Aortic heart disease code ICD 10. Mitral heart defects. Congenital heart defects

There is a huge difference between acquired cardiac disorders and congenital developmental anomalies, as they are in different ICD classes. Despite the fact that disturbances in the flow of arterial and venous blood will be the same, 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 class congenital anomalies 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 Funnel valve stenosis pulmonary artery
• 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. Vices in which infancy Only palliative operations are possible: 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 and [ 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)

Location of the heart in the left half chest with the apex directed to the left, but with transposition of the others 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 International classification diseases of the 10th revision (ICD-10) was adopted as a single regulatory document to take into account morbidity, reasons for the population’s visits 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. 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. It could be hers complete absence, presence of holes, change in size ratio.

Acquired aortic heart defects are most often provoked by infectious (angina, sepsis, pneumonia, syphilis) and autoimmune processes (rheumatism, lupus erythematosus, dermatomyositis). But others also highlight less frequent illnesses, which contribute to the development of the pathological condition. These include hypertension, atherosclerosis, age-related changes in blood vessels, calcification of the walls, 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 is 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.

Exists clinical classification, which distinguishes 5 stages of the disease. These include:

1. 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 of cardio-vascular system.
2. Stage of latent heart failure. Patients note limitation physical activity. The electrocardiogram shows mild signs of left ventricular hypertrophy, the aorta is dilated, and the development of cardiac volume overload is observed.
3. 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.
4. Stage of decompensation. Even with light exertion, shortness of breath and 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. 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 it is noted complex symptom carotid dancing, heart pain, a combination of decreased diastolic pressure and increased systolic.

TO general symptoms can be attributed:

• fatigue;
• headache;
• dizziness with sudden movements;
• fatigue;
• noise in ears;
• loss of consciousness;
• development of edema in the area lower limbs;
• 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 patient examinations.

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.

Wherein 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 anamnesis and interpreting the results of the study will help a qualified doctor reach Right way, make a 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 return it to normal. arterial pressure.

In this regard, it is appointed medicines such pharmacological groups: 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. The doctor's lecture is methodological material 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.

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

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

• Signs
• Causes
• 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, the 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;
• common infectious diseases respiratory tract, constant cough;
• cyanosis - turning blue skin 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 survey measure pressure in the right ventricle. 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 various drugs 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 sounds in the heart of a newborn, the duct is closed with 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 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 medicines, stop smoking and drinking alcohol, and beware 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 – infectious disease, which affects the heart valves and is dangerous for complications.
• Myocardial infarction, in which necrosis of an area 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 valve 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 retardation in development.

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 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 birth defects 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:

Causes

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, a defect of the interatrial and interventricular septa is formed, and abnormalities of the sex chromosomes 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 these 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, the 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 its manifestation with each strain. The 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, in children with this pathology, tachycardia or arrhythmia is detected, including external manifestations include sweating, shortness of breath and pulsation of blood vessels in the neck.

When chronic disorder The baby lags behind his peers in weight and 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. 1. Defects of the interatrial and interventricular septa (enrichment of the small circle).
2. 2. Defects characterized by “depletion” of the pulmonary circulation (for example, isolated pulmonary stenosis).
3. 3. Depletion of the systemic circulation (for example, aortic stenosis or coarctation).
4. 4. Without hemodynamic disturbance.

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

1. 1. Enrichment of the pulmonary circulation (for example, transposition of the great vessels).
2. 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 is sick chronic pathologies, capable of being 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 at such risk are referred to ultrasonography. 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 it is necessary additional research father.

Congenital defects have common Clinical signs. They often appear right 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, during a highly specialized medical examination, and for young men, when they are registered at 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. 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. 2. Heart failure. Characterized by attacks of suffocation. The intensity of such attacks depends on each specific case.
3. 3. Systemic oxygen starvation (hypoxia). Characterized by disruption of oxygen supply to tissues. As a result, children lag behind physically 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. 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 the right decision. The operation is prescribed based on the ICD 10 specification for congenital heart disease.

• Under the supervision of doctors. If the defects are not so serious, regular medical checkup in order to prevent the 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 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.

An isolated defect is one defect of one valve, for example, mitral regurgitation.

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

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.

On average, the latent period from the moment of rheumatic heart disease (carditis) to the development clinical manifestations the defect is about 20 years old, 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. 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).

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

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 specification 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 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 with mitral insufficiency Without obvious predominance: stages and indications for surgical treatment, as with mitral insufficiency Mitral valve prolapse 1.34.1 Aortic stenosis: Rheumatic 1.06.0 Non-rheumatic 1.35.0 (with specification 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 insufficiency:

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:

Rheumatic aortic stenosis with insufficiency 1.06.2 Non-rheumatic aortic (valvular) stenosis with insufficiency 1.35.2 (with clarification 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 and the date indicated. surgical treatment, nature of complications. 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 normally sized hole, 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, diastolic pressure increases in it. 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 occurs or with the release of a small amount of mucous sputum, often mixed with blood (hemoptysis). With high pulmonary hypertension, patients experience weakness, 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, as amended) Appearance patients with moderately severe mitral stenosis was 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, 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) 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 second 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 has 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, mitral annulus area, 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

Diagnosis and assessment of the severity of associated valves

Repeated examination of patients diagnosed with mitral valve

noses 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.

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

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

The cause of the defect is usually rheumatic damage to the left atrioventricular (mitral) valve.
With rheumatism, everyone is involved in the pathological process structural elements heart - endocardium (including heart valves), myocardium, pericardium and vascular system. However, the course of the disease is usually determined by the degree of damage to the valve apparatus.
The fibrous tissue that forms on the valve causes uneven thickening of the valves, which become denser and less mobile. Cicatricial wrinkling of the overgrown tissue often shortens the valves, causing valve insufficiency to develop. In this case, damage to the valves with fibrous compaction and shortening, and changes in the subvalvular apparatus due to cicatricial shortening of the chords and sclerotic changes in the papillary muscles also play a role. In later stages of development of the defect, calcium salts are deposited on the valve leaflets, which increases its rigidity and leads to a sharp limitation of mobility.
However, rheumatic endocarditis does not always cause a defect; sometimes the process ends in complete recovery or develops into marginal sclerosis of the valve, without disruptive its functions.
Adhesion and then fusion of the mitral valve leaflets is the main cause of mitral stenosis. The fusion lines of the valves are called commissures. Sometimes several years pass from the onset of endocarditis to the formation of pronounced stenosis. According to foreign authors, pure mitral stenosis often develops in cases where the rheumatic process is relatively mild.
In addition to the main cause of stenosis formation (rheumatic valve damage), there are also secondary nonspecific factors. These, according to a number of authors, include hemodynamic effects to which a working valve is constantly exposed; in this case, tears occur in the internal layers of the valves, especially in the area of ​​the commissures. The places of tears are covered with blood clots, and their further organization leads to fusion of the valves and progression of the defect.
When the left atrioventricular orifice is narrowed, the flow of blood from the left atrium into the left ventricle becomes difficult; part of the blood (residual volume) remains in the atrium, which causes its overflow.
With mitral valve insufficiency, part of the blood from the left ventricle at the moment of systole penetrates back into the atrium (regurgitation), which again causes its overflow.
Due to increased blood supply and high blood pressure in the cavity of the left atrium, the latter increases in size, and its muscle hypertrophies.
With pure mitral stenosis, the left atrium enlarges moderately and only in rare cases reaches enormous sizes (atriomegaly). In this case, reflex rhythm disturbances may occur - atrial fibrillation, atrial extrasystoles. The left atrium (especially its appendage) with mitral stenosis is the site of frequent localization of parietal thrombi.
An important place in the clinical picture of mitral stenosis is occupied by impaired pulmonary circulation, since this increases pressure in the left atrium, then in the pulmonary veins, capillaries and in the pulmonary artery system, and then in the right ventricle of the heart, which leads to its hypertrophy.
Since the pressure in the pulmonary veins and capillaries is increased, blood plasma is transudated into the interstitial tissue of the lungs, and sometimes into the lumen of the alveoli, and this causes a picture of stagnation in the pulmonary circle, characteristic of decompensated mitral stenosis, with hemoptysis and chronic interstitial pulmonary edema. Sometimes, against this background, there is a proliferation of connective tissue around the alveoli with the subsequent development of fibrosis, which further complicates pulmonary ventilation and gas exchange.
Due to the fact that the muscle of the right ventricle hypertrophies, it usually expands somewhat (myogenic dilatation). The consequence of this expansion may be the development of relative tricuspid valve insufficiency.
In this case, congestion from the right ventricle spreads to the right atrium, into the systemic circulation, which is clinically manifested by swelling of the neck veins, congestive liver, and edema. Thus, with decompensated mitral stenosis, total heart failure occurs over time.
With mitral regurgitation, the left atrium sharply enlarges, since part of the blood entering the left ventricle returns back to the atrium during systole. During ventricular diastole, the entire blood mass flows from the left atrium into the left ventricle, which expands and hypertrophies. Increased pressure in the left atrium creates increased pressure in the pulmonary circle, which again causes hypertrophy of the right ventricle.

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 it is?

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 exercise, 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 stasis big 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 abdominal cavity(symptom of “frog belly”), 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 with either arterial insufficiency or venous stagnation (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:

1. Stage of the disease - 1 or 2;
2. Early execution of the operation;
3. Registration with a cardiologist;
4. Age up to 60 years;
5. 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 preparation for surgery, which is the only effective method treatment.

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.

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

For people far from medicine, the phrase hypertension code according to ICD 10 does not mean anything. Even if the person himself suffers from this terrible disease. Many people understand that we are talking about high blood pressure, but what does the code with the strange abbreviation ICD have to do with it and why is it with the number 10 remains a mystery to them.

Everything is quite simple - each disease has its own code in a special disease classifier. There are several codes in this list for various manifestations of hypertension, and the incomprehensible ICD is a simple and understandable thing.

Despite the differences in the provision medical services different countries There is a unified international classification of diseases. It contains an impressive list of various diseases, accepted internationally.

The World Health Organization has been working on the creation of such classifiers for many years. The full name of this document (ICD) 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 letter and numeric meanings corresponding to a specific disease. One code contains 1 letter and 2 numbers indicating the disease, and the third number is 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 currently in effect, which is why it is designated 10. This version of the classification emerged as a result of long-term international cooperation through the search for compromises that are convenient for everyone. The consent of the parties is necessary to achieve the goals of the ICD.

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 statistical data on diseases and makes it possible to compare international data.

Thanks to this regulatory document, conditions for comparative analysis statistics on diseases and deaths occurring at different times in many countries. The appearance of codes has significantly simplified this task; now there is no need to write the full name of the disease, but rather indicate the corresponding code.

The international classifier allows us to determine the epidemiological situation, the prevalence of certain diseases, including the frequency of sharply “younger” hypertension. Arterial hypertension code according to ICD 10 describes more than one common disease; the code may differ due to the concept of target organs damaged by this disease.

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

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

The following organs are often affected by hypertension:

• Eyes;
• Kidneys;
• Heart;
• Brain.

In each of the organs, under the influence of high pressure, many processes can occur - all this is related to the work of the vessels that are primarily exposed to the negative effects of hypertension.

According to WHO, hypertension is in class IX, which includes diseases of the circulatory system. Hypertension code ICD 10, depending on the type, is designated by a code from I10 to I15, not including I14. With the exception of I10, each code has a qualifying 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 this is hypertension with predominantly simultaneous damage to the kidneys and heart. There is also a secondary unspecified hypertensive disease.

ICD 10 codes for various types of arterial hypertension

Hypertension code ICD 10, designated I11, including I11.0 and I11.9, denotes diseases with predominant damage to the heart. This subgroup does not include combinations of heart and kidney damage; they belong to codes I13 and have 4 internal codes - I13.0, I13.1, I13.2 and I13.9

I12 codes are for hypertension with renal involvement. The international classification distinguishes hypertension with development renal failure against the background of high blood pressure (I12.0). Code I12.9 indicates hypertension with kidney damage without the development of insufficiency of their functions.

The alphanumeric designations I15.0, I15.1, I15.2, I15.8, I15.9 hide various variations of secondary hypertensive disease. For primary hypertension, code I10 is assigned. Hypertensive crises are usually noted this way.

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

Hypertensive crisis according to ICD

A hypertensive crisis according to ICD 10 code refers to essential hypertension, although a sharp rise in pressure, life-threatening, can also occur with secondary manifestations of the disease. Code I10 is sometimes changed to other codes for hypertensive diseases after the diagnosis has been clarified. Quite often this occurs with hypertension, which affects both the heart and kidneys.

In Russia there is still no legally established classification of hypertensive crises. In the USA and a number of other countries, crises in hypertensive patients are divided into two types:

• Complicated;
• Uncomplicated.

The first of them requires urgent hospitalization, regardless of the ICD 10 code. The second can be treated at home, followed by treatment in a hospital. And this data can also be subjected to statistical processing.

Many countries have their own statistical centers that process various data. Thanks to the availability of disease classifications, 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 about any disease - hypertension according to ICD 10 occupies several different codes, and not 20-25 definitions with the names of specified diseases.

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

Prevention of hypertension

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

Proper nutrition with sufficient amounts of minerals and vitamins, normal physical activity, optimal weight and moderate salt intake can seriously help avoid hypertension. If you exclude excessive stress, alcohol abuse and smoking, then the likelihood of hypertension will become even less. And then there will be no need to worry about what ICD 10 code for hypertension will be.

Diagnosis and treatment of heart defects

The heart is a powerful muscle pump that works tirelessly. Its size is not much larger than a human fist. This organ consists of four chambers: the upper pair are 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 pass in one direction.

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

There are two groups: congenital and acquired defects.

Acquired vices

According to the International Classification of Diseases (ICD), 10th revision, acquired defects belong to sections 105–108 of the classifier. ICD is normative document, used to take into account morbidity, the reasons why the population turns to medical structures, as well as causes of mortality.

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

In 90 percent of cases, acquired heart defects arise 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 detected (no more than 1%).

Why do acquired defects occur?

Most common reasons development of such defects:

• rheumatism;
• infective endocarditis;
• atherosclerosis;
• syphilis;
• sepsis;
• cardiac ischemia;
• connective tissue diseases of a degenerative nature.

Classification of valve defects

There are different classification systems:

• by etiology: atherosclerotic, rheumatic, etc.;
• based on the degree of severity: which do not affect hemodynamics in the heart chambers, moderate and severe severity;
• according to 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. As the disease progresses, the following signs appear:

• shortness of breath is observed during physical activity (later it may appear at rest);
• pain in the heart (cardialgia);
• cardiopalmus;
• dry cough;
• swelling of the lower extremities;
• painful sensations 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);
• the voice becomes hoarse;
• a dry cough appears (a small amount of mucous sputum may form);
• heart pain (cardialgia);
• hemoptysis;
• excessive fatigue.

Aortic valve insufficiency

During the compensation stage, rapid heartbeat and pulsation behind the sternum are occasionally observed. Later the following symptoms appear:

• dizziness (possible fainting);
• cardialgia;
• shortness of breath appears during physical exertion (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 defect may not make itself felt for a long time. Only after narrowing the lumen of the aortic duct to 0.75 sq. see appear:

• pain of a compressive 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;
• Arrhythmia may occur.

Tricuspid valve stenosis

Symptoms of the disease:

1. The appearance of pulsation in the neck area.
2. Discomfort and pain in the right hypochondrium.
3. Decreased cardiac output, causing the skin to become cold.

Diagnosis and treatment

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

• general urine test;
• biochemical blood test;
• EchoCG;
• plain chest x-ray;
• contrast radiological technique;
• CT or MRI.

Acquired heart defects are treated with medication and surgery. The first option is used to correct the patient’s condition during the state of compensation of the defect or when the patient is being prepared for surgery. Drug therapy consists of a complex of drugs from various pharmacological groups (anticoagulants, cardioprotectors, antibiotics, ACE inhibitors, 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 surgical treatment of subcompensated and decompensated defects, heart defects can be subjected to the following types of intervention:

• plastic;
• saving valve;
• valve replacement with biological or mechanical prostheses;
• valve replacement with coronary bypass surgery;
• reconstruction of the aortic root;
• performing valve replacement for defects that arise as a result of infective endocarditis.

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

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

Preventive actions

In order to prevent valvular heart defects from developing, those pathologies that can provoke damage to the heart valves should be promptly treated, as well as healthy image life, which implies:

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

Congenital heart defects

According to the ICD 10th revision, congenital defects belong to section Q20-Q28. In the USA, the classification of heart muscle diseases is used with the codes “SNOP”; the International Society of Cardiology uses the code “ISC”.

What are congenital defects, 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 heart muscle, which occurs during the period from the 2nd to the 8th week of pregnancy, is called a congenital defect. According to statistics, this pathology is found in one baby out of a thousand. Achievements modern medicine make it possible to detect defects at the stage of perinatal development or immediately after birth. However, congenital heart defects remain unrecognized in 25% of cases, which is due to the physiological characteristics of the child or the difficulties of diagnosis. That is why it is so important to monitor the child’s condition, which will allow the disease to be identified in the early stages and treatment to begin. This task falls on the shoulders of the 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 valve.

The mechanism of development of the anomaly

In newborns, heart disease has several phases:

1. Adaptation: the child’s body goes through an adaptation period to the hemodynamic disturbances caused by the defect. If severe circulatory disorders occur, significant hyperfunction of the heart muscle occurs.
2. Compensation: is temporary, improvements in motor functions and general condition of the child are observed.
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 capillary-trophic insufficiency syndrome, 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

The congenital defect is accompanied by the following symptoms:

• the outer skin has a bluish or pale color (more often this is noticeable in the nasolabial area, on the fingers and toes). During breastfeeding, crying or straining of the child, these symptoms are especially pronounced;
• the baby is lethargic or restless when attached to the breast;
• the baby is not gaining weight well;
• often regurgitates 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;
• a bulge is visible in the area of ​​the heart.

Such signs should be a signal to immediately consult a doctor for an examination. During the initial examination, the pediatrician, having determined the heart murmur, 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.

According to indications, additional diagnostic methods, for example, cardiac probing. But there must be good reasons for this: for example, preliminary tests did not reveal the full clinical picture.

Treatment of birth defects

Children with a congenital defect must be observed by a local pediatrician and cardiologist. How many times should a child undergo a medical examination? In the first year of life, examinations by specialists are carried out quarterly. After your child is one year old, you need to be examined every six months. An examination should be performed monthly if the heart defect 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 doses, while the volume of food should be reduced by one meal.
3. Walks in the open air.
4. Light physical activity, but no signs of discomfort should appear in the child’s behavior.
5. Severe frost or direct Sun rays are a contraindication.
6. Prevention of infectious diseases.
7. Rational nutrition: control the amount of liquid absorbed, table salt, inclusion in the diet of foods that are rich in potassium (dried apricots, raisins, baked potatoes, etc.).

Congenital defects are treated with surgical and therapeutic methods. More often medications used to prepare a child for surgery or treatment after it.

Surgery is recommended if there is a severe heart defect. Moreover, depending on its type, the operation can be performed using a minimally invasive technique or with the child connected to a machine for artificial blood circulation 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 finally eliminating the problem.

If the operation is performed 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 advice from 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 status of the adults themselves. You need to take a responsible approach to your health, under no circumstances tempt fate or hope for luck in matters that concern it.

No one can say exactly how long a person with a heart defect can live. In each individual case, the answer to this question will be different. When people need surgery but stubbornly refuse it, the question that arises is not how long the 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 the right approach and adequate choice of treatment that 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 for an established diagnosis.

It is known that this cancer 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. Stomach cancer is one of the leading causes of death (about 10% in the world and 14% in Russia), therefore the information related to it is always relevant, especially for our country.

Stomach cancer is common along with lung, intestinal, skin oncological diseases 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, and in Russia, Brazil, and Japan it is high.

Russia shows the following ratios of survival to disease stages:

Stage 1 is detected in 10-20% of people, 60-80% of whom overcome the five-year period;
Stage 2 and 3 with local lesions lymphatic system 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 5-7% probability.

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

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

Often, diagnostic failures are associated with the similarity of symptoms of gastrointestinal and cardiac 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, ulcers, cholecystitis, pancreatitis, which are characterized by vomiting, gastrointestinal bleeding and pain.

Incorrect diagnosis and the absence of obvious signs prevents timely recognition of the main cause of deviations in older people.

The doctor and the patient should be alert to the following observed sensations characteristic of small cancer (two or three points at least):

Permanent heaviness and discomfort in the abdomen, belching, heartburn;
substernal pain felt in the back, difficulty swallowing;
prolonged pain in the abdominal area that is not relieved by medications;
constant fatigue and weakness with the slightest physical activity, dizziness;
decreased appetite up to aversion to food and rapid weight loss, change in mood for the worse (depression);
aversion to meat and fish, atypical pickiness in food;
rapid saturation with a very small amount of food, with no satisfaction;
abdominal enlargement due to fluid accumulation (ascites);
pale skin (anemia);
slight increase in temperature over a long period of time;
flatulence and defecation disorders (gas formation and unhealthy stool).

The patterns inherent in the disease have been identified 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;
severe 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 about a quarter of patients;
blanching of the mucous membranes - approximately 40%.

It is worth noting that depending on where the cancerous tumor develops, different signals are observed. This does not exclude general symptoms.

1. A malignant formation closer to the esophagus is accompanied by heart pain and restriction of swallowing function until the cessation of food intake, and dehydration progresses.
2. The affected middle region of the digestive organ is characterized by developing anemia (lack of hemoglobin) and gastric bleeding, which in its abundance changes the color and consistency of stool to pitch-black, liquid (and foul-smelling).
3. Damage closer to the duodenum has consequences such as stool disorders, vomiting and belching with the smell of a rotten egg.

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

The development of malignant tumors is a long process that goes through many stages. By highlighting the stages, the following systematization can be given.

1. Progression of mutations under the influence of carcinogens.
2. Pre-cancer illnesses.
3. Activation of oncology against the background of the influence of carcinogens and precancerous diseases.

Stage I

Internal causes include immune, infectious, age-related and hereditary factors. For example, people with blood group II get sick 20% more often, Ahelicobacter infection increases the chance of developing a cancer several times; After overcoming the fifty-year age threshold, the risks increase manifold.

External causes of the first stage include diet. Unlimited eating of spicy, salty, hot, fried, smoked, canned food, and pickled vegetables is dangerous. It should also be noted in this regard that there is no measure in the use of drugs (antibiotics, analgesics, hormonal drugs), excess starch, nitrates, nitrites, synthetic substances entering the body food additives(dyes, flavors, flavor enhancers). Finally, tobacco and strong alcohol have been proven to be unconditionally harmful in this regard.

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 stability of mucous membranes, and vitamin B12 and folic acid participate in normal cell division.

Stage II

III stage

The previous factors, in interaction with currently 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.

Emergence process malignant tumor not studied deeply enough. The absence of symptoms may last for years.

Gastric pathologies are varied.

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

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

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

Thus, the most common adenocarcinoma develops as follows:

Stage 1 - cancer cells do not go deeper into muscle tissue, they may spread to neighboring lymph nodes;
Stage 2 - the tumor begins to penetrate deep into the wall of the stomach, the lymph nodes are damaged;
Stage 3 - 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 shapes. In this regard, there are various definitions.

Signet ring cell carcinoma

This aggressive disease is of the diffuse type with squamous cell changes. It is characterized by a slight predominance of women among patients, as well as peaks of occurrence between 40-50 and 60-70 years. Almost half of the patients have blood group II. No relationship has been found with bad habits and external unfavorable factors, but the species is more often observed in cities.

Infiltrative cancer

A type of carcinoma with unclear boundaries of the neoplasm, one of the most malignant. The lesion is localized mainly in the thickness of the gastric wall. The foci of cancer cells are located 5-8 cm from each other. There is a noticeable hereditary predisposition and the possibility of development in relatively young people. Clinical stage accompanied by disturbances of peristalsis and vomiting. The tumor is stone-like and often spreads metastases.

Poorly differentiated cancer

In addition to the above 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 may be improved in accordance with the latest research.

Malignant tumors World Organization Health care divides into 11 types according to cellular forms. In 90% of cases or more, adenocarcinoma occurs - a neoplasm of glandular cells.

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

There is such a concept - screening - regular examination even in the absence of symptoms, which contributes to the timely detection of tumors. 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 bulb is inserted into the stomach through the mouth. The mucous membrane is collected from the area and the sample is sent to the laboratory (biopsy), which allows for an accurate diagnosis. The effectiveness of gastroscopic examinations 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) is a more advanced form of gastroscopy, in which the duodenum; the method can be modified with optical attachments (up to the possibility of observing the cellular level), however, it is inconvenient for differentiating benign and malignant neoplasms;
radiography of the gastrointestinal tract - for this, the patient ingests a contrast solution (barium) covering the mucous membrane, after which clear radiographs are obtained, showing even minor changes (the X-ray method can also be used for the chest, skull, limbs to identify metastases);
CT ( CT scan) and PET (positron emission tomography), which allows you to take X-rays from different angles and give a clear picture, to determine the spread of cancer formations with the help of radiopharmaceuticals (radioisotopes), used due to their selective concentration;
MRI (magnetic resonance imaging), which makes it possible to study layer by layer 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 stomach through an incision to determine the boundaries of the spread of a cancer cell formation in the abdominal cavity and the possibility of its removal, and tissue and fluid can be collected for examination;
Ultrasound (ultrasound), which helps detect the tumor and lesion itself lymph nodes, neighboring organs - can be carried out from the outside (including using degassed liquid to fill the organ under study) and from the inside (with an endoscopic probe);
tumor markers, once a diagnosis has been established, used to assess the response of tumor tissues to therapy;
tests - biochemical, immunological and general blood tests, stool occult blood test and urine test.

Science is making a lot of efforts to find the best means to combat the disease. So, in foreign cancer centers drugs with a “targeted” effect (destroying mutated tissues) are used - 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, endoscopic resection is performed (the instrument is inserted through the mouth or a minimal opening is performed). In simple cases, cauterization of tumors is used using electrothermal and laser effects.

2. Subtotal gastrectomy involves removing 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, palliative surgery is used - resection of cancer 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 low doses) is used before and after surgery, in the first case - neoadjuvant (to facilitate resection), in the second - adjuvant (to destroy cancer cells). Side effects Radiation usually causes bowel problems and nausea, but in some cases the method will help avoid surgery.

Often with radiation therapy Chemotherapy is also used (the same two types - neoadjuvant and adjuvant), the complex of which, with little chance of cure, prolongs the patient’s life and alleviates symptoms, but in general has a negative effect on the body. The consequences of chemotherapy (removable by restoration) are baldness, weight loss, liver damage from toxins, hematopoietic disorders, immunosuppression, etc. The effect is produced by antitumor antibiotics, cytotoxins and cytostatics in various combinations(two or three courses at different intervals).

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

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

Treatment tactics are chosen depending on the degree of carcinogenesis. Surgery is most often used in combination with chemotherapy.

Lifestyle and diet for patients

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

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

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

Alcohol, tobacco, coffee and food that cause irritation of the gastrointestinal mucosa are excluded. Due to the body losing a large amount of fluid (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 is no swelling).

Prevention

Don't forget the importance of a healthy diet.

To reduce your chances of developing cancer, you should strive to follow these tips:

Reducing the harmful effects of polluted environments and chemical compounds, attention to the quality of vegetables used for food (exclusion of carcinogens and nitrates);
consumption of milk, fresh foods containing vitamins and microelements;
reducing the amount of fatty, fried, spicy, smoked foods, preservatives, salt;
natural diet (avoiding overeating and irregular meals);
avoidance bad habits;
moderate medication use;
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 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 is 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:

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;
• headache;
• dizziness with sudden movements;
• fatigue;
• noise in ears;
• 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
• Causes
• 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, the 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 an area 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.