Aortic insufficiency. Aortic valve insufficiency: types of disease and treatment regimens Aortic valve dimensions

Aortic insufficiency is a pathology in which the aortic valve leaflets do not close completely, as a result of which the return flow of blood into the left ventricle of the heart from the aorta is disrupted.

This disease causes many unpleasant symptoms - chest pain, dizziness, shortness of breath, irregular heartbeat and more.

The aortic valve is a valve in the aorta, which consists of 3 leaflets. Designed to separate the aorta and left ventricle. In a normal state, when blood flows from this ventricle into the aortic cavity, the valve closes tightly, creating pressure due to which ensures the flow of blood through thin arteries to all organs of the body, without the possibility of reverse outflow.

If the structure of this valve is damaged, it closes only partially, which leads to the backflow of blood into the left ventricle. Wherein organs stop receiving the required amount of blood for normal functioning, and the heart has to contract more intensely to compensate for the lack of blood.

As a result of these processes, aortic insufficiency is formed.

According to statistics, this Aortic valve insufficiency occurs in approximately 15% of people having any heart defects and often accompanies diseases such as the mitral valve. As an independent disease, this pathology occurs in 5% of patients with heart defects. Most often it affects males, as a result of exposure to internal or external factors.

Useful video about aortic valve insufficiency:

Causes and risk factors

Aortic insufficiency occurs when the aortic valve is damaged. The reasons that lead to its damage may be the following:

Other causes of the disease, which are much less common, can be: connective tissue diseases, rheumatoid arthritis, ankylosing spondylitis, diseases of the immune system, long-term radiation therapy for the formation of tumors in the chest area.

Types and forms of the disease

Aortic insufficiency is divided into several types and forms. Depending on the period of formation of the pathology, the disease can be:

• congenital– occurs due to poor genetics or the adverse effects of harmful factors on a pregnant woman;
• acquired– appears as a result of various diseases, tumors or injuries.

The acquired form, in turn, is divided into functional and organic.

• functional– formed when the aorta or left ventricle dilates;
• organic– occurs due to damage to valve tissue.

1, 2, 3, 4 and 5 degrees

Depending on the clinical picture of the disease, aortic insufficiency occurs in several stages:

1. First stage. It is characterized by the absence of symptoms, a slight enlargement of the heart walls on the left side, with a moderate increase in the size of the left ventricular cavity.
2. Second stage. The period of latent decompensation, when pronounced symptoms are not yet observed, but the walls and cavity of the left ventricle are already quite increased in size.
3. Third stage. The formation of coronary insufficiency, when partial reflux of blood from the aorta back into the ventricle already occurs. Characterized by frequent pain in the heart area.
4. Fourth stage. The left ventricle contracts weakly, which leads to congestion in the blood vessels. Symptoms such as shortness of breath, lack of air, swelling of the lungs, heart failure are observed.
5. Fifth stage. It is considered the pre-mortem stage, when it is almost impossible to save the patient’s life. The heart contracts very weakly, resulting in blood stagnation in the internal organs.

Danger and complications

If treatment does not begin in a timely manner, or the disease occurs in an acute form, pathology can lead to the development of the following complications:

• – a disease in which an inflammatory process forms in the heart valves as a result of the impact of pathogenic microorganisms on the damaged valve structures;
• lungs;
• heart rhythm disturbances - ventricular or atrial extrasystole, atrial fibrillation; ventricular fibrillation;
• thromboembolism – the formation of blood clots in the brain and other organs, which can lead to strokes and heart attacks.

When treating aortic insufficiency surgically, there is a risk of developing complications such as implant destruction, endocarditis. Surgical patients often have to take medications for life to prevent complications.

Symptoms

Symptoms of the disease depend on its stage. In the initial stages, the patient may not experience any discomfort, since only the left ventricle is subject to stress - a fairly powerful part of the heart that can withstand disruptions in the circulatory system for a very long time.

As the pathology develops, the following symptoms begin to appear:

• Pulsating sensations in the head, neck, increased heartbeat, especially in a supine position. These signs arise due to the fact that a larger volume of blood enters the aorta than usual - the blood that returned to the aorta through a loosely closed valve is added to the normal amount.
• Pain in the area of ​​the heart. They can be compressive or squeezing and appear due to impaired blood flow through the arteries.
• Cardiopalmus. It is formed as a result of a lack of blood in the organs, as a result of which the heart is forced to work at an accelerated rhythm to compensate for the required volume of blood.
• Dizziness, fainting, severe headaches, vision problems, ringing in the ears. Characteristic of stages 3 and 4, when blood circulation in the brain is disrupted.
• Weakness in the body, increased fatigue, shortness of breath, heart rhythm disturbances, increased sweating e. At the beginning of the disease, these symptoms occur only during physical exertion, later they begin to bother the patient even in a calm state. The appearance of these signs is associated with impaired blood flow to the organs.

The acute form of the disease can lead to overload of the left ventricle and the formation of pulmonary edema, coupled with a sharp decrease in blood pressure. If surgical care is not provided during this period, the patient may die.

When to see a doctor and which one

This pathology requires timely medical attention. If you notice the first signs - increased fatigue, throbbing in the neck or head, pressing pain in the sternum and shortness of breath - you should consult a doctor as soon as possible. This disease is treated therapist, cardiologist.

Diagnostics

To make a diagnosis, the doctor examines the patient’s complaints, his lifestyle, anamnesis, then the following examinations are carried out:

• Physical examination. Allows you to identify such signs of aortic insufficiency as: pulsation of the arteries, dilated pupils, dilation of the heart to the left side, enlargement of the aorta in its initial section, low blood pressure.
• Urine and blood analysis. With its help, you can determine the presence of concomitant disorders and inflammatory processes in the body.
• Biochemical blood test. Shows the level of cholesterol, protein, sugar, uric acid. Necessary to detect organ damage.
• ECG to determine heart rate and heart size. Find out everything about.
• Echocardiography. Allows you to determine the diameter of the aorta and pathologies in the structure of the aortic valve.
• Radiography. Shows the location, shape and size of the heart.
• Phonocardiogram for the study of heart murmurs.
• CT, MRI, CCG- to study blood flow.

Treatment methods

In the initial stages, when the pathology is mild, patients are prescribed regular visits to a cardiologist, an ECG examination and an echocardiogram. Moderate form of aortic insufficiency is treated with medication, the goal of therapy is to reduce the likelihood of damage to the aortic valve and the walls of the left ventricle.

First of all, drugs are prescribed that eliminate the cause of the pathology. For example, if the cause is rheumatism, antibiotics may be indicated. The following are prescribed as additional means:

• diuretics;
• ACE inhibitors – Lisinopril, Elanopril, Captopril;
• beta blockers - Anaprilin, Tranzikor, Atenolol;
• angiotensin receptor blockers - Naviten, Valsartan, Losartan;
• calcium blockers – Nifedipine, Corinfar;
• drugs to eliminate complications resulting from aortic insufficiency.

In severe forms, surgery may be prescribed. There are several types of surgery for aortic insufficiency:

• aortic valve plastic surgery;
• aortic valve replacement;
• implantation;
• Heart transplantation is performed for severe heart damage.

If aortic valve implantation has been performed, patients are prescribed Lifelong use of anticoagulants - Aspirin, Warfarin. If the valve was replaced with a prosthesis made of biological materials, anticoagulants will need to be taken in short courses (up to 3 months). Plastic surgery does not require taking these medications.

To prevent relapses, antibiotic therapy, strengthening the immune system, and timely treatment of infectious diseases may be prescribed.

Forecasts and preventive measures

The prognosis for aortic insufficiency depends on the severity of the disease, as well as on what disease caused the development of the pathology. Survival of patients with severe aortic insufficiency without symptoms of decompensation approximately equals 5-10 years.

The stage of decompensation does not give such comforting prognoses– drug therapy is ineffective and most patients, without timely surgical intervention, die within the next 2-3 years.

Measures to prevent this disease are:

• prevention of diseases that cause damage to the aortic valve - rheumatism, endocarditis;
• hardening of the body;
• timely treatment of chronic inflammatory diseases.

Aortic valve insufficiency – an extremely serious disease that cannot be left to chance. Folk remedies won't help matters here. Without proper drug treatment and constant monitoring by doctors, the disease can lead to severe complications, including death.

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

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).

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

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

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

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 speeds of opening and closing of the leaflets (narrow peaks E and 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).

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

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 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 characteristics:

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, separated 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,