Muscular apical VSD. Treatment of ventricular septal defect. How is the treatment carried out?

VSD is a defect interventricular septum hearts. This pathology is quite common and represents an anomaly within the cardiac organ. This anomaly is expressed in the hole in the septum between the left and right ventricles.

This intrauterine developmental defect occurs in 17% to 42% of cases of intrauterine pathology. The pattern of occurrence depending on the sex of the child was not monitored.

The defect can occur as an independent deviation or tetralogy of Fallot (blue heart defect). Tetralogy of Fallot includes 4 congenital heart defects.

Defects in the wall of a small scale (3 mm - 10 mm) practically do not cause discomfort in the organ, and after several years self-healing occurs.

When big hole It is recommended to correct it surgically. Pathology in the septum causes pneumonia in acute form, which manifests itself with systematic frequency, as well as constant shortness of breath and colds out of season.

Classification of pathological changes

This classification of pathology, in which biological fluid is discharged from the left ventricle into the right ventricle:

• Congenital heart defect - congenital heart disease - VSD;
• Component of a combined congenital disorder;
• Complicated myocardial infarction.

According to focal localization, pathology is divided into:

• The defect is perimembranous;
• Defect muscle tissue;
• The defect is subaortic.

Separation by hole diameter:

• The hole is larger than the aortic diameter - BJDP;
• The size is half the diameter of the aorta - SJP;
• A hole with a diameter less than a third of the aortic lumen - MJP.

Etiology of VSD

During fetal development in utero in the 1st trimester, a hole appears in the dividing wall of the right and left ventricles. During this period, a comparison of individual parts of the heart organ occurs, their correct connection into one harmonious organ.

If at this stage there is an impact on the unformed organ of factors of an endogenous nature, as well as exogenous ones, a defect of an organ that is not correctly formed, or not fully formed, occurs in the interventricular septum.

Reasons for the fetus to have an organ that is not formed correctly - VSD pathology:

• Genetic hereditary factor - the likelihood of having children with pathologies of the heart organ increases in those families where children have already been born with pathologies and anomalies of the heart type;
• Infection in a woman during the development of a child in utero - ARVI, as well as infectious mumps, smallpox, viral rubella;
• During the period of bearing the unborn child, the woman took antibacterial drugs, antimicrobial agents, as well as antiepileptic drugs, hormonal drugs;
• Living in poor environmental conditions;
• Intoxication of the body with alcohol;
• Drug intoxication;
• Radiation;
• Toxicosis during pregnancy at the beginning of the 1st trimester;
• Fasting during pregnancy;
• Insufficient consumption of foods rich in vitamins and microminerals;
• Pregnancy after the age of forty, when the body experiences age-related changes in the hormonal sphere;
• Diseases endocrine system- hyperglycemia;
• Disease thyrotoxicosis;
• Constantly being tense and stressed;
• Rebooting the body, which is reflected in severe fatigue.

How does a cardiac anomaly (VSD) affect blood flow?

The focus of the VSD defect in the wall between the ventricles of the cardiac organ is localized in the heart muscle, or in the area of ​​the membrane (membranous defect). The opening of the hearth varies from 0.5 centimeters to 3.0 centimeters. The shape of the hole can be a circle, or it can be in the form of a slot.

If the lesion is no more than one centimeter, then this does not in any way affect the functioning of the heart organ or blood flow. The person does not feel any signs of abnormal heart function.

If the holes in the septum are more than one centimeter, then disturbances occur in the blood flow system.

At the moment of systole of the left-sided ventricle, biological fluid enters the opening in an increased amount under a certain pressure, then enters the right-sided ventricle, which leads to its pathology and hypertrophy of its walls.

Also, under the influence of improper blood flow, the pulmonary vessel expands, through which venous blood enters the lungs. The pressure in the pulmonary vessel increases and the pressure in the arteries of the pulmonary organ increases accordingly.

These arteries spontaneously create a spasm so as not to overload the lung with blood. The consequence of this may be pulmonary failure.

During diastole, the left-sided ventricle contains less blood than its right-sided neighbor. The left ventricle ejects blood better and is better emptied.

IN in this case The left ventricle receives a new portion of blood from two sources:

• From the right-sided ventricle through the pathological opening of the VSD;
• From the left atrium.

This situation in the bloodstream creates the prerequisites for the development of pathology of the left ventricle - hypertrophy of its wall and pathology interatrial septum.

With the constant release of blood into the bloodstream through the left ventricle, which is diluted with venous blood, there is a lack of oxygen in the bloodstream, leading to hypoxia of the tissue cells of the internal organs.

Violations normal functioning blood flow inside the heart organ can cause the formation of blood clots and, with the help of the blood flow, transfer blood clots to the organs of the respiratory system and to the brain.

Clinical manifestations of VSD depend on the size of the defect, the duration of the pathology, the compensatory capabilities of the organ, as well as the degree and speed of blood flow damage, and changes in hemodynamics.

Symptoms for small foci of VSD defect

Small foci of a VSD defect are considered to have an opening radius of up to one centimeter, or based on individual characteristics aortic diameter size. These are abnormalities of the lower part of the septum.

With this VSD defect, the child is born at the right time, without any deviations or impairments in development, both physical and mental.

Only from the first minutes after birth are sounds heard in the heart organ. This noise can even be heard from the back. At this stage, this is the only sign of clinical manifestation of VSD. Very rarely a vibrating state is felt when placing a hand on the chest.

This vibration depends on the fact that the biological fluid passes through the small interventricular diameter of the pathology. Until one year of age, the small hole may close.

At an older age, the noise weakens when the child is in a sitting or standing position, as well as after exertion of the body. This occurs due to almost tight compression of the opening of this pathology, spontaneous closure occurs.

Symptoms of medium defects and large lesions of VSD

Medium-sized foci of defects include holes with a diameter of one centimeter to two centimeters, and large foci of pathology include holes from two centimeters to three centimeters. Many patients with this pathology (up to 45%) have low body weight - muscle wasting.

As a child grows up, a lack of muscle tissue occurs, which leads to dystrophy of varying degrees - from the first degree (mild) to the third (severe) degree of muscle disease.

This phenomenon occurs because muscle tissue does not receive the required amount of oxygen and muscle hypoxia develops. The second cause of dystrophy is a decreased appetite in such children and this results in a lack of calories.

Signs of VSD in newborns:

• Difficulty sucking reflex - the child often stops sucking the breast;
• Shortness of breath when sucking the breast;
• The baby's skin is very pale;
• A bluish tint near the mouth, which becomes more noticeable when the child cries;
• Large amount of sweat, especially during breastfeeding.

A quarter of newborns show signs of blood flow deficiency, which can cause death.

In the future, such children get sick respiratory diseases, rotovirus infections, bronchial diseases, inflammatory processes in the lung tissues, as well as pathologies in the pulmonary blood flow.

Shortness of breath in a newborn child becomes constant, such a child lags behind in physical development from peers and cannot lead active image life.

Symptoms of VSD in a child aged three years:

• The child’s constant complaints of chest pain;
• The child feels interruptions in work heart rate;
• Nosebleeds;
• Fainting;
• A bluish tint around the nose and mouth;
• Blue discoloration appears on the tips of the fingers and toes;
• Shortness of breath in horizontal position causing inconvenience during sleep;
• Persistent dry cough;
• Physical retardation in growth and muscle tissue gain.

With the auscultation technique, low-pitched noises are heard in the myocardium, as well as wheezing in the lower parts of the lung lobes.

Sign of swelling on lower limbs in children they do not appear.

Signs in an adult

In adults, signs of VSD and heart failure are:

• Shortness of breath on exertion and at rest;
• Wet cough;
• Chest pain;
• Abnormal heart rhythm - arrhythmia.

If a VSD is detected in a woman during intrauterine pregnancy, it is urgently necessary to undergo a comprehensive diagnostic study of the cardiac organ and blood flow system in order to establish the exact diameters of the pathology focus.

If the focus of the defect is small, then the birth process will go away on its own, and no disturbances in the heart are expected throughout the entire period of pregnancy.

If the defect is medium in size, then the following disorders in the body may develop during pregnancy:

• Heart failure;
• Insufficiency of the blood flow system;
• Hypoxia of internal organs;
• Swelling;
• Disturbance in the rhythm of the heart muscle - arrhythmia;
• Dyspnea.

Oxygen deficiency during pregnancy affects the intrauterine formation of the fetus. With hypoxia of mother and child, the risk of intrauterine development pathology increases.

At this point, the mother needs to take cardiac medications, which are toxic to the fetus.

Therefore, a child often inherits heart defects of congenital etiology from his mother. With a large-diameter VSD, women are strictly prohibited from giving birth to a child. Treatment of heart defects must be carried out before planning pregnancy.

Stages

• Stage No. 1. VSD manifests itself as an increase in the size of the heart organ, as well as stagnant blood in the bloodstream and in the vessels of the lungs. Timely diagnosis of pathology and qualified therapy are necessary. The complicated form of the disease at this stage is acute pneumonia and swelling of lung tissue;
• Stage No. 2. Clinical manifestations of heart disease at this stage are pulmonary artery spasm. A spasmodic state appears in the coronary vessels. This is a response to overstretching of these vessels from high pressure blood;
• Stage No. 3. This stage develops in the absence of therapy for VSD and has difficult character course of the disease. The disease cardiosclerosis develops in an irreversible form. This is the stage of inoperable cardiosclerosis.

Division by clinical signs

According to the clinical manifestations and course of VSD pathology, it is divided into two types:

Development of a disease that occurs asymptomatically. It is possible to identify this pathology in this course of the disease only by determining the sound tonality.

With the development of VSD, the volume of the cardiac organ increases, and the second pulmonary heart sound can be detected. With this tone, a small opening in the septum between the cardiac ventricles is determined.

Observation by a cardiologist is necessary for no less than 12 calendar months.

If during the observation period the noise in the cardiac organ disappears, and other symptoms of the pathology do not appear, then the septal opening itself has closed.

If the noise occurs at a later stage, surgical intervention is possible. In 5% of newborn babies who have birth defect heart muscle, by the age of one year the defect (hole) between the heart ventricles heals on its own.

Large size defect of the opening of the septum between the ventricles of the heart with a symptomatic course of the disease, and with manifestations of cardiac failure. With this degree of disease, it is easy to diagnose using echocardiography.

When diagnosing a VSD, possible concomitant pathologies are identified, and the doctor prescribes drug therapy.

Conservative treatment methods in most cases give positive results. If this treatment ineffective, then using surgical intervention the defect is corrected.

Complicated form

A complicated form of VSD is changes in the heart organ without proper professional treatment.

Complicated heart disease is manifested by the following diseases:

• Muscle tissue hypotrophy is a tissue disorder that leads to loss of body weight. In a child with this pathology, the physical development and performance of organs and all body systems decreases. Heart defects are the main cause of the disease malnutrition. In severe malnutrition, the child develops muscle tissue dystrophy. Treatment of malnutrition has a clear target direction - to restore balance nutrients in the child’s body, in accordance with his age. A sick child is treated with drugs that increase appetite and hormonal therapy;
• Eisenmenger syndrome is a disease of pulmonary hypertension, which has an irreversible process. When developed together with VSD, it gives rise to severe cardiac pathology. Symptoms include: pain in the area chest, loss of consciousness and fainting, cough. Treatment method: surgery;
• Bacterial endocarditis- inflammation in the inner lining of the heart organ caused by staphylococcal infection. The disease manifests itself as intoxication, fever, difficulty breathing, and skin rash, asthenia. Treatment of this disease- this is taking antibacterial drugs, thrombolytic agents, immunostimulants;
• Aortic insufficiency- a pathology of a congenital or acquired nature, which manifests itself in incomplete closure of the aortic valve. Treatment for this pathology is valve replacement;
• Aortic aneurysm;
• Pneumonia, which tends to recur constantly;
• Atrial fibrillation;
• Cardiac failure;
• Embolism of the coronary arteries;
• Pulmonary embolism;
• Myocardial infarction;
• Lung abscess;
• Ischemic stroke;
• Heart block;
• Death.

Diagnostics

Diagnostic testing of the disease - includes examination of the patient and instrumental methods examinations. Using the auscultation method, the cardiologist detects heart murmurs and determines their tone.

Based on heart murmurs, a preliminary diagnosis can be made - VSD.

In order to make an accurate diagnosis and correctly draw up a treatment regimen, you need to undergo an instrumental study:

• Echocardiography (ultrasound)- a method for detecting the source of the defect, its size, as well as the direction of pressure in the bloodstream. The heart chambers and blood flow are examined;
• Electrocardiography— determines the consequences of the defect: ventricular hypertrophy, arrhythmia, as well as pathology in the sinus node;
• Phonocardiography is a technique for determining heart murmurs and their tonality. Even noises that are not detected by auscultation are detected;
• Dopplerography— primary diagnostic technique. Evaluates the blood flow indicator, the functioning of the valves that operate in the pathology of VSD;
• X-ray- with VSD, the size of the cardiac organ is increased, so the X-ray shadow will reveal the exact size of the increase;
• Angiocardiography is a complex study for VSD, which consists of injecting a special substance into the heart. This technique determines the exact size of the defect;
• Pulse oximetry- determination of oxyhemoglobin in the body, its amount in blood plasma;
• Tomography (magnetic resonance)- this is a technique that more accurately determines all the parameters of the cardiac organ, as well as a septal defect in VSD, and deviations that are caused by a heart defect;
• Catheterization of the cardiac organ- this method of diagnosing the heart muscle from the inside allows you to see the exact location of the defect and its size.

Therapeutic measures for VSD

If small child the hole has not closed until 12 calendar months of life, but does not increase, then it is carried out drug treatment. Such little patient under the supervision of a doctor until the age of three.

Small areas of the defect heal on their own, and there is no need to take medications. If the defect remains the same, then you need to take medications.

Drug therapy does not lead to a reduction in the focus of the defect, but prevents the transition of VSD to a complicated form.

Prescribed groups of drugs:

• Cardiac glycosides- able to increase the functionality of the myocardium and regulate the heart rhythm - the drug Digoxin, Korglykon;
• Diuretics- reduce blood pressure index ( blood pressure), and also remove excess fluid from the body - Indapamide, Furosemide;
• Group of cardioprotectors- improves myocardial nutrition, increases its work - medication Riboxin, Panangin;
• Anticoagulants- do not allow blood clots to form - the drug Phenilin;
• Beta blockers- normalize proper contraction of the heart muscle - the drug Bisoprol;
• ACE inhibitors- Captopril.

Cardiac surgery

Indications for surgical intervention in the cardiac organ:

• Congenital myocardial defects that accompany VSD;
• There is no positive dynamics in drug treatment;
• Heart failure with relapses;
• Pneumonia is constantly recurring;
• Down syndrome;
• The volume of the skull increases;
• Pulmonary hypertension;
• Large size DMZHB.

The following techniques have shown good results in the treatment of VSD in cardiac surgery:

• Plastic surgery to correct a congenital defect - a patch is applied to the hole and sewn on (large holes), small holes are simply sewn together. This technique refers to open heart surgery;
• Correction of the endovascular method - this technique is not an open operation on the organ, so it is less traumatic. Through a vein incision in the thigh, a mesh is installed using a catheter to close the lumen;
• Palliative technique is used in pediatrics from the first days of a baby’s life. Cardiac surgeons narrow the lumen in the pulmonary artery, and in this way reduce the pressure in the artery. This is an intermediate operation that can give the child a chance for normal development.

Disability with congenital heart disease

Children get disability due to congenital heart disease after surgical intervention on the heart, as well as with the defect Tetralogy of Fallot, and with other complex defects.

Disability for children is established within the following periods: 6 calendar months, one and a half years, 5 years and up to 16 years of age.

After 16 years, the child passes medical commission and receives disability according to adult criteria.

Preventive actions

A woman should begin preventive measures to prevent VSD pathology before conceiving a child. Before planning a pregnancy, it is worth getting your body vaccinated and performing laboratory tests.

During the period of bearing a child, especially in the first trimester of intrauterine development of the fetus, a woman must avoid hypothermia, viruses (chickenpox, measles, rubella) and infections that can negatively affect the intrauterine development of the heart organ and vascular system.

Self-medication during pregnancy is contraindicated. During this period, any medications that are not prescribed by a doctor can cause a number of pathologies in the unborn child.

Prognosis of VSD

In most cases, the life prognosis for this disease is favorable. Up to 65% of defects heal in the first year of life; the main thing is to make a timely diagnosis and take measures to eliminate the pathology.

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

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

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

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

Schematic representation of a ventricular septal defect.

Causes of VSD

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

The mechanism of development of hemodynamic disturbances (blood movement)

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

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

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

Symptoms of VSD

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

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

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

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

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

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

Complications of VSD:

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

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

Infectious (bacterial) endocarditis– damage to the endocardium (the inner lining of the heart) and heart valves caused by infection (most often bacterial). In patients with a VSD, the risk of developing infective endocarditis is approximately 0.2% per year. It usually occurs in older children and adults; more often with small VSDs, which is caused by endocardial injury due to the high speed of the pathological discharge of blood. Endocarditis can be provoked 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 spreads to the aortic and tricuspid valves.

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

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

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

Heart failure.

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

Instrumental diagnosis of VSD

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

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

3. Echocardiography (ultrasonography 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 indirect signs this defect (increase in the size of the ventricles of the heart and left atrium, increase in the thickness of the wall of the right ventricle and others). Doppler echocardiography allows us to identify another direct sign of the defect - pathological blood flow through the VSD into systole. In addition, it is possible to assess blood pressure in the pulmonary artery, the magnitude and direction of pathological blood discharge.

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

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

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

Treatment of VSD

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

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

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

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

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

Prognosis for VSD

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

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

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

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

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

Surgeon M.E. Kletkin

A ventricular septal defect (VSD) is a hole located in the wall that serves to separate the cavities of the right and left ventricles.

General information

This condition results in abnormal mixing (shunting) of blood. In cardiological practice, such a defect is the most common congenital pathology hearts. Critical conditions with VSD develop with a frequency of twenty-one percent. IN equally Both male and female children are susceptible to this defect.

VSD in the fetus can be isolated (that is, the only existing anomaly in the body) or part of complex defects (atresia of the tricuspid valve, transposition of vessels, common arterial trunks, tetralogy of Fallot).

In some cases, the interventricular septum is completely absent; this defect is called a single ventricle of the heart.

VSD Clinic

Symptoms of a ventricular septal defect often appear in the first days or months after the baby is born.

The most common manifestations of the defect include:

• shortness of breath;
• cyanosis of the skin (especially fingertips and lips);
• decreased appetite;
• cardiopalmus;
• fatigue;
• swelling in the abdomen, feet and legs.

VSD at birth may be asymptomatic if the defect is small enough, and appear only in more advanced stages. late dates(six years or more). Symptoms directly depend on the size of the defect (hole), however, the doctor should be alert to noises heard during auscultation.

VSD in the fetus: causes

Any congenital heart defects appear due to disturbances in the development of the organ in the early stages of embryogenesis. Important role at the same time, it belongs to external environmental and genetic factors.

With VSD in the fetus, an opening is determined between the left and right ventricles. Muscle layer The left ventricle is more developed than the right, and therefore oxygen-rich blood from the cavity penetrates into the right and mixes with oxygen-depleted blood. As a result, less oxygen reaches organs and tissues, which ultimately leads to chronic oxygen starvation of the body (hypoxia). In turn, the presence of additional blood volume in the right ventricle entails its dilatation (expansion), myocardial hypertrophy and, as a consequence, the occurrence of cardiac right ventricular failure and pulmonary hypertension.

Risk factors

The exact causes of VSD in the fetus are unknown, but an important factor is family history (that is, the presence of a similar defect in close relatives).

In addition, factors that are present during pregnancy also play a huge role:

Classification

There are several options for the location of the VSD:

• Conoventricular, membranous, perimembranous VSD in the fetus. It is the most common location of the defect and accounts for approximately eighty percent of all such defects. A defect is detected on the membranous part of the septum between the ventricles with probable spread to the outlet, septal and inlet sections; under the aortic valve and the tricuspid valve (its septal leaflet). Quite often, aneurysms occur in the membranous part of the septum, which subsequently leads to closure (complete or partial) of the defect.
• Trabecular, muscular VSD in the fetus. Found in 15-20% of all similar cases. The defect is completely surrounded by muscles and can be located in any part of the muscular part of the septum between the ventricles. Several such pathological holes can be observed. Most often, such VSDs in the fetus close spontaneously spontaneously.
• Subpulmonary, subarterial, infundibular, and crestal openings of the outflow tract account for approximately 5% of all such cases. The defect is localized under the outlet or cone-shaped sections of the septum. Quite often, this VSD due to prolapse of the right leaflet is combined with aortic insufficiency;
• Defects in the area of ​​the afferent tract. The hole is located in the area of ​​the inlet septum, directly under the area of ​​attachment of the ventricular-atrial valves. Most often, the pathology accompanies Down syndrome.

Most often single defects are found, but multiple defects in the septum are also found. VSD can be involved in combined cardiac defects, such as tetralogy of Fallot, transposition of the vessels and others.

According to size, the following defects are distinguished:

• small (symptoms are not expressed);
• average (the clinic appears in the first months after childbirth);
• large (usually decompensated, with vivid symptoms, severe course and complications that can lead to death).

Complications of VSD

If the size of the defect is small, clinical manifestations may not occur at all, or the holes may spontaneously close immediately after birth.

For larger defects, the following serious complications may occur:

• Characterized by the development of irreversible changes in the lungs as a result of pulmonary hypertension. This complication can develop in both young and older children. In this condition, part of the blood moves from the right to the left ventricle through a hole in the septum, because due to hypertrophy of the myocardium of the right ventricle, it turns out to be “stronger” than the left. Therefore, blood depleted of oxygen reaches the organs and tissues, and, as a result, develops chronic hypoxia, manifested by a bluish tint (cyanosis) of the nail phalanges, lips and skin generally.
• Heart failure.
• Endocarditis.
• Stroke. It can develop with large septal defects due to turbulent blood flow. Blood clots may form, which can subsequently clog the blood vessels of the brain.
• Other heart pathologies. Arrhythmias and valve pathologies may occur.

VSD in the fetus: what to do?

Most often, such heart defects are detected during a second routine ultrasound. However, there is no need to panic.

• You need to lead a normal life and not be nervous.
• The attending physician should carefully monitor the pregnant woman.
• If the defect is detected during the second planned ultrasound, the doctor will recommend waiting for the third examination (at 30-34 weeks).
• If a defect is detected on the third ultrasound, another examination is prescribed before birth.
• Small (for example, VSD 1 mm in the fetus) openings can close spontaneously before or after birth.
• Consultation with a neonatologist and fetal ECHO may be required.

Diagnostics

The presence of a defect can be suspected by auscultation of the heart and examination of the child. However, in most cases, parents learn about the presence of such a defect even before the baby is born, during routine ultrasound examinations. Quite large defects (for example, a 4 mm VSD in a fetus) are usually detected in the second or third trimester. Small ones can be detected after birth by chance or when clinical symptoms appear.

A diagnosis of VSD in a newborn or older child or adult can be made based on:

• Patient's complaints. This pathology is accompanied by shortness of breath, weakness, heart pain, and pale skin.
• History of the disease (time of appearance of the first symptoms and their relationship with stress).
• Life history (complicated heredity, maternal illnesses during pregnancy, and so on).
• General examination (weight, height, age-appropriate development, skin tone, etc.).
• Auscultation (murmurs) and percussion (expansion of the boundaries of the heart).
• Blood and urine examination.
• ECG data (signs of ventricular hypertrophy, conduction and rhythm disturbances).
• X-ray examination (changed shape of the heart).
• Vetriculography and angiography.
• EchoCG (i.e. ultrasound of the heart). This study allows you to determine the localization and size of the defect, and with Doppler measurements (which can be carried out even in the prenatal period) - the volume and direction of blood through the hole (even if the congenital heart disease - VSD in the fetus is 2 mm in diameter).
• Catheterization of the cardiac cavities. That is, inserting a catheter and using it to determine the pressure in the vessels and cavities of the heart. According to the data, a decision is made on further tactics of patient management.
• MRI. Prescribed in cases where it is uninformative.

Treatment

When a VSD is detected in the fetus, a wait-and-see approach is followed, since the defect can spontaneously close before birth or immediately after birth. Subsequently, if the diagnosis is maintained, such a patient is managed by cardiologists.

If the defect does not interfere with blood circulation and general condition the patient is simply observed. In case of large holes that interfere with the quality of life, a decision is made to perform surgery.

Surgical interventions for VSD can be of two types: palliative (restriction of pulmonary blood flow in the presence of combined defects) and radical (complete closure of the opening).

Operation methods:

• On open heart(for example, with tetralogy of Fallot).
• Cardiac catheterization with controlled application of a patch to the defect.

Prevention of ventricular septal defect

Specific preventive measures The fetus does not have a VSD, however, in order to prevent congenital heart disease, it is necessary:

Forecast

For small VSDs in the fetus (2 mm or less), the prognosis is favorable, since such openings often close spontaneously. In the presence of large defects, the prognosis depends on their location and the presence of a combination with other defects.

A ventricular septal defect is a congenital or acquired heart defect consisting of incomplete separation of the cavities of the right and left ventricles. As a result, part of the blood from one ventricle (usually from the left, as it is stronger) enters the other and disrupts the normal functioning of the heart and blood circulation in the body.

Ventricular septal defect most often occurs in utero, in in rare cases Such pathology is formed during life. This defect can be considered in two ways:

1. Isolated, arising as independent problem, congenital or acquired origin,

2. How component some other combined defects.

During life, this defect can occur as a result of myocardial infarctionlocalized in the area of ​​the septum.

Ventricular septal defect occurs in approximately 20-25% of cases of all congenital heart defects, in one out of a thousand newborns. With the development of technologies for caring for premature newborns and seriously ill children, the frequency of defects in last years increases.

Causes

Heart defects, including ventricular septal defects, occur in the earliest stages of heart development from 3-4 to 8-10 weeks of intrauterine life.

The main causes of violations are considered to be external and internal unfavorable factors. Several key points stand out:

• genetic predisposition, especially in families with existing heart defects or diseases
• viral infections transferred to early dates pregnancy, especially dangerous are rubella, measles, influenza and herpes
• drinking alcohol, smoking
• taking medications with embryotoxic effects (antibiotics, anti-epileptic drugs, some sedatives)
• Availability diabetes mellitus with sharp fluctuations in blood glucose
• work in hazardous industries (gas stations, paint and varnish plants, chemical plants)
• stress factors

Kinds

Depending on the size of the defect in the interventricular septum, we can distinguish:

• small defect or Tolochinov-Roger disease (hole size from 1-2 mm to 1 cm),
• a large defect measuring more than half the size of the aortic orifice or more than 1 cm.

Based on the location of the hole in the septum, three types of defect are distinguished:

• membranous. The defect is located in the area upper segment interventricular septum, under the aortic valve. Usually small in size and can close spontaneously as the child grows.
• muscular. The defect is located in the muscular part of the septum, far enough from the valves and conduction system of the heart. Can close independently in small sizes.
• supra-ridge. Located in the area of ​​​​the border of the efferent vessels of the right and left ventricles, it usually does not close on its own.

What happens when there is vice

In the cavity of the right ventricle, the blood pressure during contraction is several times lower than in the left.

If there is a defect in the interventricular septum, blood moves from the left ventricle to the right during contraction. As a result, the pressure in it increases, and it is transmitted to the vessels of the pulmonary (pulmonary) circulation. Blood rich in oxygen also enters there, and big circle At the same time, he does not receive enough blood.

Constant overload of the right ventricle leads to its failure and pulmonary hypertension. Gradually, the vessels of the pulmonary circulation are sclerosed (replaced by inextensible and impermeable to gases connective tissue) and occur irreversible changes in the lungs.

Symptoms of ventricular septal defect

The first manifestations of the defect can develop already in the first days or weeks of life. Especially with a large defect and pronounced discharge of blood into the right ventricle.

Manifest:

• cyanosis (blue discoloration) of the skin, limbs and face, aggravated by crying,
• loss of appetite, sluggish sucking with frequent interruptions,
• violation of weight gain, slow rate of development,
• the occurrence of shortness of breath,
• fatigue, such children sleep a lot,
• the formation of edema in the legs, feet and abdomen,
• tachycardia.

Sometimes, with small defects in the septum, signs may not appear externally, however, they are detected when listening to the heart in the form of rough murmurs.

Diagnostics

A defect can be suspected by examining the child and listening to the heart. But usually parents learn about heart defects in advance, even before the birth of the child, during screening ultrasounds during pregnancy. Big sizes The defect can be detected on ultrasound in the second or third trimester.

If a heart murmur is detected after birth, a course of examinations is prescribed:

• Ultrasound of the heart with Dopplerometry (study of blood flow),
• X-ray of the chest to determine the size of the heart and possible defects,
• Puloximetry - measurement of oxygen concentration in capillary blood.
• cardiac catheterization with contrast X-ray examination, measurement of pressure in the chambers of the heart,
• MRI of the heart to determine the structure of the heart and the size of the defect, the presence of complications.

Treatment of ventricular septal defects

Cardiologists and cardiac surgeons are involved in the diagnosis and treatment of defects.

For minor defects in the septum, a wait-and-see approach can be chosen - often the defects close on their own. If the hole does not interfere with life, health and does not interfere with blood circulation, it is actively monitored without performing surgery.

If the defect is large, the normal functioning of the heart and blood circulation are disrupted, it is necessary to decide on heart surgery.

In preparation for surgery, medications can be used that help regulate heart rhythm, stabilize blood pressure, maintain myocardial nutrition, and regulate blood clotting.

Surgery for significant ventricular septal defects is performed when the child is able to adequately tolerate anesthesia and can recover quickly.

There are several methods, these include:

• cardiac catheterization with the introduction of a catheter through the femoral vein to the cavities of the heart and the application of a patch to the defect area under the control of ultrasound and other devices. Helps well with small and muscle defects.
• open heart surgery. It is used for a combined defect (tetralogy of Fallot) or for a significant, low-lying defect that cannot be covered with one patch. During this operation, the child is connected to a heart-lung machine.

Today, through cardiac surgery, it is possible to save the lives of those children who were previously doomed to suffering and death at an early age. After the operation, children begin to develop as normal and continue to live a normal life.

Complications and prognosis

With small defects in the heart of 1-2 mm, children can grow as usual and not show any symptoms; with more significant defects, signs of the defect may be observed, which without treatment can turn into complications.

The main ones include Eisenmenger syndrome - irreversible consequences of pulmonary hypertension with vascular sclerosis and the death of a child from heart and respiratory failure

Other serious complications include:

• formation of heart failure,
• development of inflammation of the inner lining of the heart - endocarditis,
• strokes, due to an increase in blood pressure in the pulmonary circulation and the formation of uneven blood flow with thrombus formation,
• disorders of the valvular apparatus and the formation of valvular heart defects.

Ventricular septal defect is the most common congenital heart defect. Ventricular septal defects occur with equal frequency in both sexes. In most cases they are diagnosed in infancy due to a rough heart murmur. In 25-40%, spontaneous closure of the ventricular septal defect occurs, of which 90% occur before the age of 8 years. The degree of functional impairment depends on the magnitude of shunt and pulmonary vascular resistance. If there is a left to right shunt, but the ratio of pulmonary to systemic blood flow (QP/QS)< 1,5:1, то легочный кровоток возрастает незначительно и повышения легочного сосудистого сопротивления не происходит. При больших дефектах межжелудочковой перегородки (QP/QS >2:1) pulmonary blood flow and pulmonary vascular resistance significantly increase; pressures in the right and left ventricles are equalized. As pulmonary vascular resistance increases, a change in the direction of discharge (from right to left) is possible, which is manifested by cyanosis, a symptom of drumsticks; the risk of paradoxical embolism increases. In the absence of treatment, right and left ventricular failure and irreversible changes in the pulmonary vessels (Eisenmenger syndrome) develop.

A. Types

1. Membranous(75%): located in the upper part of the interventricular septum immediately below the aortic valve and the septal leaflet of the tricuspid valve. They often close spontaneously.

2. Muscular(10%): located in the muscular part of the septum, at a considerable distance from the valves and conduction system. Muscular ventricular septal defects are multiple, fenestrated, and often close spontaneously.

3. Supracrestal(ventricular septal defects of the right ventricular outflow tract, 5%): located above the supraventricular crest (a muscle bundle that separates the cavity of the right ventricle from its outflow tract). Often accompanied by aortic insufficiency. They do not close spontaneously.

4. AV channel(defect AV septum, defect of the interventricular septum of the afferent tract of the right ventricle, 10%): found in the posterior part of the interventricular septum near the site of attachment of the mitral and tricuspid valves. Often found in Down syndrome. A ventricular septal defect is combined with an atrial septal defect of the ostium primum type and malformations of the cusps and chords of the mitral and tricuspid valves. Doesn't close spontaneously.

B. Clinical picture.The first manifestation is usually a rough heart murmur. Small ventricular septal defects are often asymptomatic and may go unrecognized. With large ventricular septal defects, delays in physical development and frequent respiratory infections are often observed. In those rare cases when a patient with a large ventricular septal defect survives into adolescence and adulthood, there are symptoms of right and left ventricular failure (shortness of breath, swelling of the legs, orthopnea). Eisenmenger syndrome (irreversible pulmonary hypertension due to left-to-right shunting) may present with dizziness, syncope, hemoptysis, brain abscesses, and chest pain.

IN. Course and prognosis in the absence of treatment

1. Small ventricular septal defects:life expectancy does not change significantly, but the risk of infective endocarditis increases.

2. Medium-sized ventricular septal defects:heart failure usually develops in childhood; with spontaneous closure or reduction in size, improvement occurs. Severe pulmonary hypertension is rare.

3. Large ventricular septal defects(without a pressure gradient between the ventricles, or non-restrictive): in most cases diagnosed at an early age, in 10% they lead to Eisenmenger syndrome; Most patients die in childhood or adolescence. Maternal mortality during pregnancy and childbirth with Eisenmenger syndrome exceeds 50%; in 3.3% of cases, direct relatives of patients with ventricular septal defects also have this defect.

G. Physical examination

1. Appearance.In heart failure, weakness and cachexia are observed; depressions are often found in the lower part of the anterior chest wall, the so-called Harrison's furrows (displacement of areas of the chest as a result of chronic shortness of breath). When dumping from right to left, there is cyanosis and a symptom of drumsticks.

2. Pulse.With small defects of the interventricular septum, the pulse in the peripheral arteries is normal, the pulsation of the jugular veins is also not changed. In pulmonary hypertension, distension of the jugular veins, high-amplitude A waves (atrial contraction with a rigid right ventricle) and, sometimes, wave V (tricuspid regurgitation) on the jugular venogram are observed.

3. Palpation.Strengthened apical impulse. Trembling at the left lower edge of the sternum.

4. Auscultation.Rough pansystolic murmur at the left lower sternal border. Pathological splitting of the second tone as a result of prolongation of the ejection period of the right ventricle. With supracrestal defects of the interventricular septum there is a diastolic murmur of aortic insufficiency.

D. Non-invasive studies

1. ECG.With a large discharge from left to right: overload of the left atrium and left ventricle, deviation of the electrical axis to the left. With pulmonary hypertension: overload of the right ventricle, deviation of the electrical axis to the right.

2. Chest X-ray.For small defects of the interventricular septum: normal. With a large left-to-right shunt: enlarged left ventricle, increased pulmonary vascular pattern due to increased pulmonary blood flow. With pulmonary hypertension: marked enlargement of the trunk and proximal parts of the pulmonary artery with a sharp narrowing of the distal branches, depletion of the pulmonary vascular pattern.

3. EchoCG.Two-dimensional echocardiography is performed for the purpose of direct visualization of the ventricular septal defect, identifying pathology of the mitral and aortic valves, enlarged heart chambers, concomitant congenital defects. Using a Doppler study (including color), the magnitude and direction of the discharge are assessed, and the pressure in the pulmonary artery is calculated.

E. Invasive research.Cardiac catheterization and coronary angiography are performed to confirm the diagnosis, measure pulmonary artery pressure and rule out coronary artery disease (if appropriate and before surgery). The amount of shunt can be assessed qualitatively using left ventriculography and quantitatively by oxygen saturation in the right ventricle (in contrast to atrial septal defects, instead of oxygen saturation of mixed venous blood, the average saturation value in the right atrium is used).

AND. Treatment

1. Medication.At asymptomatic and normal pressure in the pulmonary artery (even with large ventricular septal defects), conservative treatment is possible. If spontaneous closure does not occur by 3-5 years of age, surgical correction is indicated. For congestion in the lungs, use hydralazine (or sodium nitroprusside for emergency therapy), which reduces peripheral vascular resistance to a greater extent than pulmonary vascular resistance, which leads to a decrease in left-to-right shunt and improvement of the condition. For right ventricular failure, diuretics are prescribed. Before and within 6 months after uncomplicated surgical correction ventricular septal defect, prevention of infective endocarditis is indicated. Heart failure and pulmonary hypertension in young children.

V. In adults - QP/QS > 1.5:1.Surgical treatment is ineffective for severe pulmonary hypertension, when the ratio of pulmonary vascular resistance to total peripheral vascular resistance is 0.9.