Cough

Definition of bicuspid aortic valve as a congenital heart defect. Mitral heart defects ICD 10 defect with mitral insufficiency

II Acquired heart defects.

Heart defect– this is an anatomical change in the valve apparatus of the heart or the interatrial, interventricular septum and other defects.

Based on their origin, defects are divided into:

Congenital– arise as a result of disruption of the formation of the heart and blood vessels in the embryonic period.
Purchased– acquired changes in the heart valves, leading to dysfunction 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 vice– one defect of one valve, for example, mitral insufficiency.

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

Decompensated defect– complaints of circulatory failure of the left ventricular or right ventricular type appear.

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 regurgitation- inability of the left atrioventricular valve to prevent the reverse movement of blood from the left ventricle into the left atrium during systole of the ventricles of the heart, that is, incomplete closure of the valves of the MV.

Mitral valve prolapse (MVP)- pathological sagging (bending) of one or both mitral valve leaflets 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 diseases 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 life.

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

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

CLASSIFICATION.

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

PATHOGENESIS

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

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

from 2000-2015. REGISTER OF MEDICINES 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

Stage V - terminal

Mitral regurgitation

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 disease (Rheumatic mitral stenosis with insufficiency: 1.05.2) C predominance of stenosis: stages and indications for surgical treatment, as in mitral stenosis With predominance of insufficiency: stages and indications for surgical treatment, as in mitral regurgitation Without obvious predominance: stages and indications for surgical treatment, as in mitral regurgitation Mitral valve prolapse 1.34.1 Aortic stenosis: Rheumatic 1.06.0 Non-rheumatic 1.35.0 (with specification of etiology) Stage I - full compensation Stage II - latent heart failure Stage III - relative coronary insufficiency GU stage - severe left ventricular failure Stage V - terminal Aortic failure:

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

stage - subcompensation

stage - decompensation

Stage V - terminal Combined aortic disease:

Rheumatic aortic stenosis with insufficiency 1.06.2 Non-rheumatic aortic (valvular) stenosis with insufficiency 1.35.2 (with specification of etiology) With predominant stenosis: stages and indications for surgical treatment correspond to those for aortic stenosis With predominant insufficiency: stages and indications for surgical treatment correspond to those for aortic insufficiency 216

Without obvious predominance: stages and indications for surgical treatment correspond to those for aortic stenosis. Tricuspid stenosis:

Rheumatic 1.07.0 Non-rheumatic 1.36.0 (with specification 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 stenosis of the tricuspid valve with insufficiency 1.36.2 (with specification of etiology) Pulmonary artery stenosis 1.37.0 Pulmonary valve insufficiency 1.37.1 Combined pulmonary valve disease (Pulmonary 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 the 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” when there is stenosis and insufficiency of one valve and “combined” when several valves are affected. If there are several defects, they are listed, and the defect whose severity is greater is indicated first - for example, aortic valve insufficiency, mitral valve disease with a predominance of stenosis.

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

Degrees of valve calcification

Individual lumps of calcium in the thickness of commissures or valves

Significant calcification of the valves and commissures without water

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

For patients who have undergone heart valve surgery, the pre-existing defect should be identified, the date of surgical treatment, and the nature of complications should be indicated. For example, operated mitral heart disease with predominant stenosis, closed commissurotomy (date) or operated aortic valve disease with predominant insufficiency. Aortic valve replacement (specify type of prosthesis and date).

Along with heart defects caused by organic changes in the valve, there are dysfunctions of the valve in the form of relative insufficiency or relative stenosis. The cause of relative valve insufficiency may be a decrease in the tone of the papillary muscles or impaired function of the circular muscles, which normally reduce the lumen of the orifice during systole. With a decrease in the tone of these muscles, the opening remains large during systole, and even unchanged valve leaflets cannot completely cover it. The most typical is relative mitral valve insufficiency in aortic disease, which gives rise to talk about “mitralization of aortic disease.” Relative insufficiency of the valves of the great vessels is observed with an increase in the perimeter of the fibrous ring, in which the area of the valve leaflets is insufficient to completely cover the mouths 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 hole of normal size, for example, with severe regurgitation of the mitral or aortic valves. The addition of relative valve insufficiency or relative stenosis, despite changes in auscultatory signs and the course of the disease, does not provide grounds for designating the defect as combined.

Mitral stenosis

The defect was first 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 usually forms at a young age and is more often observed in women (80%).

Etiology. Mitral stenosis occurs as a result of 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, or myxoma of the left atrium.

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

219 Fig. 18. Mitral valve (no F. Netter, 1969, as amended) then when the edges of the fibrous thickened valve fusion, 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 threads with their fusion, thickening, shortening - sharply limits the mobility of the valve; with significant involvement of subvalvular formations, the narrowing has the appearance of a “fish mouth” (Fig. 20). In some patients, double narrowing is detected - fusion of the valves and tendon threads. If the defect persists for a long time, the valve becomes calcified.

Pathological physiology. Normally, the area of the atrioventricular opening is 4-6 cm2; the opening has a significant reserve area, and only its reduction by more than 2 times can cause a noticeable hemodynamic disturbance. The smaller the area of the hole, 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”) activates compensatory mechanisms that ensure sufficient cardiac performance. With mitral stenosis, blood moves from the left atrium to Fig. 19. Heart valves (according to F. Netter, 1969, with modifications) 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) leaflet, 2 - commissural leaflets, 3 - posterior leaflet, 4 - fibrous ring; D - tricuspid ManaH: 1 _ anterior leaflet, 2 - septal leaflet, 3 - posterior leaflet, 4 - fibrous ring Fig. 20. EchoCG of mitral stenosis (B-mode, orifice 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). The pressure in the left atrium increases compensatoryly, the atrial myocardium hypertrophies, and its cavity expands. Due to the fact that the left atrium cannot cope with the increased load, further growth Fig. 21. Normal blood pressure (mm Hg) in different parts of the heart and blood vessels (systolic/diastolic) leads to a retrograde increase in pressure in the pulmonary veins and capillaries, and 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 small pulmonary arteries occurs at the precapillary level (“second barrier”) - the Kitaev reflex, which protects the capillary network of the lungs from overflow with blood. Subsequently, as a result of prolonged vascular spasm, organic degeneration of the vascular walls occurs, hypertrophy develops, as well as sclerosis of the walls of the pulmonary arterioles, capillaries, and lung parenchyma. A persistent pulmonary “second barrier” appears. Hemodynamic disturbances are aggravated by weakening of the left atrium 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, and diastolic pressure in it increases. Subsequently, an increase in pressure in the pulmonary artery and the development of myocardial wear syndrome causes the appearance of right ventricular failure and relative tricuspid valve insufficiency (Fig. 22).

The clinical picture of mitral stenosis depends on the stage of the disease and the state of circulatory compensation. With compensatory hyperfunction of the left atrium, patients usually have no complaints and can perform significant physical activity.

With an increase in pressure in the pulmonary circulation, complaints of shortness of breath and a feeling of palpitations during physical activity appear. With a sharp increase in pressure in the capillaries, attacks of cardiac asthma develop, a dry cough or with the release of a small amount of mucous sputum occurs, often mixed with blood (hemoptysis). With high pulmonary hypertension, patients experience weakness and increased fatigue, due to the fact that in conditions of mitral stenosis (“the first barrier”) during physical activity 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 modifications) The appearance of patients with moderate mitral stenosis is not changed. With severe stenosis and increasing symptoms of pulmonary hypertension, typical Facies mitralis is observed: “mitral” flush on the cheeks against the background of pale facial skin, cyanosis of the lips, tip of the nose, and ears. In patients with high pulmonary hypertension, cyanosis increases during physical activity, and a grayish coloration of the skin (“ashy cyanosis”) appears, which is due to low cardiac output. The area of the heart in the lower part of the sternum often bulges and pulsates due to the formation of a “heart hump” caused by hypertrophy and dilatation of the right ventricle and its increased impact on the anterior chest wall. Along the left edge of the sternum in the third or fourth intercostal space, pulsation of the outflow tracts of the right ventricle may 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 tremor is detected - “cat's purring” - a phenomenon caused by low-frequency vibrations of the blood as it passes through the narrowed mitral orifice.

Mitral stenosis is diagnosed based on the characteristic melody of heart sounds and murmurs. The intensified (popping) 1st sound at the apex of the heart and the opening sound of the mitral valve (opening click), appearing 0.08-0.11 s after the 2nd sound, create a characteristic melody of mitral stenosis - the rhythm of a quail. A flapping first sound is heard only in the absence of gross deformations of the valves (in the absence of fibrosis and calcification of the valve). The opening tone of the mitral valve remains the same when atrial fibrillation occurs. With increased pressure in the pulmonary artery in the second intercostal space to the left of the sternum, an accent of the second tone is heard, often with bifurcation, which is caused by the non-simultaneous closure of the pulmonary artery and aortic valves.

Characteristic auscultatory symptoms of mitral stenosis include diastolic murmur, which can occur at various periods of diastole. Protodiastolic murmur occurs at the beginning of diastole due to the movement of blood through a narrowed opening as a result of a pressure gradient in the left atrium - left ventricle; its character is low, rumbling (its palpatory equivalent is “cat purring”). The noise can be of varying duration, its intensity gradually decreases. Presystolic murmur occurs at the end of diastole due to active atrial systole; when atrial fibrillation appears, the murmur disappears. Pre-systolic murmur is usually short, has a rough, scraping timbre, has an increasing character, and ends with a clapping sound. It should be noted that diastolic murmurs with mitral stenosis are heard in a limited area and are not carried out, therefore, an insufficiently thorough search for the place of best auscultation of the mitral valve can be a source of diagnostic errors.

The electrocardiogram with minor mitral stenosis is not changed. As the defect progresses, signs of overload of the left atrium (Pmitrale), hypertrophy of the right ventricle appear in the form of increased amplitude of the QRS complex waves in the corresponding leads in combination with an altered final part of the ventricular complex (flattening, inversion of the T wave, decrease in segment 57) in the same leads. Heart rhythm disturbances (atrial fibrillation, atrial flutter) are often recorded.

A phonocardiogram for diagnosing 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 murmurs in diastole are detected. The duration of the interval from the beginning of the second sound to the opening tone of the mitral valve (II sound - QS) ranges from 0.08 to 0.12 si and shortens to 0.04-0.06 s as the stenosis progresses. As the pressure in the left atrium increases, the ?-l tone interval lengthens, reaching 0.08-0.12 s. Various diastolic murmurs are recorded (pre-, meso- and proto-diastolic). The phonocardiographic picture of mitral stenosis is shown in Fig. 23. The importance of phonocardiography increases in conditions of the tachysystolic form of atrial fibrillation, when with normal auscultation it is difficult to attribute the auscultated murmur to one or another phase of the cardiac cycle.

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

decrease in the speed of early diastolic covering of the anterior

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

decrease in the amplitude of opening of the mitral valve leaflet

(up to 8 mm or less);

enlargement of the left atrium cavity (antero-posterior size

can increase up to 70 mm);

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

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

Rice. 24. EchoCG for mitral stenosis (M-mode) 1. Diagnosis of mitral stenosis, assessment of the severity of hemodynamic disturbances (pressure gradient value, area of the mitral annulus, pulmonary artery pressure), as well as determination of the size and function of the right ventricle.

Rice. 25. EchoCG for mitral stenosis (B-mode)

Assessing the condition of the mitral valve to determine whether

knowledge for performing percutaneous balloon valvotomy of the left

atrioventricular opening.

Diagnosis and assessment of the severity of associated valves

ny defeats.

Repeated examination of patients diagnosed with mitral valve

nosas whose clinical picture of the disease develops over time

has changed.

Assessment of hemodynamics and pressure gradient in the lungs

artery using Doppler echocardiography at rest in patients

com in case of discrepancy between objective and instrumental results

new research methods.

Catheterization of the cardiac cavities plays a supporting role. In some patients with mitral stenosis, invasive methods are required to accurately diagnose the defect. Indications for cardiac catheterization for 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.

Assessing the severity of mitral regurgitation in patients

in whom percutaneous mitral balm is expected to be performed

pubic valvotomy, in cases where clinical data are against

speak echocardiographic.

Assessment of the state of the pulmonary artery, left atrium and diastolic pressure in the left ventricular cavity when clinical symptoms

There is a huge difference between acquired cardiac disorders and congenital developmental anomalies, as they are in different ICD classes. Although the disturbances in arterial and venous blood flow will be the same, the treatment and etiological factors will be completely different.

Congenital heart disease may not require therapeutic measures, but more often planned operations are performed or even urgent ones in case of serious, incompatible with life, inconsistencies with the norm.

VSP encoding

Heart defects are in the class of congenital anomalies of the structure of the body in the block of anomalies of the circulatory system. VSP 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 cardiac chambers and their connections (for example, various clefts of the oval window);
Q21 – pathologies of the cardiac septum (defects of the atrial and interventricular septa 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, dextracardia, etc.).

Each of the listed points requires further differentiation, which will allow us to 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 ICD, congenital heart disease implies some kind of blood flow disturbance.

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

Congenital heart defects ICD 10

Small anomalies of heart development

Small anomalies of heart development: Brief description

Minor anomalies of cardiac development (MACD) are anatomical congenital changes in the heart and great vessels that do not lead to gross dysfunction of the cardiovascular system. A number of MARS are unstable and disappear with age.

Etiology

Hereditary determined connective tissue dysplasia. A number of MARS are dysembryogenetic in nature. The influence of various environmental factors (chemical, physical effects) cannot be excluded.

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

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

Q24.9 Congenital heart defect, unspecified

Other diagnoses in the ICD 10 section

Q24.0 Dextrocardia
Q24.1 Levocardia
Q24.2 Triatrial heart
Q24.3 Infundibular stenosis of the pulmonary valve
Q24.4 Congenital subaortic stenosis

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

Heart defects.congenital (classification)

Classification of congenital heart disease by severity classes (J. Kirklin et al. 1981) Class I. It is possible to perform a planned operation later than 6 months: VSD, ASD, radical correction for tetralogy of Fallot class II. A planned operation can be performed within 3–6 months: radical correction for VSD, open atrioventricular canal (PAVC), palliative correction for class III TF. A planned operation can be performed within a period of up to several weeks: radical correction for transposition of the great vessels (TMS) class IV. Emergency surgery with a maximum preparation period of several days: radical correction for total anomalous pulmonary vein drainage (TAPDV), palliative correction for TMS, VSD, OAVC class V. The operation is performed urgently due to cardiogenic shock: various types of defects in the decompensation stage.

Classification of congenital heart disease 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 diseases, etc. Group 3. Poor prognosis (mortality during the first year of life is 36–52%): TMS, coarctation and stenosis of the aorta, tricuspid valve atresia, TADLV, single ventricle of the heart, OAVC, origin of the aorta and pulmonary artery from the right ventricle, etc. Group 4. Extremely unfavorable prognosis (mortality during the first year of life is 73–97%): hypoplasia of the left ventricle, pulmonary atresia with an intact interventricular septum, common truncus arteriosus, etc.

Classification of congenital heart disease according to the possibility of radical correction (Turley K. et al. 1980) group 1. Defects for which only radical correction is possible: aortic stenosis, pulmonary artery stenosis, TADLV, triatrial heart, coarctation of the aorta, patent ductus arteriosus, aortic pulmonary septal defect, ASD, mitral valve stenosis or insufficiency group 2. Defects in which the advisability of radical or palliative surgery depends on the anatomy of the defect, the age of the child and the experience of the cardiology center: various variants of TMS, pulmonary atresia, common truncus arteriosus, tetralogy of Fallot, OAVC, VSD group 3. Defects for which only palliative operations are possible in infancy: a single ventricle of the heart, some variants of the origin of the great vessels from the right or left ventricle with pulmonary stenosis, atresia of the tricuspid valve, atresia of the mitral valve, hypoplasia of the ventricles of the heart.

Abbreviations OAVC - patent atrioventricular canal TMS - transposition of the great vessels TADLV - total anomalous drainage of the pulmonary veins.

ICD-10 Q20 Congenital anomalies [malformations] of the heart 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 aliya [ developmental defects] 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 of the atria with localization inversion (Q89.3)

The location of the heart in the left half of the chest with the apex directed 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

Incorrect position of the heart

Congenital:

cardiac anomaly NOS
heart disease NOS

In Russia, the International Classification of Diseases, 10th revision (ICD-10) has been adopted as a single normative document for recording morbidity, reasons for the population's visits to medical institutions of all departments, and 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. No. 170

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

With changes and additions from WHO.

Processing and translation of changes © mkb-10.com

ICD 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 maternity hospital) and acquired form (manifests in adulthood).

Features of valve operation

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

The valve is located between the left chamber of the heart and the aorta. Externally, the heart valves look like pockets that surround the fibrous ring. Due to this structure, the load developed under the influence of blood is distributed evenly across 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 ability to contract.

The lumen of the opening of our anatomical formation differs from the diameter of the valve, which is called bicuspid (mitral-aortic). During ventricular systole, the blood pressure increases significantly, and therefore the valve experiences heavy 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 congenitality, which may be caused by infectious diseases suffered by the mother during pregnancy. They can appear in utero or in the first days of the baby’s life. A defect in one of the heart valves develops. This may be its complete absence, the presence of holes, or a change in the size ratio.

Acquired aortic heart defects are most often provoked by infectious (angina, sepsis, pneumonia, syphilis) and autoimmune processes (rheumatism, lupus erythematosus, dermatomyositis). But there are other less frequent diseases that contribute to the development of the 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 a combined type. Aortic stenosis is a pathological condition that is characterized by structural changes in the cusp, manifested by a sharp narrowing of the aortic mouth. This leads to the development of increased tension in this area and a decrease in cardiac blood output into the aorta.

Insufficiency is a pathological condition that represents a violation of the closure of the valves, which is formed as a result of their exposure to cicatricial processes or changes in the fibrous ring. It is characterized by a decrease in cardiac output, the passage of blood from the aorta back into the ventricular cavity, 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 left ventricular valves.

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

Full compensation stage. The patient makes no complaints, even if for him sport is the meaning of life, and he performs moderate physical activity every day, but upon external examination, slight changes in the cardiovascular system are noted.
Stage of latent heart failure. Patients note limitation of physical activity. The electrocardiogram shows mild signs of left ventricular hypertrophy, the aorta is dilated, and the development of cardiac volume overload is observed.
Subcompensation stage. During physical activity, patients note the appearance of shortness of breath, headache, and dizziness. The electrocardiogram shows left ventricular hypertrophy. Anatomical changes in the valves are noted. Hemodynamics are also reduced.
Stage of decompensation. Even with light exertion, shortness of breath and attacks of cardiac asthma occur.
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. Every doctor uses it when making a diagnosis.

Symptoms of aortic disease

Symptoms of aortic valve disease depend on the type. With stenosis, patients complain of palpitations, arrhythmias, pain in the cardiac region and shortness of breath, which can result in pulmonary edema. On auscultation, a systolic murmur is heard over the aortic orifice. In case of insufficiency, a complex symptom of carotid dancing, heart pain, and a combination of decreased diastolic pressure and increased systolic pressure are noted.

Common symptoms include:

fatigue;
headaches;
dizziness with sudden movements;
fatigue;
tinnitus;
loss of consciousness;
development of edema in the lower extremities;
increased pulsation in the area of large arteries;
increased heart rate.

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 external examination (propaedeutics deals with this) and instrumental research methods. When examining, doctors should pay attention to the skin and the pulsation of the central and peripheral arteries. Determination of the apex beat also has diagnostic significance (displaces in the 6-7 intercostal space). Diastolic murmur, weakening of the first and second sounds, the presence of vascular phenomena (auscultatory Traube sound) - these are all aortic heart defects.

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

electrocardiography;
phonocardiography;
echocardiography;
radiography;
Dopplerography.

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

Treatment

Collecting an anamnesis and 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 medicinal and surgical. The first type of therapy is used only in case of minor changes, which consists in prescribing medications that improve the flow of oxygen to the heart muscle, eliminate the sign of arrhythmia, and also normalize blood pressure.

In this regard, medications of the following pharmacological groups are prescribed: antianginal drugs, diuretics, antibiotics. The most relevant drugs that help normalize heart rate are Nitrolong, Sustak, Trinitrolong. They eliminate pain and prevent the development of angina pectoris by increasing blood oxygen saturation.

When the volume of circulating blood increases, it is customary to prescribe diuretics, as 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 treatment, there is a predominance of antibiotics of penicillin origin: Bicillin-1, Bicillin-2, Bicillin-3, as well as a drug from the glycopeptide group - Vancomycin.

You must always remember that the indication, dosage, combination and frequency of administration of a particular drug should be prescribed by the attending physician, whose recommendation is rule number one. A doctor’s lecture is a teaching material for every patient. After all, even minor fluctuations in dosage can lead to ineffective therapy or even a deterioration in health.

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

There are several options for surgery: balloon valvuloplasty and valve implantation. The main disadvantage of the first method is its possible repeated narrowing. If there is a concomitant pathology (or contraindications), the operation is not performed.

Cardiovascular system defects are a pressing problem for the entire population. This is the second most common pathology among cardiac diseases.

Timely implementation of drug therapy or surgical intervention significantly improves the quality of life and its duration, and reduces the development of many complications.

Patent ductus arteriosus (PDA) in children: what is this pathology?

Signs
Reasons
Diagnosis
Treatment
Prevention

Children are not immune from congenital anomalies, so it is important for parents to know what signs may indicate certain developmental defects. For example, about such a pathology as patent 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 because it provides fetal circulation necessary for the fetus, which does not breathe air in the womb. After the baby is born, a small duct closes in the first two days after birth and turns into a cord of connective tissue. In premature babies, this period can last up to 8 weeks.

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

By what signs can one suspect that the duct remains open?

The main symptoms in children under one year of age are shortness of breath, rapid heartbeat, slow weight gain, pale skin, sweating, and 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 when the duct is open, instead of rushing to the organs.

The severity of symptoms depends on the diameter of the duct. If it has a small diameter, the disease may be asymptomatic: this is due to a slight deviation from normal pressure in the pulmonary artery. With a large diameter of the open vessel, the symptoms are more severe and are characterized by several other 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 screaming, breathes quickly and holds his breath when crying and eating, then it is necessary to urgently consult a pediatrician, cardiologist or cardiac surgeon.

If a patent ductus arteriosus has not been diagnosed in a newborn, then as the child grows, the symptoms usually worsen. In children over one year of age and adults, the following signs of PDA can be observed:

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

For what reasons does the ductus arteriosus not close?

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

a number of other congenital heart defects (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;
infection with rubella during pregnancy;
chemical and radiation effects on a pregnant woman;
consumption of alcoholic beverages and drugs by pregnant women;
taking medications during pregnancy.

Moreover, statistics show that this pathology occurs twice as often in girls 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 noises do not stop after two days, the examination is continued using other methods.

A chest x-ray shows changes in the lung tissue, expansion of the cardiac borders and vascular bundle. High load on the left ventricle is detected using an ECG. To detect an increase in the size of the left ventricle and atrium, echocardiography or ultrasound of the heart is performed. To determine the volume of blood discharged and the direction of its flow, Doppler echocardiography is needed.

In addition, the pulmonary artery and aorta are probed, with the probe passing through the open duct from the artery into the aorta. During this examination, the pressure in the right ventricle is measured. Before performing aortography, a contrast agent is injected into the aorta with a catheter, which enters the pulmonary artery with the blood.

Early diagnosis is very important, since the risk of complications and severe consequences is very high, even with an asymptomatic course.

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

Treatment depends on the patient’s age, severity of symptoms, diameter of the pathological duct, existing complications and concomitant congenital malformations. The main methods of treatment: medication, catheterization, ligation of the duct.

Conservative treatment is prescribed in case of mild symptoms, in the absence of complications and other congenital defects. Treatment of patent ductus arteriosus with various drugs is carried out before the age of one year under constant medical supervision. For treatment, drugs can be used: non-steroidal anti-inflammatory drugs (ibuprofen, indomethacin), antibiotics, diuretics.

Catheterization 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 carries out all actions using a long catheter, which is inserted into a large artery.

Often, a patent ductus arteriosus is treated surgically by ligating it. If a defect is detected while listening to extraneous murmurs in the heart of a newborn, the duct is closed through surgery when the child reaches the age of 1 year in order to avoid possible infectious diseases. If necessary (with a large diameter of the duct and heart failure), the operation can be performed on a newborn, but it is optimal to do it before the age of three.

Don't forget about prevention

In order to protect the unborn child from developing PDA, during pregnancy you should avoid taking medications, stop smoking and drinking alcohol, and be wary of infectious diseases. If there are congenital heart defects in family members and relatives, you need to contact a geneticist even before the moment of conception.

What's the prognosis?

The vice is dangerous because there is a high risk of death. Patent ductus arteriosus can be complicated by a number of diseases.

Bacterial endocarditis is an infectious disease that affects the heart valves and can cause complications.
Myocardial infarction, in which necrosis of a section of the heart muscle occurs due to impaired blood circulation.
Heart failure develops when the diameter of the unclosed ductus arteriosus is large if left untreated. Signs of heart failure, which is accompanied by pulmonary edema, include: shortness of breath, rapid breathing, high pulse, low blood pressure. This condition poses a threat to the child's life and requires hospitalization.
Aortic rupture is the most severe complication of PDA, leading to death.

What is congenital heart disease

Congenital heart disease refers to the isolation of diseases that are combined by anatomical defects of the heart or valvular apparatus. Their formation begins during the process of intrauterine development. The consequences of defects lead to disturbances in intracardiac or systemic hemodynamics.

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

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 only and is NOT a guide to action!
Only a DOCTOR can give you an ACCURATE DIAGNOSIS!
We kindly ask you NOT to self-medicate, but to 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, every year in the world 0.8-1.2% of the total number of newborns are born with this pathology. Moreover, these defects account for about 30% of the total number of diagnosed congenital defects in fetal development.

Often the pathology in question is not the only disease. Children are also born with other developmental disorders, of which a third are musculoskeletal defects. Taken together, all the violations lead to a rather sad picture.

Congenital heart defects include the following list of defects:

Reasons

Among the causes of this pathology in newborns, I highlight the following factors:

constitute 5% of all identified 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 autosomal trisomy, an atrial and interventricular septal defect is formed, and sex chromosome abnormalities lead to coarctation of the aorta.

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

occupy up to 2% of all identified cases;
This includes viral diseases, taking 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, the child develops a heart septal defect;
amphetamines and anticonvulsants used have a negative effect;
Any medications must be approved by the attending physician.

The cause of pathology in newborns in the form of maternal diseases during pregnancy accounts for 90% of cases. Risk factors also include toxicosis during pregnancy in the first trimester, threats of miscarriage, genetic predisposition, endocrine system disorders 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 influence on pulmonary blood flow plays a key role.

In practice, experts divide the heart pathologies under consideration into three groups.

Hemodynamic disturbance

When the listed factors-causes are exposed and manifested in the fetus during development, characteristic disturbances occur in the form of incomplete or untimely closure of the membranes, underdevelopment of the ventricles and other anomalies.

Intrauterine development of the fetus is distinguished by the functioning of the ductus arteriosus and the oval window, which is in an open state. The defect is diagnosed when they still remain open.

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

Such phenomena are explained by the time of closure of the communication between the systemic and pulmonary circulation, individual characteristics and other defects. As a result, pathology can make itself felt some time after birth.

Treatment methods for heart disease are described in this article.

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

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

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

Symptoms

Symptoms appear depending on the type of anomaly, the nature and time of development of circulatory disorders. When the cyanotic form of the pathology develops in a sick child, a characteristic blueness of the skin and mucous membranes is noted, which increases in appearance with each strain. White defect 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 to breastfeed, and if he starts sucking, he quickly gets tired. Often, children with this pathology are diagnosed with tachycardia or arrhythmia; external manifestations include sweating, shortness of breath and pulsation of neck vessels.

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

Diagnostic measures

The disease in question is determined by using several methods of examining the child:

How to treat congenital heart disease

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

Treatment methods and methods depend on the types and severity of the pathology in question. If an anomaly of the interatrial or interventricular septum is detected, the child undergoes plastic surgery or suturing.

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

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

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

The anomaly itself does not disappear. It talks about the possibility of performing Fontannes, Senning and other types of operations. If surgery does not help in treatment, they resort to a heart transplant.

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

Prevention

Preventive actions for the development of this pathology in children should include careful planning of pregnancy, complete exclusion of unfavorable factors, as well as a preliminary examination to identify a risk factor.

Women who are on such an unfavorable list must undergo a comprehensive examination, which includes ultrasound and timely chorionic villus biopsy. If necessary, issues of indications for termination of pregnancy should be addressed.

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

A description of mitral heart disease can be found at the link.

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 reaching their first birthday.

Then comes a period of compensation, during which mortality rates drop to 5% of cases. It is important to identify the 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 intrauterine development of a child. It includes anatomical defects of the heart, valve apparatus, blood vessels, etc. Appears immediately after the birth of a child or has hidden symptoms.

Let's 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 defects. There are more than a hundred categories in this classifier alone. Conventionally, they are divided into “white” and “blue”.

White congenital heart disease - without mixing arterial and venous blood. There are 4 groups of such diseases:

1. Defects of the interatrial and interventricular septa (enrichment of the small circle).
2. Defects characterized by “depletion” of the pulmonary circulation (for example, isolated pulmonary stenosis).
3. Depletion of the systemic circulation (for example, aortic stenosis or coarctation).
4. Without hemodynamic disturbances.

With “blue” congenital heart disease, mixing of arterial and venous blood is observed. There are 2 groups of defects:

1. Enrichment of the pulmonary circulation (for example, transposition of the great vessels).
2. Depletion 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 defect. 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 suffered from in the first trimester of pregnancy (8-10 weeks are critical);
bad habits of the mother (drinking alcohol and smoking). Recently, the pathogenicity of paternal smoking has been proven;
maternal and paternal drug use (critical period of pregnancy - first trimester);
unfavorable hereditary predisposition;
pregnancy after 35 years;
high age of the father;
if the woman has had many abortions;
if a woman suffers from chronic pathologies that can be transmitted to the fetus.

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

A pregnant woman should know what is most harmful to her health. In some cases, additional examination of the father is necessary.

The congenital defect has common clinical signs. They often appear from a very 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, during a highly specialized medical examination, and for young men - when registering with a recruiting station. Some children may suffer from shortness of breath, bluish lips and skin, and frequent fainting.

A doctor can often detect the presence of a heart murmur by listening. However, not all heart defects can be distinguished by murmurs.

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

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 pale skin (or, conversely, blue discoloration) and excessive swelling of blood vessels. In addition, excessive pulsation can often be seen. The appearance of specific tones during auscultation is characteristic (they are noticeable only to specialists). The ECG shows characteristic changes and lengthening of the waves.
2. Heart failure. Characterized by attacks of suffocation. The intensity of such attacks depends on each specific case.
3. Systemic oxygen starvation (hypoxia). Characterized by a violation of the supply of oxygen to tissues. As a result, children lag behind in physical and mental development. The symptom of drumsticks (Hippocrates' fingers, often observed in tetralogy of Fallot with thickening of the phalanges in the form of a flask) and watch glasses (the so-called Hippocrates' nail with deformation of the nail plate) develops. It resembles the appearance of a watch glass. Sometimes a person may feel the plate moving.
4. Respiratory disorders of varying degrees of intensity and severity.

ICD 10 congenital heart defect

The ICD 10 specification for 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 is.

Thanks to progress in the field of surgery, 85% of newborns have an excellent opportunity to live a full and happy life, and adults have a chance to find a new life with a healthy heart. This fantastic information gives hope to all of us.

Types of heart defects

Let's find out how many types of heart defects there actually are. The UK National Health Service will help us with this, which has identified more than 30 positions, but it’s worth talking about only the 2 most important:

Congenital heart defect, ICD code 10 (Q20-Q28) blue type, more precisely, with cyanosis.

Unlike the first type, the blood is quite saturated with oxygen, however, it circulates in the body in an unusual way. In newborns, symptoms do not appear immediately, but over time. Blood pressure exceeds the permissible norm, 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 birth defects.

How to cure congenital heart disease?

Often such 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 correct solution. The operation is prescribed based on the ICD 10 specification for congenital heart disease.

Under the supervision of doctors. If the defects are not as severe, regular medical examinations 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 with specialists if anything worries you. Take care of your health, practice good habits and love the people around you.

There is no need to give up on yourself and accept the fact that you will always have to live with heart failure. We live in the 21st century, when it is possible to cure almost any disease or disorder. The main thing is to believe in a bright future and never give up hope, because it dies last.

ICD 10 acquired heart disease

Mitral stenosis.

II Acquired heart defects.

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

Based on their origin, defects are divided into:

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 dysfunction and hemodynamics; acquired defects are a complication of various diseases.

Combined defect is 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 - complaints of circulatory failure of the left ventricular or right ventricular type appear.

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 into the left atrium during ventricular systole, that is, incomplete closure of the MV valves.

Mitral valve prolapse (MVP) is a pathological sagging (bending) of one or both mitral valve leaflets 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 diseases 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.

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

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

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

c. REGISTER OF MEDICINES 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 1.06.1 Non-rheumatic 1.35.1 (with specification of etiology) Stage I - full compensation Stage II - latent heart failure

Stage V - terminal Combined aortic disease:

Without obvious predominance: stages and indications for surgical treatment correspond to those for aortic stenosis. Tricuspid stenosis:

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

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

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

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

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

Degrees of valve calcification

Individual lumps of calcium in the thickness of commissures or valves

Significant calcification of the valves and commissures without water

Mitral stenosis

In the region of the apex of the heart or somewhat laterally, diastolic tremor is detected - “cat's purring” - a phenomenon caused by low-frequency vibrations of the blood as it passes through the narrowed mitral orifice.

decrease in the speed of early diastolic covering of the anterior

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

decrease in the amplitude of opening of the mitral valve leaflet

(up to 8 mm or less);

enlargement of the left atrium cavity (antero-posterior size

can increase up to 70 mm);

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

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

Rice. 25. EchoCG for mitral stenosis (B-mode)

Assessing the condition of the mitral valve to determine whether

knowledge for performing percutaneous balloon valvotomy of the left

Diagnosis and assessment of the severity of associated valves

Repeated examination of patients diagnosed with mitral valve

nosas whose clinical picture of the disease develops over time

Assessment of hemodynamics and pressure gradient in the lungs

artery using Doppler echocardiography at rest in patients

com in case of discrepancy between objective and instrumental results

new research methods.

The need for percutaneous mitral balloon

valvotomy in properly selected patients.

Assessing the severity of mitral regurgitation in patients

in whom percutaneous mitral balm is expected to be performed

pubic valvotomy, in cases where clinical data are against

Assessment of the state of the pulmonary artery, left atrium and diastolic pressure in the left ventricular cavity when clinical symptoms

Combined heart defects are a group of chronic progressive diseases characterized by damage to two or more heart valves.

They account for 6.4% of cases of cardiac pathology, of which 93% are causally related to rheumatism and represent a simultaneous narrowing of the opening of one valve and insufficiency of the second.

Combined defects are always a consequence of chronic diseases affecting the endocardium (endocarditis, syphilis, atherosclerosis), and are characterized by a rapid deterioration of the patient’s condition.

An isolated defect is one type of defect in one valve (for example), combined - two types of defect in one valve (stenosis +), combined - a lesion of any type in two or more valves (+ aortic insufficiency).

Can a combined defect be combined at the same time? A combined defect may be part of a combined one (for example, stenosis and insufficiency of the mitral valve in combination with aortic insufficiency). A combined defect cannot be combined at the same time, since it affects several valves, while a combined defect affects only one.

Let's look at the 3 most common combined heart defects that can develop during life, and also give their ICD-10 codes.

Aortic-mitral valve disease

ICD-10 code: I08.0

What is it?

It is a combination with mitral insufficiency. Stenosis always develops first, and insufficiency of the second valve is secondary. Occurrence - 1.2 cases per 100,000 population.

Both valves belong to the left half of the heart, so the defect is characterized by impoverishment of the systemic circulation. Stenosis causes insufficient blood flow into the aorta, which quickly leads to hypoxia of the internal organs and (compensation). A compensatory increase in the force of contractions when it is impossible to pump blood into the aorta leads to increased load on the mitral valve, which is initially healthy (subcompensation).

Since the heart is not able to overcome the stenotic narrowing, the increased work of the second valve is not enough to replenish the blood flow, and its insufficiency develops with symptoms of congestion in the lungs (decompensation).

Symptoms

For mitral-aortic heart disease characterized by a combination of pulmonary and extrapulmonary symptoms. The skin is pale at first, later becomes bluish, and always cold. Patients experience chilliness regardless of the air temperature, complain of fainting, transient visual and hearing impairment, decreased urine output, enlarged liver, and hemoptysis.

Compensation. Shortness of breath during physical activity, interruptions in heart function, headaches, pallor, hair loss.
Subcompensation. The condition worsens when lying down, sleep is disturbed. Patients breathe through their mouths, lose weight, and are forced to wear warm clothes out of season. Swelling appears (patients limit water intake, which does not lead to an improvement in the condition), and the urine darkens.
Decompensation. Severe swelling of the legs and enlarged liver. Hemoptysis, turning into fear of death, stupor. and barely palpable. High risk of suffocation during pulmonary edema or fibrillation.

Diagnostics

Inspection. Pale bluish cold skin, shortness of breath, noisy breathing, wet cough (later with blood).
Palpation. Dense swelling of the legs and enlarged liver. High systolic pressure combined with low diastolic (for example, 180 over 60). The more pronounced the defect, the more frequent the pulse.
Percussion. Expansion of the borders of the heart up and to the left. Dulling of lung sounds due to fluid accumulation.
Auscultation. Mixed systole-diastolic murmur, decreased volume of 2 tones and increased volume of 1 tone, additional tones.
ECG. High amplitude and splitting of the R or P waves (ST segment widening).
Radiography. Shift of the heart borders to the left, fluid in the lungs.
Ultrasound. A method for confirming the diagnosis, allowing one to determine the type and severity of damage to both valves, as well as the degree of backflow of blood, by the location of which the predominance of the defect is judged.

Treatment

Treatment tactics for combined aortic valve disease are determined by complaints, clinical picture and ultrasound data. Indications for treatment depend on the stage: compensation - drug therapy, subcompensation - surgery, decompensation - palliative care.

Conservative therapy is suitable only at stage 1 and includes: beta-blockers (bisoprolol), antiarrhythmics (amiodarone), cardiac glycosides (in exceptional cases). No drug can completely compensate for stenosis, so it is impossible to cure the defect without surgery.
Surgical treatment is carried out at stage 2 in the absence of contraindications (acute conditions, old age). The operation of choice is valve replacement.

Mitral-tricuspid defect

ICD-10 code: I08.1.

Characteristic

This combined defect is represented by a combination of mitral valve stenosis with. Failure always develops secondarily within 2-3 years after stenosis. Occurrence - 4 cases per 100,000 population. The disease is characterized by rapid development.

The defect affects both halves of the heart, and therefore causes damage to the pulmonary system with venous stagnation in a large circle. Stenosis causes congestion in the lungs with an increase in pressure in them and (compensation). The load from the dilated ventricle is transferred to the tricuspid valve (subcompensation), the gradual thinning and stretching of which causes venous stagnation throughout the body (decompensation).

The defect is characterized by a rapid deterioration of the condition, a combination of cyanosis with simultaneous swelling of the superficial veins, and the development of dense and warm edema.

Clinical picture

Compensation. Dizziness, tinnitus, headaches and decreased vision, palpitations, shortness of breath, loss of appetite.
Subcompensation. Periodic wet cough at rest, inability to perform physical work, selection of shoes and clothes that do not fit, paresthesia (pins and needles), numbness of the extremities.
Decompensation. Severe swelling of the lower extremities, fluid in the abdominal cavity (frog belly symptom), enlarged liver, pulmonary edema.

How is it diagnosed?

Inspection. Diffuse cyanosis, dilated retinal veins (confirmed by an ophthalmologist), enlarged liver and legs.
Palpation. Dense warm swelling, tortuosity of superficial veins.
Percussion. Expansion of the borders of the heart upward and to the right.
Auscultation. Strengthening of 1 tone above the pulmonary artery, systole-diastolic murmur, rhythm disturbances.
ECG. Shift of the heart axis to the right, enlargement of the right ventricle (split R wave), arrhythmias.
Radiography. Expansion of the heart shadow to the right and upward, congestion in the lungs.
Ultrasound. A method for confirming the diagnosis, allowing to identify the degree of stenosis and backflow of blood, pulmonary edema, and the degree of insufficiency of the second valve. The predominance of the defect is localized in the valve where the reverse flow of blood is more pronounced.

Treatment

The choice of therapy is based on the stage of the disease and the number of complaints. Indications: compensation - drug treatment, subcompensation - surgical, decompensation - symptomatic.

Conservative therapy is indicated in the compensation stage. With its help, you can prepare the patient for surgery (but not cure). It includes: beta-blockers, diuretics and ACE inhibitors (perindopril, furosemide), antiarrhythmics (amiodarone), cardiac glycosides (rarely).
The operation is indicated in the subcompensation stage and in the absence of contraindications(age over 70 years, acute conditions). The method of choice is replacement of both valves or a combination of valvuloplasty with prosthetics.

Three-valve defect

ICD-10 code: I08.3.

Description

Combination of aortic stenosis with mitral and tricuspid valve insufficiency. Occurrence - 1 case per 100,000 population. The disease is characterized by extremely rapid decompensation (within 1 year).

Both circles of blood circulation are affected. Depending on which half of the heart the predominant lesion is located, the disease will begin either with arterial insufficiency or with venous stasis (compensation), always supplemented by an increase in pressure in the lungs and involvement of neighboring valves in the process (subcompensation). Lung congestion leads to increased pressure in the right ventricle and rapid depletion of the right ventricle, causing blood to pool and veins to dilate throughout the body (decompensation).

The prognosis is unfavorable due to the rapid depletion of myocardial fibers. Distinctive signs are early pulmonary edema, a tendency to pneumonia, weight gain, disorders of consciousness, digestion and urination.

Characteristic signs

Compensation. Paleness, quickly turning into blueness of the skin. Transient swelling of the legs, shortness of breath, decreased blood pressure.
Subcompensation. Interruptions in heart function, difficulty walking, shortness of breath at rest, constant headaches, loss of appetite. Worsening at night. The swelling rises to the knees and does not subside.
Decompensation. Loss of consciousness, decreased amount of urine, thinning and vulnerable skin, stupor, lack of response to any cardiac medications.

Diagnostics

Inspection. Noisy shortness of breath, difficulty speaking, wheezing, cough streaked with blood.
Palpation. The skin is warm, the swelling is dense. The liver protrudes from under the edge of the costal arch. A cardiac impulse, a “frog belly”, a decrease in pressure, and a rapid pulse are detected.
Percussion. Expansion of all boundaries of the heart, dullness of pulmonary sound (pulmonary edema).
Auscultation. Constant blowing noise superimposed on the “quail” rhythm, decreased volume of tones, moist rales.
ECG. , signs of hypertrophy of the ventricles and atria (bifurcation and increased amplitude of the P and R waves).
Radiography. Fluid accumulation in the lungs, spherical heart (cardiomegaly).
Ultrasound. Method of confirming the diagnosis. Ultrasound reveals the type of combination and the magnitude of the stenosis, as well as the degree of reverse blood flow. Depending on which valve has the greatest backflow, the predominance of the defect is determined.

How are they treated?

The choice of method depends on the complaints and general condition. The disease quickly leads to decompensation, so it is important to detect the patient in an early period. Indication for drug treatment is preparation for surgery, for surgery - subcompensation.

Conservative therapy is used in stage 1. It is impossible to cure the defect without surgery. Drugs used: cardiac glycosides (digoxin), diuretics, antiarrhythmics, adrenergic blockers.
Surgical treatment is indicated in the subcompensated stage and often combines commissurotomy (separation of fused folds), valvuloplasty (valve expansion) and prosthetics, which are performed in several stages.

Prognosis and life expectancy

The prognosis for life is relatively favorable if the following conditions are met:

Stage of the disease - 1 or 2;
Early execution of the operation;
Registration with a cardiologist;
Age up to 60 years;
There are no concomitant diseases.

Without treatment, the life of patients is limited to 3-5 years from the moment of development of the disease. As a rule, conservative therapy is used as a preparation for surgery, which is the only effective treatment method.

The decompensated stage of any defect in all patients leads to death within 0.5-1 year (death from pulmonary edema).

Combined heart disease is a severe complex of syndromes caused by simultaneous damage to several valve structures. The pathology is characterized by a progressive course and gradual loss of all cardiac functions, a variety of complaints and clinical manifestations. Treatment of combined defects should be immediate, comprehensive and lifelong.

Features of valve operation

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

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

The essence of aortic defects

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. Every doctor uses it when making a diagnosis.

Symptoms of aortic disease

Common symptoms include:

fatigue;
headaches;
dizziness with sudden movements;
fatigue;
tinnitus;
loss of consciousness;
development of edema in the lower extremities;
increased pulsation in the area of large arteries;
increased heart rate.

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

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

electrocardiography;
phonocardiography;
echocardiography;
radiography;
Dopplerography.

Treatment

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

Cardiovascular system defects are a pressing problem for the entire population. This is the second most common pathology among cardiac diseases.

Timely implementation of drug therapy or surgical intervention significantly improves the quality of life and its duration, and reduces the development of many complications.

Patent ductus arteriosus (PDA) in children: what is this pathology?

Signs
Reasons
Diagnosis
Treatment
Prevention

By what signs can one suspect that the duct remains open?

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

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

For what reasons does the ductus arteriosus not close?

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

a number of other congenital heart defects (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;
infection with rubella during pregnancy;
chemical and radiation effects on a pregnant woman;
consumption of alcoholic beverages and drugs by pregnant women;
taking medications during pregnancy.

Moreover, statistics show that this pathology occurs twice as often in girls 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 noises do not stop after two days, the examination is continued using other methods.

Early diagnosis is very important, since the risk of complications and severe consequences is very high, even with an asymptomatic course.

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

Don't forget about prevention

What's the prognosis?

The vice is dangerous because there is a high risk of death. Patent ductus arteriosus can be complicated by a number of diseases.

Bacterial endocarditis is an infectious disease that affects the heart valves and can cause complications.
Myocardial infarction, in which necrosis of a section of the heart muscle occurs due to impaired blood circulation.
Heart failure develops when the diameter of the unclosed ductus arteriosus is large if left untreated. Signs of heart failure, which is accompanied by pulmonary edema, include: shortness of breath, rapid breathing, high pulse, low blood pressure. This condition poses a threat to the child's life and requires hospitalization.
Aortic rupture is the most severe complication of PDA, leading to death.