Aortic insufficiency. Characteristics of valve movement by echocardiography. Normal EchoCG (echocardioscopy) Divergence of the aortic valve leaflets is normal

Definition: aortic valve insufficiency (aortic insufficiency) is a heart defect in which the semilunar cusps of the aortic valve do not completely close the aortic opening during diastole of the left ventricle. As a result, blood flows back from the aorta into the left ventricle (aortic regurgitation).

Etiology of aortic insufficiency:- against the background of a number of diseases, anatomical changes in the aortic valve occur, leading to its insufficiency. Against the background of rheumatic endocarditis, wrinkling and shortening of the semilunar valves occurs as a result of the inflammatory-sclerotic process. In infectious (septic) endocarditis (ulcerative endocarditis), partial disintegration occurs with the formation of defects, followed by scarring and shortening of the valve leaflets. With syphilis, atherosclerosis and some systemic connective diseases (rheumatoid arthritis, ankylosing spondylitis), the main role in the formation of aortic insufficiency is played mainly by damage to the aorta itself. As a result of the expansion of the aorta and its valve ring, the semilunar valves are retracted with their incomplete closure. It is extremely rare that aortic insufficiency occurs against the background of a closed chest injury with rupture or tear of the valve leaflets.

Due to the fact that the valve leaflets do not completely close the lumen of the aortic ostium, during diastole blood enters the left ventricle not only from the left atrium, but also from the aorta due to reverse blood flow (aortic regurgitation) during diastolic relaxation of the left ventricle, the pressure in it is lower than in the aorta. This leads to overfilling and greater distension of the left ventricle during diastole. During systole, the left ventricle contracts with greater force, throwing an increased volume of blood into the aorta. Volume load causes an increase in the work of the left ventricle, which leads to its hypertrophy. Thus, hypertrophy and then dilatation of the left ventricle occurs. Increased cardiac output in systole and aortic regurgitation in diastole, leading to a sharper than normal drop in pressure in the aorta and arterial system during the diastolic period. An increased systolic blood volume compared to the norm causes an increase in systolic blood pressure; the return of part of the blood to the ventricle leads to a more rapid drop in diastolic pressure, the values ​​of which become lower than normal. A sharp fluctuation in pressure in the arterial system causes increased pulsation of the aorta and arterial vessels.

The defect is compensated by the increased work of the powerful left ventricle, so the health of patients can remain satisfactory for a long time. However, over time, complaints appear.

The main complaints may be: - pain in the heart area, similar to angina pectoris. They are caused by coronary insufficiency due to an increase in oxygen demand against the background of myocardial hypertrophy and increased work of the left ventricle, as well as a decrease in blood supply to the coronary arteries with low diastolic pressure in the aorta.

Dizziness: sensations of “noise” and “pulsation” in the head occur as a result of a malnutrition of the brain against the background of sharp fluctuations in blood pressure and low diastolic pressure. When the defect is decompensated, symptoms of heart failure appear: decreased tolerance to physical activity, inspiratory shortness of breath, palpitations. As heart failure progresses, the following may occur: - cardiac asthma, pulmonary edema.

Examination (a number of symptoms are revealed):

1. Paleness of the skin (low blood supply to the arterial system during diastole due to reduced diastolic blood pressure).

2. Pulsation of peripheral arteries (increased systolic blood pressure against the background of a larger than normal stroke volume of the left ventricle; and a rapid decrease in diastolic blood pressure against the background of aortic regurgitation).

Pulsation: carotid arteries (“carotid dance”); subclavian, brachial, temporal, etc.

Rhythmic shaking of the head, synchronous with the arterial pulse (Muse's symptom) - occurs in severe aortic insufficiency due to pronounced vascular pulsation due to mechanical transmission of vibrations.

A rhythmic change in the color of the nail bed when pressing on the end of the nail (Quincke's capillary pulse). A more accurate name is pseudocapillary Quincke's pulse, because It is not the capillaries that pulsate, but the smallest arteries and arterioles. It is noted in cases of severe aortic insufficiency.

The following have a similar origin: - pulsatory hyperemia of the soft palate, pulsation of the iris, rhythmic increase and decrease in the area of ​​redness of the skin after friction.

When examining the heart area, the apical impulse is often noticeable, enlarged in area and shifted downward and to the left (the result of increased work against the background of the volume load of the hypertrophied left ventricle).

Palpation

On palpation, a displacement of the apical impulse is determined in the sixth, sometimes in the seventh, intercostal space, outward from the midclavicular line. The apical impulse is strengthened, diffuse, lifting, dome-shaped, which indicates a large enlargement of the left ventricle and its hypertrophy.

Percussion

Percussion reveals a shift in the borders of cardiac dullness to the left. In this case, the configuration of cardiac dullness is determined by percussion, which has a pronounced cardiac waist (aortic configuration).

Auscultation

A characteristic auscultatory sign of aortic insufficiency is a diastolic murmur heard in the aorta (2nd intercostal space to the right of the sternum) and at the Botkin-Erb point. This noise is blowing in nature, protodiastolic. It weakens towards the end of diastole, as blood pressure in the aorta drops and blood flow slows (therefore, the noise is of a decreasing nature, with a maximum severity at the beginning of diastole.)

Auscultation also reveals: weakening of the first sound at the apex (during systole of the left ventricle there is no period of closed valves, with incomplete closure of the aortic valve leaflets, which reduces the intensity of tension at the beginning of systole) (phase of isometric contraction, and leads to a weakening of the valve component of the first sound) . The second sound on the aorta is also weakened, and with significant damage to the mitral valve leaflets, the second sound may not be heard at all (a decrease in the contribution of the aortic valve leaflets to the formation of the valve component of the second sound). In some cases, with syphilitic and atherosclerotic lesions of the aorta, the II tone may remain quite loud, and even its accent may be noted.

With aortic insufficiency, murmurs of functional origin may be heard. This is a systolic murmur at the apex, caused by relative mitral valve insufficiency against the background of left ventricular dilatation and stretching of the fibrous mitral valve ring, which leads to its incomplete closure, although the mitral valve leaflets remain intact. Diastolic murmur (presystolic murmur - Flint murmur) may appear relatively less frequently at the apex. It is associated with the fact that functional stenosis of the left atrioventricular orifice occurs, due to the fact that the jet of aortic regurgitation lifts the anterior leaflet of the mitral valve, located closer to the outflow tract of the left ventricle, and causes the closure of the atrioventricular orifice, which creates an obstacle to transmitral diastolic blood flow.

Study of pulse and blood pressure.

The arterial pulse in aortic insufficiency, due to increased systolic output of the left ventricle and large fluctuations in blood pressure, becomes fast, high, large (pulsus celler, altus, magnus). Blood pressure changes as follows: systolic increases (increased stroke output), diastolic decreases (a more pronounced and rapid decrease in blood pressure in diastole due to the reverse flow of blood from the aorta into the left ventricle against the background of aortic regurgitation). Pulse blood pressure (the difference between systolic and diastolic) increases.

Sometimes, when measuring blood pressure, a so-called “infinite tone” may be noted (when the pressure in the manometer cuff reaches zero, Korotkoff sounds remain). This is explained by the sound of the first tone on the peripheral artery when an increased pulse wave passes through the section of the vessel compressed by the stethoscope.

When listening to arteries, the first sound above the arteries (carotid, subclavian) becomes louder due to the passage of a larger pulse wave (increases systolic output), while the first sound can be heard on arteries more distant from the heart (brachial, radial). As for the femoral artery, with severe aortic insufficiency, two tones are sometimes heard (double Traube sound), which is associated with vibrations of the vascular wall, both during systole and during diastole (reverse blood flow against the background of aortic regurgitation). With aortic insufficiency above the femoral artery, when it is compressed with a stethoscope, two murmurs can be heard (one in systole, the other in diastole) - the double Vinogradov-Durozier murmur. The first of these noises is stenotic noise, due to the passage of a pulse wave through a vessel narrowed by a stethoscope. The genesis of the second murmur is probably associated with the movement of blood towards the heart in diastole against the background of aortic regurgitation.

Data from additional research methods.

Physical examination data (palpation, percussion) indicate hypertrophy and dilatation of the left ventricle are confirmed by additional research methods.

On ECG signs of left ventricular hypertrophy appear (deviation of the electrical axis of the heart to the left, deep S waves in the right chest leads, high R waves in the left chest leads, an increase in the time of internal deviation in the left chest leads). Changes in the final part of the ventricular complex, as a result of hypertrophy and overload of the left ventricle (downward depression of the ST segment in combination with an asymmetric negative or biphasic T wave in I, AVL and left precordial leads).

During X-ray examination– enlargement of the left ventricle with an emphasized cardiac waist (aortic configuration), expansion of the aorta and increased pulsation.

During phonocardiographic study (PCG)– above the aorta, a decrease in the amplitude of sounds is detected, especially a second and decreasing diastolic murmur with a maximum at the beginning of diastole.

It should be noted that currently FCG is used relatively rarely and has an auxiliary value. This is due to the fact that the emergence of such a modern method as Doppler echocardiography (including color Doppler echocardiography) provides much more information (not only qualitative, indicating the presence of aortic insufficiency, but also quantitative, by which one can judge the magnitude of aortic regurgitation and the severity of the defect) .

Echocardiography, Doppler echocardiography.

An echocardiographic study reveals signs indicating intracardiac hemodynamic disturbances characteristic of this defect: an increase in the cavity of the left ventricle, hypertrophy of its myocardium, increased systolic excursion of its walls, indicating a volume load on the left ventricle. When examining in M ​​mode at the level of the mitral valve leaflets, an increase in the cavity of the left ventricle, hypertrophy of its myocardium, and increased systolic excursion of its walls may be noted, indicating a volume load on the left ventricle. When examining in M ​​mode at the level of the mitral valve leaflets, a peculiar sign may be noted during echolocation of the anterior leaflet, associated with its vibrations under the influence of the jet of aortic regurgitation (flutter - symptom).

Doppler echocardiographic examination makes it possible to directly confirm aortic insufficiency: - both the presence of the latter and the degree of its severity (see section “Echocardiography for heart defects”.

Thus, by evaluating the data obtained from physical and additional methods of examining the patient, it is possible, in accordance with the proposed algorithm, to analyze the results obtained in order to finally establish aortic insufficiency as a heart defect with its clinical characteristics.

The algorithm for assessing examination data provides for the identification of three groups of signs of this heart defect:

1. Valve signs that directly confirm an existing valve defect:

A. Physical: - on auscultation, diastolic (protodiastolic) noise and weakening of the second sound on the aorta and at the Botkin-Erb point.

B. Additional methods: on FCG - in the aorta there is a decrease in the amplitude of sounds, especially the second tone; diastolic, decreasing murmur.

Doppler echocardiography: signs of aortic regurgitation (mild, moderate, severe regurgitation)

2. Vascular signs:

“Carotid Dance”; Musset's symptom; changes in blood pressure (increased systolic, decreased diastolic, increased pulse pressure). Listening to the “infinite tone” when determining blood pressure using the Korotkoff method. Changes in arterial pulse (pulsus celler, altus, magnus). Double Traube tone, double Vinogradov-Durozier noise. Quincke's sign (pseudo-capillary pulse), pulsatory hyperemia of the soft palate, pulsation of the iris.

3. Left ventricular signs (signs of hypertrophy and

volume overload on the entire left ventricle.

A. Physical:

Shift down and to the left of the apical impulse. The apical impulse is strengthened, lifting, dome-shaped. Percussion shift of cardiac dullness to the left. Aortic configuration of cardiac dullness with a pronounced cardiac waist.

B. Additional methods:

X-ray examination - confirms the physical data (expanded shadows of the heart to the left, aortic configuration); expansion and pulsation of the aorta.

ECG - signs of hypertrophy and systolic overload of the left ventricle.

ECHO-CG – signs of left ventricular dilatation (increased end-diastolic volume); increased systolic excursion of the walls of the left ventricle, hypertrophy of its myocardium.

The above three groups of signs are mandatory for aortic insufficiency as a heart defect.

As for vascular signs, characteristic changes in pulse and blood pressure are sufficient to establish aortic insufficiency as a heart defect. Such signs as Muset's symptom, Quincke's symptom; the double murmur of Vinogradov-Durozier et al. does not always occur and is usually found in severe aortic insufficiency.

After a diagnosis of heart disease has been established, clinical and anamnestic data suggest its etiology.

If there are signs of heart failure, indicate the symptoms indicating its presence, and also in the formulation of the clinical diagnosis indicate the stage of congestive heart failure according to N.D.’s classification. Strazhesko, V.Kh. Vasilenko and her NYHA functional class.

Aortic stenosis (stenosis of the aortic mouth).

Definition: Aortic stenosis is a heart defect in which there is an obstacle to the expulsion of blood into the aorta during contraction of the left ventricle as a result of a decrease in the area of ​​the aortic ostium. Aortic stenosis occurs when the cusps of the aortic valve fusion, or appears as a result of cicatricial narrowing of the aortic opening.

Etiology: there are three main causes of aortic stenosis: rheumatic endocarditis, the most common cause, degenerative aortic stenosis (sclerosis, calcification occurs against the background of the atherosclerotic process), valve rings and aortic valve leaflets), congenital aortic stenosis (including with a bicuspid aortic valve ).

With rheumatic etiology of aortic valve stenosis, there is usually concomitant aortic insufficiency, often plus mitral valve disease.

The mechanism of hemodynamic disorders.

Normally, the area of ​​the aortic mouth is 2-3 cm. Clinical manifestations occur when the aortic mouth is narrowed by 3-4 times - less than 0.75 cm, and with an area of ​​the aortic opening of 0.5 cm, aortic stenosis is considered critical. If the degree of narrowing of the aortic opening is small, then no significant circulatory disturbance occurs. If there is an obstacle to the expulsion of blood into systole, the left ventricle has to contract with great tension, resulting in a systolic pressure gradient between the left ventricle and the aorta. The increased pressure gradient provides the desired value of the stroke volume of the left ventricle when blood is expelled through the narrowed orifice during the allotted time interval (the ejection period). That is, there is a resistance load during the expulsion of blood, which significantly increases the mechanical work of the left ventricle and causes its pronounced hypertrophy. Hemodynamic disorders are caused by the organic capabilities of the left ventricle and cause its pronounced hypertrophy. Hemodynamic disorders are caused by a limitation in the ability of the left ventricle to adequately increase cardiac output when it comes to intense physical activity. If the degree of stenosis is small, then incomplete systolic emptying of the left ventricle may occur. This leads to the fact that during diastole, a normal amount of blood from the left atrium enters the incompletely emptied left ventricle (increased atrial systole for adequate filling of the hypertrophied left ventricle with increased diastolic pressure). Hyperfunction of the left atrium can lead to its dilatation. Changes in the left atrium can cause atrial fibrillation, which in turn can dramatically worsen intracardiac hemodynamics in aortic stenosis. Over time, with the development of cardiac decompensation and impaired emptying of the left chambers of the heart, the increased pressure in them is retrogradely transmitted to the pulmonary veins and to the venous knee of the pulmonary circulation. Subsequently, venous stagnation of blood occurs in the pulmonary circulation, as well as an increase in pressure in the pulmonary artery system as a result of the Kitaev reflex. This in turn leads to a load on the right ventricle with subsequent decompensation and dilation, increased pressure in the right atrium and the development of congestion in the systemic circulation.

Clinical picture.

Aortic stenosis can be a compensated heart defect for many years and does not cause any complaints even with heavy physical exertion. This is explained by the large compensatory capabilities of the powerful left ventricle. However, with pronounced narrowing of the aortic mouth, characteristic clinical symptoms appear. In patients with severe aortic stenosis, a classic triad of symptoms is observed: - angina pectoris; fainting during physical exertion; development of heart failure (which initially occurs of the left ventricular type). The occurrence of angina pectoris even with absolutely normal coronary arteries in aortic stenosis is associated with relative coronary insufficiency of the hypertrophied left ventricle (discrepancy between the increased myocardial oxygen consumption and the degree of its vascularization).

A certain role may be played by the Venturi effect, which consists in the suction effect of a blood stream when passing through a stenotic valve at the level of the ostia of the coronary arteries. A certain role may be played by the absence of an increase in cardiac output adequate to physical activity (“fixed stroke volume”), which is reflected in an adequate increase in coronary blood flow for an intensively working hypertrophied left ventricle. Fainting during physical activity occurs due to dilation of blood vessels in working muscles and redistribution of blood flow to the muscles with a simultaneous decrease in blood supply to the brain. As for the signs of left ventricular failure, they are first a consequence of impaired diastolic relaxation of the left ventricle; in the later stages, systolic dysfunction also develops.

The appearance of the above clinical symptoms indicates both the presence of significant stenosis and the onset of decompensation. After the appearance of the above clinical symptoms, the life expectancy of patients with aortic stenosis rarely exceeds 5 years (after the onset of angina 5 years, after the appearance of fainting 3 years, after the appearance of signs of heart failure - 1.5 - 2 years). Thus, the occurrence of any of these symptoms is an absolute indication for surgical treatment.

The general purpose of the lesson: - to train students based on physical and additional examination data: to identify the presence of aortic heart disease (aortic stenosis), to give a general clinical description of this defect, indicating its possible etiology and prognosis.

1. Complaints. Identification of complaints characteristic of aortic stenosis (see above - clinical picture).

2. Inspection. Pallor of the skin is typical for patients with aortic stenosis, which is associated with low blood supply to the arterial system.

3. Palpation. The apical impulse, due to powerful hypertrophy of the left ventricular myocardium, is shifted to the left, less often downward, high, resistant, lifting “dome-shaped”. When palpating the heart area, in some cases, systolic trembling (“cat’s purring”) is detected in the second intercostal space to the right of the sternum and above the manubrium of the sternum. This phenomenon is due to the fact that the high-speed turbulent blood flow passing through the narrowed opening of the aortic valve ring causes its vibration, which is mechanically transmitted to the surrounding tissues. The systolic nature of the tremor is confirmed by the fact that it begins immediately after the first sound and coincides with the arterial pulse.

4. Percussion. Reveals a shift of the boundaries of relative cardiac dullness to the left. At the same time, the severity of the cardiac waist is emphasized and the contours of cardiac dullness acquire a characteristic aortic configuration, which is associated with an increase in the significantly hypertrophied left ventricle.

5. Auscultation. Above the aorta (2nd intercostal space to the right of the sternum), the second tone is weakened. The reason is severe deformation, thickened leaflets of the aortic valve, leading to decreased mobility and “slamming speed.” In the case of immobility of the fused aortic valve leaflets, the second sound may not be heard at all. With aortic stenosis of atherosclerotic origin, if it is not clearly expressed, the second sound above the aorta, on the contrary, can be enhanced (the dense walls of the aorta better reflect the sound when the valve leaflets slam shut). Aortic stenosis is characterized by a systolic murmur in the aorta (second intercostal space to the right of the sternum), which is associated with blood flow through the narrowed opening of the aortic ostium. This noise in the direction of blood flow is well carried out on the carotid arteries, and in some cases, is heard in the interscapular space. Systolic murmur with aortic stenosis has all the distinctive features of “organic” noise - loud, persistent, long-lasting, rough timbre. In some cases, the noise is so loud that it can be heard from all points of auscultation, but the epicenter of this noise will be located above the places where the aortic valve is heard (the second intercostal space to the right of the sternum and the Botkin-Erb point, i.e. the 2nd and 5th auscultation point), with the noise volume decreasing as it moves away from the specified auscultation points.

At the apex (1st point of auscultation), a weakening of the first tone may be noted, which is associated with excessive hypertrophy of the left ventricle and, as a consequence, slow contraction during systole (systole lengthens).

After the onset of heart failure, there is usually a decrease in the volume and duration of the systolic murmur (a decrease in the linear and volumetric velocity of blood flow against the background of decreased contractility of the left ventricle).

6. Study of pulse and blood pressure. An obstacle to the expulsion of blood from the left ventricle leads to a decrease in the speed of volumetric blood flow in systole, blood passes into the aorta slowly and in smaller quantities. This leads to the fact that with aortic stenosis the arterial pulse is small, slow, rare (pulsus parvus, tardus et rarus).

Systolic blood pressure usually decreases, diastolic blood pressure does not change or increases, so pulse pressure will be reduced.

II. ECG data. Signs of noticeably pronounced hypertrophy of the left ventricle are recorded (deviation of the electrical axis of the heart to the left, deep S waves in the right chest leads, high R waves in the left chest leads. A change in part of the ventricular complex is noted as a consequence of hypertrophy and overload of the left ventricle (sloping depression of the ST segment in combination with an asymmetric negative or biphasic T wave in I, aVL and left chest leads.

X-ray examination.

The heart, due to the increase in the fourth arc of the left contour, acquires a peculiar shape - a “boot” or “duck”. There is an expansion of the aorta in the ascending section (poststenotic expansion). Signs of defoliation of the aortic valve leaflets are often found.

Phonocardiography (PCG). As a method, PCG currently has only an auxiliary value and is used relatively rarely, since its diagnostic capabilities are inferior to such modern methods as echocardiography and Doppler echocardiography.

On FCG, changes in heart sounds characteristic of this defect are noted: - a decrease in the amplitude of the first sound recorded at the apex of the heart and a decrease in the second sound above the aorta. Especially typical for aortic stenosis is a systolic murmur with a characteristic diamond-shaped shape (increasing-decreasing systolic murmur).

Sphygmography (recording vibrations of the artery wall). The sphygmogram of the carotid artery shows a slower rise and fall of the pulse wave (slow pulse), a low amplitude of the pulse waves and a characteristic jaggedness of their peaks (a curve resembling a “cockscomb” due to the reflection of fluctuations associated with the conduction of systolic noise to the vessels of the neck).

As a diagnostic method, sphygmography is currently used very rarely, since there are modern highly informative research methods, which were discussed above.

Ultrasound research methods (echocardiography, Doppler echocardiography).

These methods are the most informative of all additional research methods. Thanks to them, it is possible to obtain reliably not only a qualitative characteristic (the presence of a heart defect), but also to provide fairly complete information about the severity of the defect, the compensatory capabilities of the heart, prognosis, etc. etc.

Echocardiography (ECHO CG)

With ECHO CG in two-dimensional mode (B-mode) and one-dimensional (M-Mode) thickenings, deformations of the aortic valve leaflets, a decrease in their mobility during systolic opening, and often signs of calcification in the area of ​​the aortic valve ring and valve leaflets are noted.

Doppler echocardiography (Doppler – ECHO – KG).

Doppler ECHO-CG reveals high-speed turbulent systolic aortic flow through a narrowed aortic ostium. Despite the reduced volumetric velocity of systolic transaortic blood flow, the linear velocity (m/sec) increases due to the narrowing.

With the help of Doppler ECHO CG, it is possible to determine the main indicators characterizing the severity of the defect.

Maximum velocity of systolic blood flow through the aortic valve ring (normal £ 1.7 m/sec).

Pressure gradient between the left ventricle and the aorta (taking into account the speed of blood flow according to Bernoulli’s formula - see section echocardiography).

The severity of aortic stenosis is indicated by:

Aortic valve ostial area (AVA)

In addition to changes in the aortic valve, echocardiography provides information about left ventricular hypertrophy, which occurs with this heart defect.

Aortic stenosis is characterized by pronounced hypertrophy of the left ventricular myocardium in the absence of significant dilatation of its cavity, and therefore the end-diastolic and end-systolic volume (EDV and ESV) of the ventricle for a long time differs little from the norm. The thickness of the interventricular septum (IVS) and the posterior wall of the left ventricle (PLW) are markedly increased.

In addition, against the background of pronounced hypertrophy of the left ventricle, in the absence of dilatation of the latter, an increase in the cavity of the left atrium may be noted (a decrease in the elasticity of the hypertrophied left ventricle and impaired filling during the period of diastolic relaxation creates an additional load on the atrium during its systole and makes emptying difficult).

In advanced cases of aortic stenosis, when myogenic dilatation of the left ventricle and its decompensation develop, the echocardiogram shows an increase in the cavity of the left ventricle, in some cases with the development of relative mitral regurgitation, which, together with an enlarged left atrium, resembles the changes that occur with mitral regurgitation ( mitral insufficiency). In this case, they talk about “mitralization” of the aortic defect.

With aortic stenosis, changes in the aorta can also be detected on the echocardiogram - poststenotic dilatation of the aorta (caused by an increase in the linear velocity of blood flow through the narrowed aortic opening).

Since aortic stenosis is “the most surgical heart defect” and surgical treatment is the only promising one, the presence of severe aortic stenosis (according to the pressure gradient and the degree of narrowing of the aortic valve opening) is an indication for consultation with a cardiac surgeon.

III. General assessment of symptoms identified during physical and additional examination in accordance with the general plan of the diagnostic algorithm.

Diagnostic algorithm: provides for the identification of the following signs of aortic stenosis:

1. Valvular signs: direct valvular signs of aortic stenosis are: rough systolic murmur and systolic tremor in the 2nd intercostal space to the right of the sternum, weakening of the second tone. The noise radiates to the vessels of the neck, and can radiate to all points of auscultation (austed over the entire region of the heart).

Confirmation of valvular signs by additional examination methods: - on FCG above the aortic valve - diamond-shaped systolic murmur; with echocardiography - the aortic valve leaflets are compacted, their systolic opening is reduced, high-speed turbulent flow through the aortic mouth, an increase in the systolic pressure gradient between the left ventricle and the aorta.

2. Vascular signs (due to a characteristic hemodynamic disorder): small, slow, rare pulse; decrease in systolic and pulse blood pressure. Against this background, there may be signs of insufficient blood supply to the brain and heart (headaches, dizziness, fainting, attacks of angina). The sphygmogram of the carotid artery shows a slow rise of anacrota, a “cock’s crest” at the apex, a slow descent of catacrota, and a weak expression of incisura.

3. Left ventricular signs: (pronounced hypertrophy of the left ventricular myocardium: - shifted to the left, strengthened, high, resistant apical impulse, aortic configuration of the heart. Data: ECG (signs of hypertrophy and systolic overload of the left ventricle), echocardiography (thickening of the walls of the left ventricle, increase in its mass myocardium).

IV. The diagnosis is formulated with a presumable indication of the etiology of the defect. The severity of the defect and prognosis are indicated. If cardiac decompensation is present, indicate the stage of heart failure.

Tricuspid valve insufficiency.

Insufficiency of the tricuspid (three-leaf) valve (tricuspid insufficiency) can be either organic or relative.

Organic tricuspid insufficiency is based on damage to the tricuspid valve leaflets (rheumatic endocarditis), and very rarely, rupture of the capillary muscles of the tricuspid valve (as a result of trauma).

In the case of rheumatic etiology of tricuspid insufficiency, the latter is usually combined with damage to other heart valves, and is never isolated. As an isolated defect, tricuspid valve insufficiency is possible only with infective endocarditis (comparatively less common than other valve lesions in this disease).

Relative insufficiency of the tricuspid valve is more common and appears when the right atrioventricular orifice is stretched against the background of dilatation of the right ventricle of any origin, while the valve leaflets remain intact.

The mechanism of hemodynamic disorders.

During right ventricular systole, due to incomplete closure of the valve leaflets, some of the blood returns back to the right atrium (tricuspid regurgitation). Since the usual amount of blood from the vena cava enters the atrium at the same time, the latter stretches against the background of an increase in blood volume. During diastole, an increased volume of blood also enters the right ventricle from the right atrium, since that part of the blood that returned to the atrium during systole is added to the normal amount. The right ventricle increases in volume, the load on it increases.

When working under conditions of volume loading of the right ventricle and right atrium, hypertrophy of their myocardium occurs. Thus, with tricuspid insufficiency, compensation is supported by increased work of the right parts of the heart.

Clinical picture.

Considering the relatively small mass of the right ventricle compared to the left and its lower compensatory potential, signs of right ventricular failure with symptoms of stagnation in the systemic circulation appear relatively quickly (swelling of the lower extremities, enlarged liver; in severe cases, anasarca, hydrothorax, hydropericardium, ascites, cardiac cirrhosis liver).

The indicative basis of action (BAA) of a student at the patient’s bedside implies:

General plan for independent work: students work in a room with

The anterior leaflet of the mitral valve without signs of pathology is recorded in the second standard position of the sensor in the form of the letter M.
For a more complete understanding and subsequent interpretation of parameters, reflecting the mechanism of the mitral valve, we consider it appropriate to provide a descriptive description of the movement according to the diagram.

General excursion of the mitral valve is determined in systole by the vertical displacement of the valves in the SD interval, diastolic discrepancy is determined horizontally in the interval of the SD segment. The speed of early diastolic opening and closing is calculated graphically using the method described above by constructing tangents to the corresponding sections of the mitral valve movement curve.

Semilunar valves. The aortic valves and the aorta itself are located in the IV standard position of the sensor. In diastole, the valves are recorded on the echocardiogram in the form of a “snake” in the center of the aortic lumen. The divergence of the aortic valves in systole resembles a “diamond-shaped figure.”

Systolic aortic valve divergence equal to the distance between their terminal sections facing the lumen of the aorta. The lumen of the aorta in systole and diastole is determined by the outlines of its inner surface in the corresponding phases of the cardiac cycle relative to the ECG.

Left atrium, like the aorta, is recorded in the IV standard position of the sensor. The echocardiogram shows almost only the posterior wall of the left atrium. Its anterior wall in echocardiography is considered to coincide with the posterior surface of the aorta. According to these signs, the size of the cavity of the left atrium is determined.

Normal EchoCG (echocardioscopy)

Average echocardiographic parameters are normal(according to literature):
Left ventricle.
The thickness of the posterior wall of the left ventricle is 1 cm in diastole and 1.3 cm in systole.
The end-diastolic size of the left ventricular cavity is 5 cm.
The final systolic size of the left ventricular cavity is 3.71 cm.
The rate of contraction of the posterior wall of the left ventricle is 4.7 cm/s.
The relaxation rate of the posterior wall of the left ventricle is 10 cm/s.

Mitral valve.
The total excursion of the mitral valve is 25 mm.
Diastolic divergence of the mitral leaflets (at the level of point E) is 26.9 mm.
The opening speed of the transition flap (EG) is 276.19 mm/s.
The speed of early diastolic closure of the anterior wall is 141.52 mm/s.

The valve opening duration is 0.47±0.01 s.
The opening amplitude of the front leaf is 18.42±0.3& mm.
The lumen of the base of the aorta is 2.52±0.05 cm.
The size of the cavity of the left atrium is 2.7 cm.
End diastolic volume - 108 cm3.

The final systolic volume is 58 cm3.
Stroke volume - 60 cm3.
Exile faction - 61%.
The speed of circular contraction is 1.1 s.
The mass of the left ventricular myocardium is 100-130 g.

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Normally, the AC consists of three crescents. In 0.5% of the population, a congenital bicuspid valve is found, which is prone to degenerative changes with the development of combined aortic disease in the form of regurgitation and stenosis (Fig. 1). In addition, these people have an increased risk of aortic dissection. A bicuspid valve can be diagnosed during a routine echocardiogram. In elderly patients, as well as with long-term arterial hypertension, focal sclerotic changes in the AV often occur without significant obstruction. Minimal aortic regurgitation is also common, especially in old age.

Rice. 1. Typical view of a congenital bicuspid aortic valve (parasternal cross-section). The arrow indicates the round shape of the valve opening

Aortic stenosis is the most common severe valvular heart disease in the European population and is an indication for surgical treatment. The disease begins with focal sclerosis, which, spreading, leads to severe thickening, calcification and immobility of the aortic semilunar cusps. These changes are well recognized by echocardiography. The presence of even mild aortic stenosis, in which only a slight acceleration of blood flow is noted (maximum speed ‹2.5 m/s), leads to a clear deterioration in the cardiovascular prognosis. Severe aortic stenosis (aortic orifice area <1.0 cm2 or area index <0.6 cm2) requires careful assessment of clinical symptoms or signs of deterioration in LV function, the appearance of which becomes an indication for aortic valve replacement. The most important EchoCG indicators characterizing the severity of aortic stenosis are the average and maximum gradients on the aortic valve, as well as the area of ​​the aortic opening, which is usually calculated using the blood flow continuity equation:

SАО = SLVOT × VTILVOT / VTI,

where SАО is the area of ​​the aortic opening; SLVOT is the cross-sectional area of ​​the LV outflow tract, calculated through its diameter D, as π × D2/4; VTILVOT - time integral of linear velocity in the LV outflow tract (calculated in pulsed Doppler mode); VTI is the time integral of the linear velocity of blood flow through the AV (calculated in constant-wave Doppler mode; Fig. 2).

Rice. 2. A - the principle of the flow continuity equation. From the law of conservation of mass it follows that the product of the cross-sectional area and the average flow velocity or the integral of its velocity (v) is constant for each section of the pipe, which is reflected in the equation of blood flow continuity in the upper left corner of the figure. The aortic orifice area is calculated by solving the equation for CSA2.

B - an example of using the blood flow continuity equation in severe aortic stenosis.

I) Aortic stenosis (arrow) in parasternal longitudinal section; note concentric LV hypertrophy.

II) Enlarged image of the AC region with measurement of the diameter of the LV outflow tract (D) at a distance of 2 cm from the AC annulus.

III) Recording of blood flow in the LV outflow tract in pulsed Doppler mode with calculation of the velocity integral over time (VTILVOT).

IV) Recording of blood flow through the AV in continuous wave Doppler mode with calculation of the velocity time integral (VTIAS). From the blood flow continuity equation, the aortic orifice area (A) is calculated using the formula: A = π × (D2/4) × VTILVOT / VTIAS, which is 0.6 cm2 and corresponds to severe stenosis.

Sometimes, especially with transesophageal echocardiography, the area of ​​the narrowed aortic opening can be determined directly by the planimetric method. It must be remembered that the area of ​​the aortic opening does not depend on stroke volume, therefore, in case of impaired LV function, it remains the only reliable indicator for assessing the severity of aortic stenosis.

Sometimes, in cases of severe LV dysfunction and suspected severe aortic stenosis, stress echocardiography with dobutamine helps clarify valve function and prognosis.

Among all valve defects, aortic regurgitation is the most difficult for EchoCG assessment of its severity. The causes of aortic regurgitation may be dilation of the ascending aorta (for example, with Marfan syndrome), valve calcification, infective endocarditis, degenerative changes such as prolapse, rheumatic disease, etc. The semi-quantitative severity of aortic regurgitation can be assessed in the following ways (Fig. 3):

• assessment of valve morphology and degree of LV enlargement;
• determination of the ratio of the width of the base of the regurgitation jet to the diameter of the LV outflow tract in the parasternal longitudinal section (≥65% - a sign of severe regurgitation);
• calculation of the half-life of the pressure gradient between the aorta and the LV from the flow of aortic regurgitation recorded in continuous-wave Doppler mode (half-life of the pressure gradient <250 ms is a characteristic sign of severe regurgitation);
• recording of holodiastolic reverse blood flow in the descending aorta (from the supraclavicular approach) with an end-diastole velocity >16 cm/s indicates severe regurgitation.

Rice. 3. Aortic regurgitation.

A - parasternal longitudinal section: the regurgitant jet (in diastole) occupies the entire outflow tract of the LV.

B - enlarged transesophageal long-axis image of the aortic valve: prolapse of the non-coronary aortic crescent (arrow).

B - aortic regurgitation in continuous wave Doppler mode. The white line indicates the slope corresponding to the decrease in the diastolic velocity of aortic regurgitation, from which the half-life of the pressure gradient between the aorta and LV can be determined.

D - pulsed Doppler study of blood flow in the descending aorta from the supraclavicular approach: a clear holodiastolic reverse flow (the arrow indicates reverse blood flow that continues until the end of diastole). VoA is the ascending aorta.

An important part of the examination of patients with moderate and severe aortic regurgitation is the assessment of LV function (size and EF) and the diameter of the ascending aorta.

Signs of damage to the aortic valve in infective endocarditis are vegetation, newly emerging aortic regurgitation, structural defects of the semilunar valves and the transition of the process to perivalvular tissue with the formation of para-aortic abscesses and fistulas (for example, between the aortic root and left atrium). Such complications are especially well recognized during transesophageal examination.

Frank A. Flachskampf, Jens-Uwe Voigt and Werner G. Daniel

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 enlarged 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.