Mkb 10 defect with mitral insufficiency. Mitral heart disease

Four percent of patients with malformations of the cardiovascular system are diagnosed with congenital heart disease bicuspid aortic valve. The disease has an ICD-10 code - “Q 23.1. Bicuspid aortic valve. Congenital aortic insufficiency".

The disease is included in the class of congenital anomalies (malformations) of the aortic and mitral valves (Q23).

The reasons

The essence of this defect is the incomplete closure of the valve leaflets during diastole. Because of this, the blood flow partially returns back from the aorta to the left ventricle.

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Incomplete closure occurs due to the fact that instead of three movable flaps in the valve, there are only two. This pathology occurs in the prenatal period during the formation of the organs of the fetus at 6-8 weeks of gestation.

Two of the three leaflets fuse and take over the functions of the missing part of the aortic valve.

Causes of abnormal development of the aortic valve leaflets:

• infectious diseases during pregnancy (flu, rubella);
• exposure to radiation, exposure during x-ray examination;
• negative environmental factors;
• stressful situations, psycho-emotional shocks;
• smoking during pregnancy, taking alcoholic beverages;
• hereditary predisposition to the disease, the presence of a defect in one of the parents,
• genetically determined connective tissue pathologies in the child's parents (Marfan's syndrome, osteoporosis, aortoannular ectasia, cystic fibrosis).

When managing pregnancy and giving birth to parents with a predisposition to a disease such as congenital heart disease, bicuspid aortic valve, it is necessary to conduct a thorough diagnosis in order to take timely measures to maintain the child's cardiac activity and prevent complications.

Symptoms

For several years, a congenital disease may not show any symptoms. Subjective manifestations appear as the child grows up and the load on the growing organism increases. Cases of detection of this pathology already in adolescence and adulthood have been recorded.

Symptoms of congenital aortic insufficiency:

• Feeling of a strong pulsation, the work of your heart in the neck, head and directly in the projection of the heart. Especially strong manifestations occur when the patient is in a supine position. The cause of this symptom is high cardiac output and high pulse pressure.
• Sinus tachycardia, which manifests itself as a rapid heartbeat.
• Frequent fainting and dizziness associated with physical activity and sudden changes in body position. The cause of this symptom is cerebrovascular insufficiency. Appears with pronounced changes in the structure of the valve.
• Shortness of breath, which initially occurs with significant physical exertion, and later at rest. When the systolic function of the left ventricle falls, it manifests itself in the form of orthopnea. As a result of the development of the disease, cardiac asthma and pulmonary edema cause asthma attacks.
• Rapid fatigue, general weakness.
• Visual impairment.
• Retrosternal pain in the region of the heart, not associated with physical and emotional overload. Appears at rest, with a pronounced aortic valve defect, is pressing or compressive in nature, lasts a long time, does not disappear after taking nitroglycerin. Night attacks of pain are usually tolerated more severely by patients, accompanied by profuse sweating. The cause of the symptom is ventricular hypertrophy.

Most of the symptoms are caused by a violation of hemodynamics, that is, the blood circulation passes through a pathologically altered path, enters the aorta, passing through the ventricle.

This violation can be detected only with hardware diagnostics of congenital pathology of the aortic valve.

Diagnostics

Instrumental methods are of great importance for the diagnosis of the disease, however, a visual examination by a cardiologist of a patient with suspected aortic valve insufficiency can reveal signs of the disease.

First of all, it is cyanosis and acrocyanosis skin when the skin becomes pale or its individual areas acquire a blue tint.

Increased pulsation is also a sign of the disease.

Instrumental methods for diagnosing a congenital aortic valve defect:

The most informative study is ultrasound, based on its results, further treatment tactics are built.

When a bicuspid aortic valve defect is accompanied by aortic regurgitation (blood flow in the opposite direction of normal movement), young men of military age on the basis of this diagnosis are required to receive a deferment from the army.

Such a pathology gives them the right to be enrolled in the reserve and issue a military ID marked "category B, limited fit." If signs of regurgitation are not found, then the presence of a bilateral aortic valve is not an obstacle to military service.

Treatment of congenital heart disease - bicuspid aortic valve

Determination of treatment tactics depends on the severity of symptoms of aortic insufficiency. With little or no symptoms of the disease, good exercise tolerance, treatment may not be required. The cardiologist will put the patient on a dispensary record and prescribe regular ultrasound to monitor the condition of the heart.

If heart failure is not pronounced, it is carried out conservative treatment. The use of medicines will help improve the quality of life of the patient, if necessary, stabilize his condition with indications for surgical treatment.

With pronounced symptoms of aortic insufficiency, the patient is indicated for surgical intervention with the replacement of the aortic valve. result surgical operation will be the installation of a prosthetic aortic valve.

Types of artificial aortic valves:

Methodology modern operations does not provide for open intervention in the chest. The artificial valve is inserted percutaneously, by transcatheter implantation of the prosthesis through the subclavian or femoral artery. It is possible to insert the prosthesis through the apex of the heart (transpically).

Possible complications of valve replacement surgery:

• thromboembolism of arteries in the area of ​​the surgical field;
• destruction of a biological prosthesis, its calcification;
• infective endocarditis - inflammation of the endocardium due to bacteria entering the bloodstream during the operation;
• disruption of normal blood flow due to the formation of blood clots in the area of ​​the prosthesis;
• the appearance of paravular fistulas.

After prosthetic surgery, constant medication is required to reduce blood clotting and anticoagulant therapy.

Patients who have undergone aortic valve replacement surgery should continue with dental or endoscopic interventions before manipulations with a prophylactic course of antibiotic therapy.

Forecast

Prediction of the course of the disease and life expectancy of patients with congenital pathology of the aortic valvular apparatus depends on the following factors:

• dynamics of changes in the work of the aortic valve;
• the degree of manifestation of coronary or heart failure,
• patient compliance with the recommendations of the attending physician on lifestyle correction, dosing of physical and psycho-emotional stress.

The prognosis of viability in newly diagnosed aortic valve disease is:

To improve the prognosis of the course of the disease, it is necessary to observe preventive measures. They include optimizing the regime of work and rest, introducing foods rich in vitamins into the diet, regular walks and feasible physical education in the fresh air, and regulating the psycho-emotional load.

It is important not to infectious diseases heart, such as endocarditis, prevent rheumatism, hardening the body.

Conducted on doctor's orders drug therapy so that pathological changes do not progress. For professional sports, congenital aortic valve disease may be a contraindication, since during intense physical exertion, the volume of blood that passes along the wrong path (regurgitation) increases.

Timely diagnosis of congenital aortic valve disease will help to choose the right tactics for its treatment. Compliance with the recommendations of a cardiologist will help stop the progression of the disease, prepare for surgery, and improve the prognosis for the development of the disease.

II Acquired heart defects.

Heart disease- this is an anatomical change in the valvular apparatus of the heart or interatrial, interventricular septum and other defects.

By origin, the vices are divided:

• Congenital- arise as a result of a violation of the formation of the heart and blood vessels in the embryonic period.
• Acquired- acquired changes in the heart valves, leading to impaired function and hemodynamics, acquired defects are a complication of various diseases.

Combined vice- a combination of two defects of one valve. For example, mitral stenosis and mitral insufficiency.

Combined vice- a combination of defects of several valves, for example, mitral stenosis and aortic insufficiency.

Isolated vice- one defect of one valve, for example, mitral insufficiency.

Compensated vice- no complaints, no signs of circulatory failure.

Decompensated defect- there are complaints of circulatory failure of the left ventricular or right ventricular type.

MITRAL HEART DEFECTS.

mitral stenosis- narrowing of the left atrioventricular orifice, which prevents the physiological flow of blood from it into the left ventricle during systole of the left atrium.

Mitral insufficiency- the inability of the left atrioventricular valve to prevent the reverse movement of blood from the left ventricle to the left atrium during ventricular systole, that is, incomplete closure of the MV valves.

Prolapse mitral valve(PMK)- pathological sagging (flexion) of one or both leaflets of the mitral valve into the left atrium during left ventricular systole.

I05.0 Mitral stenosis, rheumatic.

I05.1 Rheumatic mitral valve insufficiency

I05.2 Mitral stenosis with insufficiency

I05.8 Other disorders of the mitral valve (mitral insufficiency)

I05.9 Mitral valve disease, unspecified

EPIDEMIOLOGY and ETIOLOGY.

■mitral stenosis almost always occurs as a result of an acute rheumatic attacks, more often in women.

On average, the latent period from the moment of rheumatic heart disease (carditis) to the development of clinical manifestations of the defect is about 20 years, so the disease manifests itself between 30 and 40 years of age.

■Mitral insufficiency. Causes: MVP, rheumatism (30%), atherosclerosis, infective endocarditis, trauma, connective tissue diseases. At men mitral insufficiency is noted more often.

■PMK. Causes: rheumatism, infections, ischemic heart disease.

CLASSIFICATION.

• Mitral stenosis classification the severity is based on the severity of the narrowing of the left atrioventricular orifice (mild, moderate and severe stenosis).
• Mitral regurgitation classification the degree of severity is determined by the volume of regurgitant blood (4 degrees of mitral insufficiency).

PATHOGENESIS

Through the narrowed left atrioventricular orifice, not all blood enters the left ventricle (LV) during systole of the left atrium (LA), as a result, an excess volume of blood is formed in the left atrium (remaining after systole and again coming from the pulmonary veins during subsequent diastole) , this leads to left atrial hypertrophy (compensation stage), over time, the atrial myocardium is depleted, the left atrial cavity expands, decompensation develops, as a result, pressure in the ICC increases and hypertrophy of the right ventricle (RV) develops, and then the right atrium (RA).

I51.9 Heart disease, unspecified: description, symptoms and treatment

from 2000-2015. REGISTER OF DRUGS OF RUSSIA ® RLS ®

Classification of acquired heart defects

(Adopted at the VI Congress of Cardiologists of Ukraine, Kyiv, 2000) Mitral stenosis:

Rheumatic 1.05.0 Non-rheumatic 1.34.2 (with clarification of etiology) Stage I - compensation Stage II - pulmonary congestion

stage - right ventricular failure

stage - dystrophic

V stage - terminal

Mitral insufficiency

Rheumatic 1.05.1 Non-rheumatic 1.34.0 (with clarification of etiology) Stage I - compensation Stage II - subcompensation Stage III - right ventricular decompensation Stage IV - dystrophic Stage V - terminal Combined rheumatic mitral defect (Rheumatic mitral stenosis with insufficiency: 1.05.2) C predominance of stenosis: stages and indications for surgical treatment, as in mitral stenosis With a predominance of insufficiency: stages and indications for surgical treatment, as in mitral insufficiency No clear predominance: stages and indications for surgical treatment, as in mitral insufficiency Mitral valve prolapse 1.34.1 Aortic stenosis: Rheumatic 1.06.0 Non-rheumatic 1.35.0 (with specification of etiology) Stage I - complete compensation Stage II - latent heart failure Stage III - relative coronary insufficiency GU stage - severe left ventricular failure Stage V - terminal Aortic insufficiency:

Rheumatic 1.06.1 Non-rheumatic 1.35.1 (with clarification of etiology) Stage I - complete compensation Stage II - latent heart failure

stage - subcompensation

stage - decompensation

Stage V - terminal Combined aortic defect:

Rheumatic aortic stenosis with insufficiency 1.06.2 Non-rheumatic aortic (valvular) stenosis with insufficiency 1.35.2 (with specification of etiology) Stenosis-predominant: stages and indications for surgical treatment are the same as those for aortic stenosis Insufficiency-dominant: stages and indications for surgical treatment are the same with aortic insufficiency 216

Without a clear predominance: the stages and indications for surgical treatment correspond to those for aortic stenosis Tricuspid stenosis:

Rheumatic 1.07.0 Non-rheumatic 1.36.0 (with clarification of etiology) Tricuspid insufficiency:

Rheumatic 1.07.1 Non-rheumatic 1.36.1 (with specification of etiology) Combined tricuspid defect:

Rheumatic tricuspid stenosis with insufficiency 1.07.2 Non-rheumatic tricuspid valve stenosis with insufficiency 1.36.2 (with specified etiology) Pulmonary artery stenosis 1.37.0 Pulmonary valve insufficiency 1.37.1 Combined valvular disease of the pulmonary artery (Pulmonary artery stenosis with valve insufficiency 1.37.2 ) Combined heart defects:

Combined damage to the mitral and aortic valves 1.08.0 Combined damage to the mitral and tricuspid valves 1.08.1 Combined damage to the aortic and tricuspid valves 1.08.2 Combined damage to the mitral, aortic and tricuspid valves 1.08.3 The severity of "simple" defects is determined by three degrees:

I degree - insignificant II degree - moderate III degree - pronounced.

The severity of defects in accordance with their clinical and instrumental characteristics are given below for individual nosological forms of heart defects.

It should be noted that heart disease is considered "combined" in the presence of stenosis and insufficiency of one valve and "combined" in case of damage to several valves. If there are several defects, they are listed, with the first indicating the defect, the severity of which is greater - for example, aortic valve insufficiency, mitral defect with a predominance of stenosis.

Given that valve kalydinosis determines the tactics of surgical intervention, it is proposed to distinguish 3 degrees of kalydinosis (Knyshov G.V. BendetYa.A. 1996).

Degrees of valve calcification

Separate clumps of calcium in the thickness of the commissures or valves

Significant calcification of valves and commissures without

valve ring attraction III +++ Massive calcification of the valve with the transition to the annulus fibrosus, and sometimes to the aortic wall and ventricular myocardium. In the diagnosis, it is also necessary to take into account the etiological cause of the defect (rheumatism, infective endocarditis, atherosclerosis), the degree of heart failure.

For patients who underwent surgery on the heart valves, it is necessary to indicate the previous defect, indicate the date surgical treatment the nature of the complications. For example, operated mitral heart disease with a predominance of stenosis, closed commissurotomy (date) or operated aortic valve disease with a predominance of insufficiency. Aortic valve replacement (specify type of prosthesis and date).

Along with heart defects caused by organic changes in the valve, there are violations of valve function in the form of relative insufficiency or relative stenosis. The cause of relative insufficiency of the valve may be a decrease in the tone of the papillary muscles or a violation of the function of the circular muscles, which normally reduce the lumen of the hole during systole. With a decrease in the tone of these muscles, the opening during systole remains large, and even unchanged valve leaflets cannot completely cover it. The most typical is the relative insufficiency of the mitral valve in aortic disease, which gave grounds to speak of "mitralization of aortic disease". Relative valvular insufficiency main vessels observed with an increase in the perimeter of the fibrous ring, in which the area of ​​​​the cusps of the valves is insufficient to completely cover the mouths of the vessels (more often relative insufficiency of the pulmonary valve). Relative stenosis occurs when sharp increase blood flow through an opening of normal size, for example, with severe mitral or aortic valve insufficiency. The addition of relative valve insufficiency or relative stenosis, despite changes in auscultatory signs and the course of the disease, does not give grounds for designating the defect as combined.

mitral stenosis

For the first time, the defect was described by Viussens in 1715. When it occurs, an obstacle is created to the movement of blood from the left atrium to the left ventricle. Mitral stenosis is the most common rheumatic heart disease. The defect is usually formed at a young age and is more often observed in women (80%).

Etiology. Mitral stenosis occurs due to long-term rheumatic endocarditis, an extremely rare cause of mitral stenosis is infective endocarditis. Narrowing or closure of the mitral orifice can be caused by a thrombus, polyp, left atrial myxoma.

Pathological anatomy. Pathological changes in the mitral valve in the rheumatic process are complex and varied. The valve defect is based on sclerotic processes, which involve the leaflets, annulus fibrosus, chords and papillary muscles (Fig. 18). The narrowing of the opening occurs initially due to gluing of the adjoining edges of the valves, primarily along their poles adjacent to the fibrous ring (Fig. 19), where mobility is limited, with the formation of commissures. In the future, the fusion of the valves extends to the middle of the hole, gradually narrowing it. In parallel, fibrous changes in the structures of the valvular apparatus occur, they become rigid and inactive. At the same time, the fibrous ring becomes sclerosed and loses its elasticity. If the process is localized mainly in the valve leaflets,

219 Fig.18. Mitral valve (no F. Netter, 1969, with changes), then when the edges of the fibrous thickened valve are fused, a diaphragm with a slit-like opening is formed - stenosis in the form of a "button loop" (in 85% of cases). Involvement of subvalvular structures in the pathological process - damage to tendon filaments with their fusion, thickening, shortening - sharply limits the mobility of the valve, with significant involvement of subvalvular formations, the narrowing looks like a "fish mouth" (Fig. 20). In some patients, a double narrowing is found - the fusion of the valves and tendon filaments. With prolonged existence of the defect, calcification of the valve occurs.

pathological physiology. Normally, the area of ​​the atrioventricular opening is 4-6 cm2, the opening has a significant area reserve, and only its decrease by more than 2 times can cause a noticeable hemodynamic disturbance. The smaller the hole area, the heavier clinical manifestations mitral stenosis. The "critical area", at which noticeable hemodynamic disorders begin, is 1-1.5 cm2.

The resistance to blood flow created by the narrowed mitral orifice (the “first barrier”) sets in motion compensatory mechanisms that ensure sufficient heart performance. With mitral stenosis, the movement of blood from the left atrium in Fig.19. Heart valves (according to F. Netter, 1969, with changes) A ​​- pulmonary valve: 1 - anterior leaflet, 2 - right leaflet, 3 - left leaflet; B - aortic valve: 1 - right (coronary) cusp, 2 - left (coronary) cusp, 3 - posterior (non-coronary) cusp; B - mitral valve: 1 - anterior (aortic) cusp, 2 - commissural cusps, 3 - posterior cusp, 4 - fibrous ring; D - tricuspid ManaH: 1 - anterior leaflet, 2 - septal leaflet, 3 - posterior leaflet, 4 - annulus fibrosus 20. Echocardiography of mitral stenosis (B-mode, opening area = 1.2 cm2) the ventricle accelerates due to an increase in the pressure gradient between the left atrium and the left ventricle (Fig. 21). Compensatory pressure in the left atrium increases, the atrial myocardium hypertrophies, its cavity expands. Due to the fact that the left atrium cannot cope with the increased load, further growth 21. Blood pressure (mm Hg) in different parts of the heart and blood vessels in normal (systolic / diastolic) pressure in it leads to a retrograde increase in pressure in the pulmonary veins and capillaries, arterial hypertension occurs in the pulmonary circulation. When the pressure in the left atrium is above a certain level, due to irritation of the receptor apparatus in the walls of the left atrium and pulmonary veins, a reflex narrowing of the small pulmonary arteries occurs at the precapillary level (“second barrier”) - the Kitaev reflex, which protects the capillary network of the lungs from overflowing with blood. In the future, due to prolonged vascular spasm, an organic degeneration of the walls of the vessels occurs, hypertrophy develops, as well as sclerosis of the walls of the pulmonary arterioles, capillaries, and lung parenchyma. There is a persistent pulmonary "second barrier". Hemodynamic disturbances are exacerbated by weakening of the left atrial myocardium. High pressure in the pulmonary artery (up to 80 mm Hg and above) leads to compensatory hypertrophy, and then dilatation of the right ventricle, it increases diastolic pressure. In the future, an increase in pressure in the pulmonary artery and the development of myocardial wear syndrome causes the appearance of right ventricular failure and relative insufficiency of the tricuspid valve (Fig. 22).

The clinical picture of mitral stenosis depends on the stage of the disease, the state of circulatory compensation. With compensatory hyperfunction of the left atrium, patients usually do not complain, they can perform significant physical activity.

With an increase in pressure in the pulmonary circulation, there are complaints of shortness of breath and a feeling of palpitations during physical exertion. With a sharp increase in pressure in the capillaries, attacks of cardiac asthma develop, dry or with separation a large number mucous sputum cough, often with an admixture of blood (hemoptysis). With high pulmonary hypertension, patients experience weakness, increased fatigue, due to the fact that in the conditions of mitral stenosis ("first barrier") during exercise, there is no adequate increase in cardiac output (the so-called fixation of cardiac output).

Rice. 22. Mitral stenosis (according to F. Netter, 1969, with changes) Appearance patients with moderately severe mitral stenosis is not changed. With severe stenosis and an increase in symptoms of pulmonary hypertension, typical Facies mitralis is observed: a “mitral” blush on the cheeks against the background of pale skin of the face, cyanosis of the lips, nose tip, auricles. In patients with high pulmonary hypertension, cyanosis increases during exercise, and a grayish coloration of the skin (“ashy cyanosis”) appears, which is due to low cardiac output. The region of the heart in the lower part of the sternum often bulges and pulsates due to the formation of a "heart hump" due to hypertrophy and dilatation of the right ventricle and its increased impacts on the anterior chest wall. On the left edge of the sternum in the third-fourth intercostal space, a pulsation of the output tracts of the right ventricle can be observed, associated with its hemodynamic overload in conditions of pulmonary hypertension.

In the region of the apex of the heart, or somewhat laterally, diastolic trembling is determined - "cat's purr" - a phenomenon caused by low-frequency fluctuations of blood when it passes through a narrowed mitral opening.

Mitral stenosis is diagnosed based on the characteristic melody of tones and heart murmurs. Amplified (flapping) I tone at the apex of the heart and the mitral valve opening tone (opening click), appearing 0.08-0.11 s after tone II, create a characteristic melody of mitral stenosis - a quail rhythm. Flapping I tone is heard only in the absence of gross deformities of the valves (in the absence of fibrosis and calcification of the valve). The mitral valve opening tone persists even when atrial fibrillation occurs. With an increase in pressure in the pulmonary artery in the second intercostal space to the left of the sternum, an accent of the II tone is heard, often with a bifurcation, which is due to the non-simultaneous slamming of the valves of the pulmonary artery and aorta.

The characteristic auscultatory symptoms in mitral stenosis include diastolic murmur, which may occur in different periods diastole. Protodiastolic murmur occurs at the beginning of diastole due to the movement of blood through the narrowed hole as a result of a pressure gradient in the left atrium - left ventricle, its character is low, rumbling (its palpatory equivalent is "cat's purr"). The noise can be of different duration, its intensity gradually decreases. Presystolic murmur occurs at the end of diastole due to active atrial systole, with the appearance of atrial fibrillation, the murmur disappears. The pre-systolic murmur is usually short, rough, scraping timbre, has a growing character, ends with a clapping I tone. It should be noted that diastolic murmurs in mitral stenosis are heard in a limited area and are not carried out, therefore, an insufficiently thorough search for the place of the best auscultation of the mitral valve can be a source of diagnostic errors.

Electrocardiogram with minor mitral stenosis is not changed. As the defect progresses, there are signs of left atrial overload (Pmitrale), right ventricular hypertrophy in the form of an increased amplitude of the QRS complex teeth in the corresponding leads in combination with an altered end part of the ventricular complex (flattening, T wave inversion, segment 57 decrease) in the same leads. Heart rhythm disturbances (flicker, atrial flutter) are often recorded.

Phonocardiogram for the diagnosis of mitral stenosis is of great importance. With mitral stenosis, a change in the intensity of the first tone, the appearance of an additional tone (a click of the opening of the mitral valve), as well as the appearance of noise in diastole, are detected. The duration of the interval from the beginning of the II tone to the opening tone of the mitral valve (II tone - QS) ranges from 0.08 to 0, 12 si shortens to 0.04-0.06 s with the progression of stenosis. As the pressure in the left atrium increases, the interval?-l tone lengthens, which reaches 0.08-0.12 s. Various diastolic murmurs are recorded (pre-, meso- and proto-diastolic). The phonocardiographic picture in mitral stenosis is shown in fig. 23. The value of phonocardiography increases in the conditions of the tachysystolic form of atrial fibrillation, when during normal auscultation it is difficult to attribute the auscultated murmur to any or another phase of the cardiac cycle.

Rice. 23. Phonocardiogram for mitral and aortic heart disease (according to F. Netter, 1969, with changes) Echocardiography can be a verifying method for mitral stenosis, in which the following changes are observed: unidirectional (P-shaped) movement of the anterior and posterior mitral valve leaflets forward ( normally, the posterior leaflet moves posteriorly during diastole; Fig. 24);

Decreased rate of early diastolic occlusion of the anterior

mitral valve leaflets (up to 1 cm/s);

decrease in the amplitude of the opening of the mitral valve leaflet

(up to 8 mm or less);

enlargement of the left atrial cavity (anteroposterior size

can be increased up to 70 mm);

Valve thickening (fibrosis and calcification; Fig. 25).

Experts from the American College of Cardiology (1998) developed indications for echocardiography in mitral stenosis:

Rice. 24. Echocardiography in mitral stenosis (M-mode) 1. Diagnosis of mitral stenosis, assessment of the severity of hemodynamic disorders (pressure gradient value, mitral ring area, pressure in the pulmonary artery), as well as determining the size and function of the right ventricle.

Rice. 25. Echocardiography in mitral stenosis (B-mode)

Assessment of the mitral valve to determine if

for percutaneous balloon valvotomy of the left

atrioventricular orifice.

Diagnosis and assessment of severity of associated valve

ny defeats.

Re-examination of patients diagnosed with mitral steatosis

nose, which clinical picture disease over time

has changed.

Assessment of the state of hemodynamics and pressure gradient in the lung

artery using Doppler echocardiography at rest in patients

goods in case of discrepancy between the results of objective and instrumental

research methods.

Catheterization of the cavities of the heart plays an auxiliary role. In some patients with mitral stenosis, an accurate diagnosis of the defect requires invasive methods. Indications for cardiac catheterization in mitral stenosis, developed by experts from the American College of Cardiology (1998), are given below.

The need for percutaneous mitral balloon

valvotomy in properly selected patients.

Assessment of the severity of mitral regurgitation in patients

who are expected to perform a mitral percutaneous ball

pubic valvotomy, when clinical evidence is against

speak echocardiographically.

Evaluation of the state of the pulmonary artery, left atrium and diastolic pressure in the cavity of the left ventricle, when the clinical symptom

1. Purposes of disease classification
2. MKB 10 codes for various kinds arterial hypertension
3. Hypertensive crisis according to mcb
4. Prevention of hypertension

For people who are far from medicine, the phrase hypertension code for microbial 10 does not mean anything. Even if the person himself suffers from this formidable disease. Many understand that we are talking about high blood pressure, but where does the code with the strange abbreviation microbial and why it is with the number 10 remain a mystery to them.

Everything is quite simple - each disease has its own code in a special classifier of diseases. For various manifestations of hypertension in this list, several codes are assigned at once, and an incomprehensible microbial is a simple and understandable thing.

Despite differences in delivery medical services different countries there is a single international classification of diseases. It contains an impressive list of various diseases, accepted at the international level.

The procedure for creating such classifiers has been carried out by the World Health Organization for many years. The full name of this document (icb) is more detailed - "International Statistical Classification of Diseases and Related Health Problems".

All diseases are divided into 21 classes depending on body systems, groups of diseases and human conditions. Each class has its own letters and digital values corresponding to a particular disease. One code contains 1 letter and 2 digits indicating the disease, and the third digit carries only a clarifying diagnosis.

WHO began to oversee the medical classification of diseases in 1948 after the 6th revision. The tenth revision of the ICD is now in force, which is why it is designated by the number 10. This version of the classification has emerged as a result of long-term international cooperation by searching for compromises that are convenient for all. The consent of the parties is necessary to achieve the objectives of the ICB.

Purposes of disease classification

At the moment, the unified classifier of diseases and health problems has only two goals - collecting statistics and facilitating work with data. The ICD provides uniform methodological approaches to disease statistics and makes it possible to compare international data.

Thanks to this normative document, conditions began to appear all over the world for a comparative analysis of statistical data on diseases and mortality occurring at different times in many countries. The appearance of codes has greatly facilitated this task, now there is no need to write the full name of the disease, but it is enough to indicate the code corresponding to it.

The international classifier allows you to determine the epidemiological situation, the prevalence of certain diseases, including the frequency of sharply “rejuvenated” hypertension. arterial hypertension icb 10 code describes more than one common disease, the code may differ due to the concept of target organs damaged by this disease.

Arterial hypertension is a very common cardiovascular disease and the frequency of its manifestations increases with age. In some countries and regions, the percentage of the elderly is as high as 65, and that of young people is about 20.

Despite the fact that the frequency increases with age, but hypertension does not change the ICD code for young people and the elderly. This applies to all types of disease - hypertension can disable various organs, and each of these types has its own code.

Hypertension often affects the following organs:

• Eyes;
• kidneys;
• Heart;
• Brain.

In each of the organs, under the influence of increased pressure, many processes can occur - all this is connected with the work of the vessels that are exposed to the negative effects of hypertension in the first place.

According to WHO, hypertension is in class IX, which includes diseases of the circulatory system. Hypertension code μb 10, depending on the type, is indicated by the code from I10 to I15, not including I14. With the exception of I10, each cipher has a clarifying third digit for a specific diagnosis.

Although it is not entirely correct to talk about specifics - there are also unspecified types of arterial hypertension. Most often it is hypertension with predominant simultaneous damage to the kidneys and heart. There is also a secondary unspecified hypertensive disease.

ICD 10 codes for different types of arterial hypertension

Hypertension cipher microbial 10, denoted by I11, including I11.0 and I11.9 denotes diseases with a primary lesion of the heart. This subgroup does not include combinations of heart and kidney damage, they belong to I13 codes and have 4 internal codes - I13.0, I13.1, I13.2 and I13.9

Codes I12 are for hypertension with kidney damage. International classification allocates hypertension with the development kidney failure against the background of high blood pressure (I12.0). Under the code I12.9, hypertension is indicated with kidney damage without the development of insufficiency of their functions.

Behind the alphanumeric designations I15.0, I15.1, I15.2, I15.8, I15.9, various variations of secondary hypertensive disease are hidden. The code for primary hypertension is I10. Hypertensive crises are usually noted in this way.

Read the full article about the symptoms and first aid for hypertensive crisis here.

Hypertensive crisis according to mcd

The hypertensive crisis, according to the microbial code 10, refers to essential hypertension, although a sharp jump in pressure, life threatening may also occur in secondary manifestations of the disease. The I10 code is sometimes changed to other codes for hypertensive diseases after the diagnosis has been clarified. Quite often this happens with hypertension, which affects the heart and kidneys at the same time.

In Russia, there is no legislatively fixed classification yet. hypertensive crises. In the USA and a number of other countries, the crisis in hypertensive patients is divided into two types:

• Complicated;
• Uncomplicated.

The first of them requires urgent hospitalization, regardless of the code for ICD 10. The second is stopped at home with subsequent treatment in a hospital. And these data can also be subjected to statistical processing.

Many countries have their own statistical centers that process various data. Due to the presence of classifications of diseases, it is possible to determine the prevalence of a particular disease in a certain region or an entire country. This allows you to quickly collect all the data on any disease - hypertension in microbial 10 occupies several different codes, and not 20-25 definitions with the names of specified diseases.

The analyzed data allows the ministries of different countries to correctly respond to a surge in a particular disease. Additional surveys are being created to identify an epidemiological disease in the initial stages, work is being carried out with the population and medical workers. Also, on the basis of such an analysis, information brochures and various materials dedicated preventive measures specific illness.

Prevention of hypertension

Hypertensive disease occupies several codes for microbial 10 at once. There are several types of hypertension, including those that can damage various organs. Codes for hypertension were determined by the World Health Organization and will later be processed by statistical centers. In order not to become another unit in statistics, it is advisable to take preventive measures in advance, especially if there is a hereditary predisposition.

Proper nutrition with enough minerals and vitamins, normal physical activity, optimal weight and moderate salt intake can seriously help to avoid hypertension. If you exclude excessive stress, alcohol abuse and smoking, then the likelihood of hypertension will become even less. And then you don’t need to worry about which microbial code 10 for hypertension will be completely unnecessary.

Diagnosis and treatment of heart defects

The heart is a powerful muscular pump that works tirelessly. Its size is not much larger than a human fist. This organ consists of four chambers: the upper pair is called the atrium, the lower ones are the ventricles. During circulation, blood passes a certain path: from the atria it enters the ventricles, then into the main arteries. Four heart valves take an active part in this process, which, opening and closing, allow blood to flow in one direction.

Heart defects are changes or disorders in the structure of an organ that change the movement of blood inside it or in the systemic and pulmonary circulation. Problems can arise with partitions, walls, valves, outgoing vessels.

There are two groups: congenital and acquired defects.

Vices acquired

According to the International Classification of Diseases (ICD) of the 10th revision, acquired defects belong to sections 105–108 of the classifier. The ICD is a regulatory document used to record morbidity, the reasons why the population turns to medical structures, as well as the causes of death.

Acquired heart defects (or valvular) are disorders in the functioning of the heart, caused by structural and functional changes in the functioning of the heart valves. Signs of such disorders are stenosis or insufficiency of the valve. The reason for their development is the defeat of autoimmune or infectious factors, overload and dilatation (increase in the lumen) of the heart chambers.

In 90 percent of cases, acquired heart defects occur as a result of rheumatism. Most often, the mitral valve is affected (up to 70% of cases), less often the aortic valve (up to 27%). The smallest percentage of tricuspid valve defects is revealed (no more than 1%).

Why do acquired defects occur?

Most common causes the development of such defects:

• rheumatism;
• infective endocarditis;
• atherosclerosis;
• syphilis;
• sepsis;
• cardiac ischemia;
• connective tissue diseases that are degenerative in nature.

Classification of valvular defects

There are various classification systems:

• on an etiological basis: atherosclerotic, rheumatic, etc.;
• based on the severity: which do not affect the hemodynamics in the cardiac chambers, the severity of moderate and severe;
• by functional form: simple, combined, combined.

How to recognize the disease

Symptoms and their severity depend on the location of the defect.

mitral valve insufficiency

At the beginning of the development of this stage, the patient does not have any complaints. When the disease progresses, the following symptoms appear:

• during physical exertion, shortness of breath is observed (later it may appear at rest);
• pain in the heart (cardialgia);
• cardiopalmus;
• dry cough;
• swelling of the lower extremities;
• pain in the right hypochondrium.

mitral valve stenosis

This pathology has the following symptoms:

• the appearance of shortness of breath during physical exertion (later appears at rest);
• voice becomes hoarse;
• a dry cough appears (may form a small amount of mucous sputum);
• heart pain (cardialgia);
• hemoptysis;
• excessive fatigue.

Aortic valve insufficiency

During the compensation stage, palpitations and pulsations behind the sternum are occasionally noted. Later, the following symptoms appear:

• dizziness (possible fainting);
• cardialgia;
• during physical exertion, shortness of breath appears (later occurs at rest);
• swelling of the legs;
• pain and feeling of heaviness in the right hypochondrium.

Aortic valve stenosis

This type of disease is extremely insidious, since such a heart disease may not make itself felt for a long time. Only after the narrowing of the lumen of the aortic duct to 0.75 sq. see appear:

• pains that are compressive in nature;
• dizziness;
• fainting states.

These are the signs of this pathological condition.

Tricuspid valve insufficiency

Main manifestations:

• cardiopalmus;
• dyspnea;
• feeling of heaviness in the right hypochondrium;
• swelling and pulsation of the jugular veins;
• arrhythmias may occur.

Stenosis of the tricuspid valve

Symptoms of the disease:

1. The occurrence of pulsation in the neck.
2. Discomfort and pain in the right hypochondrium.
3. Decreased cardiac output resulting in cold skin.

Diagnosis and treatment

In order to diagnose valvular heart disease, you should contact a cardiologist who will collect an anamnesis, examine the patient and prescribe a number of studies, including:

• general urinalysis;
• biochemical blood test;
• echocardiography;
• Plain chest x-ray;
• contrast radiological technique;
• CT or MRI.

Acquired heart defects are treated medically and surgically. The first option is used to correct the patient's condition during the defect compensation state or when the patient is being prepared for surgery. Drug therapy consists of a complex of drugs of various pharmacological groups (anticoagulants, cardioprotectors, antibiotics, ACE inhibitors and etc.). Heart defects are also treated in this way when, for some reason (one of them is medical indications), it is impossible to perform surgical intervention.

When it comes to the surgical treatment of subcompensated and decompensated defects, heart defects can be subjected to the following types of intervention:

• plastic;
• valve-preserving;
• valve replacement with biological or mechanical prostheses;
• valve replacement with coronary bypass surgery;
• aortic root reconstruction;
• valve prosthetics for defects that arose as a result of infective endocarditis.

Heart disease involves a course of rehabilitation after surgery, as well as registration with a cardiologist after discharge from the hospital. The following remedial measures may be prescribed:

• physiotherapy;
• breathing exercises;
• drugs to support immunity and prevent relapses;
• control analyses.

Preventive actions

In order for valvular heart defects not to develop, those pathologies that can provoke damage to the heart valves should be treated in a timely manner, as well as healthy lifestyle life, which includes:

• timely treatment of infectious and inflammatory diseases;
• immune support;
• giving up cigarettes and caffeine;
• getting rid of excess weight;
• motor activity.

Congenital malformations of the heart muscle

According to the ICD 10th revision, congenital malformations are classified under section Q20-Q28. In the USA, the classification of diseases of the heart muscle with the codes "SNOP" is used, the International Society of Cardiology uses the code "ISC".

What are congenital malformations, when do they occur, how to recognize them, and what methods does modern medicine use to treat them? Let's try to figure this out.

An anomaly in the structure of large vessels and the heart muscle, which occurs in the period from the 2nd to the 8th week of pregnancy, is called a congenital defect. According to statistics, such a pathology is found in one baby out of a thousand. Achievements modern medicine allow to detect defects at the stage of perinatal development or immediately after birth. However, congenital heart defects in 25% of cases remain unrecognized, which is associated with the peculiarities of the physiology of the child or the difficulties of diagnosis. That is why it is so important to monitor the condition of the child, which will identify the disease on early stages and start treatment. This task falls on the shoulders of adults who are next to the child.

Congenital heart defects include anomalies that are associated with stenosis, as well as insufficiency of the aortic, mitral, or tricuspid valves.

Anomaly Development Mechanism

In newborns, heart disease has several phases of the course:

1. Adaptation: the child's body goes through an adaptation period to the hemodynamic disturbances that the defect causes. If there are severe violations blood circulation, there is a significant hyperfunction of the heart muscle.
2. Compensation: Temporary, improvements seen motor functions and general condition child.
3. Terminal: develops when the compensatory reserves of the myocardium are exhausted and degenerative, sclerotic and dystrophic changes in the structure of the heart.

Heart disease in the compensation phase is accompanied by a syndrome of capillary-trophic insufficiency, which subsequently becomes the cause of metabolic disorders, as well as various changes in the internal organs.

How to recognize a defect in a child

A congenital defect is accompanied by the following symptoms:

• the outer skin has a bluish or pale color (more often it is noticeable in the nasolabial region, on the fingers and feet). During breastfeeding, crying or straining the child, these symptoms are especially pronounced;
• the child is lethargic or restless during attachment to the breast;
• the baby is not gaining weight well;
• often spit up when eating;
• the cry of a child, despite the fact that there are no external signs or factors that may cause such behavior;
• there are attacks of shortness of breath, rapid breathing;
• sweating;
• swelling of the upper and lower extremities;
• swelling is seen in the region of the heart.

Such signs should be a signal for an immediate visit to a doctor for an examination. During the initial examination, the pediatrician, having identified heart murmurs, will recommend further management of the case by a cardiologist.

Diagnostic measures

A birth defect can be diagnosed through a series of tests, which include:

• general blood test;
• radiography;
• EchoCG.

Additional indications may be given diagnostic methods, for example, sounding of the heart. But there must be good reasons for this: for example, preliminary analyzes did not reveal the full clinical picture.

Treatment of birth defects

Children with a congenital defect must be observed by a district pediatrician and a cardiologist without fail. How many times the child must pass medical checkup? In the first year of life, examination by specialists is carried out quarterly. After the child is one year old, you need to be examined every six months. Examination should take place monthly if the heart disease is severe.

There are a number of conditions that should be created for children with a similar problem:

1. Natural feeding with mother's milk or donor milk.
2. Increase the number of feedings by 3 meals, while the amount of food should be reduced by one meal.
3. Walks in the open air.
4. Small physical activity, while there should not be signs of an uncomfortable state in the child's behavior.
5. Severe frost or direct sunlight are contraindications.
6. Prevention of infectious diseases.
7. Rational nutrition: control over the amount of liquid absorbed, salt, inclusion in the diet of foods that are rich in potassium (dried apricots, raisins, baked potatoes, etc.).

Congenital malformation is treated with surgical and therapeutic techniques. Most often, medications are used to prepare the child for surgery or treatment after it.

Surgery is recommended if severe heart disease is present. At the same time, depending on its type, the operation can be performed using a minimally invasive technique or with the child connected to a heart-lung machine on an open heart. Certain symptoms indicate the need for surgical treatment in several stages: the first stage involves alleviating the general condition, the rest are aimed at the final elimination of the problem.

If the operation is carried out in a timely manner, the prognosis in most cases is favorable.

It is important to pay attention to the slightest signs of the disease and seek the advice of a specialist: it is better to be safe than to deal with irreversible consequences. This applies both to the monitoring of children by their parents and to the health of the adults themselves. You need to take a responsible approach to your health, in no case should you tempt fate and not hope for luck in matters that concern it.

No one can say for sure how long a person with heart disease can live. In each case, the answer to this question will be different. When people need surgery but stubbornly refuse it, the question is not how long a person will live, but how such people live. And the quality of life of a sick person is quite low.

Heart defects, both congenital and acquired, are a serious diagnosis, but with the right approach and an adequate choice of treatment, it can be corrected.

Signs of stomach cancer at an early stage

There are very serious questions about health, for example, how to identify stomach cancer, the first symptoms of which can be confused with other ailments. It is important to know what needs to be done in order to protect yourself from the development of a malignant tumor, and what are the treatment methods and prognosis with an established diagnosis.

It is known that this oncological disease is more common in people over fifty years of age and is 10-20% more common in men than in women of the same age. Gastric cancer is one of the leading causes of death (about 10% in the world and 14% in Russia), so the information related to it is always relevant, especially for our country.

Gastric cancer is common along with pulmonary, intestinal, skin cancers and malignant tumors of the mammary glands. Every year, 750 thousand people die from it in the world, while the incidence depends on geography. In Western European countries and America, for example, the frequency is low, while in Russia, Brazil, and Japan it is high.

Russia shows the following ratios of survival to stages of the disease:

Stage 1 is detected in 10-20% of people, 60-80% of whom overcome the five-year period;
2nd and 3rd stage with local involvement lymphatic system is detected in 30% of patients, 15-45% of them manage to live for five years;
Stage 4 with metastases spreading to nearby organs is found in half of the patients, for whom a favorable outcome after five years is only a 5-7% probability.

A positive prognosis, even in the case when the disease can be cured, is not always possible, since there is a tendency to relapse, which is difficult to eliminate by repeated intervention. Unfortunately, in Russia the situation is such that 35% of patients are significantly late with the examination.

The appearance of a tumor node is difficult to detect for a long time.

Often, diagnostic misses are associated with the similarity of symptoms of gastrointestinal diseases and heart diseases that are not related to oncology:

If the tumor is located in the cardiac segment (end of the esophagus), this is associated with chest pain, especially with high blood pressure in patients over 50 years of age;
if the localization of degeneration is near the duodenum, it may look like gastritis, ulcer, cholecystitis, pancreatitis, which are characterized by vomiting, gastrointestinal bleeding and pain.

Incorrect diagnosis and the absence of obvious signs do not allow time to recognize the main cause of deviations in the elderly.

The doctor and the patient should be alerted by the following observed sensations characteristic of small cancer (two or three points minimum):

Permanent heaviness and discomfort in the abdomen, belching, heartburn;
retrosternal pain felt in the back, difficulty in swallowing;
prolonged pain in the abdominal region, which is not removed by medicines;
constant fatigue and weakness at the slightest physical exertion, dizziness;
loss of appetite up to an aversion to food and rapid weight loss, a change in mood for the worse (depression);
rejection of meat and fish, atypical intelligibility in food;
fast onset satiety with very little food, with no satisfaction;
enlargement of the abdomen due to accumulation of fluid (ascites);
pale skin (anemia);
a slight increase in temperature over a long period;
flatulence and defecation disorders (gas formation and unhealthy stools).

The patterns inherent in the disease are revealed by clinical experience.

Two or three signs must be combined:

Painful sensations in the central epigastric region, as reported by two-thirds of the subjects;
strong weight loss, which is observed by half of the patients;
gag reflex and nausea accompanying food intake - within 40% of people;
nausea and bloody vomiting (signs of intoxication) - in the region of a quarter of patients;
blanching of the mucous membranes - about 40%.

It is worth noting that depending on where the cancerous tumor develops, the manifestation of various signals is observed. This does not rule out general symptoms.

1. A malignant formation closer to the esophagus is accompanied by heart pain and constraint of swallowing function up to the cessation of food intake, dehydration progresses.
2. Affected middle area digestive organ characterized by developing anemia (lack of hemoglobin) and gastric bleeding, with its profusion changing the color and consistency of feces to pitch-black, liquid (at the same time fetid).
3. Damage closer to the duodenum has consequences such as stool disorders, vomiting and belching with a rotten egg smell.

Do not forget about suspicious health problems, so as not to complicate a dangerous condition. It is necessary to notice the symptoms of stomach cancer in a timely manner and seek medical help long before the advanced stages of cancer cell development. After all, such a delay in most cases threatens death.

Development malignant formations- a long process, passing through many degrees. Highlighting the stages, the following systematization can be given.

1. Progression of mutations under the influence of carcinogens.
2. Diseases that precede cancer.
3. Activation of oncology against the background of the influence of carcinogens and precancerous diseases.

Stage I

Internal causes are immune, infectious, age and hereditary factors. For example, people with blood type II fall ill 20% more often, an A. pylori infection increases the chance of a cancerous tumor several times; after overcoming the fifty-year age threshold, there is a multiple increase in risks.

To external reasons The first step is diet. Dangerously unlimited food spicy, salty, hot, fried, smoked, canned food, pickled vegetables. In this regard, it should also be noted that there is no measure in the use of drugs (antibiotics, analgesics, hormonal drugs), an excess of starch, nitrates, nitrites, synthetic food additives (dyes, flavors, flavor enhancers) entering the body. terms of tobacco and hard alcohol.

The lack of certain nutrients and vitamins also plays a role. For example, vitamin C is responsible for the quality and quantity of hydrochloric acid, reducing bleeding, vitamin E regulates the resistance of mucous membranes, and vitamin B12 and folic acid are involved in normal cell division.

II stage

III stage

The previous factors in interaction with the yet unknown causes trigger carcinogenesis. However, it can be reliably stated that serious complications usually appear after Helicobacter pylori infection, damage to the digestive organ and the activity of carcinogens.

Origin process malignant tumor not studied in depth. The absence of symptoms can last for years.

Gastric pathologies are varied.

There is the following classification of cancers according to the principle of growth:

1. Intestinal type. Metaplasia (a transitional state) occurs, that is, the gastric mucosa shows similarities with the intestinal mucosa. It is more often observed in people of solid age and originates from chronic diseases of the gastrointestinal tract. The prognosis is relatively favorable.
2. Diffuse type (penetrating). Genetically determined. Mutated cells spread along the gastric walls, the mucosa is normal.
3. Mixed type.

In addition to forms, the degree of prevalence is also classified, which is of the greatest importance.

So, the most common adenocarcinoma develops as follows:

Stage 1 - cancer cells do not go deep into muscle tissue, they may spread to neighboring lymph nodes;
2nd stage - the penetration of the tumor deep into the wall of the stomach begins, the lymph nodes are damaged;
3rd stage - complete damage to the gastric wall, increased damage to neighboring lymph nodes, there is a possibility of infection of nearby organs;
Stage 4 - peripheral metastases.

Cell mutation can spread in different ways and have various forms. As a result, there are various definitions.

Signet cell carcinoma

This aggressive disease is diffuse type with squamous altered formation. It is characterized by a certain predominance among female patients, as well as peaks of occurrence in the intervals between 40-50 and 60-70 years. Almost half of the patients have blood type II. A relationship with bad habits and external adverse factors has not been found, however, the species is more often observed in cities.

Infiltrative cancer

A type of carcinoma with indistinct boundaries of the neoplasm, one of the most malignant. The lesion is localized mainly in the thickness of the gastric wall. The foci of oncological cells are 5-8 cm apart. Noticeable hereditary predisposition and the possibility of development in relatively young people. The clinical stage is accompanied by violations of peristalsis, vomiting. The tumor is stony, often spreading metastases.

Poorly differentiated cancer

In addition to these typologies, there is another generally accepted codification - the International Classification of Diseases (ICD 10), in which a disease is assigned a code with a subcode for clarification. ICD 10 has some shortcomings, so it is possible to improve it in accordance with the latest research.

Tumors of a malignant nature are classified by the World Health Organization into 11 types according to cellular forms. In 90% of cases or more, adenocarcinoma is found - a neoplasm of glandular cells.

Early detection of the disease is problematic, and reducing the mortality associated with it is an important task of medicine. Of great importance for detection is the vigilance of doctors general practice and their professional sensitivity. It is useful to know that many methods contribute to the correct diagnosis.

There is such a thing - screening - regular examination even in the absence of symptoms, which contributes to the timely detection of neoplasms. For this, FGS is used - fibrogastroscopy - a popular endoscopic method in which a thin and flexible tube equipped with a small video camera and a light is inserted into the stomach through the mouth. When a suspicious area is detected, the mucosa is taken and the sample is sent to laboratory (biopsy), which allows you to give an accurate diagnosis. The effectiveness of gastroscopic studies is confirmed by the experience of Japan, where mortality rates, despite the incidence rate, are low.

Diagnosis is also made using other relevant methods, such as:

FGDS (fibrogastroduodenoscopy) - more perfect form gastroscopy, in which the examination is additionally subjected to duodenum; the method can be modified with optical nozzles (up to the ability to observe the cellular level), however, it is inconvenient for differentiating benign and malignant neoplasms;
radiography of the gastrointestinal tract - for this, patients take a contrast solution (barium) inside, covering the mucous membrane, after which clear radiographs are obtained, showing even minor changes ( X-ray method can also be applied to the chest, skull, limbs to detect metastases);
CT ( CT scan) and PET (positron emission tomography), which allow X-rays to be taken from different angles and give a clear picture, to find out the spread of oncological formations using radiopharmaceuticals (radioisotopes) used due to their selective concentration;
MRI (magnetic resonance imaging), which allows layer-by-layer examination using powerful magnets - like CT, one of the most informative methods;
diagnostic laparoscopy, in which a laparoscope (a tube with a mini-camera) is inserted into the patient's abdomen through an incision to determine the boundaries of the spread of oncological formation in abdominal cavity and the possibility of its removal, while tissue and fluid can be taken for research;
Ultrasound (ultrasound), which helps to detect the tumor itself and the lesion lymph nodes, neighboring organs - can be carried out from the outside (including using a degassed liquid to fill the organ under study) and from the inside (with an endoscopic probe);
tumor markers used to assess the response of tumor tissues to therapy when the diagnosis is established;
analyzes - biochemical, immunological and general for blood, analysis of feces for occult blood and urinalysis.

Science makes a lot of effort in finding the best means fight the disease. For example, drugs with a “targeted” effect (destroying mutated tissues) are used in foreign oncological centers - immunoglobulins and enzyme inhibitors.

In Russia, the predominant method is surgical (radical). The complexity of the operation is determined by the degree of damage.

1. If the thickness of the gastric wall is not damaged, an endoscopic resection is performed (the instrument is inserted through the mouth or a minimal opening is performed). In simple cases, cauterization of neoplasms is used using electrothermal and laser exposure.

2. Subtotal gastrectomy involves the removal of the damaged part of the digestive organ, and with total gastrectomy, the stomach is cut out along with nearby tissues. It is also possible to eliminate neighboring lymph nodes and organs affected by metastases.

3. When recovery is impossible, a palliative operation is used - resection of oncological formation to alleviate the patient's condition. In hopeless cases, when the diseased areas are no longer operable, a gastrostomy is used - an opening in the anterior abdominal wall for food intake.

Radiation therapy (X-ray radiation in small doses) is used before and after surgery, in the first case - neoadjuvant (to facilitate resection), in the second - adjuvant (to destroy cancer cells). side effect Irradiation usually causes stool disorders and nausea, but in some cases the method will help to avoid surgical intervention.

Often with radiation therapy they also use chemotherapy (the same two types - neoadjuvant and adjuvant), the complex of which, with little chance of a cure, prolongs the life of the patient and alleviates the symptoms, but in general has a negative effect on the body. The consequences of chemotherapy (removable recovery) are baldness, weight loss, liver damage with toxins, hematopoiesis disorder, immune suppression, and more.

Drug treatment is also prescribed as a symptomatic therapy - for pain relief, elimination of flatulence, nausea and vomiting, normalization of digestion and strengthening of immunity.

There is also relatively new way therapy - photodynamic. It boils down to the use of light and photosensitizers (drugs used to identify affected areas). Cancer cells are exposed to laser beams(LED tubes), as a result of which a toxic reaction occurs and they die without destroying healthy tissues.

The tactics of treatment is chosen depending on the degree of carcinogenesis. Most often, surgery is used in combination with chemotherapy.

Lifestyle and diet for patients

Patients should adhere to certain lifestyle and dietary guidelines to minimize the risk of relapse:

Prolonged sleep and rest, normalization of the regime;
limitation of physical activity;
walks in the open air;
support for good mood;
spa treatment (excluding physiotherapy);
regular visits to the doctor for diagnosis and treatment;
the first 3-6 days (depending on the complexity of the operation) after surgery, it is allowed to drink only water, then liquid, pureed food is given, and only after that the diet gradually expands.

After the operation, you need to eat 4-8 times a day in small portions. Boiled, stewed and baked foods are allowed for consumption - cereals and soups, vegetables, fruits that do not contribute to clear fermentation, dairy products, bread, lean fish and meat. Whole milk and confectionery products are limited.

Excluded are alcohol, tobacco, coffee and food, irritating mucous membrane of the gastrointestinal tract. Due to the loss of a large amount of fluid by the body (due to vomiting, bleeding), up to 2 liters of water per day is recommended, and juices with pulp can help with this (especially if there are no edema).

Prevention

Don't forget the importance of a healthy diet.

To reduce the chances of cancer, you should strive to implement the following tips:

Reducing the harmful effects of a polluted environment and chemical compounds, attention to the quality of vegetables used for food (exclusion of carcinogens and nitrates);
the use of milk, fresh products containing vitamins and minerals;
reduction in the amount of fatty, fried, spicy, smoked foods, preservatives, salt;
natural diet (avoiding overeating and irregular meals);
avoidance bad habits;
moderate medication;
a thorough examination and compliance with the instructions of the attending physician in the presence of precancerous ailments.

Aortic heart disease is a pathological condition characterized by dysfunction of the aortic valve. It is divided into congenital (diagnosed in the hospital) and acquired form (manifested in adulthood).

Features of the functioning of the valve

Our heart has 4 valves: mitral (or bicuspid), tricuspid, aortic and pulmonary. According to ICD - 10, non-rheumatic leaflet lesions have the code I35.

The valve is located between the left chamber of the heart and the aorta. Externally, the cardiac valves look like pockets that surround the annulus fibrosus. Due to this structure, the load developing under the action of blood is distributed evenly on all walls. It opens when the left ventricle contracts and closes when it relaxes. Through it enriched with oxygen arterial blood spreads throughout the body.

The valve is passive. This is due to the fact that there are no muscle fibers in the structure, that is, there is no possibility to contract.

The lumen of the opening of our anatomical formation differs from the diameter of the valve, which is called bicuspid (mitral-aortic). With ventricular systole, the blood pressure increases significantly, and therefore the valve experiences a strong load and its wear also increases significantly. This underlies the pathological condition.

The essence of aortic defects

The reasons for the development of this pathology are divided into two groups. The first includes congenital, which may be due to the transferred infectious diseases of the mother during pregnancy. They can appear in utero or in the first days of a baby's life. A defect in one of the heart valves develops. It could be her complete absence, the presence of holes, the change in the aspect ratio.

Acquired aortic heart defects are most often provoked by infectious (tonsillitis, sepsis, pneumonia, syphilis) and autoimmune processes (rheumatism, lupus erythematosus, dermatomyositis). But there are other less frequent diseases that contribute to the development of a pathological condition. These include hypertension, atherosclerosis, age-related changes vessels, wall calcification, surgical operations.

There are several types of defects: stenosis, insufficiency and combined form. Stenosis of the aortic orifice is a pathological condition characterized by structural changes in the leaflet, manifested by a sharp narrowing of the aortic orifice. This leads to the development of an increase in tension in this area and a decrease in cardiac output of blood into the aorta.

Deficiency is a pathological condition, which is a violation of the closure of the valves, which is formed as a result of exposure to cicatricial processes or a change in the fibrous ring. It is characterized by a decrease in cardiac output, the passage of blood from the aorta back into the cavity of the ventricle, which contributes to its overfilling and overstrain. Combined aortic heart disease contains a change in stenosis, as well as a violation of the closure of the valves of the left ventricle.

There is a clinical classification that distinguishes 5 stages of the disease. These include:

According to this classification, one can judge the degree of the pathological condition, as well as the adaptive capabilities of the human body. When making a diagnosis, every doctor uses it.

Symptoms of aortic disease

The symptoms of aortic valve disease vary by type. With stenosis, patients complain of palpitations, arrhythmias, pain in the cardiac region, and shortness of breath, which may culminate in pulmonary edema. Auscultation reveals a systolic murmur above the aortic orifice. In case of insufficiency, a complex symptom of carotid dancing, heart pain, a combination of a decrease in diastolic pressure and an increase in systolic pressure are noted.

To general symptoms can be attributed:

• fast fatigue;
• headache;
• dizziness with sudden movements;
• fast fatigue;
• noise in ears;
• loss of consciousness;
• development of edema in the lower extremities;
• increased pulsation in the area of ​​large arteries;
• promotion heart rate.

The symptoms are varied, so it often happens that it is not enough to make a correct diagnosis. As a result, doctors are resorting to additional methods examinations of patients.

Diagnostics

Diagnosis is based on an external examination (propaedeutics is engaged in this) and instrumental research methods. When examining doctors, they should pay attention to the skin, to the pulsation of the central and peripheral arteries. The definition of the apex beat also has diagnostic significance (it shifts to the 6th-7th intercostal space). Diastolic murmur, weakening of the first and second tone, the presence of vascular phenomena (Traube's auscultatory tone) are all aortic heart disease.

In addition to routine clinical analyzes blood and urine, there are several more instrumental diagnostic methods:

• electrocardiography;
• phonocardiography;
• echocardiography;
• radiography;
• dopplerography.

Wherein pathological condition The electrocardiogram shows left ventricular hypertrophy. This is mainly due to the compensatory mechanisms of the body due to its increased stress. The results of radiography indicate the expansion of the aorta, the left ventricle, which leads to the development of a change in the axis of the heart, there is a shift of the apex to the left. Identification of pathological heart murmurs is possible using the phonocardiography method. Echocardiography determines the size of the ventricles, the presence of anatomical defects.

Treatment

Taking an anamnesis, interpreting the results of the study will help a qualified doctor get on the right track, make the correct diagnosis and begin treatment of the patient, which is divided into medical and surgical. The first type of therapy is used only in case of minor changes, which consists in prescribing drugs that improve the flow of oxygen to the heart muscle, eliminate the sign of arrhythmia, and also normalize blood pressure.

In this regard, appointed medicines such pharmacological groups: antianginal drugs, diuretics, antibiotics. The most relevant drugs that contribute to the normalization of the heart rhythm are Nitrolong, Sustak, Trinitrolong. They eliminate pain, prevent the development of angina pectoris by increasing blood oxygen saturation.

With an increase in the volume of circulating blood, it is customary to prescribe diuretics, since they significantly reduce this indicator. These include Lasix, Torasemide, Britomar. Antibiotic therapy is used in case of infectious causes of development (with exacerbation of tonsillitis, pyelonephritis). In the treatment, there is a predominance of antibiotics of penicillin origin: "Bicillin-1", "Bicillin-2", "Bicillin-3", as well as the preparation of the group of glycopeptides - "Vancomycin".

It must always be remembered that the indication, dosage, how to combine and the frequency of taking a particular drug should be prescribed by the attending physician, whose recommendation is the number one rule. The doctor's lecture is the methodological material of each patient. After all, even slight fluctuations in dosage can lead to ineffective therapy or even to a deterioration in health.

Surgical treatment of the heart muscle is used in advanced cases, when the leaflet area is less than one and a half square centimeters.

There are several options for the operation: balloon valvuloplasty and valve implantation. The main disadvantage of the first technique is its possible re-narrowing. In the presence of concomitant pathology (or contraindications), the operation is not performed.

vices of cardio-vascular system This is a real problem for the entire population. This is the second most common pathology among cardiac diseases.

Carrying out on time drug therapy or surgical intervention significantly improves the quality of life and its duration, reduces the development of many complications.

Open ductus arteriosus (OAP) in children: what is this pathology

• signs
• The reasons
• Diagnosis
• Treatment
• Prevention

Children are not immune from congenital anomalies, so it is important for parents to know what signs may indicate certain malformations. For example, about such a pathology as an open ductus arteriosus in newborns.

The ductus arteriosus is a small vessel that connects the pulmonary artery to the fetal aorta, bypassing the pulmonary circulation. This is normal before birth as it provides the fetal circulation needed for a fetus that does not breathe air in the womb. After the birth of a child, a small duct closes in the first two days after birth and turns into a strand of connective tissue. In premature babies, this period can last up to 8 weeks.

But there are times when the duct remains open and leads to disruption of the lungs and heart. More often this pathology is observed in premature babies and is often combined with other congenital malformations. If the ductus arteriosus remains open for 3 or more months, we are talking about such a diagnosis as PDA (open ductus arteriosus).

By what signs can one suspect that the duct has remained open?

The main symptoms in children under one year old are shortness of breath, palpitations, slow weight gain, pale skin, sweating, difficulty feeding. The reason for their appearance is heart failure, which occurs due to congestion of the vessels of the lungs, to which blood returns with an open duct, instead of rushing to the organs.

The severity of symptoms depends on the diameter of the duct. If it has a small diameter, an asymptomatic course of the disease is possible: this is due to a slight deviation from the norm of pressure in the pulmonary artery. With a large diameter of the open vessel, the symptoms are more severe and are characterized by several more signs:

• hoarse voice;
• cough;
• frequent infectious diseases of the respiratory system (pneumonia, bronchitis);
• weight loss
• poor physical and mental development.

Parents should know that if a child is slowly gaining weight, gets tired quickly, turns blue when crying, breathes frequently and holds his breath when crying and eating, then an urgent need to contact a pediatrician, cardiologist or cardiac surgeon.

If a patent ductus arteriosus has not been diagnosed in a newborn, the symptoms tend to get worse as they grow. In children from one year old and adults, the following signs of PDA can be observed:

• frequent breathing and lack of air even with minor physical exertion;
• frequent infectious diseases respiratory tract, persistent cough;
• cyanosis - blue discoloration of the skin of the legs;
• weight deficit;
• quick fatigue even after short outdoor games.

What are the reasons why the ductus arteriosus does not close?

Until now, doctors can not give an exact answer to this question. It is assumed that risk factors for abnormal development include:

• a number of other congenital heart diseases (congenital heart defects);
• premature birth;
• insufficient body weight of the newborn (less than 2.5 kg);
• hereditary predisposition;
• oxygen starvation fetus;
• genomic pathologies, such as Down syndrome;
• diabetes mellitus in a pregnant woman;
• rubella infection during childbearing;
• chemical and radiation effects on a pregnant woman;
• the use of pregnant alcoholic beverages and drugs;
• taking medication during pregnancy.

Moreover, statistics show that in girls this pathology occurs twice as often as in boys.

How do doctors make a diagnosis?

First of all, the doctor listens to the newborn's heart with a stethoscope. If the noise does not stop after two days, the examination is continued by other methods.

On the chest radiograph, changes in the lung tissue, expansion of the cardiac borders and the vascular bundle are visible. High load on the left ventricle is detected by ECG. To detect an increase in the size of the left ventricle and atrium, echocardiography or ultrasound of the heart is performed. Doppler echocardiography is needed to determine the volume of the discharged blood and the direction of its current.

In addition, probing of the pulmonary artery and aorta is performed, while the probe passes through the open duct from the artery into the aorta. During this examination, the pressure in the right ventricle is measured. Before aortography, a contrast agent is injected into the aorta with a catheter, which enters the pulmonary artery with blood.

Early diagnosis is very important because the risk of complications and severe consequences is very high, even in asymptomatic cases.

Spontaneous closure of an abnormal ductus arteriosus can occur in children under 3 months of age. In a later period, self-healing is almost impossible.

Treatment is carried out depending on the age of the patient, the severity of symptoms, the diameter of the pathological duct, the existing complications and concomitant congenital malformations. The main methods of treatment: medication, catherization, ligation of the duct.

Conservative treatment is prescribed in case of unexpressed symptoms, in the absence of complications and other congenital malformations. Treatment of the open ductus arteriosus with various drugs is carried out at the age of up to a year under constant medical supervision. For treatment, drugs can be used: anti-inflammatory non-steroidal (ibuprofen, indomethacin), antibiotics, diuretics.

Catherization is performed for adults and children over the age of one year. This method is considered effective and safe in terms of complications. The doctor performs all actions using a long catheter, which is inserted into a large artery.

Often, an open ductus arteriosus is treated surgically - bandaged. If a defect is detected while listening to extraneous heart sounds in a newborn, the duct is closed by surgery when the child reaches the age of 1 year to avoid possible infectious diseases. If necessary (with a large diameter of the duct and heart failure), the operation can also be performed on a newborn, but it is optimal to do them at the age of up to three years.

Don't Forget About Prevention

In order to protect the unborn child from the development of PDA, during gestation, you should avoid taking medicines, stop smoking and drinking alcohol, be afraid of infectious diseases. In the presence of congenital heart defects in family members and relatives, you need to turn to genetics even before the moment of conception.

What is the prognosis?

Vice is dangerous because the risk of death is high. An open ductus arteriosus can be complicated by a number of diseases.

• Bacterial endocarditis is an infectious disease that affects the heart valves and can lead to complications.
• Myocardial infarction, in which necrosis of a section of the heart muscle occurs due to impaired blood circulation.
• Heart failure develops with a large diameter of an open ductus arteriosus in the absence of treatment. Among the signs of heart failure, which is accompanied by pulmonary edema, should be called: shortness of breath, rapid breathing, high pulse, low blood pressure. This state poses a threat to the life of the child and requires hospitalization.
• Aortic rupture is the most severe complication of PDA, leading to death.

There is a huge difference between acquired cardiac disorders and congenital malformations, as they are in different classes of the ICD. Despite the fact that arterial and venous blood flow disorders will be the same, the treatment and etiological factors will be completely different.

CHD may not require therapeutic measures, but elective surgeries are more often performed or even urgent ones in case of serious, incompatible with life inconsistencies with the norm.

GSP encoding

Heart defects are in the class of congenital anomalies in the structure of the body in the block of anomalies of the circulatory system. The GSP in ICD 10 branches into 9 sections, each of which also has subparagraphs.

However, heart problems include:

• Q20 - anatomical disorders in the structure of the heart chambers and their connections (for example, various non-closure of the oval window);
• Q21 - pathologies of the cardiac septum (defects of the atrial and interventricular septum, and others);
• Q22 - problems with the pulmonary and tricuspid valves (insufficiency and stenosis);
• Q23 - pathologies of the aortic and mitral valves (insufficiency and stenosis);
• Q24 - other congenital heart defects (change in the number of chambers, dextrocardia, and so on).

Each of the listed items requires further differentiation, which will determine the treatment plan and prognosis for the child. For example, with lesions of the valves, there may be phenomena of insufficiency or stenosis. In this case, the hemodynamic features of the disease will differ.

In the ICD, congenital heart disease implies any disturbance of blood flow.

That is why in all encodings a complete inversion of organs or their structures with full functioning is excluded.

Congenital heart defects mkb 10

Anomalies of heart development small

Anomalies of development of the heart small: Brief description

Minor heart anomalies (MARS) are anatomical congenital changes in the heart and great vessels that do not lead to gross violations of the cardiovascular system. The MARS series is unstable and disappears with age.

Etiology

Hereditarily determined connective tissue dysplasia. A number of MARS have a disembryogenetic character. The impact of various environmental factors (chemical, physical impact) is not excluded.

Code according to the international classification of diseases ICD-10:

Q20. 9 - Congenital malformation of cardiac chambers and connections, unspecified

Q24.9 Congenital heart disease, unspecified

Other diagnoses in ICD section 10

• Q24.0 Dextrocardia
• Q24.1 Levocardia
• Q24.2 Triatrial heart
• Q24.3 Funnel stenosis of pulmonic valve
• Q24.4 Congenital subaortic stenosis

The information posted on the site is for reference only and is not official.

Heart defects.congenital (classification)

CHD classification according to severity classes (J. Kirklin et al. 1981) Class I. It is possible to carry out a planned operation later than 6 months: VSD, ASD, radical correction in class II tetralogy of Fallot. Elective surgery can be performed within 3–6 months: radical correction in VSD, open atrioventricular canal (AVC), palliative correction in class III TF. Elective surgery can be performed within a few weeks: radical correction in transposition of the great vessels (TMS) class IV. Emergency surgery with a maximum preparation time of several days: radical correction for total anomalous pulmonary venous drainage (TADLV), palliative correction for TMS, VSD, OAVK class V. The operation is carried out urgently in connection with cardiogenic shock: various types of defects in the stage of decompensation.

Classification of CHD by prognostic groups (Fyler D. 1980) Group 1. Relatively favorable prognosis (mortality during the first year of life does not exceed 8–11%): patent ductus arteriosus, VSD, ASD, pulmonary stenosis, etc. Group 2. Relatively unfavorable prognosis (mortality during the first year of life is 24–36%): tetralogy of Fallot, myocardial disease, etc. Group 3. Unfavorable prognosis (mortality during the first year of life is 36–52%): TMS, coarctation and aortic stenosis, tricuspid valve atresia, TALVV, single ventricle, OAVK, aortic and pulmonary artery origin from the right ventricle, etc. Group 4. Extremely unfavorable prognosis (mortality during the first year of life is 73–97%): left ventricular hypoplasia, pulmonary artery atresia with intact interventricular septum, common arterial trunk, etc.

Classification of CHD according to the possibility of radical correction (Turley K. et al. 1980) Group 1. Defects in which only radical correction is possible: aortic stenosis, pulmonary artery stenosis, TALVV, three-atrial heart, aortic coarctation, patent ductus arteriosus, aortopulmonary septal defect, ASD, stenosis or insufficiency of the mitral valve, group 2. Defects in which the expediency of radical or palliative surgery depends on the anatomy of the defect, the age of the child and the experience of the cardiological center: various types of TMS, pulmonary atresia, common arterial trunk, tetralogy of Fallot, OAVK, VSD group 3. The vices in which infancy only palliative operations are possible: a single ventricle of the heart, some variants of the main vessels from the right or left ventricle with pulmonary artery stenosis, tricuspid valve atresia, mitral valve atresia, ventricular hypoplasia of the heart.

Abbreviations OAVK - open atrioventricular canal TMS - transposition of the great vessels TADLV - total anomalous pulmonary venous drainage.

ICD-10 Q20 Congenital anomalies [malformations] of the cardiac chambers and connections Q21 Congenital anomalies [malformations] of the cardiac septum Q22 Congenital anomalies [malformations] of the pulmonary and tricuspid valves Q23 Congenital anomalies [malformations] of the aortic and mitral valves Q24 Other congenital anomalies [ malformations] of the heart.

Other congenital anomalies [malformations] of the heart (Q24)

Excludes: endocardial fibroelastosis (I42.4)

Excluded:

• dextrocardia with localization inversion (Q89.3)
• atrial appendage isomerism (with asplenia or polysplenia) (Q20.6)
• mirror image atrial arrangement with localization inversion (Q89.3)

Location of the heart in the left side of the chest with the apex pointing to the left, but with transposition of other internal organs (situs viscerum inversus) and heart defects, or corrected transposition of the great vessels.

Congenital coronary (arterial) aneurysm

Wrong position of the heart

Congenital:

• cardiac anomaly NOS
• heart disease NOS

In Russia, the International Classification of Diseases of the 10th revision (ICD-10) is accepted as a unified normative document to account for morbidity, the reasons for the population's appeals to medical institutions all departments, causes of death.

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. #170

The publication of a new revision (ICD-11) is planned by WHO in 2017 2018.

With amendments and additions by WHO.

Processing and translation of changes © mkb-10.com

Mkb 10 acquired aortic heart disease

What is aortic heart disease?

Aortic heart disease is a pathological condition characterized by dysfunction of the aortic valve. It is divided into congenital (diagnosed in the hospital) and acquired form (manifested in adulthood).

Features of the functioning of the valve

Our heart has 4 valves: mitral (or bicuspid), tricuspid, aortic and pulmonary. According to ICD - 10, non-rheumatic leaflet lesions have the code I35.

The valve is located between the left chamber of the heart and the aorta. Externally, the cardiac valves look like pockets that surround the annulus fibrosus. Due to this structure, the load developing under the action of blood is distributed evenly on all walls. It opens when the left ventricle contracts and closes when it relaxes. Through it, oxygenated arterial blood is distributed throughout the body.

The valve is passive. This is due to the fact that there are no muscle fibers in the structure, that is, there is no possibility to contract.

The lumen of the opening of our anatomical formation differs from the diameter of the valve, which is called bicuspid (mitral-aortic). With ventricular systole, the blood pressure increases significantly, and therefore the valve experiences a strong load and its wear also increases significantly. This underlies the pathological condition.

The essence of aortic defects

The reasons for the development of this pathology are divided into two groups. The first includes congenital, which may be due to the transferred infectious diseases of the mother during pregnancy. They can appear in utero or in the first days of a baby's life. A defect in one of the heart valves develops. This may be its complete absence, the presence of holes, a change in the size ratio.

Acquired aortic heart defects are most often provoked by infectious (tonsillitis, sepsis, pneumonia, syphilis) and autoimmune processes (rheumatism, lupus erythematosus, dermatomyositis). But there are other less frequent diseases that contribute to the development of a pathological condition. These include hypertension, atherosclerosis, age-related changes in blood vessels, calcification of the walls, and surgical operations.

There are several types of defects: stenosis, insufficiency and combined form. Stenosis of the aortic orifice is a pathological condition characterized by structural changes in the leaflet, manifested by a sharp narrowing of the aortic orifice. This leads to the development of an increase in tension in this area and a decrease in cardiac output of blood into the aorta.

Deficiency is a pathological condition, which is a violation of the closure of the valves, which is formed as a result of exposure to cicatricial processes or a change in the fibrous ring. It is characterized by a decrease in cardiac output, the passage of blood from the aorta back into the cavity of the ventricle, which contributes to its overfilling and overstrain. Combined aortic heart disease contains a change in stenosis, as well as a violation of the closure of the valves of the left ventricle.

There is a clinical classification that distinguishes 5 stages of the disease. These include:

1. full compensation stage. The patient does not complain, even if sport is the meaning of life for him, and he performs moderate physical activity daily, but during an external examination, mild changes in the cardiovascular system are noted.
2. Stage of latent heart failure. Patients note the limitation of physical activity. On the electrocardiogram, there are slight signs of left ventricular hypertrophy, the aorta is dilated, and the development of heart volume overload is also observed.
3. subcompensation stage. During physical exertion, patients note the appearance of shortness of breath, headache, dizziness. Electrocardiogram shows left ventricular hypertrophy. Anatomical changes in the valves are noted. Also reduced hemodynamics.
4. stage of decompensation. Even with light exertion, shortness of breath, attacks of cardiac asthma occur.
5. Terminal stage. Heart failure progresses, dystrophy is observed in all major organs.

According to this classification, one can judge the degree of the pathological condition, as well as the adaptive capabilities of the human body. When making a diagnosis, every doctor uses it.

Symptoms of aortic disease

The symptoms of aortic valve disease vary by type. With stenosis, patients complain of palpitations, arrhythmias, pain in the cardiac region, and shortness of breath, which may culminate in pulmonary edema. Auscultation reveals a systolic murmur above the aortic orifice. In case of insufficiency, a complex symptom of carotid dancing, heart pain, a combination of a decrease in diastolic pressure and an increase in systolic pressure are noted.

Common symptoms include:

• fast fatigue;
• headache;
• dizziness with sudden movements;
• fast fatigue;
• noise in ears;
• loss of consciousness;
• development of edema in the lower extremities;
• increased pulsation in the area of ​​large arteries;
• increase in heart rate.

The symptoms are varied, so it often happens that it is not enough to make a correct diagnosis. In this regard, doctors resort to additional methods of examining patients.

Diagnostics

Diagnosis is based on an external examination (propaedeutics is engaged in this) and instrumental research methods. On examination, doctors should pay attention to the skin, to the pulsation of the central and peripheral arteries. The definition of the apex beat also has diagnostic significance (it shifts to the 6th-7th intercostal space). Diastolic murmur, weakening of the first and second tone, the presence of vascular phenomena (Traube's auscultatory tone) are all aortic heart disease.

In addition to routine clinical blood and urine tests, there are several more instrumental diagnostic methods:

• electrocardiography;
• phonocardiography;
• echocardiography;
• radiography;
• dopplerography.

In this pathological condition, left ventricular hypertrophy is noted on the electrocardiogram. This is mainly due to the compensatory mechanisms of the body due to its increased stress. The results of radiography indicate the expansion of the aorta, the left ventricle, which leads to the development of a change in the axis of the heart, there is a shift of the apex to the left. Identification of pathological heart murmurs is possible using the phonocardiography method. Echocardiography determines the size of the ventricles, the presence of anatomical defects.

Treatment

Taking an anamnesis, interpreting the results of the study will help a qualified doctor get on the right track, make the correct diagnosis and begin treatment of the patient, which is divided into medical and surgical. The first type of therapy is used only in case of minor changes, which consists in prescribing drugs that improve the flow of oxygen to the heart muscle, eliminate the sign of arrhythmia, and also normalize blood pressure.

In this regard, drugs of such pharmacological groups are prescribed: antianginal drugs, diuretics, antibiotics. The most relevant drugs that contribute to the normalization of the heart rhythm are Nitrolong, Sustak, Trinitrolong. They eliminate pain, prevent the development of angina pectoris by increasing blood oxygen saturation.

With an increase in the volume of circulating blood, it is customary to prescribe diuretics, since they significantly reduce this indicator. These include Lasix, Torasemide, Britomar. Antibiotic therapy is used in case of infectious causes of development (with exacerbation of tonsillitis, pyelonephritis). In the treatment, there is a predominance of antibiotics of penicillin origin: "Bicillin-1", "Bicillin-2", "Bicillin-3", as well as the preparation of the group of glycopeptides - "Vancomycin".

It must always be remembered that the indication, dosage, how to combine and the frequency of taking a particular drug should be prescribed by the attending physician, whose recommendation is the number one rule. The doctor's lecture is the methodological material of each patient. After all, even slight fluctuations in dosage can lead to ineffective therapy or even to a deterioration in health.

Surgical treatment of the heart muscle is used in advanced cases, when the leaflet area is less than one and a half square centimeters.

There are several options for the operation: balloon valvuloplasty and valve implantation. The main disadvantage of the first technique is its possible re-narrowing. In the presence of concomitant pathology (or contraindications), the operation is not performed.

Defects of the cardiovascular system is an urgent problem of the entire population. This is the second most common pathology among cardiac diseases.

Carrying out on time drug therapy or surgical intervention significantly improves the quality of life and its duration, reduces the development of many complications.

Open ductus arteriosus (OAP) in children: what is this pathology

• signs
• The reasons
• Diagnosis
• Treatment
• Prevention

Children are not immune from congenital anomalies, so it is important for parents to know what signs may indicate certain malformations. For example, about such a pathology as an open ductus arteriosus in newborns.

The ductus arteriosus is a small vessel that connects the pulmonary artery to the fetal aorta, bypassing the pulmonary circulation. This is normal before birth as it provides the fetal circulation needed for a fetus that does not breathe air in the womb. After the birth of a child, a small duct closes in the first two days after birth and turns into a strand of connective tissue. In premature babies, this period can last up to 8 weeks.

But there are times when the duct remains open and leads to disruption of the lungs and heart. More often this pathology is observed in premature babies and is often combined with other congenital malformations. If the ductus arteriosus remains open for 3 or more months, we are talking about such a diagnosis as PDA (open ductus arteriosus).

By what signs can one suspect that the duct has remained open?

The main symptoms in children under one year old are shortness of breath, palpitations, slow weight gain, pale skin, sweating, difficulty feeding. The reason for their appearance is heart failure, which occurs due to congestion of the vessels of the lungs, to which blood returns with an open duct, instead of rushing to the organs.

The severity of symptoms depends on the diameter of the duct. If it has a small diameter, an asymptomatic course of the disease is possible: this is due to a slight deviation from the norm of pressure in the pulmonary artery. With a large diameter of the open vessel, the symptoms are more severe and are characterized by several more signs:

• hoarse voice;
• cough;
• frequent infectious diseases of the respiratory system (pneumonia, bronchitis);
• weight loss
• poor physical and mental development.

Parents should know that if a child slowly gains weight, gets tired quickly, turns blue when crying, breathes often and holds his breath when crying and eating, then you should urgently contact a pediatrician, cardiologist or cardiac surgeon.

If a patent ductus arteriosus has not been diagnosed in a newborn, the symptoms tend to get worse as they grow. In children from one year old and adults, the following signs of PDA can be observed:

• frequent breathing and lack of air even with minor physical exertion;
• frequent respiratory infections, persistent cough;
• cyanosis - blue discoloration of the skin of the legs;
• weight deficit;
• quick fatigue even after short outdoor games.

What are the reasons why the ductus arteriosus does not close?

Until now, doctors can not give an exact answer to this question. It is assumed that risk factors for abnormal development include:

• a number of other congenital heart diseases (congenital heart defects);
• premature birth;
• insufficient body weight of the newborn (less than 2.5 kg);
• hereditary predisposition;
• oxygen starvation of the fetus;
• genomic pathologies, such as Down syndrome;
• diabetes mellitus in a pregnant woman;
• rubella infection during childbearing;
• chemical and radiation effects on a pregnant woman;
• the use of pregnant alcoholic beverages and drugs;
• taking medication during pregnancy.

Moreover, statistics show that in girls this pathology occurs twice as often as in boys.

How do doctors make a diagnosis?

First of all, the doctor listens to the newborn's heart with a stethoscope. If the noise does not stop after two days, the examination is continued by other methods.

On the chest radiograph, changes in the lung tissue, expansion of the cardiac borders and the vascular bundle are visible. High load on the left ventricle is detected by ECG. To detect an increase in the size of the left ventricle and atrium, echocardiography or ultrasound of the heart is performed. Doppler echocardiography is needed to determine the volume of the discharged blood and the direction of its current.

In addition, probing of the pulmonary artery and aorta is performed, while the probe passes through the open duct from the artery into the aorta. During this examination, the pressure in the right ventricle is measured. Before aortography, a contrast agent is injected into the aorta with a catheter, which enters the pulmonary artery with blood.

Early diagnosis is very important because the risk of complications and severe consequences is very high, even in asymptomatic cases.

Spontaneous closure of an abnormal ductus arteriosus can occur in children under 3 months of age. In a later period, self-healing is almost impossible.

Treatment is carried out depending on the age of the patient, the severity of symptoms, the diameter of the pathological duct, the existing complications and concomitant congenital malformations. The main methods of treatment: medication, catherization, ligation of the duct.

Conservative treatment is prescribed in case of unexpressed symptoms, in the absence of complications and other congenital malformations. Treatment of the open ductus arteriosus with various drugs is carried out at the age of up to a year under constant medical supervision. For treatment, drugs can be used: anti-inflammatory non-steroidal (ibuprofen, indomethacin), antibiotics, diuretics.

Catherization is performed for adults and children over the age of one year. This method is considered effective and safe in terms of complications. The doctor performs all actions using a long catheter, which is inserted into a large artery.

Often, an open ductus arteriosus is treated surgically - bandaged. If a defect is detected while listening to extraneous heart sounds in a newborn, the duct is closed by surgery when the child reaches the age of 1 year to avoid possible infectious diseases. If necessary (with a large diameter of the duct and heart failure), the operation can also be performed on a newborn, but it is optimal to do them at the age of up to three years.

Don't Forget About Prevention

In order to protect the unborn child from the development of PDA, during gestation, one should avoid taking medications, stop smoking and drinking alcohol, and be wary of infectious diseases. In the presence of congenital heart defects in family members and relatives, you need to turn to genetics even before the moment of conception.

What is the prognosis?

Vice is dangerous because the risk of death is high. An open ductus arteriosus can be complicated by a number of diseases.

• Bacterial endocarditis is an infectious disease that affects the heart valves and can lead to complications.
• Myocardial infarction, in which necrosis of a section of the heart muscle occurs due to impaired blood circulation.
• Heart failure develops with a large diameter of an open ductus arteriosus in the absence of treatment. Among the signs of heart failure, which is accompanied by pulmonary edema, should be called: shortness of breath, rapid breathing, high pulse, low blood pressure. This condition poses a threat to the life of the child and requires hospitalization.
• Aortic rupture is the most severe complication of PDA, leading to death.

What is congenital heart disease

Under congenital heart disease understand the isolation of diseases that are combined with anatomical defects of the heart or valvular apparatus. Their formation begins in the process of intrauterine development. The consequences of defects lead to violations of intracardiac or systemic hemodynamics.

Symptoms differ depending on the type of pathology. The most common signs are a pale or blue tint to the skin, a heart murmur, and physical and mental retardation.

It is important to diagnose the pathology in time, since such disorders provoke the development of respiratory and heart failure.

• All information on the site is for informational purposes and is NOT a guide to action!
• Only a DOCTOR can make an EXACT DIAGNOSIS!
• We kindly ask you DO NOT self-medicate, but make an appointment with a specialist!
• Health to you and your loved ones!

Congenital heart defects - ICD-10 code Q24 - include various pathologies of the cardiovascular system, accompanied by changes in blood flow. Subsequently, heart failure is often diagnosed, which leads to death.

According to statistics, 0.8-1.2% of the total number of newborns with the presented pathology is born annually in the World. Moreover, these defects account for about 30% of the total number of diagnosed birth defects in the development of the fetus.

Often the pathology under consideration is not the only disease. Children are born with other developmental disorders, where the third part is occupied by defects in the musculoskeletal system. In a complex, all violations lead to a rather sad picture.

Congenital heart defects include the following list of defects:

The reasons

Among the causes of the presented pathology in newborns, I single out the following factors:

• make up 5% of all detected cases;
• chromosomal aberrations often provoke the development of various intrauterine pathologies, as a result of which the child is born sick;
• in the case of trisomy of autosomes, a defect of the interatrial and interventricular septa is formed, and anomalies of the sex chromosomes lead to coarctation of the aorta.

• make up 2-3% of cases;
• the presented factor often provokes the occurrence of defects in the organs of the body;
• heart defects in such cases are only part of the possible dominant or recessive syndromes.

• occupy up to 2% of all detected cases;
• here they distinguish diseases of a viral nature, the use of illegal drugs and harmful addictions of the mother during pregnancy, radiation and radiation, and other harmful effects on human health in general;
• caution should be exercised in the first 3 months of pregnancy.

• against the background of a woman's alcohol addiction, a defect in the septa of the heart is formed in a child;
• adversely affect the use of amphetamines and anticonvulsants;
• any medicinal products must be subject to the approval of the attending physician.

The cause of pathology in newborns in the form of maternal diseases during pregnancy is 90% of cases. Risk factors also include toxicosis during pregnancy in the first trimester, threats of miscarriage, genetic predisposition, disorders endocrine system and "inappropriate" age for pregnancy.

Classification

Depending on the principle of changes in hemodynamics, there is a certain classification of the presented pathology. The classification includes several types of heart disease, where the key role is played by the effect on pulmonary blood flow.

In practice, experts subdivide the considered pathologies of the heart into three groups.

Violation of hemodynamics

Under the influence and manifestation of the listed factors-causes, the fetus in the process of development has characteristic disturbances in the form of incomplete or untimely closure of the membranes, underdevelopment of the ventricles and other anomalies.

The intrauterine development of the fetus is distinguished by the functioning of the arterial duct and the oval window, which is in the open state. The defect is diagnosed when they are still open.

The presented pathology is characterized by the absence of manifestation in fetal development. But after birth, characteristic disorders begin to appear.

Similar phenomena are explained by the time of closing the message between the large and small blood circulation, individual characteristics and other defects. As a result, pathology can make itself felt some time after birth.

Methods for the treatment of heart disease are described in this article.

Often, hemodynamic disorders are accompanied by respiratory infections and other concomitant diseases. For example, the presence of pathology of the pale type, where arteriovenous emission is noted, provokes the development of hypertension of the small circle, while the pathology of the blue type with a venoarterial shunt contributes to hypoxemia.

The danger of the disease in question lies in the high mortality rate. So, a large discharge of blood from a small circle, provoking heart failure, in half of the cases ends in the death of a baby even before the age of one, which is preceded by a lack of timely surgical care.

The condition of a child older than 1 year is noticeably improving due to a decrease in the amount of blood entering the pulmonary circulation. But at this stage, sclerotic changes in the vessels of the lungs often develop, which gradually provokes pulmonary hypertension.

Symptoms

Symptoms manifest themselves depending on the type of anomaly, the nature and time of development of circulatory disorders. During the formation of the cyanotic form of pathology in a sick child, a characteristic cyanosis of the skin and mucous membranes is noted, which increases its manifestation with each voltage. White vice is characterized by pallor, constantly cold hands and feet of the baby.

The baby himself with the presented disease differs from others in hyperexcitability. The baby refuses the breast, and if he starts to suck, he quickly gets tired. Often, in children with the presented pathology, tachycardia or arrhythmia is detected, sweating, shortness of breath and pulsation of the vessels of the neck are among the external manifestations.

In the case of a chronic disorder, the baby lags behind peers in weight, height, and there is a physical lag in development. As a rule, congenital heart disease at the initial stage of diagnosis is auscultated, where heart rhythms are determined. In the further development of the pathology, edema, hepatomegaly and other characteristic symptoms are noted.

Diagnostic measures

The disease under consideration is determined by the use of several methods of examining a child:

How to treat congenital heart disease

The presented disease is complicated by the operation of a sick child up to one year of age. Here, specialists are guided by the diagnosis of cyanotic pathologies. In other cases, operations are postponed because there is no danger of developing heart failure. Cardiology specialists work with the child.

Methods and methods of treatment depend on the types and severity of the pathology in question. If an anomaly of the intercardiac or interventricular septum is detected, the child undergoes plasty or suturing.

In the case of hypoxemia, at the initial stage of treatment, specialists perform palliative intervention, which involves the imposition of intersystemic anastomoses. Such actions can significantly improve blood oxygenation and reduce the risk of complications, as a result of which further elective surgery will take place with favorable indicators.

Aortic malformation is treated by resection or balloon dilatation of the coarctation of the aorta, or plastic stenosis. In the case of an open ductus arteriosus, a simple ligation is performed. Pulmonary artery stenosis undergoes open or endovascular valvuloplasty.

If a newborn is diagnosed with a heart disease in a complicated form, where it is impossible to talk about a radical operation, specialists resort to actions to separate the arterial and venous ducts.

The elimination of the anomaly itself does not occur. It talks about the possibility of carrying out the operation of Fontenne, Senning and other varieties. If the operation does not help in the treatment, they resort to a heart transplant.

As for the conservative method of treatment, here they resort to the use of drugs, the action of which is aimed at preventing attacks of shortness of breath, acute left ventricular failure and other heart damage.

Prevention

The preventive actions for the development of the presented pathology in children should include careful planning of pregnancy, the complete exclusion of adverse factors, as well as a preliminary examination to identify a risk factor.

Women who fall into such an unfavorable list should undergo a comprehensive examination, where ultrasound and a timely biopsy of the chorion are isolated. If necessary, questions of indications for termination of pregnancy should be addressed.

If a pregnant woman is already informed about the development of pathology during the development of the fetus, she should undergo a more thorough examination and consult an obstetrician-gynecologist and a cardiologist much more often.

A description of mitral heart disease can be found here.

From here you can learn about patent ductus arteriosus in children.

Forecasts

According to statistics, mortality due to the development of congenital heart disease occupies a leading position.

In the absence of timely assistance in the form of surgical intervention, 50-75% of children die before they reach their first birthday.

Then comes the compensation period, during which the mortality rate drops to 5% of cases. It is important to identify pathology in a timely manner - this will improve the prognosis and condition of the child.

What does congenital heart disease mean according to ICD 10?

ICD code 10 congenital heart disease is a group of diseases that arose during the period of intrauterine development of a child. It includes anatomical defects of the heart, valvular apparatus, blood vessels, etc. It appears immediately after the birth of a child or has hidden symptoms.

Consider the main causes of this group of diseases, symptoms, consequences and methods of treatment.

According to ICD 10, there are a huge number of vices. There are more than a hundred rubrics in this classifier alone. Conventionally, they are divided into "white" and "blue".

White CHD - no mixing of arterial and venous blood. There are 4 groups of such diseases:

1. 1. Defects of the interatrial and interventricular septa (enrichment of the small circle).
2. 2. Defects characterized by "impoverishment" of the pulmonary circulation (for example, isolated pulmonary stenosis).
3. 3. Impoverishment of the systemic circulation (for example, aortic stenosis or coarctation).
4. 4. Without violation of hemodynamics.

With "blue" CHD, mixing of arterial and venous blood is observed. There are 2 groups of vices:

1. 1. Enrichment of the pulmonary circulation (for example, transposition of the great vessels).
2. 2. Impoverishment of the pulmonary circulation (for example, tetralogy of Fallot).

Each disease has its own code, thanks to which you can easily identify it.

Doctors know many reasons why a child develops a congenital heart disease. According to medical data obtained on the basis of many years of research, the main causes of birth defects are:

• infectious pathologies that the mother had in the first trimester of pregnancy (weeks 8-10 are critical);
• maternal bad habits (drinking and smoking). Recently, the pathogenicity of paternal smoking has been proven;
• drug use by mother and father (critical period of pregnancy - first trimester);
• unfavorable hereditary predisposition;
• pregnancy after 35 years;
• high age of the father;
• if a woman has had many abortions;
• if a woman suffers from chronic pathologies that can be transmitted to the fetus.

It must be remembered that all these reasons are factors of increased risk of congenital heart disease. That is why all pregnant women who are at such a risk are sent for an ultrasound examination. It should confirm or exclude congenital anomalies of the heart of the unborn child.

A pregnant woman should be aware of what is most harmful to health. In some cases, an additional study of the father is necessary.

Congenital malformation has common Clinical signs. Often they appear from the very beginning. early age. It also happens that a child or his parents do not notice these signs throughout his life. A person learns about their presence, for example, at a highly specialized medical examination, and young men - when they register for a recruiting station. Some children may suffer from shortness of breath, blue lips and skin, and frequent fainting.

A doctor can often determine the presence of a heart murmur by listening. However, not all heart defects can differ in noise.

All clinical manifestations of the disease combine 4 groups of symptoms:

1. 1. Cardiac symptoms. These include pain in the heart (cardialgia), palpitations, shortness of breath, and sometimes heart failure. Examination of such patients most often reveals pallor of the skin (or vice versa, its blue), excessive swelling of the vessels. In addition, excessive pulsation can often be seen. The appearance of specific tones during auscultation is characteristic (they are noticeable only to narrow specialists). On the ECG, characteristic changes and lengthening of the teeth are noticeable.
2. 2. Heart failure. Characterized by attacks of suffocation. The intensity of such attacks depends on each specific case.
3. 3. Systemic oxygen starvation (hypoxia). It is characterized by a violation of the supply of oxygen to the tissues. Because of this, children lag behind in physical and mental development. A symptom of drumsticks develops (Hippocratic fingers, often observed in Fallot's tetrad with thickening of the phalanges in the form of a bulb) and watch glasses (the so-called Hippocratic nail with deformation of the nail plate). It resembles the look of a watch glass. Sometimes a person can feel the mobility of the plate.
4. 4. Respiratory disorders varying degrees intensity and expression.

ICD 10 congenital heart disease

The specification of microbial 10 congenital heart disease is one of the sections of the assessment tool that was introduced by the Russian healthcare system in 1999. It allows you to assess how serious a particular disease associated with heart failure.

Thanks to progress in the field of surgery, 85% of newborns get a great opportunity to live a full and happy life, and adults get a chance to gain new life with a healthy heart. This fantastic information gives hope to each of us.

Types of heart defects

Let's find out how many types of heart disease actually exist. The National Health Service of Great Britain, which has identified more than 30 positions, will help us with this, but it is worth talking about only the 2 most important ones:

• Congenital heart disease, microbial code 10 (Q20-Q28) blue type, more precisely, with cyanosis.

Unlike the first type, the blood is sufficiently saturated with oxygen, however, it circulates in the body in an unusual way. In newborns, symptoms do not appear immediately, but over time. Arterial pressure exceeds the allowable rate, forcing the heart to work in emergency mode.

The patient may experience frequent and rapid fatigue, dizziness, shortness of breath and pulmonary hypertension.

In addition, genetic diseases such as Down syndrome and infectious diseases (rubella) can become the basis for the development of congenital malformations.

How to cure congenital heart disease?

Often these problems do not require serious treatment and go away on their own. But there are exceptions in which surgery and a course of medications are the only right solution. The operation is prescribed based on the specification of microbial 10 congenital heart disease.

• Under the supervision of doctors. If the defects are not so severe, regular medical check-ups may be required to prevent progression of the disease.

• A catheter is a long, flexible tube that is inserted into the heart. This method is considered safe for the baby and does not require any major surgical incisions in the chest area.

• Surgery or heart transplant. It is used only when a person's life depends on it.

Be sure to consult a specialist if you have any concerns. Take care of your health, stick to good habits, and love the people around you.

No need to give up on yourself and put up with the fact that you will always have to live with heart failure. We live in the XXI century, when it is possible to cure almost any disease or deviation. The main thing is to believe in a brighter future and never give up hope, because it dies last.

Mkb 10 acquired heart disease

mitral stenosis.

II Acquired heart defects.

Heart disease is an anatomical change in the valvular apparatus of the heart or interatrial, interventricular septum and other defects.

By origin, the vices are divided:

• Congenital - arise as a result of a violation of the formation of the heart and blood vessels in the embryonic period.
• Acquired - acquired changes in the heart valves, leading to impaired function and hemodynamics, acquired defects are a complication of various diseases.

Combined defect - a combination of two defects of one valve. For example, mitral stenosis and mitral insufficiency.

Combined defect - a combination of defects of several valves, for example, mitral stenosis and aortic insufficiency.

Isolated defect - one defect of one valve, for example, mitral insufficiency.

Compensated defect - no complaints, no signs of circulatory failure.

Decompensated defect - there are complaints of circulatory failure of the left ventricular or right ventricular type.

MITRAL HEART DEFECTS.

Mitral stenosis is a narrowing of the left atrioventricular orifice, which prevents the physiological flow of blood from it into the left ventricle during systole of the left atrium.

Mitral insufficiency is the inability of the left atrioventricular valve to prevent the reverse movement of blood from the left ventricle to the left atrium during ventricular systole, that is, incomplete closure of the MV cusps.

Mitral valve prolapse (MVP) is a pathological sagging (flexion) of one or both leaflets of the mitral valve into the left atrium during left ventricular systole.

I05.0 Mitral stenosis, rheumatic.

I05.1 Rheumatic mitral valve insufficiency

I05.2 Mitral stenosis with insufficiency

I05.8 Other disorders of the mitral valve (mitral insufficiency)

I05.9 Mitral valve disease, unspecified

EPIDEMIOLOGY and ETIOLOGY.

■mitral stenosis almost always occurs as a result of an acute rheumatic attack, more often in women.

On average, the latent period from the moment of rheumatic heart disease (carditis) to the development of clinical manifestations of the defect is about 20 years, so the disease manifests itself between 30 and 40 years of age.

■Mitral insufficiency. Causes: MVP, rheumatism (30%), atherosclerosis, infective endocarditis, trauma, connective tissue diseases. In men, mitral insufficiency is noted more often.

• The classification of mitral stenosis according to severity is based on the severity of the narrowing of the left atrioventricular orifice (mild, moderate and severe stenosis).
• The classification of mitral insufficiency according to the severity is determined by the volume of regurgitant blood (4 degrees of mitral insufficiency).

Through the narrowed left atrioventricular orifice, not all blood enters the left ventricle (LV) during systole of the left atrium (LA), as a result, an excess volume of blood is formed in the left atrium (remaining after systole and again coming from the pulmonary veins during subsequent diastole) , this leads to left atrial hypertrophy (compensation stage), over time, the atrial myocardium is depleted, the left atrial cavity expands, decompensation develops, as a result, pressure in the ICC increases and hypertrophy of the right ventricle (RV) develops, and then the right atrium (RA).

I51.9 Heart disease, unspecified: description, symptoms and treatment

c. REGISTER OF DRUGS OF RUSSIA ® RLS ®

Classification of acquired heart defects

(Adopted at the VI Congress of Cardiologists of Ukraine, Kyiv, 2000) Mitral stenosis:

Rheumatic 1.05.0 Non-rheumatic 1.34.2 (with clarification of etiology) Stage I - compensation Stage II - pulmonary congestion

stage - right ventricular failure

Rheumatic 1.05.1 Non-rheumatic 1.34.0 (with clarification of etiology) Stage I - compensation Stage II - subcompensation Stage III - right ventricular decompensation Stage IV - dystrophic Stage V - terminal Combined rheumatic mitral defect (Rheumatic mitral stenosis with insufficiency: 1.05.2) C predominance of stenosis: stages and indications for surgical treatment, as in mitral stenosis With a predominance of insufficiency: stages and indications for surgical treatment, as in mitral insufficiency No clear predominance: stages and indications for surgical treatment, as in mitral insufficiency Mitral valve prolapse 1.34.1 Aortic stenosis: Rheumatic 1.06.0 Non-rheumatic 1.35.0 (with specification of etiology) Stage I - complete compensation Stage II - latent heart failure Stage III - relative coronary insufficiency GU stage - severe left ventricular failure Stage V - terminal Aortic insufficiency:

Rheumatic 1.06.1 Non-rheumatic 1.35.1 (with clarification of etiology) Stage I - complete compensation Stage II - latent heart failure

Stage V - terminal Combined aortic defect:

Rheumatic aortic stenosis with insufficiency 1.06.2 Non-rheumatic aortic (valvular) stenosis with insufficiency 1.35.2 (with specification of etiology) Stenosis-predominant: stages and indications for surgical treatment are the same as those for aortic stenosis Insufficiency-dominant: stages and indications for surgical treatment are the same with aortic insufficiency 216

Without a clear predominance: the stages and indications for surgical treatment correspond to those for aortic stenosis Tricuspid stenosis:

Rheumatic 1.07.0 Non-rheumatic 1.36.0 (with clarification of etiology) Tricuspid insufficiency:

Rheumatic 1.07.1 Non-rheumatic 1.36.1 (with specification of etiology) Combined tricuspid defect:

Rheumatic tricuspid stenosis with insufficiency 1.07.2 Non-rheumatic tricuspid valve stenosis with insufficiency 1.36.2 (with specified etiology) Pulmonary artery stenosis 1.37.0 Pulmonary valve insufficiency 1.37.1 Combined valvular disease of the pulmonary artery (Pulmonary artery stenosis with valve insufficiency 1.37.2 ) Combined heart defects:

Combined damage to the mitral and aortic valves 1.08.0 Combined damage to the mitral and tricuspid valves 1.08.1 Combined damage to the aortic and tricuspid valves 1.08.2 Combined damage to the mitral, aortic and tricuspid valves 1.08.3 The severity of "simple" defects is determined by three degrees:

I degree - insignificant II degree - moderate III degree - pronounced.

The severity of defects in accordance with their clinical and instrumental characteristics are given below for individual nosological forms of heart defects.

It should be noted that heart disease is considered "combined" in the presence of stenosis and insufficiency of one valve and "combined" in case of damage to several valves. If there are several defects, they are listed, with the first indicating the defect, the severity of which is greater - for example, aortic valve insufficiency, mitral defect with a predominance of stenosis.

Given that valve kalydinosis determines the tactics of surgical intervention, it is proposed to distinguish 3 degrees of kalydinosis (Knyshov G.V. BendetYa.A. 1996).

Degrees of valve calcification

Separate clumps of calcium in the thickness of the commissures or valves

Significant calcification of valves and commissures without

valve ring attraction III +++ Massive calcification of the valve with the transition to the annulus fibrosus, and sometimes to the aortic wall and ventricular myocardium. In the diagnosis, it is also necessary to take into account the etiological cause of the defect (rheumatism, infective endocarditis, atherosclerosis), the degree of heart failure.

For patients who underwent surgery on the heart valves, it is necessary to indicate the previously existing defect, indicate the date of surgical treatment, the nature of complications. For example, operated mitral heart disease with a predominance of stenosis, closed commissurotomy (date) or operated aortic valve disease with a predominance of insufficiency. Aortic valve replacement (specify type of prosthesis and date).

Along with heart defects caused by organic changes in the valve, there are violations of valve function in the form of relative insufficiency or relative stenosis. The cause of relative insufficiency of the valve may be a decrease in the tone of the papillary muscles or a violation of the function of the circular muscles, which normally reduce the lumen of the hole during systole. With a decrease in the tone of these muscles, the opening during systole remains large, and even unchanged valve leaflets cannot completely cover it. The most typical is the relative insufficiency of the mitral valve in aortic disease, which gave grounds to speak of "mitralization of aortic disease". Relative insufficiency of the valves of the main vessels is observed with an increase in the perimeter of the fibrous ring, in which the area of ​​the valve cusps is insufficient to completely cover the orifices of the vessels (more often relative insufficiency of the pulmonary valve). Relative stenosis occurs in cases of a sharp increase in blood flow through a normal-sized opening, for example, with severe mitral or aortic valve insufficiency. The addition of relative valve insufficiency or relative stenosis, despite changes in auscultatory signs and the course of the disease, does not give grounds for designating the defect as combined.

mitral stenosis

For the first time, the defect was described by Viussens in 1715. When it occurs, an obstacle is created to the movement of blood from the left atrium to the left ventricle. Mitral stenosis is the most common rheumatic heart disease. The defect is usually formed at a young age and is more often observed in women (80%).

Etiology. Mitral stenosis occurs due to long-term rheumatic endocarditis, an extremely rare cause of mitral stenosis is infective endocarditis. Narrowing or closure of the mitral orifice can be caused by a thrombus, polyp, left atrial myxoma.

Pathological anatomy. Pathological changes in the mitral valve during the rheumatic process are complex and varied. The valve defect is based on sclerotic processes, which involve the leaflets, annulus fibrosus, chords and papillary muscles (Fig. 18). The narrowing of the opening occurs initially due to gluing of the adjoining edges of the valves, primarily along their poles adjacent to the fibrous ring (Fig. 19), where mobility is limited, with the formation of commissures. In the future, the fusion of the valves extends to the middle of the hole, gradually narrowing it. In parallel, fibrous changes in the structures of the valvular apparatus occur, they become rigid and inactive. At the same time, the fibrous ring becomes sclerosed and loses its elasticity. If the process is localized mainly in the valve leaflets,

219 Fig.18. Mitral valve (no F. Netter, 1969, with changes), then when the edges of the fibrous thickened valve are fused, a diaphragm with a slit-like opening is formed - stenosis in the form of a "button loop" (in 85% of cases). Involvement of subvalvular structures in the pathological process - damage to tendon filaments with their fusion, thickening, shortening - sharply limits the mobility of the valve, with significant involvement of subvalvular formations, the narrowing looks like a "fish mouth" (Fig. 20). In some patients, a double narrowing is found - the fusion of the valves and tendon filaments. With prolonged existence of the defect, calcification of the valve occurs.

pathological physiology. Normally, the area of ​​the atrioventricular opening is 4-6 cm2, the opening has a significant area reserve, and only its decrease by more than 2 times can cause a noticeable hemodynamic disturbance. The smaller the hole area, the more severe the clinical manifestations of mitral stenosis. The "critical area", at which noticeable hemodynamic disorders begin, is 1-1.5 cm2.

The resistance to blood flow created by the narrowed mitral orifice (the “first barrier”) sets in motion compensatory mechanisms that ensure sufficient heart performance. With mitral stenosis, the movement of blood from the left atrium in Fig.19. Heart valves (according to F. Netter, 1969, with changes) A ​​- pulmonary valve: 1 - anterior leaflet, 2 - right leaflet, 3 - left leaflet; B - aortic valve: 1 - right (coronary) cusp, 2 - left (coronary) cusp, 3 - posterior (non-coronary) cusp; B - mitral valve: 1 - anterior (aortic) cusp, 2 - commissural cusps, 3 - posterior cusp, 4 - fibrous ring; D - tricuspid ManaH: 1 - anterior leaflet, 2 - septal leaflet, 3 - posterior leaflet, 4 - annulus fibrosus 20. Echocardiography of mitral stenosis (B-mode, opening area = 1.2 cm2) the ventricle accelerates due to an increase in the pressure gradient between the left atrium and the left ventricle (Fig. 21). Compensatory pressure in the left atrium increases, the atrial myocardium hypertrophies, its cavity expands. Due to the fact that the left atrium cannot cope with the increased load, further growth 21. Blood pressure (mm Hg) in different parts of the heart and blood vessels in normal (systolic / diastolic) pressure in it leads to a retrograde increase in pressure in the pulmonary veins and capillaries, arterial hypertension occurs in the pulmonary circulation. When the pressure in the left atrium is above a certain level, due to irritation of the receptor apparatus in the walls of the left atrium and pulmonary veins, a reflex narrowing of the small pulmonary arteries occurs at the precapillary level (“second barrier”) - the Kitaev reflex, which protects the capillary network of the lungs from overflowing with blood. In the future, due to prolonged vascular spasm, an organic degeneration of the walls of the vessels occurs, hypertrophy develops, as well as sclerosis of the walls of the pulmonary arterioles, capillaries, and lung parenchyma. There is a persistent pulmonary "second barrier". Hemodynamic disturbances are exacerbated by weakening of the left atrial myocardium. High pressure in the pulmonary artery (up to 80 mm Hg and above) leads to compensatory hypertrophy, and then dilatation of the right ventricle, it increases diastolic pressure. In the future, an increase in pressure in the pulmonary artery and the development of myocardial wear syndrome causes the appearance of right ventricular failure and relative insufficiency of the tricuspid valve (Fig. 22).

The clinical picture of mitral stenosis depends on the stage of the disease, the state of circulatory compensation. With compensatory hyperfunction of the left atrium, patients usually do not complain, they can perform significant physical activity.

With an increase in pressure in the pulmonary circulation, there are complaints of shortness of breath and a feeling of palpitations during physical exertion. With a sharp increase in pressure in the capillaries, attacks of cardiac asthma develop, a cough occurs dry or with a small amount of mucous sputum, often with an admixture of blood (hemoptysis). With high pulmonary hypertension, patients experience weakness, increased fatigue, due to the fact that in the conditions of mitral stenosis ("first barrier") during exercise, there is no adequate increase in cardiac output (the so-called fixation of cardiac output).

Rice. 22. Mitral stenosis (according to F. Netter, 1969, with changes) The appearance of patients with moderately severe mitral stenosis is not changed. With severe stenosis and an increase in symptoms of pulmonary hypertension, typical Facies mitralis is observed: a “mitral” blush on the cheeks against the background of pale skin of the face, cyanosis of the lips, tip of the nose, and auricles. In patients with high pulmonary hypertension, cyanosis increases during exercise, and a grayish coloration of the skin (“ashy cyanosis”) appears, which is due to low cardiac output. The region of the heart in the lower part of the sternum often bulges and pulsates due to the formation of a "heart hump" due to hypertrophy and dilatation of the right ventricle and its increased impacts on the anterior chest wall. On the left edge of the sternum in the third-fourth intercostal space, a pulsation of the output tracts of the right ventricle can be observed, associated with its hemodynamic overload in conditions of pulmonary hypertension.

In the region of the apex of the heart, or somewhat laterally, diastolic trembling is determined - "cat's purr" - a phenomenon caused by low-frequency fluctuations of blood when it passes through a narrowed mitral opening.

Mitral stenosis is diagnosed based on the characteristic melody of tones and heart murmurs. Amplified (flapping) I tone at the apex of the heart and the mitral valve opening tone (opening click), appearing 0.08-0.11 s after tone II, create a characteristic melody of mitral stenosis - a quail rhythm. Flapping I tone is heard only in the absence of gross deformities of the valves (in the absence of fibrosis and calcification of the valve). The mitral valve opening tone persists even when atrial fibrillation occurs. With an increase in pressure in the pulmonary artery in the second intercostal space to the left of the sternum, an accent of the II tone is heard, often with a bifurcation, which is due to the non-simultaneous slamming of the valves of the pulmonary artery and aorta.

The characteristic auscultatory symptoms in mitral stenosis include diastolic murmur, which can occur at various times in diastole. Protodiastolic murmur occurs at the beginning of diastole due to the movement of blood through the narrowed hole as a result of a pressure gradient in the left atrium - left ventricle, its character is low, rumbling (its palpatory equivalent is "cat's purr"). The noise can be of different duration, its intensity gradually decreases. Presystolic murmur occurs at the end of diastole due to active atrial systole, with the appearance of atrial fibrillation, the murmur disappears. The pre-systolic murmur is usually short, rough, scraping timbre, has a growing character, ends with a clapping I tone. It should be noted that diastolic murmurs in mitral stenosis are heard in a limited area and are not carried out, therefore, an insufficiently thorough search for the place of the best auscultation of the mitral valve can be a source of diagnostic errors.

Electrocardiogram with minor mitral stenosis is not changed. As the defect progresses, there are signs of left atrial overload (Pmitrale), right ventricular hypertrophy in the form of an increased amplitude of the QRS complex teeth in the corresponding leads in combination with an altered end part of the ventricular complex (flattening, T wave inversion, segment 57 decrease) in the same leads. Heart rhythm disturbances (flicker, atrial flutter) are often recorded.

Phonocardiogram for the diagnosis of mitral stenosis is of great importance. With mitral stenosis, a change in the intensity of the first tone, the appearance of an additional tone (a click of the opening of the mitral valve), as well as the appearance of noise in diastole, are detected. The duration of the interval from the beginning of the II tone to the opening tone of the mitral valve (II tone - QS) ranges from 0.08 to 0, 12 si shortens to 0.04-0.06 s with the progression of stenosis. As the pressure in the left atrium increases, the interval?-l tone lengthens, which reaches 0.08-0.12 s. Various diastolic murmurs are recorded (pre-, meso- and proto-diastolic). The phonocardiographic picture in mitral stenosis is shown in fig. 23. The value of phonocardiography increases in the conditions of the tachysystolic form of atrial fibrillation, when during normal auscultation it is difficult to attribute the auscultated murmur to any or another phase of the cardiac cycle.

Rice. 23. Phonocardiogram for mitral and aortic heart disease (according to F. Netter, 1969, with changes) Echocardiography can be a verifying method for mitral stenosis, in which the following changes are observed: unidirectional (P-shaped) movement of the anterior and posterior mitral valve leaflets forward ( normally, the posterior leaflet moves posteriorly during diastole; Fig. 24);

Decreased rate of early diastolic occlusion of the anterior

mitral valve leaflets (up to 1 cm/s);

decrease in the amplitude of the opening of the mitral valve leaflet

(up to 8 mm or less);

enlargement of the left atrial cavity (anteroposterior size

can be increased up to 70 mm);

Valve thickening (fibrosis and calcification; Fig. 25).

Experts from the American College of Cardiology (1998) developed indications for echocardiography in mitral stenosis:

Rice. 24. Echocardiography in mitral stenosis (M-mode) 1. Diagnosis of mitral stenosis, assessment of the severity of hemodynamic disorders (pressure gradient value, mitral ring area, pressure in the pulmonary artery), as well as determining the size and function of the right ventricle.

Rice. 25. Echocardiography in mitral stenosis (B-mode)

Assessment of the mitral valve to determine if

for percutaneous balloon valvotomy of the left

Diagnosis and assessment of severity of associated valve

Re-examination of patients diagnosed with mitral steatosis

nose, in which the clinical picture of the disease over time

Assessment of the state of hemodynamics and pressure gradient in the lung

artery using Doppler echocardiography at rest in patients

goods in case of discrepancy between the results of objective and instrumental

research methods.

Catheterization of the cavities of the heart plays an auxiliary role. In some patients with mitral stenosis, an accurate diagnosis of the defect requires invasive methods. Indications for cardiac catheterization in mitral stenosis, developed by experts from the American College of Cardiology (1998), are given below.

The need for percutaneous mitral balloon

valvotomy in properly selected patients.

Assessment of the severity of mitral regurgitation in patients

who are expected to perform a mitral percutaneous ball

pubic valvotomy, when clinical evidence is against

Evaluation of the state of the pulmonary artery, left atrium and diastolic pressure in the cavity of the left ventricle, when the clinical symptom