Aortic valve insufficiency: types of disease and treatment regimens. Aortic insufficiency Diagnosis and differential diagnosis

Any heart defect is associated with valve abnormalities. Aortic valve defects are especially dangerous, since the aorta is the largest and most important artery in the body. And when the operation of the apparatus that supplies oxygen to all parts of the body and the brain is disrupted, the person is practically incapacitated.

The aortic valve is sometimes formed in utero with defects. And sometimes heart defects are acquired with age. But whatever the reason for the dysfunction of this valve, medicine has already found a treatment in such cases - aortic valve replacement.

Anatomy of the left side of the heart. Functions of the aortic valve

The four-chambered structure of the heart must work in perfect harmony to perform its primary function of providing the body with nutrients and air carried by the blood. Our main organ consists of two atria and two ventricles.

The right and left parts are separated by the interventricular septum. There are also 4 valves in the heart that regulate blood flow. They open in one direction and close tightly to allow blood to flow in only one direction.

The heart muscle has three layers: endocardium, myocardium (thick muscle layer) and endocardium (outer layer). What happens in the heart? The depleted blood, which has given up all its oxygen, returns to the right ventricle. Arterial blood passes through the left ventricle. We will consider in detail only the left ventricle and the work of its main valve, the aortic.

The left ventricle is cone-shaped. It is thinner and narrower than the right one. The ventricle is connected to the left atrium through the atrioventricular orifice. The mitral valve leaflets are attached directly to the edges of the hole. The mitral valve is bicuspid.

The aortic valve (valve aortae) consists of 3 leaflets. The three valves are called: right, left and posterior semilunar (valvulae semilunares dextra, sinistra, posterior). The leaflets are formed by a well-developed duplication of the endocardium.

The atrium muscles are isolated from the ventricular muscles by a plate of right and left fibrous rings. The left fibrous ring (anulus fibrosus sinister) surrounds the atrioventricular foramen, but not completely. The anterior sections of the ring are attached to the aortic root.

How does the left side of the heart work? Blood enters, the mitral valve closes, and an impulse occurs - contraction. Contraction of the heart walls pushes blood through the aortic valve into the widest artery, the aorta.

With each contraction of the ventricle, the valves are pressed against the walls of the vessel, allowing a free flow of oxygenated blood. When the left ventricle relaxes for a split second to allow the cavity to fill with blood again, the aortic valve of the heart closes. This is one cardiac cycle.

Congenital and acquired aortic valve defects

If problems arise with the aortic valve during the baby’s intrauterine development, it is difficult to notice. Usually the defect is noticed after birth, since the baby’s blood bypasses the valve, directly into the aorta through the open ductus arteriosus. Deviations in heart development can be noticed only through echocardiography, and only from 6 months.

The most common valve abnormality is the development of 2 leaflets instead of 3. This heart defect is called a bicuspid aortic valve. The anomaly is not in any danger to the child. But 2 sashes wear out faster. And by adulthood, maintenance therapy or surgery is sometimes needed. Less commonly, a defect such as a single-leaf valve occurs. Then the valve wears out even faster.

Another anomaly is congenital aortic valve stenosis. The semilunar valves either fuse together, or the valvular fibrous ring itself, to which they are attached, is excessively narrow. Then the pressure between the aorta and the ventricle differs. Over time, the stenosis intensifies. And interruptions in the work of the heart prevent the child from fully developing; it is difficult for him to exercise even in the school gym. Severe disruption of blood flow through the aorta may at some point lead to sudden death of the child.

Acquired defects are a consequence of smoking, excessive eating, sedentary and stressful lifestyle. Since everything in the body is connected, after 45-50 years all minor ailments usually develop into diseases. The aortic valve of the heart gradually wears out in old age, as it works constantly. Exploitation of your body's resources and lack of sleep wear out these important parts of the heart faster.

Aortic stenosis

What is stenosis in medicine? Stenosis means narrowing of the lumen of a vessel. Aortic stenosis is a narrowing of the valve that separates the left ventricle of the heart from the aorta. There are minor, moderate and severe. This defect can affect the mitral and aortic valves.

With a minor valve defect, a person does not feel any pain or other warning symptoms, because the increased work of the left ventricle will be able to compensate for the poor functioning of the valve for some time. Then, when the compensatory capabilities of the left ventricle are gradually exhausted, weakness and poor health begin.

The aorta is the main blood vessel. If the valve is malfunctioning, all vital organs will suffer from lack of blood supply.

The causes of heart valve stenosis are:

  1. Congenital valve defect: fibrous membrane, bicuspid valve, narrow ring.
  2. A scar formed by the connective tissue just below the valve.
  3. Infectious endocarditis. Bacteria that enter the heart tissue change the tissue. Due to the colony of bacteria, connective tissue grows on the tissue and on the valves.
  4. Deforming osteitis.
  5. Autoimmune problems: rheumatoid arthritis, lupus erythematosus. Due to these diseases, connective tissue grows in the place where the valve is attached. Growths form on which more calcium is deposited. Calcification occurs, which we will remember later.
  6. Atherosclerosis.

Unfortunately, in most cases, aortic stenosis is fatal if valve replacement is not performed in time.

Stages and symptoms of stenosis

Doctors distinguish 4 stages of stenosis. At first, there is practically no pain or discomfort. Each stage has a corresponding set of symptoms. And the more serious the stage of development of stenosis, the sooner surgery is needed.

  • The first stage is called the compensation stage. The heart is still coping with the load. A deviation is considered minor when the valve lumen is 1.2 cm 2 or more. And the pressure is 10-35 mm. rt. Art. There are no symptoms at this stage of the disease.
  • Subcompensations. The first symptoms appear immediately after exercise (shortness of breath, weakness, palpitations).
  • Decompensation. It is characterized by the fact that symptoms appear not only after exercise, but also in a calm state.
  • The last stage is called terminal. This is the stage when strong changes have already occurred in the anatomical structure of the heart.

Symptoms of severe stenosis are:

  • pulmonary edema;
  • dyspnea;
  • sometimes attacks of suffocation, especially at night;
  • pleurisy;
  • cardiac cough;
  • pain in the chest area.

Upon examination, the cardiologist usually detects moist rales in the lungs during listening. Pulse is weak. Noises are heard in the heart, vibration created by the turbulence of blood flows is felt.

Stenosis becomes critical when the lumen is only 0.7 cm2. The pressure is more than 80 mm. rt. Art. At this time, the risk of death is high. And even an operation to eliminate the defect is unlikely to change the situation. Therefore, it is better to consult a doctor during the subcompensatory period.

Development of calcification

This defect develops due to a degenerative process in the tissue of the aortic valve. Calcification can lead to severe heart failure, stroke, and general atherosclerosis. Gradually, the aortic valve leaflets become covered with calcareous growth. And the valve calcifies. That is, the valve flaps no longer close completely, but also open weakly. When a bicuspid aortic valve is formed at birth, calcification quickly renders it inoperable.

And also calcinosis develops as a consequence of disruption of the endocrine system. Calcium salts, when they do not dissolve in the blood, accumulate on the walls of blood vessels and on the heart valves. Or a kidney problem. Polycystic kidney disease or nephritis also leads to calcification.

The main symptoms will be:

  • aortic insufficiency;
  • dilatation of the left ventricle (hypertrophy);
  • interruptions in heart function.

A person must monitor his health. Chest pain and increasingly frequent periodic attacks of angina should be a signal to undergo a cardiac examination. Without surgery for calcinosis, in most cases a person dies within 5-6 years.

Aortic regurgitation

During diastole, blood from the left ventricle flows into the aorta under pressure. This is how the large circle of blood circulation begins. But with regurgitation, the valve “releases” blood back into the ventricle.

Valve regurgitation, or aortic valve regurgitation, in other words, has the same stages as valve stenosis. The reasons for this condition of the valves are either an aneurysm, or syphilis, or the mentioned acute rheumatism.

Symptoms of deficiency are:

  • low pressure;
  • dizziness;
  • frequent fainting;
  • swelling of the legs;
  • slow heart rate.

Severe failure leads to angina and ventricular enlargement, as with stenosis. And such a patient also needs valve replacement surgery in the near future.

Valve seal

Stenosis can form due to the fact that endogenous factors cause the appearance of various growths on the valve leaflets. The aortic valve becomes compacted, and problems begin in its operation. The causes of hardening of the aortic valve can be many untreated diseases. For example:

  • Autoimmune diseases.
  • Infectious lesions (brucellosis, tuberculosis, sepsis).
  • Hypertension. Due to prolonged hypertension, tissues become thicker and coarser. Therefore, over time, the lumen narrows.
  • Atherosclerosis is the clogging of tissues with lipid plaques.

Tissue compaction is also a common sign of aging. The consequence of compaction will inevitably be stenosis and regurgitation.

Diagnostics

Initially, the patient must provide all the necessary information to make a diagnosis to the doctor in the form of an accurate description of the ailments. Based on the patient's medical history, the cardiologist prescribes diagnostic procedures to know additional medical information.

Must be assigned:

  • X-ray. The shadow of the left ventricle increases. This can be seen in the arc of the heart's contour. Signs of pulmonary hypertension are also visible.
  • ECG. The examination reveals ventricular enlargement and arrhythmia.
  • Echocardiography. On it, the doctor notices whether or not there is sealing of the valve flaps and thickening of the walls of the ventricle.
  • Probing cavities. The cardiologist must know the exact value: how much the pressure in the aortic cavity differs from the pressure on the other side of the valve.
  • Phonocardiography. Heart murmurs (systolic and diastolic murmurs) are recorded.
  • Ventriculography. Prescribed to detect mitral valve insufficiency.

With stenosis, an electrocardiogram shows disturbances in the rhythm and conduction of biocurrents. On the x-ray you can clearly see signs of darkening. This indicates congestion in the lungs. You can clearly see how dilated the aorta and left ventricle are. And coronary angiography shows that the amount of blood ejected from the aorta is less. This is also an indirect sign of stenosis. But angiography is only done for people over 35 years old.

The cardiologist also pays attention to symptoms that are visible even without instruments. Pale skin, Musset's sign, Müller's sign - such signs indicate that the patient most likely has aortic valve insufficiency. Moreover, the bicuspid aortic valve is more susceptible to insufficiency. The doctor must take into account congenital characteristics.

What other signs can suggest a diagnosis to a cardiologist? If, when measuring pressure, the doctor notices that the upper pressure is much higher than normal, and the lower (diastolic) is too low, this is a reason to refer the patient for echocardiography and an x-ray. Extra noise during diastole, heard through a stethoscope, also does not bode well. This is also a sign of deficiency.

Treatment with drugs

To treat deficiency at the initial stage, drugs of the following classes can be prescribed:

  • peripheral vasodilators, which include nitroglycerin and its analogues;
  • diuretics are prescribed only for certain indications;
  • calcium channel blockers, such as Diltiazem.

If the pressure is very low, nitroglycerin preparations are combined with Dopamine. But beta blockers are contraindicated in case of aortic valve insufficiency.

Aortic valve replacement

Surgeries to replace the aortic valve are now being carried out quite successfully. And with minimal risk.

During the operation, the heart is connected to a heart-lung machine. The patient is also given complete anesthesia. How can a surgeon perform this minimally invasive surgery? There are 2 ways:

  1. The catheter is inserted directly into the femoral vein and ascends towards the aorta against the flow of blood. The valve is secured and the tube is removed.
  2. The new valve is inserted through an incision in the left chest. An artificial valve is inserted, and it slides into place, passing through the apical part of the heart, and is easily removed from the body.

Minimally invasive surgery is suitable for those patients who have concomitant diseases, and the chest cannot be opened. And after such an operation, a person immediately feels relief, since the defects are eliminated. And if there are no complaints about your health, you can be discharged within a day.

It should be noted that artificial valves require constant use of anticoagulants. Mechanical ones can cause blood clotting. Therefore, after the operation, Warfarin is immediately prescribed. But there are also valves made from biological materials that are more suitable for humans. If a valve is installed from porcine pericardium, the drug is prescribed only for a few weeks after the operation, and then discontinued, as the tissue takes root well.

Aortic balloon valvuloplasty

Aortic balloon valvuloplasty is sometimes prescribed. This is a painless operation based on the latest developments. The doctor monitors all ongoing actions through special X-ray equipment. A catheter with a balloon is passed to the mouth of the aorta, then the balloon is installed in place of the valve and expanded. This eliminates the problem of valve stenosis.

Who is the operation indicated for? First of all, such an operation is performed on children with a congenital defect, when a single or bicuspid aortic valve is formed instead of a tricuspid one. It is indicated for pregnant women and people before another heart valve transplant.

After this operation, the recovery period is only 2 days to 2 weeks. Moreover, it is very easily tolerated and is suitable for people with poor health, and even for children.

Aortic insufficiency is a pathological change in the functioning of the heart, characterized by non-closure of the valve leaflets. This leads to reverse blood flow from the aorta to the left ventricle. Pathology has serious consequences.

If you do not get treatment on time, then everything becomes complicated. Organs do not receive the required amount of oxygen. This causes the heart to beat faster to make up for the shortfall. If you do not intervene, the patient is doomed. After a certain time, the heart enlarges, then swelling appears, and due to pressure surges inside the organ, the left atrium valve may fail. It is important to consult a therapist, cardiologist or rheumatologist in time.

Aortic insufficiency is divided into 3 degrees. They differ in the divergence of the valve flaps. At first glance, it looks simple. This:

  • Sinuses of Valsalva - they are located behind the aortic sinuses, just behind the valves, which are often called semilunar sinuses. The coronary arteries begin from this place.
  • The fibrous ring is highly durable and clearly separates the beginning of the aorta and the left atrium.
  • There are three semilunar valves; they continue the endocardial layer of the heart.

The doors are arranged in a circular line. When the valve closes in a healthy person, there is completely no gap between the valves. The degree and severity of aortic valve insufficiency depends on the size of the convergence gap.

First degree

The first degree is characterized by mild symptoms. The discrepancy between the valves is no more than 5 mm. It feels no different from the normal state.

Aortic valve insufficiency of the 1st degree manifests itself with mild symptoms. With regurgitation, the blood volume is no more than 15%. Compensation occurs due to increased impulses of the left ventricle.

Patients may not even notice pathological manifestations. When the disease is in the compensation stage, therapy may not be carried out; preventive actions are limited. Patients are prescribed observation by a cardiologist, as well as regular ultrasound checks.

Second degree

Aortic valve insufficiency, which belongs to the 2nd degree, has symptoms with a more pronounced manifestation, while the divergence of the valves is 5-10 mm. If this process occurs in a child, then the signs are subtle.

If, when aortic insufficiency occurs, the volume of blood returning is 15-30%, then the pathology is classified as a second-degree disease. Symptoms are not severe, but shortness of breath and rapid heartbeat may occur.

To compensate for the defect, the muscles and valve of the left atrium are used. In most cases, patients complain of shortness of breath with light exertion, increased fatigue, strong heartbeat and pain.

During examinations using modern equipment, increased heartbeat is detected, the apical impulse moves slightly downward, and the boundaries of cardiac dullness expand (to the left by 10-20 mm). When using X-ray examination, downward enlargement of the left atrium is visible.

Using auscultation, you can clearly hear murmurs along the sternum on the left side - these are signs of an aortic diastolic murmur. Also, with the second degree of insufficiency, systolic murmur appears. As for the pulse, it is increased and pronounced.

Third degree

The third degree of insufficiency, also called severe, has a discrepancy of more than 10 mm. Patients require serious treatment. More often, surgery is prescribed followed by drug therapy.

When the pathology is at stage 3, the aorta loses more than 50% of the blood. To compensate for the loss, the heart organ increases its rhythm.

Basically, patients often complain of:

  • shortness of breath at rest or with minimal exertion;
  • pain in the cardiac region;
  • increased fatigue;
  • constant weakness;
  • tachycardia.

Research reveals a strong increase in the size of the borders of cardiac dullness down and to the left. Displacement also occurs in the right direction. As for the apical impulse, it is intensified (spread out).

In patients with the third degree of insufficiency, the epigastric region pulsates. This indicates that the pathology involved the right chambers of the heart.

During the examination, a pronounced systolic, diastolic and Flint murmur appears. They can be heard in the area of ​​the second intercostal space on the right side. They have a distinct character.

It is important to seek medical help from therapists and cardiologists at the first, even minor, symptoms.

Symptoms, signs and causes

When aortic valve insufficiency begins to develop, symptoms do not appear immediately. This period is characterized by the absence of serious complaints. The load is compensated by the left ventricular valve - it is able to resist reverse flow for a long time, but then it stretches and becomes slightly deformed. Already at this time, pain, dizziness and rapid heartbeat occur.

The first symptoms of deficiency:

  • there is a certain sensation of pulsation of the neck veins;
  • strong tremors in the heart area;
  • increased frequency of contraction of the heart muscle (minimization of reverse blood flow);
  • pressing and squeezing pain in the chest area (with strong reverse blood flow);
  • the occurrence of dizziness, frequent loss of consciousness (occurs when there is poor oxygen supply to the brain);
  • the appearance of general weakness and decreased physical activity.

During a chronic disease, the following symptoms appear:

  • pain in the cardiac region even in a calm state, without stress;
  • during exercise, fatigue appears quite quickly;
  • constant ringing in the ears and a feeling of strong pulsation in the veins;
  • the occurrence of fainting during a sudden change in body position;
  • severe headache in the front area;
  • pulsation of arteries visible to the naked eye.

When the pathology is in a decompensatory degree, metabolism in the lungs is disrupted (often observed by the appearance of asthma).

Aortic insufficiency is accompanied by severe dizziness, fainting, as well as pain in the chest cavity or its upper parts, frequent shortness of breath and irregular heartbeat.

Causes of the disease:

  • congenital aortic valve defect.
  • complications after rheumatic fever.
  • endocarditis (the presence of bacterial infection of the inside of the heart).
  • changes with age - this is explained by wear and tear of the aortic valve.
  • an increase in the size of the aorta - a pathological process occurs with hypertension in the aorta.
  • hardening of the arteries (as a complication of atherosclerosis).
  • aortic dissection, when the inner layers of the main artery separate from the middle layers.
  • impaired functionality of the aortic valve after its replacement (prosthetics).


Less common reasons include:

  • aortic valve injuries;
  • autoimmune diseases;
  • consequences of syphilis;
  • ankylosing spondylitis;
  • manifestations of diffuse type diseases associated with connective tissues;
  • complications after the use of radiation therapy.

It is important to consult a doctor at the first manifestations.

Features of the disease in children

Many children do not notice problems for a long time and do not complain about illness. Most of the time they do well, but it doesn't last long. Many are still able to engage in sports training. But the first thing that torments them is shortness of breath and increased heart rate. If these symptoms occur, it is important to immediately contact a specialist.

At first, unpleasant sensations are noticed with moderate loads. In the future, aortic valve insufficiency occurs even in a calm state. Worried about shortness of breath, strong pulsation of the arteries located in the neck. Treatment must be of high quality and timely.

Symptoms of the disease may appear as murmurs in the area of ​​the largest artery. As for physical development, in children it does not change with insufficiency, but there is a noticeable pallor of the facial skin.

When examining the echocardiogram, aortic valve insufficiency is expressed as a moderate increase in the lumen at the mouth of the artery. There are also noises in the area of ​​the left side of the chest, which indicates the progress of the discrepancy between the lobes of the semilunar valves (more than 10 mm). Strong shocks are explained by the increased work of the left ventricle and atrium in compensation mode.

Diagnostic methods

To correctly assess changes in the functionality of the heart and its systems, you need to undergo high-quality diagnostics:

  1. Dopplerography;
  2. X-ray (effectively detects pathological changes in valves and heart tissue);
  3. echocardiography;
  4. phonocardiography (determines murmurs in the heart and aorta);

During the inspection, specialists pay attention to:

  • complexion (if it is pale, this means insufficient blood supply to small peripheral vessels);
  • rhythmic dilation of the pupils or their constriction;
  • state of the tongue. Pulsations change its shape (noticeable upon examination);
  • shaking of the head (involuntary), which occurs in rhythm with the heart (this is caused by strong shocks in the carotid arteries);
  • visible pulsation of the cervical vessels;
  • heart beats and their strength upon palpation.

The pulse is unstable, there are decreases and increases. By using auscultation of the heart organ and its vessels, murmurs and other signs can be identified more quickly and accurately.

Treatment

At the very beginning, aortic insufficiency may not require special treatment (first degree); only prevention methods are applicable. Later, therapeutic or cardiac treatment is prescribed. Patients must follow the recommendations of specialists regarding the way they organize their life activities.

It is important to limit physical activity, stop smoking or drinking alcohol, and be systematically examined with an ultrasound or ECG.

When treating the disease with medication, doctors prescribe:


If the disease is in the last stage, then only surgical intervention will help.

Cases when a patient needs urgent consultation with a surgeon:

  • when the state of health has sharply deteriorated, and the reverse ejection towards the left ventricle is 25%;
  • in case of disturbances in the functioning of the left ventricle;
  • when 50% of blood volume is returned;
  • a sharp increase in the size of the ventricle (more than 5-6 cm).

Today there are two types of operations:

  1. Surgical intervention associated with implantation. It is performed when the backflow of the aortic valve is more than 60% (it is worth noting that today biological prostheses are almost never used).
  2. Operation in the form of intra-aortic balloon counterpulsation. It is done when there is slight deformation of the valve leaflets (at 30% blood ejection).

Aortic insufficiency may not occur if preventive actions aimed against rheumatic, syphilis and atherosclerotic pathologies are taken in a timely manner.

It is surgical help that helps get rid of the problems in question. The timeliness and quality of taking measures can greatly increase the chance of a person returning to normal life.

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Incomplete closure of the aortic valve leaflets during diastole, leading to reverse flow of blood from the aorta into the left ventricle. Aortic insufficiency is accompanied by dizziness, fainting, chest pain, shortness of breath, frequent and irregular heartbeat. To diagnose aortic insufficiency, chest X-ray, aortography, echocardiography, ECG, MRI and CT of the heart, cardiac catheterization, etc. are performed. Treatment of chronic aortic insufficiency is carried out conservatively (diuretics, ACE inhibitors, calcium channel blockers, etc.); in severe symptomatic cases, plastic surgery or replacement of the aortic valve is indicated.

General information

Aortic insufficiency (aortic valve insufficiency) is a valve defect in which during diastole the semilunar cusps of the aortic valve do not close completely, resulting in diastolic regurgitation of blood from the aorta back into the left ventricle. Among all heart defects, isolated aortic insufficiency accounts for about 4% of cases in cardiology; in 10% of cases, aortic valve insufficiency is combined with other valvular lesions. In the vast majority of patients (55-60%), a combination of aortic valve insufficiency and aortic stenosis is detected. Aortic insufficiency is 3-5 times more common in males.

Causes of aortic insufficiency

Aortic insufficiency is a polyetiological defect, the origin of which may be due to a number of congenital or acquired factors.

Congenital aortic regurgitation develops when there is a one-, two-, or four-leaf aortic valve instead of a tricuspid one. The causes of a defect in the aortic valve can be hereditary diseases of the connective tissue: congenital pathology of the aortic wall - aortoannular ectasia, Marfan syndrome, Ehlers-Danlos syndrome, cystic fibrosis, congenital osteoporosis, Erdheim's disease, etc. In this case, incomplete closure or prolapse of the aortic valve usually occurs.

The main causes of acquired organic aortic insufficiency are rheumatism (up to 80% of all cases), septic endocarditis, atherosclerosis, syphilis, rheumatoid arthritis, systemic lupus erythematosus, Takayasu's disease, traumatic damage to the valve, etc. Rheumatic damage leads to thickening, deformation and wrinkling of the valve leaflets of the aorta, as a result of which they do not fully close during diastole. Rheumatic etiology usually underlies the combination of aortic insufficiency and mitral disease. Infective endocarditis is accompanied by deformation, erosion or perforation of the leaflets, causing a defect in the aortic valve.

The occurrence of relative aortic insufficiency is possible due to expansion of the fibrous annulus of the valve or the lumen of the aorta due to arterial hypertension, aneurysm of the sinus of Valsalva, dissecting aortic aneurysm, ankylosing rheumatoid spondylitis (ankylosing spondylitis) and other pathologies. In these conditions, separation (divergence) of the aortic valve leaflets during diastole can also be observed.

Hemodynamic disorders in aortic insufficiency

Hemodynamic disorders in aortic regurgitation are determined by the volume of diastolic regurgitation of blood through the valve defect from the aorta back to the left ventricle (LV). In this case, the volume of blood returning to the LV can reach more than half of the cardiac output.

Thus, with aortic insufficiency, the left ventricle fills during diastole both as a result of the flow of blood from the left atrium and as a result of aortic reflux, which is accompanied by an increase in diastolic volume and pressure in the LV cavity. The volume of regurgitation can reach up to 75% of the stroke volume, and the end-diastolic volume of the left ventricle increases to 440 ml (with a norm of 60 to 130 ml).

The expansion of the cavity of the left ventricle helps to stretch the muscle fibers. To expel the increased blood volume, the force of ventricular contraction increases, which, if the myocardium is in satisfactory condition, leads to an increase in systolic output and compensation for altered intracardiac hemodynamics. However, long-term operation of the left ventricle in the hyperfunction mode is invariably accompanied by hypertrophy and then dystrophy of cardiomyocytes: a short period of tonogenic dilatation of the LV with an increase in blood outflow is replaced by a period of myogenic dilatation with an increase in blood inflow. The final result is the formation of mitralization of the defect - relative mitral valve insufficiency caused by LV dilatation, dysfunction of the papillary muscles and expansion of the fibrous ring of the mitral valve.

In conditions of compensation for aortic insufficiency, the function of the left atrium remains unimpaired. With the development of decompensation, there is an increase in diastolic pressure in the left atrium, which leads to its hyperfunction, and then to hypertrophy and dilatation. Stagnation of blood in the vascular system of the pulmonary circulation is accompanied by an increase in pressure in the pulmonary artery with subsequent hyperfunction and hypertrophy of the right ventricular myocardium. This explains the development of right ventricular failure in aortic disease.

Classification of aortic insufficiency

To assess the severity of hemodynamic disorders and the body’s compensatory capabilities, a clinical classification is used that distinguishes 5 stages of aortic insufficiency:

  • I - stage of full compensation. Initial (auscultatory) signs of aortic insufficiency in the absence of subjective complaints.
  • II - stage of latent heart failure. Characterized by a moderate decrease in exercise tolerance. According to the ECG, signs of hypertrophy and volume overload of the left ventricle are revealed.
  • III - stage of subcompensation of aortic insufficiency. Anginal pain and forced limitation of physical activity are typical. ECG and radiographs show left ventricular hypertrophy and signs of secondary coronary insufficiency.
  • IV - stage of decompensation of aortic insufficiency. Severe shortness of breath and attacks of cardiac asthma occur at the slightest exertion, and an enlarged liver is detected.
  • V - terminal stage of aortic insufficiency. It is characterized by progressive total heart failure, deep degenerative processes in all vital organs.

Symptoms of aortic insufficiency

Patients with aortic insufficiency in the compensation stage do not report subjective symptoms. The latent course of the defect can be long - sometimes for several years. The exception is acutely developed aortic insufficiency caused by dissecting aortic aneurysm, infective endocarditis and other reasons.

Symptoms of aortic insufficiency usually manifest with sensations of pulsation in the vessels of the head and neck, increased cardiac impulses, which is associated with high pulse pressure and increased cardiac output. Sinus tachycardia, characteristic of aortic insufficiency, is subjectively perceived by patients as a rapid heartbeat.

With a pronounced valve defect and a large volume of regurgitation, brain symptoms are noted: dizziness, headaches, tinnitus, visual impairment, short-term fainting (especially with a rapid change from horizontal to vertical body position).

Later, angina pectoris, arrhythmia (extrasystole), shortness of breath, and increased sweating occur. In the early stages of aortic insufficiency, these sensations are disturbing mainly during exercise, and later occur at rest. The addition of right ventricular failure manifests itself as swelling in the legs, heaviness and pain in the right hypochondrium.

Acute aortic insufficiency occurs as pulmonary edema, combined with arterial hypotension. It is associated with sudden volume overload of the left ventricle, increased LV end-diastolic pressure and decreased stroke output. In the absence of special cardiac surgical care, the mortality rate for this condition is extremely high.

Diagnosis of aortic insufficiency

Physical findings in aortic insufficiency are characterized by a number of typical signs. Upon external examination, attention is drawn to the pallor of the skin; in the later stages, acrocyanosis. Sometimes external signs of increased pulsation of the arteries are detected - “carotid dancing” (pulsation visible to the eye on the carotid arteries), Musset’s symptom (rhythmic nodding of the head in time with the pulse), Landolfi’s symptom (pulsation of the pupils), “Quincke’s capillary pulse” (pulsation of the vessels of the nail bed ), Müller's symptom (pulsation of the uvula and soft palate).

Typically visual determination of the apical impulse and its displacement in the VI-VII intercostal space; aortic pulsation is palpated behind the xiphoid process. Auscultatory signs of aortic insufficiency are characterized by diastolic murmur on the aorta, weakening of the first and second heart sounds, “accompanying” functional systolic murmur on the aorta, vascular phenomena (double Traube sound, double Durosier murmur).

Instrumental diagnosis of aortic insufficiency is based on the results of ECG, phonocardiography, X-ray studies, echocardiography (TEE), cardiac catheterization, MRI, MSCT. Electrocardiography reveals signs of left ventricular hypertrophy; with mitralization of the defect, data for left atrial hypertrophy. Using phonocardiography, altered and pathological heart murmurs are determined. An echocardiographic study reveals a number of characteristic symptoms of aortic insufficiency - an increase in the size of the left ventricle, an anatomical defect and functional failure of the aortic valve.

Signs of inoperability include an increase in LV diastolic volume to 300 ml; ejection fraction 50%, end-diastolic pressure about 40 mmHg. Art.

Prognosis and prevention of aortic insufficiency

The prognosis of aortic insufficiency is largely determined by the etiology of the defect and the volume of regurgitation. With severe aortic insufficiency without decompensation, the average life expectancy of patients from the moment of diagnosis is 5-10 years. In the decompensated stage with symptoms of coronary and heart failure, drug therapy is ineffective, and patients die within 2 years. Timely cardiac surgery significantly improves the prognosis of aortic insufficiency.

Prevention of the development of aortic insufficiency consists in the prevention of rheumatic diseases, syphilis, atherosclerosis, their timely detection and proper treatment; clinical examination of patients at risk for the development of aortic disease.

Aortic valve defects These are diseases that are associated with disruption of the structure and function of the aortic valve. They manifest themselves in incomplete closure of the valves (aortic insufficiency) or in narrowing of the aortic mouth (aortic valve stenosis).

Structure of the aortic valve

Aortic valve located on the border of the left ventricle of the heart and the aorta, the largest artery in the body. Its main task is to prevent the return of blood to the ventricle, which during its contraction went into the aorta.
The aortic valve consists of the following elements:
  • Fibrous ring– valve base. A ring of connective tissue that separates the left ventricle and the aorta.
  • Three semilunar valves- “pockets” that close tightly, blocking the lumen into the aorta.
  • Sinuses of Valsalva– the aortic sinuses, which are located behind the semilunar valve leaflets.
The basis of the valve is a fibrous ring made of elastic and dense connective tissue. It is located on the border of the left ventricle and the aorta. At this point, the aorta dilates and behind each valve leaflet there is a small sinus. Two of them give off the right and left coronary arteries.

The valves themselves look like three rounded pockets, which are located in a circle on the fibrous ring. When they open, they completely block the lumen of the aorta. The flaps are made up of connective tissue and a thin layer of muscle fibers. Moreover, the connecting fibers of collagen and elastin are arranged in bundles. This structure allows you to redistribute the load from the valve leaflets to the walls of the aorta.

Valve mechanism

The aortic valve, unlike the mitral valve, can be called passive. It opens and closes under the influence of blood flow and the pressure difference between the left ventricle and the aorta. There are no papillary muscles or chordae tendineae in this valve.

Valve opening

  • Elastin fibers, which are located on the side of the ventricle, help the valves take their original position: press against the walls of the aorta and open the passage into the aorta for blood.
  • The aortic root (the expansion at the very beginning of this artery) contracts and tightens the valves.
  • When the pressure in the ventricle exceeds the pressure in the artery, blood is pushed into the aorta and presses the valves against its walls.
Closing the valve
After the ventricle contracts, blood flow slows. In this case, small vortices, similar to whirlpools, form near the walls of the aorta, in the sinuses. It is believed that it is these vortices that push the valve leaflets away from the walls towards the middle of the aorta. This happens very quickly. Elastic flaps tightly close the lumen into the ventricle. This creates a fairly loud sound. It can be heard with a stethoscope.

The lumen of the aortic valve is much narrower than the mitral valve. Therefore, each time the ventricle contracts, it experiences greater stress and gradually wears out. This leads to the appearance of acquired arterial valve defects.

Aortic valve insufficiency or aortic insufficiency - a heart defect in which the mitral valve leaflets do not completely close the aortic opening. There remains a gap between them. Some of the blood returns back to the left ventricle through this lumen. The ventricle becomes full, stretches and begins to work worse. Blood from the lungs, which should be pumped through the heart to all organs, stagnates in the pulmonary vessels. All manifestations of the disease are associated with these processes.

Aortic valve insufficiency is the second most common heart defect, after mitral valve disease. Usually this pathology occurs in conjunction with stenosis - narrowing of the aortic lumen. Men are more likely to suffer from aortic regurgitation than women.

Causes

Aortic valve insufficiency can appear during fetal development or after birth. Therefore, the cause of the development of this defect is congenital pathologies or past illnesses.
Congenital defects develop due to the following defects:
  • two valve leaflets develop instead of three;
  • one leaf is larger than the other, stretched and sagging;
  • holes in valve flaps;
  • underdevelopment of one of the valves.
Typically, birth defects of the aorta cause minor changes in the way blood flows, but over time the valve may worsen and require treatment.

Acquired vices aortic valve cause such diseases.

Infectious diseases:

  • syphilis
  • sepsis
  • angina
  • pneumonia
Infectious diseases cause heart complications - infective endocarditis. This disease causes inflammation of the inner lining of the heart, which also makes up the valves. Bacteria accumulate on the valve flaps, most often streptococci, staphylococci and chlamydia. They form colonies. From above, these tubercles are covered with blood protein and overgrown with connective tissue. As a result, wart-like growths appear on the aortic valve pockets. They tighten the doors and prevent them from closing tightly at the right time.

Autoimmune diseases

  • rheumatism
  • lupus erythematosus
Rheumatism causes 80% of cases of aortic valve insufficiency. In autoimmune diseases, connective tissue cells multiply rapidly. Therefore, growths and thickenings appear on the valve flaps. After all, it is based on a lot of connective cells. As a result, the pockets become wrinkled and deformed, like synthetic fabric ironed with a hot iron.

Other reasons

  • atherosclerosis of the aorta
  • calcium deposits on the valve
  • hypertension
  • strong blow to the chest
  • age-related changes - expansion of the aortic root.
These factors can cause deformation or even rupture of one of the valve flaps. In the latter case, the deterioration of health occurs quickly. But for most people, aortic regurgitation develops gradually, and the condition worsens over time.

Symptoms of aortic valve insufficiency

In the first stages, you may not feel any signs of illness. The heart compensates for the slight reverse flow of blood from the aorta to the left ventricle. This can go on for decades. But gradually the aortic valve wears out, and more and more blood returns to the heart. If the volume of blood thrown into the ventricle reaches 15-30%, then well-being getting worse. The following symptoms appear:
  • Feeling of increased heartbeat;
  • Pulsation in the area of ​​large vessels throughout the body;
  • Pain in the heart area;
  • Dizziness;
  • Noise in ears;
  • Shortness of breath when performing daily activities;
  • Fainting caused by poor circulation in the brain;
  • Heaviness and pain in the right hypochondrium, associated with stagnation of blood in the liver;
  • Swelling of the legs.
Objective symptoms- these are the signs of mitral insufficiency that the doctor identifies during examination.
  • Pale skin - it is due to the fact that the small blood vessels of the skin reflexively narrow;
  • Strong pulsation of the arteries, this is especially noticeable in the carotid arteries;
  • Pulsation of the uvula and tonsils;
  • The pupils constrict during the contraction of the heart and dilate during its relaxation phase. These “pulsating” signs are due to the fact that the tone of small arteries is disturbed. They expand noticeably when a pulse wave passes through them, which appears after contraction of the ventricles.
  • Young people may develop a cardiac hump, a protrusion in the chest. This is the result of an increase in the size of the heart;
  • When palpating the chest, the doctor hears strong beats of the left ventricle under the palm of the hand;
  • Tapping reveals an increase in the size of the heart;
  • When listening with a stethoscope, the doctor hears a heart murmur as the ventricles contract. They are caused by the turbulence of blood as it passes between the deformed valve leaflets;
  • The pulse is accelerated, the vessels are dense and easily palpable;
  • Significant difference between upper and lower pressure. If normal pressure is 120/80, then with aortic insufficiency it can be 160/55. This is due to the fact that with each beat the left ventricle throws a large amount of blood into the vessels.
Objective symptoms are varied, but, unfortunately, they cannot accurately indicate that the problem is in the aortic valve:

X-ray examination– the aorta is dilated, the left and right ventricles are enlarged.

Electrocardiography- signs of left ventricular enlargement. In some people, unscheduled contractions of the ventricles appear on the cardiogram, which are knocked out of the normal rhythm of the heart - ventricular extrasystoles.

Phonocardiography Heart murmurs are heard.

  1. Systolic murmur occurs during ventricular contractions (systole). It appears when blood passes into the aorta past the modified valve leaflets. Their uneven edges create swirls, the sound of which is heard;
  2. Diastolic murmur occurs when the ventricles relax (diastole), and the pressure in them drops. Through a loosely closed valve, some of the blood returns from the aorta. At the same time, it passes noisily through a narrow hole.
Echocardiography or ultrasound of the heart allows you to identify:
  • Disturbances in the aortic valve leaflets;
  • Trembling of the mitral valve leaflets between the left atrium and the left ventricle;
  • Enlargement of the left ventricle.
Dopplerography(one of the types of cardiac ultrasound) The monitor shows blood leaking through a small hole in the aortic valve back into the left ventricle.

Diagnostics

Characteristic signs identified as a result of research help to make the correct diagnosis and distinguish aortic valve insufficiency from other heart diseases.
  1. Phonocardiography And listening detect heart murmurs during contraction and relaxation of the ventricles.
  2. Dopplerography. At dopplerography reverse flow of blood from the aorta into the left ventricle is visible.
  3. X-ray reveals an enlarged heart.
  4. Inspection. At inspection strong pulsation of the arteries is noticeable.
The patient's complaints help clarify the diagnosis. Therefore, before going to the doctor, analyze what is bothering you and try to explain your feelings as clearly as possible.

Treatment

Aortic valve insufficiency often progresses slowly, and proper treatment can help stop the progression of the disease.

Calcium antagonists: Verapamil
Prevents calcium ions from entering cells. Thanks to this, the heart contracts less strongly, needs less oxygen and has the opportunity to rest. The drug is needed if you are periodically bothered by attacks of irregular heartbeat and increased blood pressure. The first days take 40-80 mg 3 times a day. Then the dose is adjusted depending on how you feel.

Diuretics: Furosemide
Diuretics are prescribed to almost all people with this disease. They reduce the load on the heart, relieve swelling, remove salts and lower blood pressure. In the first days of treatment, 20-80 mg/day is prescribed. The dose is gradually increased to achieve improvement in well-being. The drug can be taken for a long time: every day or every other day, as directed by your doctor.

Beta blockers: Propranolol
You need this drug if aortic insufficiency is accompanied by dilation of the aortic root, heart rhythm disturbances and increased blood pressure. It blocks beta-adrenergic receptors and prevents them from interacting with adrenaline. As a result, the heart is better supplied with blood and blood pressure decreases. Take 1 tablet 40 mg 2 times a day. When there is no effect, the doctor may increase the dose. But if you have chronic liver diseases, then you need to take the drug in smaller quantities. Therefore, do not forget to tell your doctor about your health condition and the medications you are already taking.

Vasodilators: Hydralazine
This drug helps reduce tension in the walls of blood vessels, relieve spasm in small arteries and improve blood circulation. The load on the left ventricle is reduced and the pressure decreases. Take Hydralazine 10-25 mg 3-4 times a day. The dose is increased gradually to avoid side effects. This medicine should not be used if the pulse is rapid, there is mitral valve disease, atherosclerosis, or the heart has a poor supply of blood (coronary artery disease). The dose and duration of the course are determined by the doctor. This drug is often prescribed to people who are contraindicated for surgery.

Surgery

Surgery on the aortic valve will be needed for those people whose left ventricle can no longer cope with the large volume of blood that it has to pump.

With congenital aortic valve disease, which in most cases causes minor disturbances, the operation is performed after 30 years. But if the condition worsens quickly, it may be performed at an earlier age.
Age at which this operation is recommended with an acquired defect depends on changes in the valve. Usually the operation is performed on people aged 55-70 years.

Indications for surgery

  • dysfunction of the left ventricle;
  • the left ventricle has increased to 6 cm or more;
  • a large volume of blood (25%) returns from the aorta to the ventricle during its relaxation (diastole) and the person suffers from manifestations of the disease;
  • the disease is asymptomatic, there are no complaints of poor health, but about 50% of the blood returns to the ventricle.
Contraindications to the operation.
  • age over 70 years, but this issue is resolved individually;
  • More than 60% of the blood returns from the aorta to the ventricle;
  • severe chronic diseases.
Types of operation:
  1. Intra-aortic balloon counterpulsation
This operation is performed for the initial form of aortic valve insufficiency. A 2-50 ml balloon and a helium supply hose attached to it are inserted into the femoral artery. When the balloon reaches the aortic valve, it is sharply inflated. This helps align the aortic valve leaflets so they close more tightly.
  • minor changes in valve flaps;
  • reverse blood flow 25-30%.
Its virtues
  • does not require a large incision;
  • allows for faster recovery after surgery;
  • easier to tolerate.
Disadvantages of the operation
  • cannot be carried out if there are disorders in the aortic tissues: atherosclerosis, aneurysm, dissection;
  • there is no way to correct serious changes in the valve flaps;
  • there is a risk of recurrent aortic insufficiency within 5-10 years.
  1. Implantation of an artificial valve
This is the most common operation to treat aortic valve insufficiency. It experiences heavy loads, so an artificial valve made of silicone and metal is almost often installed, which does not wear out. Biological prosthesis and restoration of valve leaflets are practically not carried out.

Indications for this type of operation

  • reverse blood flow is 25-60%, if the percentage is higher, then the risk increases that after the operation the function of the left ventricle will not improve;
  • strong and numerous manifestations of the disease;
  • enlargement of the left ventricle more than 6 cm.
Its virtues
  • provides good results at any age under 70 years and with any valve lesions;
  • the vast majority of people tolerate the operation well;
  • health status improves significantly;
  • You can simultaneously get rid of arterial insufficiency.
Disadvantages of the operation
  • requires dissection of the chest and attachment of a machine for artificial circulation;
  • recovery requires 2 months;
  • The operation is not effective if severe circulatory failure occurs.
Remember that only surgery can completely cure aortic valve insufficiency. Therefore, if doctors recommend this type of treatment to you, then do not delay. The sooner you get a new valve, the better your chances of living a full and healthy life.

Aortic valve stenosis

Aortic valve stenosis – This is a heart defect in which the lumen of the aortic valve narrows. Blood cannot quickly leave the left ventricle during contraction (systole). This causes an increase in its size, pain due to increased pressure in the heart, fainting and heart failure. Without treatment, the condition will worsen over time and this can lead to dire consequences.

Causes

Aortic valve stenosis can be the result of abnormalities in the development of the fetus or be a consequence of previous diseases.

Birth defects

  • the valve has two leaflets instead of three
  • the valve consists of one leaf
  • under the valve there is a membrane with a hole
  • muscle cushion over the aortic valve

Acquired valve defects as a result of various diseases:

Infectious diseases

  • sepsis
  • pharyngitis
  • pneumonia
During infectious diseases, bacteria (mainly streptococci and staphylococci) enter the blood and are carried into the heart. Here they settle on the inner membrane and cause its inflammation - infective endocarditis. As a result, accumulations of microorganisms appear on the endocardium and valve leaflets - growths similar to warts, which narrow the lumen inside the valve or cause fusion of the leaflets.

Systemic diseases

  • rheumatism
  • systemic lupus erythematosus
  • scleroderma
Systemic diseases cause disturbances in the processes of cell division of the connective tissue that makes up the valve. Its cells divide and growths form on the valve flaps. The pockets can grow together, and this prevents the valve from opening completely.

Age-related changes

  • Calcification of the aortic valve - deposits of calcium salts along the edges of the valves.
  • Atherosclerosis is the deposition of cholesterol plaques on the inner surface of the aorta and valve.
After age 50, calcium or fatty plaques begin to deposit along the edges of the valve. They form growths, prevent the valves from closing and partially block the lumen when the valves are open. Therefore, aortic valve stenosis is often accompanied by insufficiency.

With minor changes, symptoms do not occur. If they appear, this indicates that the valve needs to be replaced.

Symptoms

Symptoms of aortic valve stenosis depend on the stage of the disease. The stage is determined based on the size of the aortic valve opening.
  • Normal area is 2-5 cm2
  • Mild stenosis orifice area greater than 1.5 cm2
  • Moderate stenosis area 1-1.5 cm2
  • Severe stenosis, opening area less than 1 cm2
Usually, the first manifestations of the disease appear when the area of ​​the hole has decreased to 1 cm 2.

Well-being

  • Pain and feeling of heaviness in the chest - angina pectoris. It appears due to the fact that pressure increases in the left ventricle and blood presses on its walls;
  • Fainting. This is the result of the fact that little blood enters the aorta through a narrow opening. The pressure in it drops, and the organs do not receive enough blood and oxygen. This is primarily felt by the brain. When he experiences oxygen starvation, the person feels weak, dizzy and loses consciousness;
  • Edema of the lower extremities is caused by circulatory failure and impaired outflow of venous blood;
  • Signs of heart failure appear as a result of dysfunction of the left ventricle:
  • Shortness of breath on exertion;
  • Shortness of breath when lying down;
  • Nocturnal coughing attacks;
  • Increased fatigue.
Objective signs or what the doctor finds
  • Pale skin due to insufficient blood supply to small vessels;
  • The pulse is slow (bradycardia) and weak;
  • When listening to the heart, a characteristic murmur is heard. It occurs between ventricular contractions. Its appearance is due to the fact that the pressure in the left ventricle increases and blood rushes into the narrow opening of the aortic valve. The higher the pressure in the ventricle, the louder the noise created by the turbulence in the blood flow;
  • The sound of the aortic valve closing is difficult to hear. This occurs because the fused valve flaps do not close tightly and quickly enough.

Instrumental examination data

Electrocardiogram helps to identify the degree of development of stenosis. With a slight narrowing of the valve, it remains normal. Otherwise, the following appears:
  • signs of enlargement of the left ventricle and thickening of its wall
  • heart rhythm disturbances
X-ray may be normal or show:
  • enlargement of the left atrium and ventricle
  • the outline of the heart resembles a shoe
  • calcium deposits on the valve or in the lower part of the aorta
Transthoracic echocardiography ( Ultrasound of the heart through the chest) can reveal:
  • enlargement of the left ventricle and thickening of its walls
  • left atrium enlargement
  • membrane below the valve
  • cushion above the valve in the aorta
  • incomplete closure of the valves
  • number of sashes
  • narrowed valve opening
Transesophageal echocardiography– the sensor is inserted into the esophagus, and it is very close to the heart. Allows you to measure the area of ​​the opening in the aortic valve.

Doppler study one of the types of cardiac ultrasound, which allows:

  • see the direction of blood flow
  • measure flow rate
  • determine the amount of blood that passes through the aortic valve
  • see the narrowing above the valve
  • identify aortic valve insufficiency - incomplete closure of its valves

Cardiac catheterization– study of the condition of the heart using a special catheter, which is inserted into its cavity through large vessels. Prescribed only to people over 50 years of age whose EchoCG data and the results of other examinations do not match. Using this method, the pressure in the chambers of the heart and the characteristics of blood movement through the aortic valve are determined.

After the first symptoms of aortic valve stenosis appear, surgery must be performed within 3-5 years. If the disease is asymptomatic and does not cause significant disturbances in the functioning of the left ventricle, the doctor will prescribe the necessary medications and the time for the next examination. Usually it is enough to undergo a cardiac ultrasound once a year.

Treatment of aortic valve stenosis

If the doctor determines that you have a slight narrowing of the aortic valve, he will prescribe treatment that will improve the oxygen supply to the heart muscle and help maintain a normal contraction rhythm and blood pressure.

Diuretics or diuretics: Torsemide
You need the drug if the doctor has detected congestion in the lungs. Torsemide reduces the amount of water in the body and the volume of blood circulating through the vessels. But diuretics are prescribed carefully and in small doses. Otherwise, it can cause a decrease in pressure in the arteries, which already receive insufficient blood. The recommended dose is 2.5 mg 1 time/day. Use in the morning, regardless of meals.

Antianginal drugs: Sustak, Nitrong
Improves blood supply to the heart and relieves pain and heaviness behind the sternum. They reduce the need for oxygen in the heart muscle and improve the blood supply to the heart. Apply 2-3 times a day with a small amount of water. Tablets should not be chewed or broken. The dose of the drug is prescribed by the doctor. Even a slight excess of it can cause deterioration and fainting due to a decrease in pressure.

Antibiotics: Bicillin-3
Prescribed for the prevention of infective endocarditis in any exacerbation of chronic diseases: tonsillitis, pyelonephritis. And before various procedures that can cause bacteria to enter the blood: tooth extraction, abortion. The drug is used 1 time, 1,000,000 units, unless the doctor prescribes a different regimen.

Surgery for aortic valve stenosis

Indications for surgery
  • signs of illness appear that reduce ability to work: weakness, shortness of breath, fatigue;
  • moderate and severe stenosis, the area of ​​the opening in the aortic valve is less than 1.5 square meters. cm;
Contraindications for surgery
  • age over 70 years;
  • severe concomitant illnesses.
Types of operations
  1. Aortic balloon valvuloplasty
A balloon is inserted through a small incision in the femoral artery, to which a helium supply hose is attached. When the device reaches the aortic valve, the balloon is inflated, and it increases the clearance between the valve leaflets.

Indications for surgery

  • childhood;
  • patients under 25 years of age without calcium deposits on the valve;
  • in adults with severe stenosis before valve replacement surgery;
  • in adulthood, if aortic valve replacement surgery is contraindicated.
Advantages of the method
  • low-traumatic method;
  • high efficiency in children;
  • does not require cardiac arrest and connection to a machine for artificial circulation;
  • allows you to recover in 7-10 days.
Disadvantages of the method
  • repeat surgery may be required within 10 years;
  • there is a risk of developing aortic insufficiency due to the fact that scars will appear on the valve flaps and they will not close tightly;
  • effectiveness in adults is 50%; after a year, narrowing may occur again.
  1. Aortic valve replacement
In place of the affected aortic valve is placed:
  1. An artificial prosthesis made of durable and high-tech materials: silicone and metal.
  2. Bioprostheses:
  • A valve transplanted from your own pulmonary artery;
  • A valve taken from the heart of a deceased person;
  • Animal bioprostheses: porcine or bovine.
Indications for aortic valve replacement
  • fainting;
  • severe weakness and fatigue;
  • violations of left ventricular contraction;
  • Only 50% of the blood passes through the narrowed aortic opening during ventricular contraction.
Advantages of the operation
  • brings significant improvements at any age;
  • low mortality rate during and after surgery;
  • during the operation, deficiencies in the functioning of the aorta can be simultaneously corrected;
  • eliminates all manifestations of the disease;
  • Life expectancy after such an operation is the same as for healthy people.
Disadvantages of the operation
  • The recovery period takes 1-2 months;
  • Bioprostheses wear out, they are installed in people over 60 years old
  • A mechanical prosthesis increases the risk of blood clots and requires constant use of blood thinning medications - anticoagulants.
Ultimately, the choice of surgery depends on your age and overall health. Listen to your doctor's recommendations and do not delay treatment - this will help you completely get rid of heart problems.
The physical properties of ultrasound determine the methodological features of echocardiography. Ultrasound of the frequency used in medicine practically does not pass through air. An insurmountable obstacle to the path of the ultrasound beam can be the lung tissue between the chest and the heart, as well as a small air gap between the surface of the sensor and the skin. To eliminate the last obstacle, a special gel is applied to the skin, displacing air from under the sensor. To exclude the influence of lung tissue, to install the sensor, select points where the heart is directly adjacent to the chest - the “ultrasound window”. This is the zone of absolute cardiac dullness (3-5 intercostal space to the left of the sternum), the so-called parasternal access, and the zone of the apical impulse (apical access). There is also a subcostal approach (at the xiphoid process in the hypochondrium) and suprasternal (in the jugular fossa above the sternum). The sensor is installed in the intercostal spaces due to the fact that ultrasound does not penetrate deep into the bone tissue and is completely reflected from it. In pediatric practice, due to the lack of ossification of cartilage, examination through the ribs is also possible.

During the examination, the patient usually lies on his back with his upper body elevated, but sometimes for better adherence of the heart to the chest wall, a lying position on the left side is used.

In patients with lung diseases accompanied by emphysema, as well as in persons with other causes of a “small ultrasound window” (massive chest, calcification of costal cartilages in elderly people, etc.), echocardiography becomes difficult or impossible. Difficulties of this kind occur in 10-16% of patients and are the main disadvantage of this method.

Ultrasound anatomy of the heart in various echolocation modes

I. One-dimensional (M-) echocardiography.

To unify studies in echocardiography, 5 standard positions have been proposed, i.e. directions of the ultrasound beam from parasternal access. 3 of them are mandatory for any study (Fig. 3).

Rice. 3. Basic standard sensor positions for one-dimensional echocardiography (M-mode).

Position I - the ultrasound beam is directed along the short axis of the heart and passes through the right ventricle, the interventricular septum, the cavity of the left ventricle at the level of the tendon filaments of the mitral valve, and the posterior wall of the left ventricle.

Standard position of sensor II - tilting the sensor slightly higher and more medially, the beam will pass through the right ventricle, the left ventricle at the level of the edges of the mitral valve leaflets.

N.M. Mukharlyamov (1987) gives the numbering of standard positions in reverse order, since research in M-mode often begins with echolocation of the aorta, then tilting the sensor downward to the remaining positions.

Image of the heart structures in the first standard position.

In this position, information is obtained about the size of the ventricular cavities, the thickness of the walls of the left ventricle, impaired myocardial contractility and the magnitude of cardiac output (Fig. 4).

pancreas– cavity of the right ventricle in diastole (normal up to 2.6 cm)

Tmzhp - swelling of the interventricular septum in diastole

Tzslzh(d)– thickness of the posterior wall of the left ventricle in diastole

CDR– end-diastolic size of the left ventricle

KSR- end-systolic size of the left ventricle

Rxs. 4. M - echocardiogram in the I standard position of the sensor.

During systole, the right ventricle and interventricular septum (IVS) move away from the transducer toward the left ventricle. The posterior wall of the left ventricle (PLW), on the contrary. moves towards the sensor. In diastole, the direction of movement of these structures is reversed, and the diastolic velocity of the LVAD is normally 2 times higher than the systolic velocity. The endocardium of the LVAD therefore describes a wave with a gentle rise and a steep descent. The epicardium of the LVAD makes a similar movement, but with a smaller amplitude. Before the systolic rise of the left ventricle, a small notch is recorded, caused by the expansion of the cavity of the left ventricle during atrial systole.

Basic indicators measured in the first stationary position.

1. End dinstolic diameter (EDD) of the left ventricle - the distance in diastole along the short axis of the heart between the endocardium of the left ventricle and the IVS at the level of the beginning of the QRS complex of a synchronously recorded ECG. The EDR is normally 4.7-5.2 cm. An increase in EDR is observed with dilatation of the left ventricular cavity, a decrease is observed with diseases leading to a decrease in its volume (mitral stenosis, hypertrophic

Cardiomyopathy).

2. End systolic diameter (ESD) of the left ventricle - the distance at the end of systole between the endocardial surfaces of the left ventricle and the IVS at the highest point of elevation of the left ventricle. The CSR is 3.2-3.5 cm in the middle. The CSR increases with dilatation of the left ventricle and with a violation of its contractility. A decrease in ESR occurs, in addition to the reasons that determine the decrease in ESR, in the case of mitral valve insufficiency (due to the volume of regurgitation).

Taking into account the fact that the left ventricle is an ellipsoid in shape, its volume can be determined by the size of the short axis. The most commonly used formula is L. Teicholtz et al. (1972).

= 7,0 * 3

V(24*D)D(cm3),

where D is the anteroposterior dimension in systole or diastole.

The difference between end-diastolic volume (EDV) and end-systolic volume (ESV) will give stroke volume ( UO):

UO - KDO - KSO (ml).

Knowing heart rate, body area ( St), other hemodynamic parameters can be determined.

Impact index (UI):

UI=UO/St

Minute volume of blood circulation ( IOC):

IOC = SV HR

Cardiac index ( SI): SI = IOC/St

3. Thickness of the left ventricle in diastole (Tslzh(d)) is normally 0.8-1.0 cm and increases with hypertrophy of the walls of the left ventricle.

4. Thickness of the left ventricle in systole (Tsl(s)), the norm is on average 1.5-1.8 cm. A decrease in Tsl(s) is observed with a decrease in myocardial contractility.

To assess the contractility of a given area of ​​the myocardium, an indicator of its systolic thickening is often used - the ratio of diastolic to systolic thickness. The norm Tzslzh(d) / Tzslzh(s) is about 65%. An equally important indicator of local myocardial contractility is the magnitude of its systolic excursion - i.e. amplitude of endocardial movement during heart contraction. The systolic excursion of the left ventricle is normal - I cm. A decrease in systolic excursion (hypokinesis) up to complete immobility (myocardial akinesia) can be observed with lesions of the heart muscle of various etiologies (IBO, cardiomyopathy, etc.). An increase in the amplitude of myocardial movement (hyperkinesis) is observed with insufficiency of the moral and aortic valves, hyperkinetic syndrome (anemia, thyrotoxicosis, etc.). Local hyperkinesis is often determined in IHD in intact areas of the myocardium as a compensatory mechanism in response to decreased contractility in the affected areas.

5. The thickness of the interventricular septum in diastole (Tmzhp(d)) is normally 0.6-0.8 cm.

6. Systolic excursion of the IVS is normally 0.4-0.6 cm and is usually half as much as the excursion of the LVSD. The reasons for hypokinesis of the IVS are similar to the reasons for the decrease in systolic excursion of the left ventricle. In addition to the above-mentioned causes of LVSD hyperkinesis, myocardial dystrophies of various etiologies in the initial stages of the disease can lead to moderate hyperkinesis of the IVS.

In some diseases, the movement of the interventricular septum changes to the opposite - not towards the left ventricular septum, as is normally observed, but parallel to it. This form of IVS movement is called “paradoxical” and occurs with severe hypertrophy of the left ventricle. “Paradoxical” movement of a limited area (IVS, apex, side wall), i.e. its “bulging” during systole, in contrast to the contraction of neighboring zones of the myocardium, is observed in left ventricular aneurysms.

To assess myocardial contractility, in addition to the measurements of the heart walls described above and the calculation of hemodynamic volumes, several highly informative indicators have been proposed (Pombo J. et al., 1971):

1. Ejection fraction is the ratio of stroke volume to end-diastolic volume, expressed as a percentage or (less commonly) as a decimal fraction:

FV =UO/KDO 100% (normal 50-75%)

2. The degree of shortening of the anteroposterior size of the left ventricle in systole (%ΔS):

%ΔS=KDR-KSR/KDR 100% (norm 30-43%)

3. The rate of piricular shortening of myocardial fibers

(Vcf). To calculate this indicator, it is first necessary to determine from the echogram the ejection time of the left ventricle, which is measured at the beginning of the systolic rise of the LVAD endocardium to its apex (Fig. 4).

Vcf =KDR-KSR/ Tee KDR (env./ With), Where Tee- period of exile

Normal value Vcf 0.9-1.45 (c/s silt s-1).

A feature of all measurements in the first standard position is the need to direct the ultrasound beam strictly perpendicular to the IVS and LVSD, i.e. along the short axis of the heart. If this condition is not met, the measurement results will be overestimated or underestimated. To eliminate such errors, it is advisable to first obtain a two-dimensional image of the heart along the long axis from a parasternal approach, then, under the control of the resulting B-scanogram, set the cursor to the desired position and expand the image in M-mode.

Image of heart structures in standard position II of the sensor (Fig. 5)

The ultrasound beam passes through the edges of the mitral valve (MV) leaflets, the movement of which provides basic information about the condition of the leaflets and disruption of the transmitral blood flow.

During ventricular systole, the valves are closed and fixed in the form of a single line (S-D interval). At the beginning of diastole (point D), blood begins to flow from the atria into the ventricles, opening the valves. In this case, the front sash moves up to the X sensor (interval D-E), the rear sash moves down in the opposite direction. At the end of the period of rapid filling, the amplitude of the divergence of the valves is maximum (point E). Then the intensity of blood flow through the mitral orifice decreases, which leads to partial closure of the leaflets (point F) in mid-diastole. At the end of diastole, transmitral blood flow increases again due to contraction of the atria, which is reflected on the echogram by the second peak of opening of the valves (point A). Subsequently, the valves close completely during ventricular systole and the cycle repeats.


Fig. 5. M-echocardiogram in the II standard position of the sensor .

Thus, due to the unevenness of the transmitral blood flow (“biphasic” filling of the left ventricle), the movement of the moral valve leaflets is represented by two peaks. The shape of the movement of the front leaf resembles the letter “M”, the rear – “W”. The posterior valvular valve is smaller than the anterior one, so the amplitude of its opening is small and its visualization is often difficult.

Clinically, both peaks of diastolic filling of the ventricles can be manifested by 3rd and 4th heart sounds, respectively.

The main indicators of the echocardiogram in the II standard position


  1. The amplitude of the diastolic opening of the anterior leaflet of the playing valve (vertical displacement of the leaflet in the D-E interval) is the norm of 1.8 cm.

  1. Diastolic divergence of the leaflets (at the height of peak E) is normal 2.7 cm. The values ​​of both indicators decrease with mitral stenosis and may increase slightly with “pure” mitral valve insufficiency.

  1. The speed of early diastolic closing of the anterior moral leaflet (determined by the slope of the E-F section). A decrease in speed (normally 13-16 cm/s) is one of the sensitive signs of the early stages of mitral stenosis.

  1. The duration of diastolic divergence of the mitral leaflets (from the moment of opening of the leaflets to the point of closure in the D-S interval) is the norm of 0.47 s. In the absence of tachycardia, a decrease in this indicator may indicate an increase in end-diastolic pressure in the left.

  1. ventricle (LVEDD). 5. Speed ​​of diastolic opening of the anterior leaflet
(determined by the slope of the D-E section and is normally 27.6 cm/s). - A decrease in the opening speed of the valves can also be an indirect sign of an increase in LVEDP.

Image of the heart structures in the third standard position of the sensor (Fig. 6).

An echogram in this position provides information about the condition of the aortic root, aortic valve leaflets, and left atrium.


Rice. 6. M-echocardiogram in the standard position of the sensor.

The ultrasound beam, passing through the anterior and posterior walls of the base of the aorta, produces an image in the form of two parallel wavy lines. Above the anterior wall of the aorta is the outflow tract of the right ventricle, below the posterior wall of the aortic root, which is also the anterior wall of the left atrium, is the cavity of the left atrium. The movement of the aortic walls in the form of parallel wills occurs due to the displacement of the aortic root along with the fibrous ring anteriorly to the sensor during systole.

In the lumen of the base of the aorta, the movement of the aortic valve leaflets (usually the right coronary leaflet above and the left coronary leaflet below) is recorded. During the ejection of blood from the left ventricle, the right coronary cusp opens forward towards the transducer (upward on the echogram), the left coronary cusp opens in the opposite direction. During the entire systole, the valves are in a fully open state, adjacent to the walls of the aorta, and are recorded on the echogram in the form of two parallel lines located at a short distance, respectively, from the anterior and posterior walls of the aorta.

At the end of systole, the valves quickly close and close, moving towards each other. As a result, the aortic valve leaflets describe a “box”-like shape during left ventricular systole. The upper and lower walls of this “box” are formed by echo signals from the aortic leaflets, which are completely open during expulsion, and the “side walls” are formed by the divergence and closure of the valve leaflets. In diastole, the aortic valve leaflets are closed and fixed in the form of one line parallel to the walls of the aorta and located in the center of its lumen. The shape of the movement of the closed valves resembles a “snake” due to vibrations of the base of the aorta at the beginning and end of ventricular diastole.

Thus, the characteristic form of movement of the aortic valve leaflets normally is the alternation of a “box” and a “snake” in the lumen of the base of the aorta.

Main indicators recorded in the III standard position of the sensor.


  1. The lumen of the aortic base is determined by the distance between the inner surfaces of the aortic walls in the middle or at the end of diastole and does not normally exceed 3.3 cm. Expansion of the lumen of the aortic root is observed in congenital defects (tetralogy of Fallot), Marfan syndrome, aortic aneurysms of various locations.

  2. Systolic divergence of the aortic valve leaflets - the distance between the open leaflets at the beginning of systole; normally 1.7-1.9 cm. The opening of the valves decreases with stenosis of the aortic mouth.

  3. Systolic excursion of the aortic walls is the amplitude of displacement of the aortic root during systole. Normally it is about 1 cm for the posterior wall of the aorta and decreases with a decrease in cardiac output.

  4. The size of the cavity of the left atrium is measured at the very beginning of ventricular diastole at the place of greatest displacement of the aortic root to the sensor. Normally, the atrial cavity is approximately equal to the diameter of the base of the aorta (the ratio of these dimensions is no more than 1.2) and does not exceed 3.2 cm. Significant dilatation of the left atrium (cavity size 5 cm or more) is almost always accompanied by the development of a permanent form of atrial fibrillation.

II. Two-dimensional echocardiography.

Image of the cardiac structures in a longitudinal section along the long axis of the heart from the parasternal approach (Fig. 7)

1 - psmk; 2 - zsmk; 3 - papillary muscle; 4 - chords.

Figure 7. Two-dimensional echocardiogram in a long-axis section from a parasternal approach.

In this projection, the base of the aorta, the movement of the aortic valve leaflets, the cavity of the left atrium, the mitral valve, and the left ventricle are clearly visualized. Normally, the leaflets of the aortic and mitral valves are thin and move in opposite directions. With defects, the mobility of the valves decreases, the thickness and echogenicity of the valves increases due to sclerotic changes. Hypertrophies of the heart parts are determined in this projection by changes in the corresponding cavities and walls of the ventricles.

Cross-section from the parasternal short-axis approach at the level of the edges of the mitral leaflets (Fig. 8)

1- PSMK; 2- ZSMK.

Rice. 8. Short-axis section from the parasternal approach at the level of the edges of the open mitral leaflets.

The left ventricle in this section looks like a circle, to which the right ventricle is adjacent in front in the form of a crescent. The projection provides foam information about the size of the left atrioventricular opening, which is normally 4-6 cm2. The distance between the commissures is normally somewhat greater than between the valves at the moment of their maximum opening. In rheumatism, due to the development of adhesions at the commissures, the intercommissural size may be smaller than the interleaflet size. Modern echocardiographs have the ability not only to determine the size, but also to directly measure the area of ​​the mitral orifice and its perimeter (Noshu W.L. et al., 197S).

Cross-section from the parasternal approach along the short axis of the heart at the level of the base of the aorta (Fig. 9)

1st right coronary leaflet;

2nd left coronary cusp;

3-non-coronary leaflet.

Rice. 9. Short axis section from the parasternal approach at the level of the aortic root.

In the center of the image is a circular slice through the aorta and all 3 leaflets of the aortic valve. Below the aorta are the cavities of the left and right atria, and above the aorta in the form of an arch is the cavity of the right ventricle. The interatrial septum, tricuspid valve, and, with a greater tilt of the sensor, one of the pulmonary artery valve leaflets are visualized.

Projection of the 4 chambers of the heart from the apical approach (Fig. 10)

1st interatrial septum

2nd interventricular septum

Rice. 10. Scheme of a two-dimensional echogram from the apical approach in the projection of 4 chambers.

The sensor is installed above the apex of the heart, so the image on the screen appears “upside down”: the atria are below, the ventricles are above. In this projection, left ventricular aneurysms and some congenital defects (ventricular and atrial septal defects) are clearly visualized.

Echocardiogram for certain heart diseases.

Rheumatic heart defects.

Mitral stenosis.

Rheumatic endocarditis leads to morphological changes in the mitral valve: the leaflets fuse along the commissures, thicken, and become inactive.

The tendon threads change fibrously and are shortened, and the papillary muscles are affected. Deformation of the leaflets and disruption of transmitral blood flow lead to a change in the shape of the leaflet movement, determined on the echogram. As stenosis develops, the transmitral blood flow ceases to be “biphasic”, as is normal, and becomes constant through the narrowed opening throughout diastole.

In this case, the mitral valve leaflets do not close in the middle of diastole and are in the maximum open state throughout its entire length. On a one-dimensional echogram, this is manifested by a decrease in the speed of early diastolic covering of the leaflets (slope of the EF section) and the transition of the normal M-shaped movement of the leaflets to a U-shaped one with severe stenosis. Clinically, in such a patient, protodiastolic and presystolic murmur, corresponding to the E- and A-peaks of the M-echogram of the mitral valve, turns into a murmur that occupies the entire diastole. In Fig. Figure 11 shows the dynamics of a one-dimensional echogram of the mitral valve during the development of moderate and severe mitral stenosis. Moderate stenosis (Fig. 11.6) is characterized by a decrease in the speed of early diastolic Covering of the anterior leaflet (EF slope), a decrease in diastolic divergence of the leaflets (marked by arrows), and a relative increase in the DC interval. Severe stenosis is manifested by a U-shaped unidirectional movement of the leaflets (Fig. 11, c).



Fig. 11 Dynamics of the M-echogram of the mitral valve during the development of stenosis: a-norm; b-moderate stenosis; c-severe stenosis.

Unidirectional movement of the leaflets is a pathognomonic sign of rheumatic stenosis. Due to adhesions along the commissures, the anterior leaflet, during opening, pulls with it a smaller posterior leaflet, which also moves towards the sensor, and not away from it, as is normal (Fig. P., Fig. 12).


Rice. 12. A-M echocardiogram in the II standard position of the sensor. Mitral stenosis. Unidirectional U-shaped movement of the valves of the valve.

B-dome-shaped movement of the PSMC on two-dimensional echocardiography (indicated by an arrow). 1 - amplitude of divergence of valve valves; 2 - PSMC; 3 - ZSMK.

A significant echographic sign of mitral stenosis is an increase in the size of the left atrium cavity, measured in the third standard position of the sensor (more than 4-5 cm, normal 3-3.2 cm).

Features of valve changes in rheumatic lesions of the edges of the valves and commissure commissures) determine the characteristic signs of stenosis on a two-dimensional echocardiogram.

The "dome-shaped" movement of the anterior leaflet is determined in a longitudinal section from the parasternal approach. It lies in the fact that the body of the valve moves with a greater amplitude than its edge (Fig. 12, B). The mobility of the edge is limited by the fusions, but the body of the valve can remain intact for a long time. As a result, at the moment of diastolic opening of the valve, the body of the leaflet filled with blood “bulges” into the cavity of the left ventricle. Clinically, at this moment, the opening click of the mitral valve is heard. The origin of the sound phenomenon is similar to the clap of a sail filled with wind or an opening parachute and is due to the fixation of the flap on both sides - the fibrous ring at the base and the adhesions at the edge. As the defect progresses, when the body of the valve also becomes rigid, the phenomenon is not determined.

Fishmouth mitral valve deformity occurs in the late stages of the disease. This is a funnel-shaped valve due to adhesions of the valves along the commissures and shortening of the tendons. threads The valves of the riveting form a “head”, and the thickened unidirectionally moving edges resemble the opening of the fish’s mouth (Fig. 13, a).

Deformation of the valve in the form of a button loop - the mitral opening is in the form of a gap formed by the compacted edges of the leaflets (pv. 13.6).

a b

Rice. 13. Typical deformations of valve leaflets in mitral stenosis.

A two-dimensional echocardiogram in a short-axis section at the level of the edges of the mitral valves at the moment of their maximum opening allows you to measure the area of ​​the mitral orifice: moderate stenosis with an area of ​​2.3-3.0 cm 2, pronounced - 1.7-2.2 cm 2, critical - 1.6 cm 2 or less. Patients with severe and critical stenosis are subject to surgical treatment.

In addition to the above direct signs of the defect, with the development of pulmonary hypertension and hypertrophy of the right heart, corresponding changes are revealed on one-dimensional and two-dimensional echocardiography.

So, the main signs of mitral stenosis on EchoCG are:

1. Unidirectional U-shaped movement of the valves on a one-dimensional echogram.

2. Dome-shaped movement of the anterior leaflet on two-dimensional echocardiography.

3. Reduced amplitude of leaflet opening on one-dimensional and two-dimensional echocardiography, reduction in the area of ​​the mitral orifice on two-dimensional echocardiography.


  1. Dilatation of the left atrium.

Mitral valve insufficiency

Compared to mitral stenosis, echocardiography is of much less importance in the diagnosis of this defect, since only indirect signs are assessed. A direct sign - a jet of regurgitation - is recorded by Doppler echocardiography.


  1. Signs of mitral valve insufficiency (MV) on one-dimensional echocardiography

  2. Increased systolic excursion of the posterior wall and interventricular septum, moderate dilatation of the cavity of the left ventricle (signs of LV volume overload).
3. Increased excursion of the posterior wall of the left atrium in the third position of the sensor (1 cm or more); moderate hypertrophy of the left atrium.

4. "Excessive" amplitude of opening of the front leaf (more than 2.7 cm).

5. Moderate decrease in the speed of early diastolic closing of the leaflets (EF slope), which, however, does not reach the degree of decrease in this indicator with stenosis.

When the NMC is “steady”, the movement of the lines remains multidirectional.

Signs of NMC on two-dimensional echocardiography should also include a violation of the closure of the leaflets, which is sometimes determined.

Mitral defect with predominant stenosis.

EchoCG corresponds to that for mitral stenosis, but changes in the left ventricle are also recorded (increased excursion of the walls, dilatation of the cavity), which is not observed with “pure” stenosis.

Mitral disease with predominant insufficiency.

In contrast to “pure” failure, unidirectional diastolic movement of the leaflets is determined. In contrast to the predominance of stenosis, the speed of early diastolic closure of the anterior leaflet (EF) is moderately reduced and its movement does not reach a U-shape (two-phase remains - peak E followed by a “plateau”).

Aortic stenosis

Sonographic diagnosis of aortic defects is difficult due to the difficulties of visualizing both intact and deformed valves and is based mainly on indirect signs.

The main symptom of aortic stenosis is a decrease in the systolic divergence of the aortic valve leaflets, their deformation and thickening. The nature of the valve deformation depends on the etiology of the defect: with rheumatic stenosis (Fig. 14.6), adhesions are determined along the commissures with a hole in the center of the valve; with atherosclerotic lesions, the bodies of the valves are deformed, between which gaps remain (Fig. 14, c). Therefore, with atherosclerotic disease, despite the pronounced auscultatory picture, the stenosis is usually not as significant as with rheumatism.


Fig. 14. Scheme of leaflet deformation during aortic stenosis, a-normal leaflets in diastole and systole; b-rheumatism atherosclerosis. PC-right coronary cusp, LC-left coronary cusp, NC-non-coronary cusp.

An indirect sign of aortic stenosis is hypertrophy of the left ventricular myocardium without enlarging its cavity, as a result of pressure overload. Wall thickness is measured in the first standard position of the sensor or on a two-dimensional echocardiography.

Aortic valve insufficiency

With this defect, dilatation of the left ventricular cavity is determined as a consequence of volume overload and an increase in the systolic excursion of its walls due to the volume of regurgitation. The flow of regurgitation can be directly recorded using Doppler echocardiography.

The regurgitation jet, heading in diastole to the open anterior mitral leaflet (Fig. 15, a - indicated by the arrow), can cause its small-amplitude flutter (Fig. 15, b - indicated by the arrow).


Fig. 15. Aortic valve insufficiency: a-two-dimensional chogram, b-one-dimensional echocardiography in the second standard position of the sensor.

Occasionally, on a two-dimensional echogram one can see an expansion of the aortic root and a violation of the diastolic closure of the valves. On a one-dimensional echogram of the base of the aorta, this corresponds to the symptom of diastolic non-closure (“separation”) of the leaflets. In Fig. Figure 16 shows a diagram of an M-echogram of the base of the aorta in a patient with a combined aortic defect. A sign of stenosis is a decrease in the amplitude of the systolic divergence of the leaflets (1), a sign of insufficiency is the diastolic “separation” of the leaflets (2). The aortic valve leaflets are thickened and have increased echogenicity.


Fig. 16 Scheme of the M-echogram of the base of the aorta with combined aortic defect.

When stenosis and failure are combined, a mixed type of left ventricular hypertrophy is also determined - its cavity increases (as with failure) and the thickness of the walls (as with stenosis).

Hypertrophic cardiomyopathy
In the diagnosis of cardiomyopathies, echocardiography plays a leading role. Depending on the predominant localization of hypertrophy, several forms of hypertrophic cardiomyopathy (PSMP) are distinguished, some of which are presented in Fig. 17;

Asymmetric hypertrophy of the interventricular septum is indicated if its thickness exceeds the thickness of the posterior wall by more than 1.3 times. The most common form (in almost 90% of all HCM) is the obstructive form, previously called “idiopathic hypertrophic subaortic stenosis” (Fig. 17, d). The thickness of the IVS in patients reaches 2-3 cm (the norm is 0.8 cm). Approaching the anterior leaflet of the mitral valve or the hypertrophied papillary muscles, it thereby creates obstruction of the outflow tract. Accelerated systolic blood flow in the obstruction zone due to hydrodynamic forces (wing effect) pulls the anterior leaflet towards the hypertrophied IVS, aggravating the stenosis of the outflow tract.

A one-dimensional echogram in the P standard position reveals the following signs of obstructive HCM (Fig. 18):

1. An increase in the thickness of the IVS and a decrease in its systolic excursion due to fibrotic changes in the myocardium.

2. Anterior systolic deflection of the mitral leaflets and the approach of the anterior leaflet to the interventricular septum.

Rice. 17. Forms of HCM:

a-asymmetric interventricular septum;

b-concentric left ventricle;

b-apical (non-obstructive);

d-asymmetrical basal sections of the IVS, the arrow indicates the area of ​​obstruction of the LV outflow tract.


Rie. 18. Echocardiogram of a patient with obstructive HCM. Increasing the thickness of the IVS. The arrow indicates the systolic deflection of the mitral leaflets to the septum.

On the echogram of the base of the aorta in the third position of the sensor, due to a decrease in cardiac output, mid-systolic closure of the aortic valve leaflets can be observed, the form of movement of which in this case resembles the M-shaped movement of the mitral leaflets (Fig. 19).


Rice. 19. Mid-systolic closure of the aortic valve leaflets (indicated by an arrow) in obstructive HCM.

Dilation of cardiomyopytia

Dilated (congestive) cardiomyopathy (DCM) is characterized by diffuse myocardial damage with dilatation to her heart cavities and a sharp decrease his contractile function (Fig. 20).


Fig.20. Scheme of echocardiography of a patient with dilated cardiomyopathy: a - two-dimensional echocardiography, pronounced dilatation of all chambers of the heart; b- M-EchoCG-hypokinesis of the IVS and LVSD, dilated cavities of the RV and LV, an increase in the distance from the anterior MV leaflet (peak E) to the septum, characteristic movement of the MV leaflets.

In addition to dilatation of cavities, decreased myocardial contractility, including a drop in ejection fraction, DCM is characterized by the formation of blood clots in dilated cavities with frequent thromboembolic complications.

Due to a decrease in the contractility of the left ventricular myocardium, LVDP increases, which is manifested on echocardiography by the characteristic movement of the mitral leaflets. The first type (Fig. 20, a) is characterized by high opening and closing speeds of the leaflets (narrow peaks E and A), a low point F. This form is described as a “diamond-shaped” movement of the mitral leaflets, which is considered characteristic of a left ventricular aneurysm against the background of coronary artery disease ( J. Burgess et al., 1973) (Fig. 21, a).

The second type, on the contrary, is characterized by a decrease in the speed of early diastolic closure of the anterior leaflet of the mitral valve, expansion of both peaks with deformation of the presystolic one due to an increase in the AS period and the appearance of a kind of “step” in this segment (Fig. 21, b - indicated by the arrow).


Rice. 21. Types of movement of the mitral valve leaflets in DCM.

The mitral valves are well located against the background of the dilated cavities of the left parts of the heart and move in antiphase (“fish pharynx” according to H. Feigenbaum, 1976).

It is often difficult to distinguish DCM from dilatation of the heart cavities in other diseases.

In the later stages of circulatory failure caused by ischemic heart disease, dilatation of not only the left, but also the right parts of the heart can also be observed. However, in IHD, left ventricular hypertrophy predominates, and the thickness of its walls is usually greater than normal. With DCM, as a rule, diffuse damage to all chambers of the heart is observed, although there are cases with predominant damage to one of the ventricles. The thickness of the walls of the left ventricle in DCM usually does not exceed the norm. Even if there is slight hypertrophy of the walls (no more than 1.2 cm), then visually the myocardium still looks “thinned” against the background of pronounced dilatation of the cavities. IHD is characterized by a “mosaic pattern” of myocardial damage: the affected hypokinetic areas are adjacent to intact ones, in which compensatory hyperkinesis is observed. In DCM, the diffuse process causes total hypokineticity of the myocardium. The degree of hypokinesis in different areas may be different due to the different degrees of their damage, but hyperkinetic zones in DCM are never detected.

An echocardiographic picture of dilation of the heart cavities, similar to DCM, can be observed in severe myocarditis, as well as in alcoholic heart disease. To make a diagnosis in these cases, it is necessary to compare echocardiographic data with the clinical picture of the disease and data from other studies.

Bibliography

1. Dvoryakovsky I.V., Chursin V.I., Safonov V.V. Ultrasound diagnostics in pediatrics. - L.: Medicine, 1987. -160 s.

2. Zaretsky V.V., Bobkov V.V., Olbinskaya L.I. Clinical echocardiography. - M.: Medicine, 1979. - 247 p.

3. Instrumental methods for studying the cardiovascular system (Handbook) / Ed. T.S. Vinogradova. - M.: Medicine, 1986. - 416 s.

4. Interpretation of a two-dimensional echocardiogram / Yu.T. Malaya, I.I. Yabluchansky, Yu.G. Gorb and others - Kharkov: Vyshcha school, 1989. 223 p.

5. Clinical ultrasound diagnostics: A guide for doctors: T.I/ N.M. Mukharlyamov, Yu.N. Belenkov, O.Yu. Ltysov and others; edited by N.M. Mukharlyamova. - M.: Medicine, 1987. - 328 p.

6. Makolkin V.I. Acquired heart defects. - M.: Medicine, 1986. - 256 s.

7. Mikhailov S.S. Clinical anatomy of the heart. - M.: Medicine, 1987. - 288 p.

8. Moiseev V.S., Sumarokov A.V., Styazhkin V.Yu. Cardiomyopathy. - M.: Medipina, 1993. - 176 p.

9. Mukharlyamov N.M. Cardiomyopathies. - M.: Medicine, 1990. - 288 p.

10. Soloviev G.M. and others. Cardiac surgery in chocardiographic research. - M.: Medicine, 1990. - 240 p.

11. Feigenbauii) H. Echogardiography. - Philadelphia: Lea and Febiger, 1976.-495p.

RHEOGRAPHY

Rheography - a bloodless method for studying blood circulation, based on graphical recording of changes in the electrical resistance of living tissues during the passage of electric current through them. An increase in blood supply to vessels during systole leads to a decrease in the electrical resistance of the studied parts of the body.

Rheography reflects the change in blood supply to the studied area of ​​the body (organ) during the cardiac cycle and the speed of blood movement in the vessels.

Arterial pressure - an integral indicator that reflects the result of the interaction of many factors, the most important of which are systolic blood volume and the total resistance to blood flow of resistive vessels. Changes in minute blood volume (MVR) are involved in maintaining a known constancy of mean pressure in the arterial system, which is determined by the relationship between the values ​​of MVR and arterial peripheral vascular resistance. Given the coordination between flow and resistance, the mean pressure is a kind of physiological constant.

The main parameters of general hemodynamics include stroke and minute blood volume, mean systemic arterial pressure, total peripheral vascular resistance, arterial and venous pressure.

Average hemodynamic pressure in mmHg.

Proper values ​​of Rdr. depend on age and gender.

In assessing the functional state of the circulatory system, the parameters of central hemodynamics are important: stroke (systolic) volume and cardiac output (minute blood volume). Stroke volume - the amount of blood that is ejected by the heart with each contraction (the norm is between 50-75 ml), cardiac output(minute blood volume) - the amount of blood ejected by the heart within 1 minute (the normal IOC is 3.5-8 liters of blood). The magnitude of the IOC depends on gender, age, changes in ambient temperature and other factors.

One of the non-invasive methods for studying central hemodynamic parameters is the tetrapolar thoracic rheography method, which is considered the most convenient for practical use in the clinic.

Its main advantages, along with high reliability - a total error of no more than 15%, include ease of registration and calculation of basic indicators, the possibility of repeated repeated studies, the total time consumption does not exceed 15 minutes. Indicators of central hemodynamics determined by tetrapolar thoracic rheography and hemodynamic indicators determined by invasive techniques (Fick method, dye dilution method, thermal dilution method) highly correlate with each other.

Determination of stroke volume of blood (SV) using transthoracic tetrapolar rheography according to Kubichek and Yu.T. Pushkar

Rheography - a bloodless method for studying blood circulation that records the electrical resistance (impedance or its active component) of living tissues, which changes with fluctuations in blood supply during the cardiac cycle at the moment an alternating current is passed through them. The method of impedance cardiography or tetrapolar thoracic rheography has become widely used abroad to determine the hemodynamics of the left ventricle of the heart.

Kubizek (1966) recorded the value of body impedance using the principle of four electrode measurements. In this case, two ring-shaped electrodes were placed on the neck and two on the chest, at the level of the xiphoid process. To implement the method, you need: rheoplethysmograph RPG 2-02, a recorder with a recording width of 40-60 mm. It is better to record volumetric rheography and its first derivative in parallel with recording an ECG (II standard lead) and PCG on the auscultatory channel.

Methodology

Calibrate the recording scale. The device provides two calibration signal values ​​for the main rheogram: 0.1 and 0.5 cm. The amplitude of the calibration signal is 1 and 5 cm/sec, respectively. The choice of the recording scale and the magnitude of the calibration signal depends on the amplitude of the differentiated rheogram.

Electrode application diagram:

The interelectrode state L is measured with a measuring tape between the middles of potential electrodes No. 2 and No. 3 along the anterior surface of the chest.

The dial indicator on the front panel of the device continuously shows the value of the base impedance (Z). With the patient breathing freely, we record 10-20 complexes.

The amplitude of the differentiated rheogram (Ad) in each of the complexes is defined as the distance (in ohms in 1 sec) from the zero line to the peak of the differentiated curve.

The average expulsion time (Ti) is defined in the same complexes as the distance between the beginning of the rapid rise of the differentiated curve to the lower point of the incisura or from the point corresponding to 15% of the height to the lower point of the incisura. Sometimes the beginning of this period can be determined by the beginning of a step on the curve, which corresponds to the end of the isometric contraction phase. When the incisura is weakly expressed, the end of the expulsion period can be determined by the beginning of the second tone on the FCG with the addition of a constant delay time of the differentiated rheogram curve by 15-20

The measured values ​​of L, Z, Ad and Ti are transferred into the formula for determining the CV:

SV - stroke volume (ml),

K - coefficient depending on the location of the electrodes, on the type of device used (for this technique

K=0.9);

G - blood resistivity (ohm/cm) N=150;

L - distance between electrodes (cm);

Z - interelectrode impedance;

Ad - amplitude of the differentiated rheogram curve

Tu - expulsion time (sec).

Voltage index - time:

TT1=SADHSSSTp.

The tetrapolar thoracic rheography method is widely used to determine the type of central hemodynamics in patients with hypertension. The distribution is usually carried out according to the cardiac index (CI). Thus, patients with a cardiac index (CI) of more than M + 15% of its value in healthy individuals belong to the hyperkinetic type of hemodynamics, respectively, with a CI of less than M - 15% of its value in healthy individuals, patients are included in the group with the hypokinetic type. With an SI value from M-15% to M+15%, the state of blood circulation is considered eukinetic.

It is now a generally accepted fact that hypertension is hemodynamically heterogeneous and requires a differentiated approach to treatment depending on the type of blood circulation.

LITERATURE

1. Kassirsky I.A. Handbook of functional diagnostics. - M.: Medicine, 1970.

2. Pushkar Yu.T., Bolypov V.M., Elizarova N.A. and others. Determination of cardiac output by the method of tetrapolar thoracic rheography and its metrological capabilities // Cardiology. - 1977. - No. 7. - p.85-90.

3. Harrison T.R. Internal illnesses. - M.: Medicine, vol. 7, 1993.

PHONOCARDIOGRAPHY

Phonocardiography (PCG) is a method of graphically recording heart sounds and murmurs and their diagnostic interpretation. FCG significantly complements auscultation and introduces many fundamentally new things into the study of heart sounds. It allows you to objectively assess the intensity and duration of heart sounds and murmurs. However, correct interpretation is possible in conjunction with the clinical picture of the disease. The sensitivity of the human ear is more significant than that of the PKG sensor. The use of channels with different frequency characteristics makes it possible to selectively register heart sounds and determine third and fourth sounds that are not audible during auscultation. Determining the shape of the noise makes it possible to establish its genesis and resolve the issue of its conductive nature at different points of the heart. Simultaneous synchronous registration of PCG and ECG reveals a number of important patterns in the relationship of heart sounds with the ECG.

Phonocardiographic research technique

FCG recording is carried out using a phonocardiograph, consisting of a microphone, an amplifier, a system of frequency filters and a recording device. A microphone located at various points in the heart region perceives sound vibrations and converts them into electrical ones. The latter are amplified and transmitted to a system of frequency filters, which select one or another group of frequencies from all heart sounds and then pass them to various recording channels, which allows selective recording of low, medium and high frequencies.

The room in which the FCG is recorded must be isolated from noise. Typically, FCG is recorded after a 5-minute rest of the subject in a supine position. Preliminary auscultation and clinical data are decisive in the selection of main and additional recording points, special techniques (recording in a lateral position, standing, after physical activity, etc.). Typically, FCG is recorded while holding the breath during exhalation, and, if necessary, at the height of inspiration and during breathing. When using airborne microphones, absolute silence is required for recording. Vibration sensors - detect and record vibrations of the chest, less sensitive, but more convenient in practical work.

Currently, the two most common frequency response systems are Maass-Weber and Mannheimer. The Maass-Weber system is used in domestic phonocardiographs, German and Austrian. The Mannheimer system is used in Swedish devices

"Mingograph".

Frequency characteristics according to Maass-Weber:

The channel with the au-cultivative characteristic has the greatest practical significance. FCG recorded on this channel is compared in detail with auscultatory data.

On channels with a low-frequency characteristic, III and IV tones are recorded; I and II tones are clearly visible in cases where they are obscured by noise on the auscultatory channel.

High-frequency noise is well recorded on the high-frequency channel. For practical work, it is good to use auscultation, low-frequency and high-frequency characteristics.

The FCG must have the following special designations (in addition to the surname of the subject, date, etc.): ECG lead (usually standard II), frequency response of channels and recording points. All additional techniques are also noted: recording in a position on the left side, after physical activity, while breathing, etc.

Normal phonocardiogram consists of oscillations of the I, II and often III and IV heart sounds. The systolic and diastolic pause on the auscultatory channel corresponds to a straight line without fluctuations, called isoacoustic.

Scheme of normal FCG. Q-I tone. a - initial, muscular component of the first tone;

B - central, valve component of tone I;

B - final component of tone I;

A - aortic component of the II tone;

P - pulmonary (pulmonalis) component of tone II

When recording FCG synchronously with an electrocardiogram, oscillations of the first tone are determined at the level of the S wave of the electrocardiogram, and the second tone - at the end of the T wave.

The normal first sound in the region of the apex of the heart and in the projection of the mitral valve consists of three main groups of oscillations. Initial low-frequency, small amplitude oscillations are the muscular component of the first tone, caused by contraction of the ventricular muscles. The central part of the first tone, or as it is called - the main segment - more frequent oscillations, large amplitude, are caused by the closure of the mitral and tricuspid valves. The final part of the first tone is a small amplitude oscillation associated with the opening of the aortic and pulmonary artery valves and vibrations of the walls of large vessels. The maximum amplitude of the first tone is determined by its central part. At the apex of the heart it is IVa "2 times greater than the amplitude of the II tone.

The beginning of the central part of the first tone is 0.04-0.06 seconds from the beginning of the Q wave of a synchronously recorded ECG. This interval is called the Q-I tone interval, the period of transformation or transformation. It corresponds to the time between the onset of ventricular excitation and the closure of the mitral valve. The greater the pressure in the left atrium, the greater the Q-I sound. Q-I tone cannot be an absolute sign of mitral stenosis; it may be a sign of myocardial infarction.

The second tone at the base of the heart is 2 times or more greater than the first tone. In its composition, the first group of oscillations, large in amplitude, corresponding to the closure of the aortic valves, the aortic component of the second tone, is often visible. The second group of oscillations, 1.5-2 times smaller in amplitude, corresponds to the closure of the pulmonary valves - the pulmonary component of the second tone. The interval between the aortic and pulmonary components is 0.02-0.04 seconds. It is caused by a physiological delay in the end of right ventricular systole.

Normal III tone is often found in young people under 30 years of age, asthenics and athletes. It is a weak and low-frequency sound and is therefore heard less frequently than recorded. The third tone is well recorded on the low-frequency channel in the form of 2-3 rare oscillations of small amplitude, following 0.12-0.18 seconds after the second tone. The origin of the III tone is associated with muscle vibrations in the phase of rapid filling of the left ventricle (left ventricular III sound) and the right ventricle (right ventricular III sound).

Normal IV tone, atrial tone is detected less frequently than III tone in the same population. It is also a weak, low-frequency sound, usually not audible during auscultation. It is determined on a low-frequency channel in the form of 1-2 rare, low-amplitude oscillations located at the end of P, synchronously recorded ECG. IV tone is caused by atrial contraction. Total gallop - a 4-beat rhythm is heard (there are 3rd and 4th tones), observed with tachycardia or bradycardia.

It is advisable to begin the analysis of FCG with a description of the tones and time intervals associated with them. Then the noises are described. All additional techniques and their effect on tones and noises are at the end of the analysis. The conclusion can be accurate, differential diagnostic, or speculative.

Pathological changes in phonocardiogram.

Pathology of tones.

Weakening of the first tone - a decrease in its amplitude has independent significance in the area of ​​the mitral and tricuspid valves. Mainly determined in comparison with the amplitude of the second tone. The weakening of the first tone is based on the following reasons: destruction of the atrioventricular valves, mainly the mitral valve, limitation of valve mobility, calcification, decreased myocardial contractile function, with myocarditis, obesity, myxedema, mitral valve insufficiency.

Strengthening the first tone occurs with fibrosis of the atrioventricular valves while maintaining their mobility, with a rapid increase in intraventricular pressure. When the P-Q I interval is shortened, the tone increases, and when the interval is lengthened, it decreases. It is observed with tachycardia (hyperthyroidism, anemia) and often with mitral valve stenosis. With complete atrioventricular block, the greatest amplitude of the first tone (“cannon” tone according to N.D. Strazhenko) is observed when the P wave is directly adjacent to the QRS complex.

Splitting of the first tone up to 0.03-0.04 seconds with an increase in both components occurs with mitral-tricuspid stenosis due to simultaneous closure of the mitral and tricuspid valves. It also occurs with bundle branch block as a result of asynchronism in ventricular contraction.

Weakening of the second tone has independent significance in the aorta, where it is caused by the destruction of the aortic valves or a sharp limitation of their mobility. A decrease in pressure in the aorta and pulmonary artery also leads to a weakening of the second tone.

Strengthening the 2nd tone on the aorta or pulmonary artery is associated with an increase in blood pressure in these vessels, compaction of the valve stroma (hypertension, symptomatic hypertension, hypertension of the pulmonary circulation, atherosclerotic changes).

Second tone splitting characterized by a stable delay of the pulmonary component, independent of the phases of breathing - a “fixed” splitting of the second tone according to the terminology of foreign authors. It occurs when the ejection phase of blood from the right ventricle is prolonged, which leads to later closure of the pulmonary valves. This occurs when there is an obstruction to the outflow of blood from the right ventricle - pulmonary artery stenosis, when the right heart is overfilled with blood. The pulmonary component of tone II increases, becomes equal to the aortic one and even exceeds it with increased blood supply to the pulmonary circulation and decreases or completely disappears with low blood supply to the pulmonary circulation. Pathological splitting of the second tone is also observed with blockade of the right bundle branch. The development of severe pulmonary hypertension with changes in the vessels of the pulmonary circulation leads to a shortening of the phase of blood expulsion from the right ventricle, to an earlier closure of the pulmonary valves and, consequently, to a decrease in the degree of splitting of the second sound. Then the large component merges with the aortic one, as a result of which a large, unsplit II tone is determined, maximally expressed in the area of ​​the pulmonary artery, which is determined upon auscultation as sharply accentuated. This II tone is a sign of severe pulmonary hypertension.

Splitting of the second sound with a delay of the aortic component is rare and is called “paradoxical”. It is caused by a sharp slowdown in the ejection phase of blood from the left ventricle with stenosis of the aortic orifice or subclasal stenosis, as well as with blockade of the left bundle branch.

Pathological III tone - large amplitude, fixed on the auscultation channel and clearly audible during auscultation, associated with increased diastolic blood flow to the ventricles or with a sharp weakening of myocardial tone (myocardial infarction). The appearance of a pathological III tone causes a three-part rhythm - a protodiastolic gallop.

Pathological IV tone is also characterized by an increase in amplitude and fixation on the auscultatory channel. Most often occurs when the right atrium is overloaded with congenital heart defects. The appearance of a pathological atrial tone causes the presystolic form of the gallop rhythm.

To characterize tones, low-frequency PCG recording is used.

Sometimes a click or late systolic click is recorded on FCG during systole. It is better heard during exhalation at the apex and at Botkin's point. Click - on the FCG, a narrow group of oscillations recorded on the mid-frequency or high-frequency channel of the FCG, at the beginning or end of systole and associated with mitral valve prolapse.

In diastole, an extraton is recorded - a click of the opening of the mitral valve (open snep "O.S.") occurs with mitral stenosis. OS - consists of 2-5 oscillations, with a duration of 0.02-0.05", necessarily visible on the high-frequency channel, at a distance of 0.03-0.11" from the beginning of the second tone. The higher the pressure in the left atrium, the shorter the distance of the second sound - 08.

With stenosis of the 3-leaf valve, the sound of the opening of the tricuspid valve is analogous to the click of the opening of the mitral valve. Short and rare, best heard on the right and left of the xiphoid process, in the fourth intercostal space to the left of the sternum. It is better heard during exhalation, and is located at a distance of 0.06" - 0.08" from the second tone.

To analyze the noise pattern, medium and high frequency channels are used.

Noise characteristic:

1. relation to the phases of the cardiac cycle (systolic and diastolic);

2. duration and form of noise;

3. temporal relationship between noise and tones;

4. frequency response

5. by duration and temporary relationships. I. Systolic: a) protosystolic;

B) mesosystolic;

B) late systolic;

D) holo or pansystolic.


Scheme of changes in tones and noises in acquired heart defects.

OS m - mitral valve opening tone;

OS t - opening tone of the tricuenidal valve;

I m - mitral component of the first tone;

I t - tricuspid component of the first tone;

1 - mitral valve insufficiency;

2 - mitral stenosis;

3 - mitral stenosis and mitral valve insufficiency;

4 - aortic valve insufficiency;

5 - stenosis of the aortic mouth;

6 - stenosis of the aortic mouth and aortic valve insufficiency;

7 - tricuspid valve insufficiency;

8 - tricuspid stenosis;

9 - tricuspid stenosis and tricuspid valve insufficiency.

Functional systolic murmurs are low-amplitude, low-frequency, spaced from the first sound by 0.05", with a duration of less than 0.5" of systole, usually of an increasing nature or have a diamond shape. For differential diagnosis, physical activity, the Valsalva maneuver is used, conductivity is taken into account, a test with amyl nitrite is an increase in functional noise.

LITERATURE

Kassirsky I.A. Handbook of functional diagnostics. - M.: Medicine, 1970. Harrison T.R. Internal illnesses. - M.: Medicine,