places, the intensity of his standing can be reduced.Since this noise is often the only manifestation of the small VSD does not have a significant impact on the health and development of the child, the situation in the medical literature had shaped the name of "much ado about nothing."
In some cases, in the third or fourth intercostal space at the left edge of the sternum can be felt shaking at the time of cardiac contraction - systolic jitter, or systolic "cat's purring."
When large defects membranous (membranous) portion of the interventricular septum symptoms of congenital heart disease usually occur immediately after childbirth, but 12 months later.Parents begin to notice difficulties in feeding the child: he has a shortness of breath, he was forced to pause and breaths, because of what may be hungry, anxiety appears.
Those born with normal weight, those children fall behind in their physical development, due to malnutrition and a decrease in the volume of circulating blood in a large circle of blood circulation (due to abnormal discharge in the right ventricle of the heart).There are severe sweating, paleness, skin mottling, cyanosis small extremities of hands and feet (peripheral cyanosis).
characteristic rapid breathing with the involvement of auxiliary respiratory muscles, paroxysmal cough that occurs with a change in body position.Develop recurring pneumonia (pneumonia), it is difficult to treat.To the left of the sternum is deformed chest - a heart shaped hump.Apical impulse is displaced to the left and down.Palpated systolic jitter in the third or fourth intercostal space at the left sternal border.Auscultation (listening to) the heart is determined by the rough systolic murmur in the third or fourth intercostal space.In children, the older age group the main clinical signs of defect are saved, they appear complaints about pain in the heart and heart palpitations, children continue to lag behind in their physical development.With age, the health and condition of many children improved.
Aortic regurgitation observed among patients with VSD in about 5% of cases.Develops, if the defect is located in such a way that makes more and sagging of one of the leaflets of the aortic valve, which leads to a combination of the defect with aortic valve regurgitation, which significantly complicates the accession course of the disease due to a substantial increase in the load on the left ventricle.Among the clinical manifestations prevails dyspnea, sometimes acute left ventricular failure develops.Auscultation of the heart is listened not only to the above systolic murmur, and diastolic (the phase of the cardiac relaxation) noise at the left sternal border.
Infundibulyarny stenosis observed in patients with VSD and about 5% of cases.Develops, if the defect is located at the rear of the interventricular septum under the so-called septal tricuspid flap (tricuspid) valve below the supraventricular crest that causes the defect to pass through a large amount of blood and trauma it supraventricular crest, which thereby increases in size, and scarring.As a consequence, there is a narrowing infundibulyarnogo department right ventricle and the formation of subvalvular stenosis of the pulmonary artery.This leads to a reduction of pathological VSD reset through from the left ventricle into the right and unloading of the pulmonary circulation, but there is a sharp increase and the load on the right ventricle.The blood pressure in the right ventricle begins to significantly increase, which gradually leads to abnormal discharge of blood from the right ventricle to the left.In marked infundibulyarnom stenosis in a patient appears cyanosis (blueness of the skin).
Infection (bacterial) endocarditis - endocardial damage (inner lining of the heart) and the heart valve, caused by an infection (usually bacterial).Patients with VSD risk of infective endocarditis is approximately 0.2% per year.There is usually in older children and adults;more often at small sizes VSD, which is caused by trauma endocardial at high abnormal blood discharge jet velocity.Endocarditis can be provoked by dental procedures, purulent skin lesions.Inflammation occurs first in the right ventricle wall, on the opposite side from the defect or the edges of the defect, and then applies the aortic valves and tricuspid.
Pulmonary hypertension - increased blood pressure in the vessels of the pulmonary circulation.In the case of congenital heart disease, it develops as a result of entering the lung vessels additional blood volume caused by abnormal discharge it through the VSD from the left ventricle to the right.Over time, worsening of pulmonary hypertension occurs in connection with the development of compensatory mechanisms - formation of a thickening of the walls of the arteries and arterioles.
Eisenmenger syndrome - podaortalnoe location of ventricular septal defect combined with sclerotic changes in the pulmonary vessels, the expansion of the trunk of the pulmonary artery and increase muscle mass and size (hypertrophy), mainly the right ventricle of the heart.
Recurring pneumonia - due to stagnation of blood in the pulmonary circulation.
Thromboembolism - acutely arising blockage of a blood vessel by a thrombus, to break away from their place of education in the heart wall and into the circulating blood.
1. Electrocardiography (ECG): In the case of small-sized VSD material changes on the electrocardiogram can not be detected.Generally, typical normal position of the heart electric axis, but in some cases it may deviate to the left or right.If the defect is large, it is more essential reflection by electrocardiography.In marked pathological discharge of blood through a defect of the heart's left ventricle into the right pulmonary hypertension without the electrocardiogram revealed signs of overload and increase the muscle mass of the left ventricle.In the case of significant pulmonary hypertension symptoms of overload of the right ventricle and the right atrium.Cardiac arrhythmias occur infrequently, usually in adult patients in the form of arrhythmia, atrial fibrillation.
2. phonocardiography (vibration recording and sound signals produced when the activity of the heart and blood vessels) allows you to record the instrumental noise and abnormal heart sounds changed, due to the presence of VSD.
3. Echocardiography (ultrasound of the heart) can not only detect direct signs of birth defects - break echo in the interventricular septum, but also to ascertain the location, number and size of defects, as well as to determine the presence of indirect signs of this defect (increased ventricular sizeand left atrium of the heart, increase in right ventricular wall thickness, etc.).Doppler echocardiography reveals another direct sign of defect - abnormal blood flow through the VSD in systole.In addition, possible to estimate the blood pressure in the pulmonary artery, the magnitude and direction of pathological shunt.
4. chest organ cells (heart and lungs).When small amounts of VSD pathological changes were determined.With significant amounts of the defect with significant discharge of blood from the left ventricle into the right to determine the increase in left ventricular dimensions and left atrium and then the right ventricle, increased pulmonary vascular pattern.With the development of pulmonary hypertension is defined by the expansion of the roots of the lungs and the pulmonary artery bulging arc.
5. catheterization of heart cavities is carried out to measure the pressure in the pulmonary artery and the right ventricle, as well as determining the blood oxygen saturation level.Characterized by a high degree of oxygen saturation (oxygenation) in the right ventricle than in the right atrium.
6. Angiocardiography - the introduction of contrast medium into the heart cavity through a special catheter.With the introduction of contrast into the right ventricle and the pulmonary artery is observed from their re-opacification, which is due to return to the right ventricle contrast with abnormal discharge of blood from the left ventricle through the VSD after passing through the pulmonary circulation.The introduction of water-soluble contrast in the left ventricle is determined by the contrast flow from the left ventricle to the right through the VSD.
With small size VSD, there are no signs of pulmonary hypertension and heart failure, normal physical development in the hope of spontaneous closure of the defect is possible to refrain from surgery.
have children early school age indication for surgical intervention are the early progression of pulmonary hypertension, stable heart failure, recurrent pneumonia, pronounced lag in physical development and body mass deficit.
Indications for surgical treatment in adults and children from 3 years are: fatigue, frequent SARS, leading to the development of pneumonia, heart failure and typical clinical picture of defect with abnormal discharge more than 40%.
Operative intervention is reduced to plastic VSD.Operation is carried out using a heart-lung machine.With a diameter of 5 mm defect it is closed by suturing the U-shaped sutures.With a diameter of 5 mm defect made its closure a patch of synthetic or specially treated biological material, which in a short time covered by its own tissues.
In cases where an open radical surgery is not immediately possible due to the high risk of surgery with cardiopulmonary bypass in children of the first months of life, with larger sizes VSD, underweight, with intractable drug correction of severe heart failure, surgical treatment is carried out intwo stages.
Surgeon Kletkin ME