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Aortic (valvular) stenosis (I35.0)

Cardiology

General information

Brief description

Aortic stenosis(aortic stenosis) is the most common acquired heart defect. It is a heart defect in the form of narrowing of the aortic opening due to pathology of the aortic valve and perivalvular structures. Normally, the area of ​​the aortic valve opening is 3-4 cm2; with severe aortic stenosis, it becomes less than 1 cm2.
Aortic stenosis causes progressive obstruction Obstruction - obstruction, blockage
left ventricular outflow tract, which leads to concentric hypertrophy Hypertrophy is the growth of an organ, its part or tissue as a result of cell proliferation and an increase in their volume
left ventricle.
Classic symptoms of aortic stenosis are heart failure, fainting, angina pectoris Angina pectoris is a form of angina pectoris in which attacks of anginal pain (pain of a pressing, squeezing or burning nature, localized behind the sternum) occur only in connection with physical activity
.

Classification

By origin:
- congenital (developmental defect);
- acquired.

By localization:
- subvalvular;
- valve;
- supravalvular.

According to the degree of circulatory disturbance:
- compensated;
- decompensated (critical).

By severity(determined by the area of ​​the valve orifice and by the systolic pressure gradient (SPG) between the left ventricle and the aorta):

Moderate stenosis - with GDM<50 мм рт.ст., площадь >1 cm 2 (norm 2.5-3.5 cm 2);
- severe stenosis - with GSD 50-80 mm Hg. (area 1-0.7 cm2);
- severe stenosis - with GSD >80 mm Hg;
- critical stenosis - with GDM up to 150 mm Hg. (area 0.7-0.5 cm2).

Aortic stenosis - ACC/AHA criteria ( American College of Cardiology/American Heart Association)

Sign	Easy	Moderate	Heavy
Flow speed (m/s)	less than 3	3-4	more than 4
Average gradient (mmHg)	less than 25	25-40	more than 40
Valve opening area (cm2)	more than 1.5	1,5-1,0	less than 1
Valve opening area index (cm 2 /m 2)			less than 0.6

Etiology and pathogenesis

Valvular aortic stenosis may be caused by several reasons:
- congenital aortic stenosis;
- rheumatism;
- bicuspid aortic valve;
- isolated calcification of the aortic valve (senile aortic stenosis).

Isolated calcification of the aortic valve is the most common cause of aortic stenosis in the United States. With this disease, calcium is deposited in the places where the valves touch. Previously, it was generally accepted that this was the result of mechanical wear of the valves, which occurs in old age. But recently, a large amount of evidence suggests the role of atherosclerosis Atherosclerosis is a chronic disease characterized by lipoid infiltration of the inner lining of elastic and mixed arteries with subsequent development of connective tissue in their wall. Clinically manifested by general and (or) local circulatory disorders
in the pathogenesis of this disease. The relationship between calcification of the aortic valve and senile aortic stenosis with risk factors for atherosclerosis such as smoking and arterial hypertension has been shown. Hypertension - 1) increased tone of the muscle or muscular layer of the wall of a hollow organ, manifested by their increased tensile strength; 2) (nrk.) - see "hypertension"
and hyperlipoproteinemia. In addition, calcification of the aortic valve can be observed in Paget's disease and in end-stage chronic renal failure.
With senile aortic stenosis, the risk of myocardial infarction and death from cardiovascular disease increases.

Bicuspid aortic valve occurs in 1-2% of people; Among first-degree relatives of a patient with a bicuspid aortic valve, its prevalence is 9%. More often observed in men.
Both stenosis and insufficiency of the bicuspid aortic valve may occur. As a rule, severe aortic stenosis develops at 40-60 years of age (only in some cases at a young age).
Bicuspid aortic valve combined with coarctation of the aorta Coarctation of the aorta is an anomaly in the development of the aorta in the form of its narrowing in a limited area, most often at the point where the arch passes into the descending section.
, with dilatation Dilatation is a persistent diffuse expansion of the lumen of a hollow organ.
of the aortic root, with it there is a predisposition to dissecting aortic aneurysm.
The unicuspid aortic valve opens through a single commissure Commissure (adhesion) - a fibrous cord formed between adjacent surfaces of organs as a result of injury or inflammatory process
; This is a very rare defect, mainly leading to severe aortic stenosis at an early age.

Rheumatic aortic stenosis usually combined with aortic insufficiency and mitral valve defects. Rheumatism is a rare cause of severe isolated aortic stenosis in developed countries.

Subvalvular aortic stenosis(subaortic stenosis) is a congenital defect (may not be present at birth). Under the aortic valve in the outflow tract of the left ventricle, as a rule, there is a membrane with a hole. This membrane often comes into contact with the anterior leaflet of the mitral valve. Less commonly, obstruction is caused not by the membrane, but by the muscular cushion in the outflow tract of the left ventricle.
The pathogenesis of subvalvular aortic stenosis is unclear. It is generally accepted that it is an adaptive reaction caused by hemodynamic disturbances in the outflow tract of the left ventricle.
Subvalvular aortic stenosis can be combined with other obstructive defects of the left heart (coarctation of the aorta, with Schon's syndrome, etc.).

Supravalvular aortic stenosis - is rare. The obstruction is located above the valve in the ascending aorta. It can develop as a result of lipoprotein deposition in severe forms of hereditary hyperlipoproteinemia, and can also be part of hereditary syndromes. For example, Williams syndrome, which is characterized by idiopathic hypercalcemia, developmental delay, short stature, grotesque facial features, multiple stenoses of the aorta and branches of the pulmonary artery).

Pathogenesis

In hemodynamic disturbances, the primary obstruction of blood outflow from the left ventricle. This results in a systolic pressure gradient between the left ventricle and the aorta. As a result of obstruction, dilatation and a decrease in stroke volume of the left ventricle develops. However, cardiac output remains normal for a long time due to compensatory developing hypertrophy of the left ventricle.
As the degree of aortic stenosis progresses, the systolic pressure in the left ventricle continues to increase, but rarely exceeds 300 mmHg. Art.

The functioning of the left atrium as an auxiliary pump prevents pressure in the pulmonary veins and pulmonary capillaries from rising to levels that would cause pulmonary congestion while maintaining left ventricular end-diastolic pressure at the elevated level necessary for effective contraction. If regular and strong contractions of the left atrium cease due to atrial fibrillation or atrioventricular dissociation, the symptoms of the disease may sharply intensify.

In the majority of patients with aortic stenosis, cardiac output at rest is maintained at a normal level, but cannot adequately increase in response to physical activity.
In the later stages of the disease, cardiac output and the pressure gradient between the left ventricle and aorta are reduced; the mean pressure in the left atrium, the wedge pressure of the pulmonary trunk, the pressure in the pulmonary trunk and the pressure in the right ventricle increase.
As a result of hypertrophy of the left ventricular muscle mass, the myocardial oxygen demand increases. Gradually, as the defect decompensates, the cavity of the left ventricle expands, first tonogenic and then myogenic dilation occurs.
Decompensation of left ventricular function indicates the onset of development of biventricular heart failure. Among the late signs of the defect is the appearance of stagnation and hypertension in the pulmonary circulation. With the “mitralization” of the defect and the development of pulmonary hypertension, the right parts of the heart are involved in the pathological process.

Epidemiology

The frequency of detection of aortic stenosis among persons under the age of 65 is 4-5%, after 65 years - about 25%, after 75 years - 48%.
Aortic stenosis has recently become the most common indication for valve surgery, which explains the interest in its treatment. This defect is detected in 25% of patients with chronic heart valve diseases. Among adult patients with clinically significant aortic stenosis, 80% are men.
The share of congenital aortic stenosis among other congenital heart defects is 3-5.5% and in about 13% of cases it is combined with other congenital heart defects.
Valvular stenosis occurs in 58% of patients, subvalvular - in 24%, and supravalvular - in 6%.

Clinical picture

Symptoms, course

With aortic stenosis, hemodynamic or clinical manifestations are rarely observed until the valve ring narrows to about 30% of normal. There may be no clinical manifestations for many years. Patients retain a fairly high working capacity, tolerate heavy physical activity well, and can play sports.

Main symptoms:

1. Dyspnea during physical activity. Shortness of breath and fatigue increase during the course of the disease and gradually limit the ability of patients to work.

2. Angina pectoris. A more pronounced obstruction to blood flow from the left ventricle increases the force of heart contractions, as a result, patients begin to feel palpitations. Attacks of angina pectoris are provoked by exercise and disappear with rest (a picture similar to angina pectoris is observed within the framework of coronary heart disease). Angina pectoris occurs in approximately 2/3 of patients with severe (critical) aortic stenosis (half of them have coronary heart disease).

3. Syncope. Syncope is typically associated with decreased cerebral blood flow during exercise when blood pressure decreases as a result of fixed cardiac output. Syncope may also be associated with baroreceptor dysfunction and the vasodepressor response to acute increases in left ventricular systolic pressure during exercise.
Hypotension Hypotonia is a decreased tone of the muscle or muscle layer of the wall of a hollow organ.
during exertion, it can manifest itself as dizziness, and patients experience a “gray veil” before their eyes. Syncope at rest may occur due to transient ventricular fibrillation, which resolves spontaneously, or as a result of transient atrial fibrillation with loss of atrial contribution to left ventricular filling, resulting in a fall in cardiac output.

Auscultation:

1. Decrease in the intensity of the aortic component in the formation of the second tone.

2. Paradoxical splitting of the second tone.

3. Systolic murmur in aortic stenosis is a characteristic ejection murmur that occurs shortly after the first sound, increases in intensity and reaches a peak in the middle of the ejection period, after which it gradually decreases and disappears just before the closure of the aortic valve.
The murmur is best heard at the base of the heart; it is often well conducted along the carotid arteries and to the apex of the heart. As left ventricular failure develops and cardiac output decreases, the murmur becomes softer or disappears completely. In this case, difficulties may arise in recognizing the disease: a clinical picture of severe left ventricular failure with low cardiac output is formed.

Diagnostics

Electrocardiography. The changes detected depend on the degree of changes in the left ventricular muscle. In the early stages of the development of the defect, there may be no changes in the ECG.
As the stenosis progresses, signs of left ventricular hypertrophy are determined in the form of an increased amplitude of the QRS complex waves in the corresponding leads, often in combination with a modified final part of the ventricular complex.
In the later stages of aortic stenosis, the ECG may show changes indicating overload of the left atrium myocardium: high split P waves. Atrioventricular conduction disturbances of varying degrees are often observed: from prolongation of the P-Q interval to complete AV block.

Phonocardiography. Systolic murmur has a characteristic rhomboid or spindle-shaped shape.

X-ray examination. Is important. In the early stages, moderate expansion of the heart to the left and lengthening of the left ventricular arch with rounding of the apex are detected. With a pronounced narrowing of the aortic opening and a long course of the defect, the heart has a typical aortic configuration. With “mitralization” of the defect (development of relative mitral valve insufficiency), an increase in the size of the left atrium and the appearance of radiological signs of stagnation in the pulmonary circulation are observed.

Echocardiographic study:
- incomplete systolic opening of the aortic valve leaflets;
- fibrosis Fibrosis is the proliferation of fibrous connective tissue, occurring, for example, as a result of inflammation.
and calcification Calcinosis (syn. calcification, calcification) - deposition of calcium salts in body tissues
valves;
- presence of a systolic gradient on the aortic valve;
- increase in the thickness of the left ventricular myocardium (up to 15 mm or more);
- increase in the anteroposterior size of the left ventricle (systolic - more than 40 mm, diastolic - more than 60 mm).
Acquired aortic stenosis can be excluded by identifying the thin and movable leaflets of the aortic valve during systole or diastole.

Indications for echocardiography for aortic stenosis (American College of Cardiology, 1998):
- diagnosis and assessment of the severity of aortic stenosis;
- assessment of the size of the left ventricle, function and/or degree of hemodynamic impairment;
- re-examination of patients who have aortic stenosis with changing symptoms;
- assessment of changes in hemodynamic disturbances and ventricular compensation over time in patients diagnosed with aortic stenosis during pregnancy;
- re-examination of patients with compensated aortic stenosis and signs of left ventricular dysfunction or hypertrophy.

Catheterization of the right sections used to get an idea of ​​the degree of compensation of the defect: it allows you to determine the pressure in the left atrium, right ventricle and pulmonary artery.
Catheterization of the left sections used to determine the degree of aortic stenosis based on the systolic gradient between the left ventricle and the aorta.

Differential diagnosis

Differential diagnosis with defects and other heart diseases is necessary, in which systolic murmur and hypertrophy of the left ventricle of the heart are determined.

In case of unclear etiology of the defect (especially in children) primarily exclude congenital aortic stenosis. Its characteristic manifestations: identification of signs of the defect in early childhood, often in combination with other congenital anomalies of the cardiovascular system (patent ductus arteriosus, coarctation of the aorta). Similar manifestations are observed with a ventricular septal defect. To differentiate it from aortic stenosis, in some cases there is a need for cardiac probing and ventriculography, which are also required to determine indications for surgical intervention.

In adults differential diagnosis is more often carried out with idiopathic hypertrophic subaortic stenosis, stenosis of the pulmonary trunk, and less often with mitral insufficiency. To make a correct diagnosis, echocardiographic examination is essential.

Complications

Infective endocarditis;

Arrhythmias;

Sudden coronary death;

Congestive heart failure;

Mental disorders;

Gastrointestinal bleeding.

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Treatment

Indications for aortic valve replacement for aortic stenosis

Indication	Class
Severe aortic stenosis with any symptoms
Severe aortic stenosis with indications for coronary artery bypass grafting (CABG), ascending aortic or other valve surgery
Severe aortic stenosis with left ventricular systolic dysfunction (left ventricular ejection fraction< 50%), не связанной с другими причинами, если нет симптомов
Severe aortic stenosis with onset of symptoms during exercise testing
Severe aortic stenosis with a decrease in arterial pressure during exercise testing, compared with its baseline level, if there are no symptoms	IIaC
Moderate aortic stenosis* with indications for CABG, ascending aortic or other valve surgery	IIaC
Severe aortic stenosis with moderate aortic valve calcification and an increase in peak velocity S of 0.3 m/s per year, if there are no symptoms	IIaC
Aortic stenosis with low pressure gradient across the aortic valve (< 40 мм рт. ст.) и дисфункцией левого желудочка при сохранении инотропного резерва	IIaC
Severe aortic stenosis with pronounced left ventricular hypertrophy (> 15 mm), not associated with arterial hypertension, if there are no symptoms	IIbC

* Moderate aortic stenosis- this is aortic stenosis with a valve opening area of ​​1.0-1.5 cm 2 (0.6-0.9 cm 2 / m 2 body surface area) or an average pressure gradient across the aortic valve of 30-50 mm Hg. Art. with unchanged blood flow through the valve.

Early aortic valve replacement - recommended for all patients with symptoms and severe aortic stenosis (however, they are also candidates for surgical intervention).
If there is an average pressure gradient across the aortic valve >40 mm Hg. Art. theoretically there is no lower limit on ejection fraction for surgery.
With low blood flow and a low gradient of aortic stenosis (significantly reduced ejection fraction and mean gradient less than 40 mm Hg), the choice of treatment tactics is more controversial. Surgical intervention is performed in patients with proven contractility reserve.

Balloon valvuloplasty considered as a “bridge” to surgery in hemodynamically unstable patients at high risk for surgery or in patients with symptomatic severe aortic stenosis who require urgent noncardiac surgery.

Drug therapy

For severe aortic stenosis drug therapy is ineffective.

Treatment Goals for asymptomatic aortic stenosis: prevention of coronary heart disease, maintenance of sinus rhythm, normalization of blood pressure.

Goal of treatment for heart failure: elimination of stagnation in the pulmonary circulation. Diuretics are prescribed with caution, since their too active use can lead to excessive diuresis, arterial hypotension, hypovolemia and a drop in cardiac output.
Nitrates can reduce blood flow to the brain and cause fainting and should be avoided or used with extreme caution.

Digoxin is used as a symptomatic treatment for left ventricular systolic dysfunction and volume overload, especially atrial fibrillation.

Vasodilators are contraindicated in aortic stenosis, since a decrease in peripheral vascular resistance with limited cardiac output can lead to fainting.

In supravalvular aortic stenosis, which is caused by severe hyperlipoproteinemia, reduction of obstruction can be achieved after plasmapheresis with removal of LDL.

Features of pharmacotherapy for aortic stenosis(according to the recommendations of the European Society of Cardiology):
1. Modification of risk factors for atherosclerosis is necessary. At the same time, an analysis of a series of retrospective studies showed mixed results from the use of statins and predominantly the benefit of ACE inhibitors.
2. There are no medications that can “delay” surgery for aortic stenosis in symptomatic patients.
3. In the presence of heart failure and contraindications to surgery, the following drugs can be used: digitalis, diuretics, ACE inhibitors or angiotensin receptor blockers. Beta blockers should be avoided.
4. In case of development of pulmonary edema in patients with aortic stenosis, nitroprusside may be used (with careful monitoring of hemodynamics).
5. With concomitant arterial hypertension, the dose of antihypertensive drugs should be carefully titrated and blood pressure monitored more often.
6. Maintaining sinus rhythm and preventing infective endocarditis are important aspects of managing patients with aortic stenosis.

Forecast

Aortic stenosis is characterized by a long period of compensation; patients are often unaware of the presence of the defect and can perform heavy physical work.
When decompensation occurs, heart failure quickly develops, often with attacks of cardiac asthma. As a result, the prognosis of the disease worsens sharply. After the onset of severe symptoms of heart failure, the average life expectancy does not exceed 1 year.
Death occurs from chronic circulatory failure, as well as suddenly due to coronary insufficiency or ventricular fibrillation (14-18% of cases).

Predictors Predictors are signs indicating the possibility of the appearance and development of a pathological process; predictive symptoms.
progression and poor prognosis for asymptomatic aortic stenosis:
1. Old age and the presence of risk factors for atherosclerosis.
2. EchoCG parameters: degree of valve calcification, peak velocity of blood ejection into the aorta (Vmax), left ventricular ejection fraction, hemodynamic progression, increase in ΔP during exercise.
Patients with significant calcification of the aortic valve and an increase in blood flow V > 0.3 m/s over the course of a year constitute a high-risk group. In the absence of surgical intervention, mortality within 2 years reaches 80%.
3. Tolerance of stress tests. The appearance of symptoms of aortic stenosis during exercise in physically active patients under the age of 70 years is a predictor of the development of symptomatic aortic stenosis within a year.

Prevention

Patients with asymptomatic aortic stenosis should be informed of the importance of promptly notifying the physician of the appearance of any clinical manifestations of the disease.
Currently, there are no preventive measures that could slow the progression of narrowing of the aortic ostium in patients with asymptomatic aortic stenosis. One possible method of such prevention is to prescribe statins.

Drug therapy is aimed at preventing complications of the disease and includes antibiotic prophylaxis of infective endocarditis and repeated rheumatic attacks. Ensure that patients with aortic disease are aware of the risk of developing infective endocarditis and understand the principles of antibiotic prophylaxis during dental and other invasive procedures.

Information

Sources and literature

1. ACC/AHA PRACTICE GUIDELINES ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease
2. Diseases of the heart and blood vessels. A guide for doctors in 4 volumes, ed. Chazova E.I., M.: Medicine, 1992
3. Internal diseases. In 10 books / trans. from English edited by Braunwald E., Isselbacher K.J., Petersdorf R.G. et al., M., Medicine, 1995
   1. pp. 224-257
4. Cardiology. National leadership / edited by Belenkov Yu.N., Oganov R.G., 2007
   1. "Acquired heart defects" Shostak N.A., Anichkov D.A., Klimenko A.A. - pp. 834-864
5. Kovalenko V.N., Nesukai E.G. Non-coronary heart diseases. Practical guide / ed. Kovalenko V.N., K.: Morion, 2001
6. Lectures on cardiovascular surgery / ed. Bockeria L.A., in 2 volumes. T. 1 -M.: Publishing house NTsSSKh im. Bakuleva A.N. RAMS, 1999
   1. pp. 311-328
7. Key provisions of the ESC recommendations for the diagnosis and treatment of valvular heart disease (acquired heart defects) (2007)
8. Guide to outpatient cardiology / ed. Belenkova Yu.N., Oganova R.G., GEOTAR-Media, 2007
   1. pp. 199-222
9. Tsukerman G.I., Burakovsky V.I. and others. Aortic valve defects, M.: Medicine, 1972

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The most common causes of organic aortic valve insufficiency are:

• Rheumatism (about 70% of cases);
• Infective endocarditis;
• More rare causes of this defect include atherosclerosis, syphilis, systemic lupus erythematosus (Libman-Sachs lupus endocarditis), rheumatoid arthritis, etc.

With rheumatic endocarditis, thickening, deformation and shrinkage of the semilunar valve leaflets occur. As a result, their tight closure during diastole becomes impossible, and a valve defect is formed.

Infectious endocarditis most often affects previously altered valves (rheumatic lesions, atherosclerosis, congenital anomalies, etc.), causing deformation, erosion or perforation of the valves.

It should be borne in mind the possibility of relative insufficiency of the aortic valve as a result of a sharp expansion of the aorta and the fibrous annulus of the valve in the following diseases:

• arterial hypertension;
• aortic aneurysms of any origin;
• ankylosing rheumatoid spondylitis.

In these cases, as a result of the expansion of the aorta, divergence (separation) of the aortic valve leaflets occurs and they also do not close during diastole.

Finally, one should be aware of the possibility of a congenital defect of the aortic valve, for example, the formation of a congenital bicuspid aortic valve or dilatation of the aorta in Marfan syndrome, etc.

Aortic valve insufficiency with congenital defects is rare and is more often combined with other congenital defects.

Aortic valve insufficiency causes a significant portion of the blood thrown into the aorta (regurgitation) to return back into the left ventricle during diastole. The volume of blood returning to the left ventricle can exceed half of the total cardiac output.

Thus, with aortic valve insufficiency, during diastole the left ventricle fills as a result of both blood flow from the left atrium and aortic reflux, which leads to an increase in end-diastolic volume and diastolic pressure in the left ventricular cavity.

As a result, the left ventricle enlarges and significantly hypertrophies (the end-diastolic volume of the left ventricle can reach 440 ml, while the norm is 60-130 ml).

Hemodynamic changes

Loose closure of the aortic valve leaflets leads to regurgitation of blood from the aorta to the LV during diastole. The reverse flow of blood begins immediately after the closure of the semilunar valves, i.e. immediately after the second sound, and can continue throughout diastole.

Its intensity is determined by the changing pressure gradient between the aorta and the LV cavity, as well as the size of the valve defect.

Mitralization of the defect- the possibility of “mitralization” of aortic insufficiency, i.e. the occurrence of relative mitral valve insufficiency with significant LV dilatation, dysfunction of the papillary muscles and expansion of the fibrous ring of the mitral valve.

In this case, the valve leaflets are not changed, but do not completely close during ventricular systole. Typically, these changes develop in the late stages of the disease, with the occurrence of LV systolic dysfunction and pronounced myogenic dilatation of the ventricle.

“Mitralization” of aortic valve insufficiency leads to regurgitation of blood from the left ventricle to the left atrium, expansion of the latter and a significant worsening of stagnation in the pulmonary circulation.

The main hemodynamic consequences of aortic valve insufficiency are:

• Compensatory eccentric hypertrophy of the LV (hypertrophy + dilatation), which occurs at the very beginning of the formation of the defect.
• Signs of left ventricular systolic failure, blood stagnation in the pulmonary circulation and pulmonary hypertension developing during decompensation of the defect.
• Some features of blood supply to the arterial vascular system of the systemic circulation:

Increased systolic blood pressure;

Reduced diastolic blood pressure;

Increased pulsation of the aorta, large arterial vessels, and in severe cases - muscular arteries (arterioles), caused by an increase in arterial filling in systole and a rapid decrease in filling in diastole;

Impaired perfusion of peripheral organs and tissues due to a relative decrease in effective cardiac output and a tendency to peripheral vasoconstriction.

• Relative insufficiency of coronary blood flow.

1. Eccentric left ventricular hypertrophy

An increase in diastolic filling of the LV with blood leads to volume overload of this part of the heart and an increase in ventricular EDV.

As a result, pronounced eccentric LV hypertrophy develops (myocardial hypertrophy + dilatation of the ventricular cavity) - the main mechanism for compensating for this defect. Over a long period of time, an increase in the force of contraction of the LV, which is due to the increased muscle mass of the ventricle and the activation of the Starling mechanism, ensures the expulsion of an increased volume of blood.

Another unique compensatory mechanism is the tachycardia characteristic of aortic insufficiency, leading to shortening of diastole and some limitation of regurgitation of blood from the aorta.

2. Cardiac decompensation

Over time, LV systolic function decreases and, despite the continued increase in ventricular EDV, its stroke volume no longer increases or even decreases. As a result, EDP in the LV, filling pressure and, accordingly, pressure in the LA and veins of the pulmonary circulation increase. Thus, stagnation of blood in the lungs when systolic dysfunction of the left ventricle occurs (left ventricular failure) is the second hemodynamic consequence of aortic valve insufficiency.

Subsequently, with the progression of LV contractility disorders, persistent pulmonary hypertension and hypertrophy develop, and in rare cases, RV failure. In this regard, it should be noted that with decompensation of aortic valve insufficiency, as well as with decompensation of aortic stenosis, clinical manifestations of left ventricular failure and blood stagnation in the pulmonary circulation always predominate, while signs of right ventricular failure are weakly expressed or (more often) completely absent.

3.

The third hemodynamic consequence of aortic valve insufficiency is the significant features of filling the arterial bed of the systemic circulation with blood, which are often detected even at the stage of compensation of the defect, i.e. even before the development of left ventricular failure. The most significant of them are:

Decrease in diastolic pressure in the aorta, which is explained by regurgitation of part of the blood (sometimes significant) in the LV

A marked increase in pulse pressure in the aorta, large arterial vessels, and in severe aortic valve insufficiency - even in muscular arteries (arterioles). This diagnostically important phenomenon occurs as a result of a significant increase in LV SV (increased systolic blood pressure) and the rapid return of part of the blood to the LV (“emptying” of the arterial system), accompanied by a drop in diastolic blood pressure. It should be noted that an increase in pulse fluctuations of the aorta and large arteries and the appearance of arteriole pulsations unusual for resistive vessels underlie numerous clinical symptoms detected in aortic valve insufficiency.

4. "Fixed" cardiac output

It was shown above that with aortic insufficiency at rest for a long time, the LV can provide expulsion into the aorta of an increased systolic blood volume, which completely compensates for the excess diastolic filling of the LV.

However, during physical activity, i.e. under conditions of even greater intensification of blood circulation, the compensatory increased pumping function of the LV is not enough to “cope” with the even greater volume overload of the ventricle, and a relative decrease in cardiac output occurs.

5. Impaired perfusion of peripheral organs and tissues

With the long-term existence of aortic valve insufficiency, a peculiar paradoxical situation arises: despite a sharp increase in cardiac output (more precisely, its absolute values), a decrease in the perfusion of peripheral organs and tissues is observed.

This is due primarily to the inability of the LV to further increase stroke volume during physical and other types of exercise (fixed stroke volume). When the defect is decompensated, a decrease in LV systolic function (both at rest and during exercise) also becomes of great importance. Finally, activation of the SAS, RAAS, and tissue neurohormonal systems, including endothelial vasoconstrictor factors, also plays a certain role in peripheral blood flow disorders.

With severe aortic regurgitation, disturbances in the perfusion of peripheral organs and tissues can also be caused by the described features of blood supply to the arterial vascular system, namely: rapid outflow of blood from the arterial system or, at least, stopping or slowing down the movement of blood through the peripheral vessels during diastole.

6. Coronary circulatory insufficiency

Particularly worth explaining is another important consequence of aortic valve insufficiency - the occurrence of coronary circulatory insufficiency, which is explained by two main reasons related to the peculiarities of intracardiac hemodynamics in this defect:

Low diastolic pressure in the aorta.
As is known, filling of the coronary vascular bed of the LV occurs during diastole, when intramyocardial tension and diastolic pressure in the LV cavity drop and, accordingly, the pressure gradient between the aorta (about 70–80 mm Hg) and the LV cavity rapidly increases (5– 10 mmHg), which determines coronary blood flow. It is clear that a decrease in aortic diastolic pressure leads to a decrease in the aortic-left ventricular gradient, and coronary blood flow decreases significantly.

The second factor leading to the occurrence of relative coronary insufficiency is the high intramyocardial tension of the LV wall during ventricular systole, which, according to Laplace's law, depends on the level of intracavitary systolic pressure and the LV radius. Pronounced dilatation of the ventricle is naturally accompanied by an increase in the intramyocardial tension of its wall. As a result, the work of the LV and the myocardial oxygen demand sharply increase, which is not fully provided by the coronary vessels operating in unfavorable conditions from a hemodynamic point of view.

Clinical manifestations

Formed aortic valve insufficiency for a long time (10–15 years) may not be accompanied by subjective clinical manifestations and may not attract the attention of the patient and the doctor. The exception is cases of acutely developed aortic valve insufficiency in patients with infective endocarditis, dissecting aortic aneurysm, etc.

One of the first clinical manifestations of the disease is unpleasant sensation of increased pulsation in the neck, in the head, as well as increased heart beats (patients “feel their heart”), especially in a lying position. These symptoms are associated with the high cardiac output and pulse pressure in the arterial system described above.

These sensations are often accompanied by rapid heartbeat, associated with sinus tachycardia characteristic of aortic valve insufficiency.

If there is a significant defect in the aortic valve, the patient may experience dizziness, a sudden feeling of lightheadedness and even a tendency to faint, especially with exertion or a rapid change in body position. This indicates cerebrovascular insufficiency caused by the inability of the LV to adequately change cardiac output (fixed stroke volume) and impaired cerebral perfusion.

Pain in the heart(angina) - can also occur in patients with a severe aortic valve defect, long before the onset of signs of LV decompensation. The pain is usually localized behind the sternum, but often differs in nature from typical angina.

They are not as often associated with certain external provoking factors (for example, physical activity or emotional stress) as angina attacks in patients with coronary artery disease. The pain often occurs at rest and is of a pressing or squeezing nature, usually lasts quite a long time and is not always well relieved with nitroglycerin. Attacks of nocturnal angina pectoris, accompanied by profuse sweating, are especially difficult for patients to tolerate.

Typical anginal attacks in patients with aortic valve insufficiency, as a rule, indicate the presence of concomitant ischemic heart disease and atherosclerotic narrowing of the coronary vessels.

The period of decompensation is characterized by the appearance of signs of left ventricular failure.

Dyspnea first appears during physical activity, and then at rest. With a progressive decline in LV systolic function, shortness of breath becomes orthopnea.

Then it is joined by attacks of suffocation (cardiac asthma and pulmonary edema). Characteristic is the appearance of rapid fatigue during exercise and general weakness. For obvious reasons, all symptoms associated with cerebral and coronary circulatory insufficiency are aggravated when left ventricular failure occurs. Finally, in more rare cases, when it persists and progresses over a long period of time pulmonary hypertension, and patients do not die from left ventricular failure, individual signs of blood stagnation in the venous bed of the systemic circulation (edema, heaviness in the right hypochondrium, dyspeptic disorders) associated with a decrease in the systolic function of the hypertrophied RV may be detected.

However, more often this does not happen and the clinical picture is dominated by the symptoms described above, caused by damage to the left side of the heart, the peculiarities of blood supply to the arterial vascular system of the systemic circulation and signs of blood stagnation in the veins of the pulmonary circulation.

Inspection

During a general examination of patients with aortic insufficiency, first of all, attention is drawn to the pallor of the skin, indicating insufficient perfusion of peripheral organs and tissues.

With a pronounced defect of the aortic valve, one can identify numerous external signs of systolic-diastolic pressure drops in the arterial system, as well as increased pulsation of large and smaller arteries:

• increased pulsation of the carotid arteries(“carotid dance”), as well as visible pulsation in the area of ​​all superficially located large arteries (brachial, radial, temporal, femoral, artery of the dorsum of the foot, etc.);
• de Musset's sign- rhythmic rocking of the head back and forth in accordance with the phases of the cardiac cycle (systole and diastole);
• Quincke's symptom(“capillary pulse”, “precapillary pulse”) - alternating redness (in systole) and blanching (in diastole) of the nail bed at the base of the nail with sufficiently intense pressure on its tip. In a healthy person, with such pressure both in systole and diastole, the pale color of the nail bed remains. A similar version of Quincke’s “precapillary pulse” is detected by pressing on the lips with a glass slide;
• Landolfi's sign- pulsation of the pupils in the form of their narrowing and dilation;
• Müller's sign- pulsation of the soft palate.

Palpation and percussion of the heart

The apical impulse is significantly enhanced due to LV hypertrophy, diffuse (“dome-shaped”) and shifted to the left and down (LV dilatation). With a pronounced defect of the aortic valve, the apical impulse can be detected in the VI intercostal space along the anterior axillary line.

Systolic tremor is often detected at the base of the heart - along the left and right edge of the sternum, in the jugular notch and even on the carotid arteries. In most cases, it does not indicate aortic stenosis accompanying aortic insufficiency, but is associated with the rapid expulsion of an increased volume of blood through the aortic valve. In this case, the opening of the aortic valve becomes relatively “narrow” for the sharply increased volume of blood ejected into the aorta during expulsion. This contributes to the occurrence of turbulence in the area of ​​the aortic valve, the clinical manifestation of which is low-frequency systolic tremor, detected by palpation, and a functional systolic murmur at the base of the heart, determined by auscultation.

Diastolic tremors in the precordial region with aortic valve insufficiency are detected extremely rarely.

Percussion in all patients with aortic insufficiency reveals a sharp shift of the left border of the relative dullness of the heart to the left. The so-called aortic configuration with an emphasized “waist” of the heart is characteristic.

Only when LA dilatation occurs, caused by “mitralization” of the defect, can the “waist” of the heart be smoothed out.

Auscultation of the heart

Typical auscultatory signs of aortic insufficiency are diastolic murmur on the aorta and at Botkin’s point, weakening of the second and first heart sounds, as well as the so-called “accompanying” systolic murmur on the aorta of a functional nature.

Changes in the first tone. Typically, the first sound at the apex is weakened as a result of a sharp volume overload of the LV and a slowdown in isovolumic contraction of the ventricle. Sometimes the first tone is split.

Changes in tone II. Depending on the etiology of the defect, tone II can either intensify or weaken until it disappears. Deformation and shortening of the valve leaflets due to rheumatism or infective endocarditis contributes to the weakening of the second sound in the aorta or its disappearance. Syphilitic damage to the aorta is characterized by an increased II tone with a metallic tint (“ringing” II tone).

Pathological III tone heard in aortic insufficiency quite often. The appearance of the third tone indicates a pronounced volume overload of the LV, as well as a decrease in its contractility and diastolic tone.

Diastolic murmur on the aorta is the most characteristic auscultatory sign of aortic insufficiency. The murmur is best heard in the 2nd intercostal space to the right of the sternum and in the 3rd–4th intercostal space at the left edge of the sternum and is carried to the apex of the heart.

Diastolic murmur in aortic insufficiency begins in the protodiastolic period, i.e. immediately after the second sound, gradually weakening throughout diastole. Depending on the degree of regurgitation, the frequency characteristic of the diastolic murmur changes: slight regurgitation is accompanied by a soft blowing, predominantly high-frequency murmur; with severe regurgitation, a mixed frequency composition of the noise is determined; severe regurgitation leads to the appearance of coarser low- and mid-frequency noise. This type of noise is observed, for example, with syphilitic lesions of the aorta.

It should be remembered that with decompensation of the defect, tachycardia, as well as with combined aortic heart disease, the intensity of the diastolic murmur of aortic insufficiency decreases.

Functional noise

Flint's functional diastolic murmur is a presystolic murmur of relative (functional) stenosis of the left atrioventricular orifice, which is occasionally heard in patients with organic insufficiency of the aortic valve.

It occurs as a result of displacement of the anterior leaflet of the mitral valve by a stream of blood regurgitating from the aorta, which creates an obstacle to the diastolic blood flow from the LA to the LV during active atrial systole.

In the genesis of this noise, vibration of the leaflets and chords of the mitral valve, which occurs as a result of the “collision” of turbulent blood flows entering the LV cavity from the aorta and left atrium, is probably also important.

At the same time, at the apex of the heart, in addition to the wired organic diastolic murmur of aortic insufficiency, presystolic amplification of the murmur is also heard - Flint's murmur.

Functional systolic murmur relative stenosis of the aortic mouth is often heard in patients with organic aortic valve insufficiency.

The murmur occurs due to a significant increase in the systolic volume of blood ejected into the LV aorta during the ejection period, for which the normal unchanged opening of the aortic valve becomes relatively narrow - a relative (functional) stenosis of the aortic mouth is formed with turbulent blood flow from the LV to the aorta.

At the same time, on the aorta and at Botkin’s point, in addition to the organic diastolic noise of aortic insufficiency, during the expulsion of blood, a functional systolic murmur is heard, which can be heard throughout the sternum, the apex of the heart and spread to the area of ​​the jugular notch and along the carotid arteries.

When examining the vascular system in patients with aortic valve insufficiency, it is necessary to pay attention to the existence of two more vascular auscultatory phenomena:

1. Durosier's sign (double Durosier murmur). This unusual auscultatory phenomenon is heard over the femoral artery in the groin area, just below the Pupart's ligament.

By simply applying a stethoscope to this area (without pressure), the femoral artery tone can be detected - a sound synchronous with the local arterial pulse. With gradual pressure with the head of the stethoscope in this area, an artificial occlusion of the femoral artery is created and a quiet and short systolic murmur begins to be heard, and then a more intense systolic murmur.

Subsequent compression of the femoral artery sometimes leads to the appearance of diastolic murmur. This second murmur is quieter and shorter than the systolic murmur. The phenomenon of Durosier's double murmur is usually explained by a higher than normal volumetric blood flow velocity or retrograde (toward the heart) blood flow in large arteries.

2. Traube double tone- a rather rare sound phenomenon when two tones are heard on a large artery (for example, femoral) (without compression of the vessel). The second tone is usually associated with reverse blood flow in the arterial system, caused by pronounced regurgitation of blood from the aorta to the LV.

Blood pressure

With aortic insufficiency, systolic blood pressure increases and diastolic blood pressure decreases, resulting in an increase in pulse blood pressure.

A decrease in diastolic pressure with aortic valve insufficiency requires comment. With direct invasive measurement of aortic blood pressure, diastolic pressure never falls below 30 mmHg. Art. However, when measuring blood pressure using the Korotkoff method in patients with severe aortic valve insufficiency, diastolic pressure is often reduced to zero. This means that during blood pressure measurements, when the pressure in the cuff decreases below the true diastolic pressure, Korotkoff sounds continue to be heard in the aorta above the artery.

The reason for this discrepancy between direct and indirect blood pressure measurements lies in the mechanisms of the appearance of Korotkoff sounds when measuring blood pressure. One way or another, Korotkoff sounds are detected by auscultation as long as intermittent blood flow remains in a large artery. In a healthy person, such a “pulsating” blood flow is artificially created by compressing the brachial artery with a cuff. When the pressure in the cuff reaches diastolic blood pressure, the difference between the speed of blood flow in the brachial artery in systole and diastole decreases, and Korotkoff sounds sharply weaken (phase IV Korotkoff sounds) and disappear completely (phase V).

Severe aortic valve insufficiency is characterized by the constant existence of a large circle of “pulsating” blood flow in the arterial system. Therefore, if you listen to the area of ​​a large artery (even without compressing it with a cuff), sometimes (with severe aortic insufficiency) you can listen to sounds reminiscent of Korotkoff sounds. It should be remembered that an “endless tone” in a large artery (or diastolic blood pressure = 0) can also be determined with a pronounced decrease in the tone of the arterial wall, for example, in patients with neurocirculatory dystonia.

In most cases, the pulse on the radial artery has characteristic features: a rapid rise (increase) of the pulse wave and an equally sharp and rapid decline are determined.

The arterial pulse becomes fast, high, large and fast (pulsus celer, altus, magnus et frequens). Such a pulse, creating an alternation of rapid and strong tension in the walls of the arteries, can lead to the fact that tones begin to be detected in the arteries, where sounds are not normally heard. Moreover, the severity of pulsus celer et magnus may be reflected in the appearance of the so-called “palmar tone”, determined on the inner surface of the patient’s hand, applied to the doctor’s ear.

Instrumental diagnostics

ECG

An electrocardiographic study reveals a rotation of the electrical axis of the heart to the left, an increase in the R wave in the left chest leads, and, subsequently, a downward displacement of the ST segment and inversion of the T wave in the standard and left chest leads.

In case of aortic valve insufficiency, the ECG shows:

• In case of aortic valve insufficiency, in most cases, signs of pronounced LV hypertrophy are revealed without its systolic overload, i.e. without changing the terminal part of the ventricular complex.
• Depression of the RS-T segment and smoothness or inversion of T wave are observed only during the period of decompensation of the defect and the development of heart failure.
• With “mitralization” of aortic insufficiency, in addition to signs of LV hypertrophy, signs of left atrial hypertrophy (R-mitrale) may appear on the ECG.

X-ray examination

In cases of aortic valve insufficiency, clear radiological signs of LV dilatation are usually detected. In the direct projection, already at the very early stages of the development of the disease, a significant lengthening of the lower arch of the left contour of the heart and a displacement of the apex of the heart to the left and down are detected.

In this case, the angle between the vascular bundle and the LV contour becomes less obtuse, and the “waist” of the heart becomes more emphasized (“aortic” configuration of the heart). In the left anterior oblique projection, a narrowing of the retrocardial space occurs.

In addition to the described radiological signs, in patients with aortic insufficiency, expansion of the ascending aorta is determined. Finally, decompensation of the defect is accompanied by the appearance of signs of venous stagnation of blood in the lungs, described above.

Echocardiography

Echocardiographic examination reveals a number of characteristic symptoms. The end-diastolic size of the left ventricle is increased. Hyperkinesia of the posterior wall of the left ventricle and the interventricular septum is determined. High-frequency flutter (tremor) of the anterior mitral valve leaflet, interventricular septum, and sometimes the posterior leaflet is recorded during diastole. The mitral valve closes prematurely, and during its opening the amplitude of movement of the leaflets is reduced.

Cardiac catheterization

During cardiac catheterization and appropriate invasive studies in patients with aortic insufficiency, an increase in cardiac output, LV EDP and the volume of regurgitation are determined. The latter indicator is calculated as a percentage relative to the stroke volume. The volume of regurgitation fairly well characterizes the degree of aortic valve insufficiency.

Diagnosis and differential diagnosis

Recognition of aortic valve insufficiency usually does not cause difficulties with diastolic murmur at Botkin's point or on the aorta, enlargement of the left ventricle and certain peripheral symptoms of this defect (high pulse pressure, increase in the pressure difference between the femoral and brachial arteries to 60-100 mm Hg ., characteristic changes in pulse).
However, diastolic murmur in the aorta and at the V point can also be functional, for example, with uremia. With combined heart defects and small aortic insufficiency, recognition of the defect can be difficult. In these cases, echocardiographic examination helps, especially in combination with Doppler cardiography.

The greatest difficulties arise in establishing the etiology of this defect. Other rare causes are also possible: myxomatous valve disease, mucopolysaccharidosis, osteogenesis imperfecta.

Rheumatic origin heart disease can be confirmed by anamnesis: approximately half of these patients have indications of typical rheumatic arthritis. Convincing signs of mitral or aortic stenosis also speak in favor of a rheumatic etiology of the defect. Detection of aortic stenosis can be difficult. Systolic murmur over the aorta, as already mentioned above, is also heard in cases of pure aortic insufficiency, and systolic trembling over the aorta occurs only with its severe stenosis. In this regard, echocardiographic examination is of great importance.

The appearance of aortic insufficiency in a patient with rheumatic mitral heart disease is always suspicious for the development infective endocarditis, although it may also be due to a relapse of rheumatism. In this regard, in such cases it is always necessary to conduct a thorough examination of the patient with repeated blood cultures. Aortic valve insufficiency of syphilitic origin has become much less common in recent years. Diagnosis is facilitated by identifying signs of late syphilis in other organs, such as damage to the central nervous system. In this case, the diastolic murmur is better heard not at the Botkin-Erb point, but above the aorta - in the second intercostal space on the right and spreads widely downwards, on both sides of the sternum. The ascending aorta is dilated. In a significant number of cases, positive serological reactions are detected, and the immobilization reaction of Treponema pallidum is of particular importance.

Aortic insufficiency may be due to atherosclerosis. With atheromatosis of the aortic arch, the valve ring expands with the appearance of slight regurgitation; atheromatous damage to the leaflets of the valve itself is less common. With rheumatoid arthritis (seropositive), aortic insufficiency is observed in approximately 2-3% of cases, and with a long course (25 years) of ankylosing spondylitis, even in 10% of patients. Cases of rheumatoid aortic insufficiency have been described long before the appearance of signs of damage to the spine or joints. Even less often, this defect is observed in systemic lupus erythematosus (according to V.S. Moiseev, I.E. Tareeva, 1980, in 0.5% of cases).

Prevalence Marfan syndrome in expressed form, according to various sources, from 1 to 4-6 per 100,000 population.
Cardiovascular pathology, along with typical changes in the skeleton and eyes, is part of this syndrome, but is difficult to detect in almost half of these patients only with the help of echocardiography. In addition to typical damage to the aorta with the development of its aneurysm and aortic insufficiency, damage to the aortic and mitral valves is possible. With a clear family predisposition and pronounced extracardiac signs of cardiovascular pathology, the syndrome is detected in childhood. If skeletal anomalies are mild, as in the patient described above, then heart damage can be detected at any age, however, usually in the third, fourth and even sixth decades of life. Changes in the aorta concern primarily the muscle layer; Necrosis with cysts are found in the wall, and fibromyc-somatous changes in the valves are possible. Aortic regurgitation often progresses gradually, but it can appear or worsen suddenly.

Cystic necrosis, without other signs of Marfan syndrome, is called Erdheim syndrome. It is believed that similar changes can simultaneously or independently occur in the pulmonary arteries, causing them the so-called congenital idiopathic dilatation. An important differential diagnostic feature that allows distinguishing aortic lesions in Marfan syndrome from syphilitic ones is the absence of its calcification. Damage to the mitral valve and chordae with their breakage occurs only in some patients, usually accompanies damage to the aorta and leads to prolapse of the mitral valve leaflets with mitral insufficiency.

A rare cause of aortic regurgitation may be Takayasu disease- nonspecific aortoarteritis, which occurs mainly in young women in the second - third decade of life and is associated with immune disorders. The disease usually begins with general symptoms: fever, weight loss, joint pain. Subsequently, the clinical picture is dominated by signs of damage to large arteries arising from the aorta, often from its arch. Due to impaired patency of the arteries, the pulse often disappears, sometimes only in one arm. Damage to the large arteries of the aortic arch can lead to cerebrovascular insufficiency and visual impairment. Damage to the renal arteries is accompanied by the development of arterial hypertension. Valvular insufficiency of the aorta may be due to dilatation of the aortic arch in patients with gangan cell arteritis. This disease develops in older people, manifesting itself as damage to the temporal arteries, which, in typical cases, are palpated in the form of a dense, painful, nodular cord. Intracardiac arteries may also be affected.

Aortic insufficiency is often combined with a variety of extracardiac manifestations, a careful analysis of which allows us to establish the nature of the heart defect.

Forecast

The life expectancy of patients, even with severe aortic insufficiency, is usually more than 5 years from the moment of diagnosis, and in half - even more than 10 years.

The prognosis worsens with the addition of coronary insufficiency (angina attacks) and heart failure. Drug therapy in these cases is usually ineffective. The life expectancy of patients after the onset of heart failure is about 2 years. Timely surgical treatment significantly improves the prognosis.

The physical properties of ultrasound determine the methodological features of echocardiography. Ultrasound of the frequency used in medicine practically does not pass through air. An insurmountable obstacle to the path of the ultrasound beam can be the lung tissue between the chest and the heart, as well as a small air gap between the surface of the sensor and the skin. To eliminate the last obstacle, a special gel is applied to the skin, displacing air from under the sensor. To exclude the influence of lung tissue, to install the sensor, select points where the heart is directly adjacent to the chest - the “ultrasound window”. This is the zone of absolute cardiac dullness (3-5 intercostal space to the left of the sternum), the so-called parasternal access, and the zone of the apical impulse (apical access). There is also a subcostal approach (at the xiphoid process in the hypochondrium) and suprasternal (in the jugular fossa above the sternum). The sensor is installed in the intercostal spaces due to the fact that ultrasound does not penetrate deep into the bone tissue and is completely reflected from it. In pediatric practice, due to the lack of ossification of cartilage, examination through the ribs is also possible.

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

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

Ultrasound anatomy of the heart in various echolocation modes

I. One-dimensional (M-) echocardiography.

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

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

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

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

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

Image of the heart structures in the first standard position.

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

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

Tmzhp - swelling of the interventricular septum in diastole

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

CDR– end-diastolic size of the left ventricle

KSR- end-systolic size of the left ventricle

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

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

Basic indicators measured in the first stationary position.

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

Cardiomyopathy).

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

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

= 7,0 * 3

V(24*D)D(cm3),

where D is the anteroposterior dimension in systole or diastole.

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

UO - KDO - KSO (ml).

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

Impact index (UI):

UI=UO/St

Minute volume of blood circulation ( IOC):

IOC = SV HR

Cardiac index ( SI): SI = IOC/St

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

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

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

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

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

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

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

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

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

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

%ΔS=KDR-KSR/KDR 100% (norm 30-43%)

3. The rate of piricular shortening of myocardial fibers

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

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

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

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

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

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

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

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

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

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

The main indicators of the echocardiogram in the II standard position

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

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

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

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

1. 
   ventricle (LVEDD). 5. Speed ​​of diastolic opening of the anterior leaflet

(determined by the slope of the D-E section and is normally 27.6 cm/s). - A decrease in the opening speed of the valves can also be an indirect sign of an increase in LVEDP.

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

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

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

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

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

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 is 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, the tricuspid valve, and, with a greater tilt of the sensor, one of the leaflets of the pulmonary artery valve 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 into 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).

Valve deformation 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 stenosis - 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 direct signs of the defect indicated above, 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 (MVI) on one-dimensional echocardiography
2. 
   Increased systolic excursion of the posterior wall and interventricular septum, moderate dilatation of the cavity of the left ventricle (signs of LV volume overload).

3. Increased excursion of the posterior wall of the left atrium in the third position of the sensor (1 cm or more); moderate hypertrophy of the left atrium.

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

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

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

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

Mitral defect with predominant stenosis.

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

Mitral disease with predominant insufficiency.

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

Aortic stenosis

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

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

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

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

Aortic valve insufficiency

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

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

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

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

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

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

Hypertrophic cardiomyopathy

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

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

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

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

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

Rice. 17. Forms of HCM:

a-asymmetric interventricular septum;

b-concentric left ventricle;

b-apical (non-obstructive);

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

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

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

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

Dilation of cardiomyopytia

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

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

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

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

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

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

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

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

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

An echocardiographic picture of dilatation 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.

References

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

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

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

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

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

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

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

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

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

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

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

RHEOGRAPHY

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

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

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

LITERATURE

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

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

General information

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

Causes of aortic insufficiency

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

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

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

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

Hemodynamic disorders in aortic insufficiency

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

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

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

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

Classification of aortic insufficiency

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

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

Symptoms of aortic insufficiency

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

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

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

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

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

Diagnosis of aortic insufficiency

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

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

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

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

Prognosis and prevention of aortic insufficiency

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

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

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 area of ​​the heart, the apical impulse is often noticeable, enlarged in area and displaced 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, which has a pronounced cardiac waist (aortic configuration), is determined by percussion.

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 falls and blood flow slows down (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 persist). 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 disturbances in intracardiac hemodynamics 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 dilation (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; double murmur of Vinogradov-Durozier et al. do not always occur and are 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 due to 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 required value of the stroke volume of the left ventricle when blood is expelled through a narrowed orifice during the allotted time interval (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 disturbances 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 dilatation, 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 lack 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 initially 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 murmur 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 reliably obtain not only a qualitative characteristic (the presence of a heart defect), but also 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 vibration 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, liver enlargement; 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