Cardiopulmonary failure ICD code 10. Cor pulmonale. What tests are needed

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

Other forms of pulmonary heart failure

Primary pulmonary hypertension

Kyphoscoliotic heart disease

Other secondary pulmonary hypertension

To indicate the underlying disease, use an additional code, if necessary.

Other specified forms of pulmonary heart failure

Excludes: Eisenmenger’s defect (Q21.8)

Pulmonary heart failure, unspecified

Chronic heart disease of pulmonary origin

Cor pulmonale (chronic) NOS

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International statistical classification of diseases and related health problems.

Pulmonary heart failure according to ICD 10

Nitrosorbide at pressure

Nitrosorbide is one of the most commonly used drugs to reduce blood pressure and relieve angina attacks. In addition, this medication is also able to combat the manifestations of heart failure and pulmonary hypertension (increased pressure in the pulmonary circulation). In accordance with the instructions, in some situations this drug can be prescribed as a component of complex treatment for arterial hypertension (high blood pressure).

Composition of the drug and form

The active component of the drug "Nitrosorbide" is the substance isosorbide dinitrate. This medication is available in tablet form. Additionally, it contains special forming substances that are responsible for the acceptable appearance of the drug and the shelf life. Nitrosorbide is produced in a dosage of 10 mg (0.01 g), available in packages of 40 or 50 tablets.

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Mechanism of action of the drug

Thanks to the drug, blood circulation in the heart improves and blood pressure decreases.

According to the instructions, isosorbide dinitrate belongs to the pharmacological group of nitrate antianginal (aimed at treating angina) medications. The mechanism of action of this medicinal substance is its effect on the wall, usually of venous vessels. Due to the action of this substance on the vascular wall, the lumen of the vessels expands, as a result of which blood circulation improves and the level of pressure in the pulmonary circulation decreases. In addition, thanks to this effect, blood circulation in the heart muscle improves and angina attacks are stopped. Isosorbide dinitrate helps to lower diastolic pressure in the cardiac ventricles, and also, to a much lesser extent, temporarily lowers the level of systemic mean arterial pressure.

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In what cases is Nitrosorbide prescribed?

• treatment and preventive therapy of angina attacks of various origins;
• component of complex treatment of chronic congestive heart failure and pulmonary hypertension;
• element of the therapeutic complex during the rehabilitation period after myocardial infarction.

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Instructions for using the medicine

According to the instructions and prescriptions of the doctor, the medicine should be taken half an hour before meals with water or placed under the tongue.

The approved instructions for the use of Nitrosorbide stipulate that the dosage volume and duration of the therapy period are determined by the attending physician for the individual patient on an individual basis. Generally, the recommended dosage of this drug is 10 mg or 20 mg 3 or 4 times a day. According to the instructions, this medicine should be taken half an hour before meals with a sufficient amount of water. The drug "Nitrosorbide" can also be taken sublingually (under the tongue). In the case of treatment of chronic heart failure and concomitant high pressure in the pulmonary circulation, it is primarily necessary to monitor hemodynamics in order to determine the volume of the required dosage of the drug. The instructions indicate that for the treatment of elderly patients, the dose may be reduced.

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Contraindications to the use of Nitrosorbide for blood pressure

The instructions for the drug "Nitrosorbide" prohibit its use in the following cases:

• personal intolerance to isosorbide dinitrate, other nitro compounds or other components of the medication;
• excessive arterial hypotension when the pressure level is less than 90 mm Hg. Art.;
• collapse, shock, acute circulatory failure;
• acute course of myocardial infarction;
• angina due to hypertrophic cardiomyopathy;
• high intracranial pressure;
• stroke;
• lactase deficiency, galactose intolerance;
• angle-closure glaucoma;
• constrictive pericarditis, mitral or aortic stenosis, cardiac tamponade;
• pulmonary edema of toxic origin, primary lung pathologies;
• severe anemia;
• simultaneous use of drugs based on phosphodiesterase inhibitors (medicines based on sildenafil, tadafil);
• severe renal and/or liver failure;
• pregnancy (1st trimester) and breastfeeding;
• childhood.

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Adverse events

In case of prolonged use of the drug "Nitrosorbide", the following side effects may develop:

• headaches, dizziness;
• changes in heart rate - tachycardia or bradycardia;
• arterial hypotension - excessive drop in blood pressure;
• facial redness, hot flashes, feeling of heat;
• peripheral edema;
• impaired concentration;
• dyspeptic disorders;
• allergic manifestations;
• “withdrawal” syndrome in case of abrupt cessation of medication;
• collapse, increased frequency of angina attacks, but in rare cases.

If any of the adverse events occur, you should contact your doctor as soon as possible.

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Intercompatibility with other medications

Nitrosorbide should not be used simultaneously with drugs based on phosphodiesterase inhibitors due to the risk of a sharp and excessive drop in blood pressure. This medication should not be combined with other vasodilators (dilators that widen the vascular lumen). In addition, according to the official instructions, it is not recommended to drink alcohol-containing drinks while using this drug, since alcohol enhances the effects of isosorbide dinitrate.

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Similar medicines

“Nitrosorbide” can be replaced with its analogues - medicines containing a similar active ingredient. The difference between them lies in the manufacturing company, trade name, and often in price and quality. Analogs of the drug “Nitrosorbide” are such medications as “Izo-Mik”, “Isoket”, “Kardiket Retard”, “Dikor Long”, “Izodinit”. It is prohibited to independently replace drugs. Only the attending physician can recommend replacing the drug.

The most common congenital heart defects in children and adults

Not all people without medical education are aware of congenital heart defects. This pathology is often detected in childhood and is difficult to treat. Drug therapy in this situation is ineffective. Many children with this pathology become disabled.

Heart defects from birth

The classification of congenital defects is known to every experienced cardiologist. This is a large group of diseases that affect various structures of the heart and blood vessels. The prevalence of this congenital pathology among children is about 1%. Some vices are incompatible with life.

In cardiology, various diseases are often combined with each other. Congenital and acquired heart defects worsen a person’s quality of life. The following types of defects are distinguished:

• accompanied by increased blood flow in the lungs;
• with normal blood flow in the pulmonary circle;
• with reduced blood supply to the lung tissue;
• combined.

There is a classification based on the presence of cyanosis. It includes congenital heart defects of the “blue” and “white” types. The most frequently diagnosed diseases are:

• open duct of Botallus;
• coarctation of the aorta;
• tetralogy of Fallot;
• valvular atresia;
• defect of the interventricular and interatrial septa;
• narrowing of the aortic lumen;
• pulmonary artery stenosis.

Main etiological factors

For congenital heart defects, the causes vary. The following etiological factors are of greatest importance:

• chromosomal disorders;
• gene mutations;
• viral infections of the mother during pregnancy;
• infection of a child with the rubella virus;
• alcohol syndrome;
• exposure to chemicals (heavy metals, pesticides, alcohol);
• irradiation;
• inhalation of polluted air;
• drinking poor quality water;
• harmful occupational factors;
• taking toxic medications during pregnancy.

The causes of heart defects often lie in external factors. Diseases such as chickenpox, herpes, hepatitis, toxoplasmosis, rubella, syphilis, tuberculosis, and HIV infection are dangerous for the unborn baby. Narcotic drugs (amphetamines) have a teratogenic effect.

Maternal smoking has an adverse effect on the development of the fetus. Congenital malformations are more often diagnosed in those children born to mothers with diabetes. Risk factors are:

• smoking;
• alcohol addiction;
• advanced age of father and mother;
• taking antibiotics in the 1st and 3rd trimesters;
• history of toxicosis;
• taking hormonal drugs.

The most frequently detected pathologies are patent ductus arteriosus and VSD.

Opening of the ductus arteriosus

During intrauterine development, the child’s cardiovascular system has its own characteristics. An example is patent ductus arteriosus. This is an anastomosis connecting the pulmonary artery and the aorta. Normally, this duct closes within 2 months after birth. This does not happen if the child’s development is impaired. Patent ductus arteriosus (PDA) persists.

Each doctor has a presentation on congenital heart defects. It should indicate that this pathology occurs quite often. In boys, PDA is diagnosed less frequently. Its share in the overall structure of congenital anomalies is about 10%. The disease is combined with another pathology - coarctation of the aorta, vasoconstriction or tetralogy of Fallot.

This heart disease is more often found in premature babies. After childbirth, it leads to a lag in physical development. In children weighing less than 1 kg, patent ductus arteriosus (PDA) is diagnosed in 80% of cases. Risk factors are:

• asphyxia during childbirth;
• burdened heredity;
• parents living in the highlands;
• carrying out oxygen therapy.

This disease belongs to the “pale” type of defects. This pathology has its own code in ICD-10. PDA is characterized by the discharge of oxygen-rich blood from the aorta into the pulmonary artery. This causes hypertension, which increases the load on the heart. This is how hypertrophy and dilatation of the left sections develop.

Patent ductus arteriosus (PDA) occurs in 3 stages. The most dangerous is grade 1. It can lead to death. Stage 2 is observed between the ages of 2 and 20 years. At this stage, overload of the right ventricle of the heart and an increase in the volume of blood volume in the pulmonary circulation system are detected. At stage 3, sclerotic changes develop in the lungs.

You need to know not only the causes of congenital heart defects, but also their symptoms. With an open duct, the following symptoms are possible:

• pale or cyanotic skin;
• disturbance of sucking;
• scream;
• straining;
• poor weight gain;
• developmental delay;
• frequent respiratory diseases;
• shortness of breath on exertion;
• heart rhythm disturbance.

Complications include the development of vascular insufficiency and inflammation of the endocardium. Many patients have no symptoms.

Aortic valve insufficiency

With congenital heart disease, the bicuspid and aortic valves can also be affected. This is a dangerous pathology that requires surgery. The aortic valve is located between the left ventricle and the aorta. Its flap closes, blocking the path for the return flow of blood. With a vice, this process is disrupted. Some of the blood rushes back into the left ventricle.

Its overflow causes stagnation of blood in the small circle. A good presentation on this topic states that the basis of hemodynamic disturbances are the following changes:

• congenital deficiency of one valve;
• valve sagging;
• different sizes of sashes;
• underdevelopment;
• the presence of a pathological hole.

This cardiac defect can be either congenital or acquired. In the first case, most often the violations are minor, but if the person is not treated, complications are possible. With this congenital heart defect, symptoms include chest pain, palpitations, swelling of the extremities, shortness of breath, tinnitus, occasional fainting, and dizziness.

Brain function is impaired. Objective signs of aortic valve insufficiency are:

• pale skin;
• pulsation of the carotid arteries;
• constriction of the pupils;
• protrusion of the chest;
• enlargement of the boundaries of the heart;
• pathological heart murmurs;
• heart rate acceleration;
• increase in pulse pressure.

All these symptoms appear if 20-30% of the blood returns back to the ventricle. Congenital malformations can appear in early childhood or later in life, when the heart cannot compensate for hemodynamic disturbances.

Aortic stenosis and atresia

In the group of congenital heart defects, the classification distinguishes coarctation of the aorta. This vessel is the largest. It has ascending and descending parts, as well as an arc. In the group of congenital heart diseases, coarctation of the aorta is common. With this pathology, a narrowing of the lumen or atresia (overgrowth) of the vessel is observed. The aortic isthmus is involved in the process.

This anomaly occurs in children. The share of this defect in the overall structure of cardiac pediatric pathology is about 7%. Most often, narrowing is observed in the area of ​​the terminal part of the aortic arch. The stenosis is shaped like an hourglass. The length of the narrowed area often reaches 5-10 cm. This pathology often leads to atherosclerosis.

Coarctation causes left ventricular hypertrophy, increased stroke volume and dilation of the ascending aorta. Collaterals (bypass network of vessels) are formed. Over time, they become thinner, which leads to the formation of aneurysms. Possible brain damage. You need to know not only what coarctation of the aorta is, but also how it manifests itself.

With this defect, the following clinical signs are revealed:

• weight gain;
• growth retardation;
• dyspnea;
• signs of pulmonary edema;
• decreased vision;
• headache;
• dizziness;
• hemoptysis;
• nosebleeds;
• convulsions;
• abdominal pain.

The clinical picture is determined by the period of development of coarctation. In the decompensation stage, severe heart failure develops. The percentage of deaths is high. Most often this is observed in older people. When brain function is impaired, neurological symptoms are pronounced. This includes chilliness of the extremities, headache, fainting, convulsions, and lameness.

Tetralogy and triad of Fallot

Congenital heart defects in adults and children include Fallot's triad. This is a combined defect that includes:

• defect of the septum between the atria;
• narrowing of the pulmonary artery;
• right ventricular hypertrophy.

The reason is a violation of embryogenesis in the 1st trimester of pregnancy. It is during this period that the heart is formed. Symptoms are caused primarily by narrowing of the pulmonary artery. This is a large vessel extending from the right ventricle of the heart. It's paired. They begin the large circle of blood circulation.

With severe stenosis, overload of the right ventricle occurs. The pressure in the cavity of the right atrium increases. The following violations occur:

• tricuspid valve insufficiency;
• decrease in minute blood volume in the pulmonary circle;
• increase in minute volume in a large circle;
• decrease in blood oxygen saturation.

Like other congenital malformations, Fallot's triad occurs hidden at an early age. A common symptom is fatigue. Along with the triad, tetralogy of Fallot often develops. It includes pulmonary stenosis, changes in the position of the aorta (dextroposition), right ventricular hypertrophy and VSD.

Tetralogy of Fallot belongs to the group of cyanotic (“blue”) defects. Its share is 7-10%. This pathology is named after the French doctor. This disease develops at 1-2 months of intrauterine development. Tetralogy of Fallot is often combined with ear abnormalities, mental retardation, internal organ defects, and dwarfism.

In the early stages, symptoms are nonspecific. Later, tetralogy of Fallot leads to dysfunction of the brain and other vital organs. The development of hypoxic coma and paresis is possible. Young children often suffer from infectious diseases. The main manifestation of the defect is cyanotic attacks accompanied by shortness of breath.

Patient examination plan

Treatment of congenital heart defects is carried out after excluding other (acquired) diseases. Any quality presentation states that the following studies are required to identify the disease:

• listening to the heart;
• percussion;
• electrocardiography;
• X-ray examination;
• registration of sound signals;
• Holter monitoring;
• coronary angiography;
• probing of cavities.

The diagnosis of congenital heart disease is made based on the results of instrumental studies. With congenital anomalies, the changes are very different. Tetralogy of Fallot shows the following symptoms:

• symptom of “drumsticks” and “watch glasses”;
• heart hump;
• rough noise in the 2-3 intercostal space to the left of the sternum;
• weakening of 2 tones in the pulmonary artery area;
• deviation of the electrical axis of the heart to the right;
• expansion of the boundaries of the organ;
• increased pressure in the right ventricle.

The main diagnostic criteria for patent ductus arteriosus are an increase in the boundaries of the myocardium, a change in its shape, simultaneous filling of the aorta and pulmonary artery with contrast, and manifestations of hypertension. If congenital malformations are suspected, brain function must be assessed. Studies such as computed tomography and magnetic resonance imaging are more informative. The valves (bicuspid, tricuspid, aortic and pulmonary) are assessed.

Therapeutic tactics for congenital defects

If there are “blue” or “white” heart defects, then radical or conservative treatment is required. If a patent ductus arteriosus is detected in a premature baby, it is necessary to use prostaglandin synthesis inhibitors. This allows you to speed up the healing of the anastomosis. If such therapy does not have an effect, then after 3 weeks of birth, surgery can be performed.

It can be open or endovascular. The prognosis for congenital and acquired heart defects is determined by the severity of hemodynamic disorders. When a person is diagnosed with tetralogy of Fallot, only surgical treatment is effective. All patients are hospitalized. When cyanotic attacks develop, the following are used:

In severe cases, an anastomosis is performed. Palliative operations are often organized. Bypass surgery is performed. The most radical and effective measure is plastic surgery of the ventricular septal defect. The patency of the pulmonary artery is necessarily restored.

If congenital coarctation of the aorta is detected, surgery should be performed early. In case of development of a critical defect, surgical treatment is indicated in the child under 1 year of age. In case of irreversible pulmonary hypertension, surgery is not performed. The most commonly used types of surgical interventions are:

• plastic reconstruction of the aorta;
• resection followed by prosthetics;
• formation of bypass anastomoses.

Thus, congenital heart abnormalities can appear both in childhood and later. Some diseases require radical treatment.

What is cardiopulmonary failure

Cardiopulmonary failure (according to ICD-10 code I27) is a disease characterized by a decrease in contractions of the heart muscle and the inability of the respiratory system to direct the required amount of oxygen into the vessels.

The disease can take an acute or chronic form. In both cases, the patient’s quality of life is significantly reduced.

The causes of the pathology may be associated with individual or systemic disorders in the functioning of the lungs and heart. The mechanism of development of the disease is due to increased pressure in the pulmonary circulation, which is responsible for the supply of oxygen to the blood.

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When blood is released into the pulmonary artery, the load on the right ventricle increases, resulting in hypertrophy (thickening of the myocardium).

Causes

Pulmonary hypertension leads to a violation of the enrichment of blood in the alveoli with oxygen. As a result, the myocardium of the right ventricle increases cardiac output in order to reduce tissue hypoxia (lack of oxygen). Over time, due to excessive stress, the muscles of the right side of the heart grow.

This period is called compensated; complications do not develop during it. If the pathology progresses, compensatory mechanisms are disrupted, which leads to irreversible changes in the heart: the stage of decompensation.

There are several groups of factors that cause the disease:

• chronic bronchitis, bronchiolitis obliterans;
• pulmonary enphysema;
• extensive pneumonia;
• sclerosis of lung tissue;
• bronchial asthma;
• chronic suppurative processes in pathologically altered bronchi.

The disease can develop with tuberculosis and pulmonary sarcoidosis.

• pulmonary artery atherosclerosis;
• tumor in the middle parts of the chest cavity;
• compression of the “right heart” by an aneurysm;
• pulmonary arteritis;
• pulmonary artery thrombosis.

• curvature of the spine in the lateral and anteroposterior direction (kyphoscoliosis);
• polio;
• ankylosing spondylitis;
• impaired innervation of the diaphragm.

Under the influence of vascular factors, the arteries narrow. This occurs due to blockage by a blood clot or thickening of the vascular walls due to the inflammatory process.

In the presence of deforming and bronchopulmonary factors, the vessels are compressed, the tone of their walls is disturbed, and the lumens are fused with connective tissue. As a result of such processes, body tissues experience a lack of oxygen.

In medical practice, the disease most often develops against the background of:

• pneumosclerosis;
• pulmonary vasculitis;
• emphysema;
• thromboembolism;
• pulmonary edema;
• pulmonary artery stenosis.

Symptoms of cardiopulmonary failure

Read about circulatory support systems in the treatment of heart failure here.

The disease has pronounced symptoms, which rarely go unnoticed.

Acute cardiopulmonary failure occurs:

• with sudden spasms or thrombosis of the pulmonary trunk;
• extensive pneumonia;
• asthmatic status;
• accumulation of air or liquid in the pleural cavity;
• severe form of incompetence of the bicuspid heart valve;
• chest injuries;
• impaired operation of the prosthetic valve.

Under the complex influence of unfavorable factors, hemodynamics are sharply disrupted. This manifests itself in the form of insufficient blood circulation of the “right heart”.

The disorder is accompanied by the following symptoms:

• rapid breathing;
• decreased blood pressure; in the acute form, collapse may occur;
• shortness of breath, difficulty breathing;
• enlarged veins in the neck;
• lack of air, suffocation;
• cold extremities;
• bluish coloration of the skin;
• cold sweat;
• chest pain.

The acute form of the disease may be accompanied by pulsation in the epigastric region of the dilated right ventricle. The x-ray shows an increase in the mediastinum to the right and upward; the electrocardiogram shows overload of the “right heart”.

When listening to the heart, the “gallop” rhythm and muffled tones are clearly revealed. In case of acute blockage of the pulmonary artery by a thrombus, pulmonary edema and pain shock rapidly develop, which can lead to rapid death.

• shortness of breath at rest, worsening when lying down;
• ischemic pain in the heart area;
• enlargement of the veins in the neck, which persists when inhaling;
• decreased blood pressure, tachycardia;
• bluish skin tone;
• enlarged liver, heaviness on the right side;
• swelling that cannot be treated.

With increasing death of all tissues (terminal state), serious damage to the brain and kidneys develops. These processes are expressed in the form of lethargy, apathy, impaired mental functions, and cessation of urine output. In the blood, due to a lack of oxygen, the concentration of hemoglobin and red blood cells increases.

Severity

The chronic form of the disease is characterized by a slow and subtle increase in symptoms. Based on this, there are four degrees of severity of the disease:

Chronic cor pulmonale ICD 10

Other forms of pulmonary heart failure (I27)

Pulmonary (arterial) hypertension (idiopathic) (primary)

In Russia, the International Classification of Diseases, 10th revision (ICD-10) has been adopted as a single normative document for recording morbidity, reasons for the population's visits to medical institutions of all departments, and causes of death.

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Chronic obstructive pulmonary disease - description, causes, symptoms (signs), diagnosis, treatment.

Short description

Chronic obstructive pulmonary disease (COPD) is a disease characterized by a partially irreversible, steadily progressive limitation of airflow caused by an abnormal inflammatory response of lung tissue to damaging environmental factors. The term “COPD” refers to a combination of chronic bronchitis and secondary emphysema.

Classification of COPD is based on the severity of the disease Stage 0 (increased risk of developing COPD): normal spirometry, chronic symptoms (cough, sputum production) Stage I (mild): FEV 1/FVC<70%. ОВФ 1 ³ 80% от должного. Наличие/отсутствие хронических симптомов (кашель, продукция мокроты) Стадия II (среднетяжёлое течение): ОФВ 1 /ФЖЕЛ <70%. 30% £ОВФ1 £ 80%от должного (IIA 50% £ ОВФ 1 £ 80%). (IIБ 30% £ ОВФ1 £ 50%). Наличие/отсутствие хронических симптомов (кашель, продукция мокроты) Стадия III (тяжёлое течение): ОФВ 1 /ФЖЕЛ <70%. ОВФ1 <30% от должного или ОВФ 1 <50% от должного, в сочетании с дыхательной недостаточностью (Р а О 2 менее 8,0 кПа в сочетании или без Р а СО 2 более 6,7 кПа при дыхании на уровне моря) или клиническими признаками правожелудочковой недостаточности.

Statistical data. 1849.2 cases in the population over 18 years of age; 548.8 cases - 15–17 years; 307.7 cases - under 14 years of age. According to WHO, the prevalence of COPD among men is 9.34/1000, and among women - 7.33/1000. People over 40 years predominate. COPD is in 6th place among the leading causes of death in the world, in 5th place in developed countries of Europe, and 4th in the USA.

Causes

Etiology. The development of COPD is promoted by smoking, occupational hazards (dust, irritants, smoke, fumes, etc.), air pollution (at home - products of fossil fuel combustion, odors of cooked food, heating appliances). Severe respiratory infections in childhood predispose to the development of COPD throughout life. The risk of developing COPD is inversely proportional to the level of socioeconomic status.

Genetic features. COPD does not develop in all individuals who have antitrypsin defects, leading to the early development of panlobular emphysema. Emphysema due to deficiency of: a 1 - antitrypsin (*107400, mutations of the PI, AAT, 14q32.1, Â genes) - liver cirrhosis, absence of a 1 - globulin peak in electrophoresis of serum proteins, a small amount of a 1 - serum antitrypsin and panlobular ( covering all sections) emphysema, more pronounced in the basal sections of the lungs. Insufficiency of a 2 - macroglobulin. (*103950, 12p13.3–p12.3, Â).

Pathogenesis. The inflammatory process is induced by various pollutants and gases. Tobacco smoke has a direct damaging effect on lung tissue and the ability to cause inflammatory changes. The chronic inflammatory process of the respiratory tract, pulmonary parenchyma and blood vessels is characterized by an increased number of macrophages, T lymphocytes and neutrophils. Activated inflammatory cells release a large number of inflammatory mediators (leukotriene B4, IL-8, TNF-a, etc.), which can damage the structure of the lungs and maintain inflammation. In addition to inflammation, an imbalance of proteolytic enzymes and antiproteinases and oxidative stress are of significant importance in the pathogenesis of COPD. Bronchitic component At an early stage in small bronchi (diameter<2 мм) обнаруживают бактериальное обсеменение, воспаление, закупорку слизью, перибронхиолярный фиброз и облитерацию При сформировавшейся патологии - гиперплазия слизистых желёз, серозное воспаление и отёк; бронхоспазм и закупорка дыхательных путей секретом приводят к бронхиальной обструкции Эмфизематозный компонент Разрушение альвеолярных стенок и поддерживающих структур ведёт к образованию значительно расширенных воздушных пространств Повышение воздушности ткани лёгких приводит к сужению дыхательных путей при динамическом спадении во время выдоха (экспираторный коллапс бронхов) Разрушение альвеолярно - капиллярной мембраны снижает диффузионную способность лёгких.

Pathomorphology. Pathological changes in large and peripheral bronchi, pulmonary parenchyma and pulmonary vessels. In the trachea, bronchi and bronchioles with a diameter of more than 2–4 mm, inflammatory cells infiltrate the surface epithelium. Hypersecretion of mucus is also observed. Damage and restoration of the bronchial wall are repeated cyclically, its structural remodeling occurs, the collagen content increases and the formation of scar tissue narrows the lumen and leads to fixed airway obstruction. Microdestruction of the pulmonary parenchyma leads to the development of centrilobular emphysema, hence dilatation and destruction of the respiratory bronchioles. Thickening of the vascular intima is their first structural change with a further increase in the content of smooth muscle elements and infiltration of the vascular wall with inflammatory cells. As COPD progresses, the accumulation of large amounts of SMC, proteoglycans and collagen contributes to further thickening of the vascular wall.

Symptoms (signs)

Complaints: epidemiological criterion for COPD is chronic productive cough lasting more than 3 months a year for 2 or more years in a row; shortness of breath of an expiratory nature, increasing over time, intensifying during an exacerbation.

Physical examination: upon examination (in later stages) the participation of accessory respiratory muscles; on auscultation - prolonged exhalation, dry scattered wheezing with quiet breathing, wheezing with forced exhalation, moist wheezing more often with exacerbation; with percussion - from a boxy tint to a distinct boxy sound. Tachycardia, accent of the second tone over the pulmonary artery.

Laboratory data: during an exacerbation, leukocytosis, increased ESR, neutrophil band shift; in severe cases - polycythemia (erythrocytosis), hypercapnia, hypoxemia, decreased content of a 1 - antitrypsin in the serum and the absence of a 1 - globulin peak in serum protein electrophoresis; bacteriological examination of sputum makes it possible to identify the causative agent of exacerbation of chronic bronchitis and exclude tuberculosis.

Instrumental data Spirometry is a criterion for diagnosis and severity (decrease in forced expiratory volume in 1 s (FEV 1) with a concomitant decrease in the Tiffno index, minimal dynamics of parameters (less than 15% of the original) after the introduction of bronchodilators; forced vital capacity is within normal limits or reduced; increase in residual lung volume; diffusion capacity within normal limits or reduced ECG: increasing signs of pulmonary hypertension, hypertrophy of the right heart, chronic pulmonary heart EchoCG: signs of pulmonary hypertension Chest X-ray in COPD reveals increased and deformed bronchopulmonary pattern, in emphysema - the heart normal size, increased airiness of the lung tissue, flattening of the diaphragm and bullous changes

Types of COPD. There are 2 classic types of COPD, which have different names. Emphysematous patients with shortness of breath (COPD type A) are classified as “pink puffers”, bronchitis patients with a characteristic cough (COPD type B) are referred to as “blue puffers”.

“Pink puffers” suffer predominantly from emphysema with a slowly progressive course, more often after 60 years of age Loss of body weight Progressive shortness of breath on exertion Productive cough Auscultation: weakened breathing, isolated wheezing Hypoxemia and hypercapnia are moderately expressed The diffusion capacity of the lungs is reduced The respiratory function indicators improve little after inhalation of bronchodilators.

“Blue edema” suffers predominantly from chronic bronchitis Productive cough Episodic shortness of breath Increased body weight at a young age Auscultation: dry rales Cor pulmonale often develops with signs of right ventricular failure Severe hypoxemia and hypercapnia as a result of fatigue of the respiratory muscles or decreased central stimulation of breathing Polycythemia Improved respiratory function after inhalation bronchodilators The diffusion capacity of the lungs is slightly affected.

More often, mixed variants are observed, combining the signs of “pink puffs” and “blue swelling”.

Diagnostics

Diagnostic tactics. The basis of diagnosis when contacting is to identify patients with chronic cough and exclude other causes of cough (sputum examination, radiography); optimal diagnosis is detection of FVD during a screening study (decrease in RVF 1).

Accompanying illnesses. aggravating the course and worsening the prognosis of COPD: obesity, sleep apnea syndrome, heart failure, diabetes, arterial hypertension.

Treatment

Treatment General tactics: stop exposure of the lungs to harmful factors. Regimen and diet: stay in the fresh air, avoid hypothermia, contact with patients with respiratory infections; annual anti-influenza and anti-pneumococcal vaccination; physical training programs Drug treatment outside of exacerbation: anticholinergic bronchodilators (ipratropium bromide) or combinations with b 2 - agonists (inhalation from a can, through a spacer or nebulizer), long-acting theophyllines. Inhaled GCs with the effectiveness of an initial two-week course of systemic steroids (improved respiratory function parameters). Expectorants with antioxidant properties (acetylcysteine, ambroxol). Regular use of cough suppressants and narcotic drugs for COPD is contraindicated. a 1 - Antitrypsin - in case of its deficiency. Long-term oxygen therapy at stage III for hypoxia (p a O 2 less than 60 mm Hg) Drug treatment for exacerbations: inhaled b 2 - short-acting agonists (salbutamol) during therapy with anticholinergic drugs (ipratropium bromide), methylxanthines with caution (serum control concentration). GC intravenously or orally (30–40 mg 10–14 days per os). Antibiotics only in the presence of purulent sputum (aminopenicillins, cephalosporins of II - IV generations, new macrolides, pneumotropic fluoroquinolones of III - IV generations). At stage III, oxygen therapy is supplemented with auxiliary ventilation Surgical treatment: bullectomy, surgical correction of pulmonary volume, lung transplantation Features of treatment in old age are determined by the presence of concomitant diseases (limitation of xanthines, sympathomimetics, combination with cardiovascular drugs) Features of management of pregnant and lactating women are associated with increasing hypoxemia for COPD (oxygenation control), possible teratogenicity of the drugs used.

Complications and their treatment. Frequent infections (antibacterial therapy); secondary pulmonary hypertension and cor pulmonale (oxygenotheria, decreased pulmonary pressure); secondary polycythemia (oxygen therapy); acute or chronic respiratory failure.

Prevention. Fighting smoking, improving production and the environment.

Course and prognosis of the disease. The course is steadily progressing. The prognosis depends on the rate of decline in FEV 1 .

Synonyms: chronic obstructive bronchitis, obstructive emphysema.

Abbreviations FEV 1 - forced expiratory volume in the first second FVC - forced vital capacity.

ICD-10 J43 Emphysema J44 Other chronic obstructive pulmonary disease

Pulmonary heart failure ICD 10

I26 Pulmonary embolism

Included: pulmonary (arteries) (veins):

I27.0 Primary pulmonary hypertension

EUPHYLLINE

Information on the drug is available only to specialists.

ICD 10

CLASS IX: DISEASES OF THE CIRCULATORY SYSTEM (I00-I99)

diseases of the endocrine system, nutritional disorders and metabolic disorders (E00-E90)

congenital anomalies, deformities and chromosomal disorders (Q00-Q99)

complications of pregnancy, childbirth and the puerperium (O00-O99)

selected conditions occurring in the perinatal period (P00-P96)

symptoms, signs and abnormalities identified by clinical and laboratory tests, not classified elsewhere (R00-R99)

systemic connective tissue disorders (M30-M36)

injuries, poisoning and some other consequences of external causes (S00-T98)

ACUTE RHEUMATIC FEVER (I00-I02)

I00 Rheumatic fever without mention of cardiac involvement

I01 Rheumatic fever with cardiac involvement

Excluded: chronic heart disease of rheumatic origin (I05-I09) without the simultaneous development of an acute rheumatic process or without phenomena of activation or relapse of this process. If you have any doubts about the activity of the rheumatic process at the time of death, you should refer to the recommendations and rules for coding mortality set out in Part 2.

I01.0 Acute rheumatic pericarditis

Excludes: pericarditis not classified as rheumatic (I30.-)

I01.1 Acute rheumatic endocarditis

I01.2 Acute rheumatic myocarditis

I01.8 Other acute rheumatic heart diseases

I01.9 Acute rheumatic heart disease, unspecified

I02 Rheumatic chorea

Included: Sydenham's chorea

I02.0 Rheumatic chorea involving the heart

I02.9 Rheumatic chorea without cardiac involvement

CHRONIC RHEUMATIC HEART DISEASES (I05-I09) I05 Rheumatic diseases of the mitral valve

Included: conditions classified under I05.0

and I05.2-I05.9, specified or unspecified as rheumatic

Excluded: cases specified as non-rheumatic (I34.-)

I05.0 Mitral stenosis

I05.1 Rheumatic mitral valve insufficiency

I05.2 Mitral stenosis with insufficiency

I05.8 Other mitral valve diseases

I05.9 Mitral valve disease, unspecified

I06 Rheumatic diseases of the aortic valve

Excluded: cases not specified as rheumatic (I35.-)

I06.0 Rheumatic aortic stenosis

I06.1 Rheumatic aortic valve insufficiency

I06.2 Rheumatic aortic stenosis with insufficiency

I06.8 Other rheumatic diseases of the aortic valve

I06.9 Rheumatic aortic valve disease, unspecified

I07 Rheumatic diseases of the tricuspid valve

Excluded: cases specified as non-rheumatic (I36.-)

I07.0 Tricuspid stenosis

I07.1 Tricuspid insufficiency

I07.2 Tricuspid stenosis with insufficiency

I07.8 Other diseases of the tricuspid valve

I07.9 Tricuspid valve disease, unspecified

I08 Lesions of several valves

Included: cases specified or unspecified as rheumatic

rheumatic diseases of the endocardium, valve unspecified (I09.1)

endocarditis, valve unspecified (I38)

I08.0 Combined lesions of the mitral and aortic valves

I08.1 Combined lesions of the mitral and tricuspid valves

I08.2 Combined lesions of the aortic and tricuspid valves

I08.3 Combined lesions of the mitral, aortic and tricuspid valves

I08.8 Other multiple valve diseases

I08.9 Multiple valve lesions, unspecified

I09 Other rheumatic heart diseases

I09.0 Rheumatic myocarditis

Excludes: myocarditis not specified as rheumatic (I51.4)

I09.1 Rheumatic diseases of the endocardium, valve unspecified

Excludes: endocarditis, valve not specified (I38)

I09.2 Chronic rheumatic pericarditis

Excludes: conditions not specified as rheumatic (I31.-)

I09.8 Other specified rheumatic heart diseases

I09.9 Rheumatic heart disease, unspecified

pulmonary hypertension (I27.0)

neonatal hypertension (P29.2)

complicating pregnancy, childbirth or the postpartum period (O10-O11, O13-O16)

involving coronary vessels (I20-I25)

I10 Essential (primary) hypertension

Excluded: with vascular damage:

I11 Hypertensive heart disease [hypertension primarily affecting the heart]

Included: any condition listed in sections I50.-, I51.4-I51.9 due to hypertension

I11.0 Hypertensive [hypertensive] disease predominantly affecting the heart with (congestive) heart failure

I11.9 Hypertensive [hypertensive] disease with predominant cardiac involvement without (congestive) heart failure

I12 Hypertensive [hypertensive] disease with predominant kidney damage

arteriosclerotic nephritis (chronic) (interstitial)

any condition specified in headings N18.-, N19.- or N26.- in combination with any condition specified in heading I10

Excludes: secondary hypertension (I15.-)

I12.0 Hypertensive [hypertensive] disease with predominant kidney damage with renal failure

I12.9 Hypertensive [hypertensive] disease with predominant kidney damage without renal failure

I13 Hypertensive [hypertensive] disease with predominant damage to the heart and kidneys

any condition specified in heading I11.-, in combination with any condition specified in heading I12.-

I13.0 Hypertensive [hypertensive] disease with predominant damage to the heart and kidneys with (congestive) heart failure

I13.1 Hypertensive [hypertensive] disease with predominant kidney damage with renal failure

I13.2 Hypertensive [hypertensive] disease predominantly affecting the heart and kidneys with (congestive) heart failure and renal failure

I13.9 Hypertensive [hypertensive] disease with predominant damage to the heart and kidneys, unspecified

I15 Secondary hypertension

Excluded: with vascular involvement:

I15.0 Renovascular hypertension

I15.1 Hypertension secondary to other renal lesions

I15.2 Hypertension secondary to endocrine disorders

I15.8 Other secondary hypertension

I15.9 Secondary hypertension, unspecified

CORONARY HEART DISEASE (I20-I25)

Included: with mention of hypertension (I10-I15)

I20 Angina [angina pectoris]

I20.0 Unstable angina

I20.1 Angina pectoris with documented spasm

I20.8 Other forms of angina

I20.9 Angina pectoris, unspecified

I21 Acute myocardial infarction

Included: myocardial infarction, specified as acute or specified duration of 4 weeks (28 days) or less after the onset of acute onset

Transported into the past (I25.2)

Specified as chronic or lasting more than 4 weeks (more than 28 days) from onset (I25.8)

some current complications after acute myocardial infarction (I23.-)

post-infarction myocardial syndrome (I24.1)

I21.0 Acute transmural infarction of the anterior myocardial wall

I21.1 Acute transmural infarction of the inferior wall of the myocardium

I21.2 Acute transmural myocardial infarction of other specified locations

I21.3 Acute transmural myocardial infarction of unspecified localization

I21.4 Acute subendocardial myocardial infarction

I21.9 Acute myocardial infarction, unspecified

I22 Recurrent myocardial infarction

Includes: recurrent myocardial infarction

Excludes: myocardial infarction, specified as chronic or with a specified duration of more than 4 weeks (more than 28 days) from onset (I25.8)

I22.0 Repeated infarction of the anterior myocardial wall

I22.1 Repeated infarction of the lower myocardial wall

I22.8 Repeated myocardial infarction of another specified location

I22.9 Recurrent myocardial infarction of unspecified localization

I23 Some current complications of acute myocardial infarction

Excluded: Conditions listed:

Not specified as current complications of acute myocardial infarction (I31.-, I51.-)

Accompanying acute myocardial infarction (I21-I22)

I23.0 Hemopericardium as an immediate complication of acute myocardial infarction

I23.1 Atrial septal defect as a current complication of acute myocardial infarction

I23.2 Ventricular septal defect as a current complication of acute myocardial infarction

I23.3 Cardiac wall rupture without hemopericardium as a current complication of acute myocardial infarction

Excluded: with hemopericardium (I23.0)

I23.4 Chordae tendinus rupture as a current complication of acute myocardial infarction

I23.5 Papillary muscle rupture as a current complication of acute myocardial infarction

I23.6 Thrombosis of the atrium, atrial appendage and ventricle of the heart as a current complication of acute myocardial infarction

I23.8 Other current complications of acute myocardial infarction

I24 Other forms of acute coronary heart disease

transient neonatal myocardial ischemia (P29.4)

I24.0 Coronary thrombosis not leading to myocardial infarction

Excludes: coronary thrombosis chronic or of established duration more than 4 weeks (more than 28 days) from onset (I25.8)

I24.1 Dressler syndrome

I24.8 Other forms of acute coronary heart disease

I24.9 Acute coronary heart disease, unspecified

Excludes: coronary heart disease (chronic) NOS (I25.9)

I25 Chronic ischemic heart disease

Excludes: cardiovascular disease NOS (I51.6)

I25.0 Atherosclerotic cardiovascular disease, as described

I25.1 Atherosclerotic heart disease

I25.2 Previous myocardial infarction

I25.3 Cardiac aneurysm

Abortion (O03-O07), ectopic or molar pregnancy (O00-O07, O08.2)

Pregnancy, childbirth and the puerperium (O88.-)

I26.0 Pulmonary embolism with mention of acute cor pulmonale

I26.9 Pulmonary embolism without mention of acute cor pulmonale

I27 Other forms of pulmonary heart failure

I27.0 Primary pulmonary hypertension

I27.1 Kyphoscoliotic heart disease

I27.8 Other specified forms of pulmonary heart failure

I27.9 Pulmonary heart failure, unspecified

I28 Other pulmonary vascular diseases

I28.0 Arteriovenous fistula of the pulmonary vessels

I28.1 Pulmonary artery aneurysm

I28.8 Other specified pulmonary vascular diseases

I28.9 Pulmonary vascular disease, unspecified

OTHER HEART DISEASES (I30-I52)

I30 Acute pericarditis

Includes: acute pericardial effusion

Excludes: rheumatic pericarditis (acute) (I01.0)

diseases specified as rheumatic (I09.2)

some current complications of acute myocardial infarction (I23.-)

postcardiotomy syndrome (I97.0)

heart injury (S26.-)

I31.0 Chronic adhesive pericarditis

I31.1 Chronic constrictive pericarditis

I31.2 Hemopericardium, not elsewhere classified

I31.3 Pericardial effusion (non-inflammatory)

I31.8 Other specified diseases of the pericardium

I31.9 Diseases of the pericardium, unspecified

I32* Pericarditis in diseases classified elsewhere

I32.0* Pericarditis in bacterial diseases classified elsewhere

I32.8* Pericarditis in other diseases classified elsewhere

I33 Acute and subacute endocarditis

acute rheumatic endocarditis (I01.1)

lesions specified as rheumatic (I05.-)

for an unknown reason, but with mention of:

Aortic valve diseases (I08.0)

Mitral stenosis or obstruction (I05.0)

I34.0 Mitral (valve) insufficiency

I34.1 Prolapse [prolapse] of the mitral valve

Excludes: Marfan syndrome (Q87.4)

I34.2 Non-rheumatic mitral valve stenosis

I34.8 Other non-rheumatic lesions of the mitral valve

I34.9 Non-rheumatic disease of the mitral valve, unspecified

I35 Non-rheumatic lesions of the aortic valve

hypertrophic subaortic stenosis (I42.1)

lesions specified as rheumatic (I06.-)

for unknown cause, but with mention of mitral valve disease (I08.0)

I35.0 Aortic (valvular) stenosis

I35.1 Aortic (valve) insufficiency

I35.2 Aortic (valvular) stenosis with insufficiency

I35.8 Other lesions of the aortic valve

I35.9 Aortic valve lesion, unspecified

I36 Non-rheumatic lesions of the tricuspid valve

without specifying the reason (I07.-)

specified as rheumatic (I07.-)

I36.0 Non-rheumatic tricuspid valve stenosis

I36.1 Non-rheumatic tricuspid valve insufficiency

I36.2 Non-rheumatic tricuspid valve stenosis with insufficiency

I36.8 Other non-rheumatic lesions of the tricuspid valve

I36.9 Non-rheumatic lesion of the tricuspid valve, unspecified

I37 Pulmonary valve lesions

Excludes: disorders specified as rheumatic (I09.8)

I37.0 Pulmonary valve stenosis

I37.1 Pulmonary valve insufficiency

I37.2 Pulmonary valve stenosis with insufficiency

I37.8 Other pulmonary valve lesions

I37.9 Pulmonary valve disease, unspecified

I38 Endocarditis, valve not specified

cases specified as rheumatic (I09.1)

endocardial fibroelastosis (I42.4)

I39.0* Lesions of the mitral valve in diseases classified elsewhere

I39.1* Lesions of the aortic valve in diseases classified elsewhere

I39.2* Lesions of the tricuspid valve in diseases classified elsewhere

I39.3* Lesions of the pulmonary valve in diseases classified elsewhere

I39.4* Multiple valvular lesions in diseases classified elsewhere

I39.8* Endocarditis, valve unspecified, in diseases classified elsewhere

I40 Acute myocarditis

I40.0 Infectious myocarditis

I40.1 Isolated myocarditis

I40.8 Other types of acute myocarditis

I40.9 Acute myocarditis, unspecified

I41* Myocarditis in diseases classified elsewhere

I41.0* Myocarditis in bacterial diseases classified elsewhere

I41.1* Myocarditis in viral diseases classified elsewhere

I41.8* Myocarditis in other diseases classified elsewhere

ischemic cardiomyopathy (I25.5)

Postpartum period (O90.3)

I42.0 Dilated cardiomyopathy

I42.1 Obstructive hypertrophic cardiomyopathy

I42.2 Other hypertrophic cardiomyopathy

I42.3 Endomyocardial (eosinophilic) diseasev I42.4 Endocardial fibroelastosis

I42.5 Other restrictive cardiomyopathy

I42.6 Alcoholic cardiomyopathy

I42.7 Cardiomyopathy due to drugs and other external factors

I42.8 Other cardiomyopathies

I42.9 Cardiomyopathy, unspecified

I43* Cardiomyopathy in diseases classified elsewhere

I43.1* Cardiomyopathy in metabolic disorders

I43.2* Cardiomyopathy in eating disorders

I43.8* Cardiomyopathy in other diseases classified elsewhere

I44 Atrioventricular [atrioventricular] block and left bundle branch block [His]

I44.0 First degree atrioventricular block

I44.1 Second degree atrioventricular block

I44.2 Complete atrioventricular block

I44.3 Other and unspecified atrioventricular block

I44.4 Block of the anterior branch of the left bundle branch

I44.5 Block of the posterior branch of the left bundle branch

I44.6 Other and unspecified bundle blockades

I44.7 Left bundle branch block, unspecified

I45 Other conduction disorders

I45.0 Right bundle branch block

I45.1 Other and unspecified right bundle branch block

tachycardia NOS (R00.0)

I47.0 Recurrent ventricular arrhythmia

I47.1 Supraventricular tachycardia

I47.2 Ventricular tachycardia

I47.9 Paroxysmal tachycardia, unspecified

I48 Atrial fibrillation and flutter

I49 Other heart rhythm disorders

bradycardia NOS (R00.1)

cardiac arrhythmia in the newborn (P29.1)

Abortion, ectopic or molar pregnancy (O00-O07, O08.8)

Obstetric surgeries and procedures (O75.4)

I49.0 Ventricular fibrillation and flutter

I49.1 Premature atrial depolarization

I49.2 Premature depolarization originating from the junction

I49.3 Premature ventricular depolarization

I49.4 Other and unspecified premature depolarization

I49.5 Sick sinus syndrome

I49.8 Other specified cardiac arrhythmias

I49.9 Heart rhythm disorder, unspecified

I50 Heart failure

consequences of heart surgery or in the presence of a cardiac prosthesis (I97.1)

heart failure in the newborn (P29.0)

conditions due to hypertension (I11.0)

Abortion, ectopic or molar pregnancy (O00-O07, O08.8)

Obstetric surgeries and procedures (O75.4)

I50.0 Congestive heart failure

I50.1 Left ventricular failure

I50.9 Heart failure, unspecified

I51 Complications and ill-defined heart diseases

any conditions listed in sections I51.4-I51.9 due to hypertension (I11.-)

With kidney disease (I13.-)

complications accompanying acute myocardial infarction (I23.-)

specified as rheumatic (I00-I09)

I51.0 Acquired cardiac septal defect

I51.1 Rupture of chordae tendons, not elsewhere classified

I51.2 Rupture of papillary muscle, not elsewhere classified

I51.3 Intracardiac thrombosis, not elsewhere classified

I51.4 Myocarditis, unspecified

I51.5 Myocardial degeneration

I51.6 Cardiovascular disease, unspecified

Excludes: atherosclerotic cardiovascular disease as described (I25.0)

I51.8 Other ill-specified heart diseases

I51.9 Heart disease, unspecified

I52* Other cardiac lesions in diseases classified elsewhere

Excludes: cardiovascular disorders NOS in diseases classified elsewhere (I98.-*)

I52.0* Other cardiac lesions in bacterial diseases classified elsewhere

I52.8* Other cardiac lesions in other diseases classified elsewhere

CEREBROVASCULAR DISEASES (I60-I69)

with mention of hypertension (conditions listed in sections I10 and I15.-)

vascular dementia (F01.-)

traumatic intracranial hemorrhage (S06.-)

transient cerebral ischemic attacks and related syndromes (G45.-)

I60 Subarachnoid hemorrhage

Includes: rupture of cerebral aneurysm

Excludes: consequences of subarachnoid hemorrhage (I69.0)

I60.0 Subarachnoid hemorrhage from the carotid sinus and bifurcation

I60.1 Subarachnoid hemorrhage from the middle cerebral artery

I60.2 Subarachnoid hemorrhage from the anterior communicating artery

I60.3 Subarachnoid hemorrhage from the posterior communicating artery

I60.4 Subarachnoid hemorrhage from the basilar artery

I60.5 Subarachnoid hemorrhage from the vertebral artery

I60.6 Subarachnoid hemorrhage from other intracranial arteries

I60.7 Subarachnoid hemorrhage from intracranial artery, unspecified

I60.8 Other subarachnoid hemorrhage

I60.9 Subarachnoid hemorrhage, unspecified

I61 Intracerebral hemorrhage

Excludes: consequences of cerebral hemorrhage (I69.1)

I61.0 Intracerebral hemorrhage in the subcortical hemisphere

I61.1 Intracerebral hemorrhage in the cortical hemisphere

I61.2 Intracerebral hemorrhage in the hemisphere, unspecified

I61.3 Intracerebral hemorrhage in the brainstem

I61.4 Intracerebral hemorrhage in the cerebellum

I61.5 Intraventricular intracerebral hemorrhage

I61.6 Intracerebral hemorrhage of multiple localization

I61.8 Other intracerebral hemorrhage

I61.9 Intracerebral hemorrhage, unspecified

I62 Other non-traumatic intracranial hemorrhage

Excludes: consequences of intracranial hemorrhage (I69.2)

I62.0 Subdural hemorrhage (acute) (non-traumatic)

I62.1 Non-traumatic extradural hemorrhage

I62.9 Intracranial hemorrhage (non-traumatic) unspecified

I63 Cerebral infarction

Includes: occlusion and stenosis of the cerebral and precerebral arteries causing cerebral infarction

Excludes: complications after cerebral infarction (I69.3)

I63.0 Cerebral infarction caused by thrombosis of precerebral arteries

I63.1 Cerebral infarction caused by embolism of precerebral arteries

I63.2 Cerebral infarction caused by unspecified occlusion or stenosis of precerebral arteries

I63.3 Cerebral infarction caused by thrombosis of cerebral arteries

I63.4 Cerebral infarction caused by cerebral artery embolism

I63.5 Cerebral infarction caused by unspecified occlusion or stenosis of cerebral arteries

I63.6 Cerebral infarction caused by cerebral vein thrombosis, non-pyogenic

I63.8 Other cerebral infarction

I63.9 Cerebral infarction, unspecified

I64 Stroke not specified as hemorrhage or infarction

Excludes: consequences of stroke (I69.4)

I65 Occlusion and stenosis of the precerebral arteries, not leading to cerebral infarction

Excludes: conditions causing cerebral infarction (I63.-)

I66.0 Occlusion and stenosis of the middle cerebral artery

I66.1 Occlusion and stenosis of the anterior cerebral artery

I66.2 Occlusion and stenosis of the posterior cerebral artery

I66.3 Occlusion and stenosis of the cerebellar arteries

I66.4 Occlusion and stenosis of multiple and bilateral cerebral arteries

I66.8 Blockage and stenosis of another cerebral artery

I66.9 Occlusion and stenosis of cerebral artery, unspecified

I67 Other cerebrovascular diseases

Excluded: consequences of listed conditions (I69.8)

I67.0 Dissection of cerebral arteries without rupture

Excludes: rupture of cerebral arteries (I60.7)

I67.1 Cerebral aneurysm without rupture

congenital cerebral aneurysm without rupture (Q28.3)

ruptured cerebral aneurysm (I60.9)

I67.2 Cerebral atherosclerosis

I67.3 Progressive vascular leukoencephalopathy

Excludes: subcortical vascular dementia (F01.2)

I67.4 Hypertensive encephalopathy

I67.5 Moyamoya disease

I67.6 Non-purulent thrombosis of the intracranial venous system

Excludes: conditions causing cerebral infarction (I63.6)

I67.7 Cerebral arteritis, not elsewhere classified

I67.8 Other specified cerebrovascular lesions

I67.9 Cerebrovascular disease, unspecified

I68* Damages of cerebral vessels in diseases classified elsewhere

I68.0* Cerebral amyloid angiopathy (E85.-+)

I68.2* Cerebral arteritis in other diseases classified elsewhere

I68.8* Other cerebral vascular lesions in diseases classified elsewhere

I69 Consequences of cerebrovascular diseases

Note: The term “consequences” includes conditions specified as such, as residual effects, or as conditions that persist for a year or more from the onset of the causative condition.

I69.0 Consequences of subarachnoid hemorrhage

I69.1 Consequences of intracranial hemorrhage

I69.2 Sequelae of other non-traumatic intracranial hemorrhage

I69.3 Consequences of cerebral infarction

I69.4 Consequences of stroke, not specified as cerebral hemorrhage or infarction

I69.8 Sequelae of other and unspecified cerebrovascular diseases

DISEASES OF ARTERIES, ARTERIOLES AND CAPILLARIES (I70-I79)

Honey. Acute cor pulmonale (ACP) is a clinical syndrome of acute right ventricular failure caused by sudden pulmonary hypertension due to pulmonary vascular obstruction. A classic example of PE. Etiology of pulmonary embolism Fat embolism, gas embolism,... ... Directory of diseases

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Honey. Chronic obstructive pulmonary disease (COPD) is a chronic pathology with progressive airway obstruction and the development of pulmonary hypertension. The term combines chronic obstructive bronchitis and emphysema. Chronical bronchitis … Directory of diseases - honey. Acute left ventricular failure is an acute weakness of the left ventricular myocardium caused by excessive load on it, leading to a decrease in the release of blood into the systemic circulation, overstretching of the left atrium and stagnation... ... Directory of diseases

Honey. Secondary pulmonary hypertension: increased pressure in the pulmonary artery above 30 mmHg. for systolic pressure and above 12 mm Hg. for diastolic pressure. Etiology Prolonged increase in pressure in the left atrium Mitral ... ... Directory of diseases

Acute cor pulmonale develops over several hours or days and, as a rule, is accompanied by symptoms of heart failure. At a slower rate of development, a subacute version of this syndrome is observed. The acute course of pulmonary embolism is characterized by the sudden development of the disease against the background of complete well-being. Severe shortness of breath, cyanosis, chest pain, and agitation appear. Thromboembolism of the main trunk of the pulmonary artery quickly, within a few minutes to half an hour, leads to the development of a state of shock and pulmonary edema.
When listening, a large number of moist and scattered dry rales are heard. Pulsation may be detected in the second or third intercostal space on the left. Characterized by swelling of the neck veins, progressive enlargement of the liver, and its pain when palpated. Acute coronary insufficiency often occurs, accompanied by pain, rhythm disturbances and electrocardiographic signs of myocardial ischemia. The development of this syndrome is associated with the occurrence of shock, compression of the veins, dilated right ventricle, and irritation of the nerve receptors of the pulmonary artery.
The further clinical picture of the disease is caused by the formation of myocardial infarction, characterized by the occurrence or intensification of chest pain associated with the act of breathing, shortness of breath, and cyanosis. The severity of the last two manifestations is less compared to the acute phase of the disease. A cough appears, usually dry or with scanty sputum. In half of the cases, hemoptysis is observed. Most patients develop an elevated body temperature, which is usually resistant to antibiotics. The examination reveals a persistent increase in heart rate, weakened breathing and moist rales over the affected area of ​​the lung.
Subacute pulmonary heart. Subacute cor pulmonale is clinically manifested by sudden moderate pain when breathing, rapidly passing shortness of breath and rapid heartbeat, fainting, often hemoptysis, and symptoms of pleurisy.
Chronic cor pulmonale. It is necessary to distinguish between compensated and decompensated chronic pulmonary heart disease.
In the compensation phase, the clinical picture is characterized mainly by the symptoms of the underlying disease and the gradual addition of signs of enlargement of the right side of the heart. In a number of patients, pulsation is detected in the upper abdomen. The main complaint of patients is shortness of breath, which is caused by both respiratory failure and the addition of heart failure. Shortness of breath increases with physical exertion, inhalation of cold air, and lying down. The causes of pain in the heart region with cor pulmonale are metabolic disorders of the myocardium, as well as relative insufficiency of coronary circulation in the enlarged right ventricle. Pain in the heart area can also be explained by the presence of a pulmonary-coronary reflex due to pulmonary hypertension and stretching of the pulmonary artery trunk. Examination often reveals cyanosis.
An important sign of cor pulmonale is swelling of the neck veins. Unlike respiratory failure, when the jugular veins swell during inhalation, in cor pulmonale the jugular veins remain swollen both during inhalation and exhalation. Characteristic pulsation in the upper abdomen, caused by an enlarged right ventricle.
Arrhythmias in cor pulmonale are rare and usually occur in combination with atherosclerotic cardiosclerosis. Blood pressure is usually normal or low. Shortness of breath in some patients with a pronounced decrease in oxygen levels in the blood, especially with the development of congestive heart failure due to compensatory mechanisms. The development of arterial hypertension is observed.
A number of patients experience the development of stomach ulcers, which is associated with a violation of the gas composition of the blood and a decrease in the stability of the mucous membrane of the stomach and duodenum.
The main symptoms of cor pulmonale become more pronounced against the background of exacerbation of the inflammatory process in the lungs. Patients with cor pulmonale have a tendency to lower their temperature, and even with exacerbation of pneumonia, the temperature rarely exceeds 37 °C.
In the terminal stage, swelling increases, there is an enlargement of the liver, a decrease in the amount of urine excreted, disorders of the nervous system occur (headaches, dizziness, noise in the head, drowsiness, apathy), which is associated with a violation of the gas composition of the blood and the accumulation of under-oxidized products.

Coronary heart disease is a pathology of the heart muscle associated with a lack of blood supply and increasing hypoxia. The myocardium receives blood from the coronary (coronary) vessels of the heart. In diseases of the coronary vessels, the heart muscle lacks blood and the oxygen it carries. Cardiac ischemia occurs when oxygen demand exceeds oxygen availability. In this case, the heart vessels usually have atherosclerotic changes.

The diagnosis of IHD is common among people over 50 years of age. With increasing age, pathology occurs more often.

Species and subspecies

Ischemic disease is classified according to the degree of clinical manifestations, susceptibility to vasodilating (vasodilating) drugs, and resistance to physical exercise. Forms of IHD:

• Sudden coronary death is associated with disorders of the myocardial conduction system, that is, with sudden severe arrhythmia. In the absence of resuscitation measures or their failure, instantaneous cardiac arrest when confirmed by eyewitnesses, or death after an attack within six hours of its onset, a diagnosis of “primary cardiac arrest with fatal outcome” is made. If the patient is successfully resuscitated, the diagnosis is “sudden death with successful resuscitation.”
• Angina pectoris is a form of coronary artery disease in which a burning pain occurs in the middle of the chest, or more precisely, behind the sternum. According to ICD-10 (International Classification of Diseases, 10th revision), angina pectoris corresponds to code I20.

It also has several subspecies:

• Angina pectoris, or stable, in which the supply of oxygen to the heart muscle is reduced. In response to hypoxia (oxygen starvation), pain and spasm of the coronary arteries occurs. Stable angina, unlike unstable angina, occurs during physical activity of the same intensity, for example, walking 300 meters at a normal pace, and is relieved with nitroglycerin preparations.
• Unstable angina (ICD code - 20.0) is poorly controlled by nitroglycerin derivatives, attacks of pain become more frequent, and the patient's exercise tolerance decreases. This form is divided into types:
  • first appeared;
  • progressive;
  • early post-infarction or post-operative.
• Vasospastic angina caused by vascular spasm without atherosclerotic changes.
• Coronary syndrome (syndrome X).

According to the international classification 10 (ICD-10), angiospastic angina (Prinzmetal's angina, variant) corresponds to 20.1 (Angina with confirmed spasm). Angina pectoris - ICD code 20.8. Unspecified angina was assigned code 20.9.

• Myocardial infarction. An attack of angina that lasts more than 30 minutes and is not relieved by nitroglycerin ends in a heart attack. Diagnosis of a heart attack includes ECG analysis, laboratory testing of the level of markers of damage to the heart muscle (fractions of the enzymes creatine phosphokinase and lactate dehydrogenase, tropomyosin, etc.). Based on the extent of the lesion, they are classified as:
  • transmural (large focal) infarction;
  • finely focal.

  According to the international classification of the 10th revision, acute infarction corresponds to code I21, its varieties are distinguished: acute extensive infarction of the lower wall, anterior wall and other localizations, unspecified localization. The diagnosis of “recurrent myocardial infarction” was assigned code I22.

• Post-infarction cardiosclerosis. Diagnosis of cardiosclerosis using an electrocardiogram is based on conduction disturbances due to cicatricial changes in the myocardium. This form of ischemic disease is indicated no earlier than 1 month from the moment of the heart attack. Cardiosclerosis is cicatricial changes that occur at the site of the heart muscle destroyed as a result of a heart attack. They are formed by rough connective tissue. Cardiosclerosis is dangerous due to the shutdown of a large part of the conduction system of the heart.

Other forms of IHD - codes I24-I25:

1. Painless form (according to the old classification of 1979).
2. Acute heart failure develops against the background of myocardial infarction or during shock conditions.
3. Heart rhythm disturbances. With ischemic damage, the blood supply to the conduction system of the heart is also disrupted.

ICD-10 code I24.0 is assigned to coronary thrombosis without infarction.

ICD code I24.1 - post-infarction Dressler syndrome.

Code I24.8 according to the 10th revision of the ICD - coronary insufficiency.

Code I25 according to ICD-10 - chronic ischemic disease; includes:

• atherosclerotic ischemic heart disease;
• previous heart attack and post-infarction cardiosclerosis;
• cardiac aneurysm;
• coronary arteriovenous fistula;
• asymptomatic ischemia of the heart muscle;
• chronic unspecified ischemic heart disease and other forms of chronic ischemic heart disease lasting more than 4 weeks.

Risk factors

The tendency to ischemia is increased with the following risk factors for ischemic heart disease:

1. Metabolic, or syndrome X, in which the metabolism of carbohydrates and fats is impaired, cholesterol levels are elevated, and insulin resistance occurs. People with type 2 diabetes are at risk for cardiovascular diseases, including angina and heart attack. If your waist circumference exceeds 80 cm, this is a reason to be more attentive to your health and nutrition. Timely diagnosis and treatment of diabetes mellitus will improve the prognosis of the disease.
2. Smoking. Nicotine constricts blood vessels, increases heart rate, and increases the heart muscle's need for blood and oxygen.
3. Liver diseases. With liver disease, cholesterol synthesis increases, this leads to increased deposition on the walls of blood vessels with further oxidation and inflammation of the arteries.
4. Drinking alcohol.
5. Physical inactivity.
6. Constantly exceeding the caloric intake of the diet.
7. Emotional stress. With anxiety, the body's need for oxygen increases, and the heart muscle is no exception. In addition, during prolonged stress, cortisol and catecholamines are released, which narrow the coronary vessels, and cholesterol production increases.
8. Lipid metabolism disorders and atherosclerosis of the coronary arteries. Diagnostics - study of the lipid spectrum of blood.
9. Syndrome of excessive colonization of the small intestine, which disrupts liver function and causes vitamin deficiency of folic acid and vitamin B12. This increases cholesterol and homocysteine ​​levels. The latter disrupts peripheral circulation and increases the load on the heart.
10. Itsenko-Cushing syndrome, which occurs with hyperfunction of the adrenal glands or with the use of steroid hormones.
11. Hormonal diseases of the thyroid gland, ovaries.

Men over 50 and women during menopause are most likely to suffer from angina and heart attacks.

Risk factors for coronary heart disease that aggravate the course of coronary heart disease: uremia, diabetes mellitus, pulmonary failure. IHD is aggravated by disturbances in the conduction system of the heart (blockade of the sinoatrial node, atrioventricular node, bundle branches).

The modern classification of coronary artery disease allows doctors to correctly assess the patient’s condition and take the right measures to treat it. For each form that has a code in the ICD, its own diagnostic and treatment algorithms have been developed. Only by freely navigating the varieties of this disease can the doctor effectively help the patient.

Hemorrhagic vasculitis is considered a disease that is a type of immune vasculitis of small vessels and is characterized by increased formation of immune complexes and increased permeability of vascular walls. This pathology can develop 2-3 weeks after acute tonsillitis, influenza or scarlet fever. Hemorrhagic vasculitis is more common in children than in adults. Children aged 4 to 12 years are especially susceptible to the disease. Boys get sick 2 times more often than girls.

Hemorrhagic vasculitis ICD 10 (according to the international classification of diseases, tenth revision) is included in the group of diseases under the code D69.0 Allergic purpura. Most photos of hemorrhagic vasculitis show that the main symptom of the disease is an allergic rash.

Etiology of the disease

The causes of hemorrhagic vasculitis in adults and children are divided into several types:

The most common causes of hemorrhagic vasculitis are associated with the influence of infectious agents.

The principle of the mechanism of formation of the disease is the formation of immune complexes, which, circulating through the bloodstream, can remain on the inner surface of the vascular walls. After this, immune complexes gradually destroy the walls of small vessels, which causes an inflammatory process of an aseptic nature and a decrease in the elasticity of the capillaries. As a result, this contributes to increased permeability of vessel walls and the formation of lumens, which lead to the formation of blood clots and fibrin deposits. Therefore, it is believed that the main symptom of vasculitis is hemorrhagic syndrome and microthrombosis.

Symptoms of the disease

Most photos of hemorrhagic vasculitis in children show that the disease begins with ordinary skin rashes. The rash is most often small-spotted in nature, located in a symmetrical order and does not disappear with pressure. The rash usually appears around the joint surfaces, in the area of ​​extension of the limbs and in the buttock area. A rash on the face, trunk, feet, or palms is quite rare. The intensity of the rash can vary - from rare and small elements to multiple ones that tend to merge. After the rashes disappear, pigmentation and severe peeling may remain in their place.

70 percent of patients exhibit symptoms of hemorrhagic vasculitis such as damage to the articular surfaces. This symptom often occurs along with rashes in the first week of the disease. Damage to joints can be minor and cause short-term pain, but it can also be more extensive, when not only large (ankle and knee) but also small articular surfaces are affected. Swelling occurs and the shape of the articular surface changes, and pain can last from 2 hours to 5 days. However, the disease does not cause severe deformation of the articular surfaces.

The third most common symptom is moderate abdominal pain, which may go away on its own within 24 hours. Typically, pain occurs at the very beginning of the disease, before rashes and joint disorders. For some, pain in the abdomen occurs suddenly in the form of intestinal colic, the location of which is difficult to determine. Painful sensations may appear several times throughout the day. In parallel with the pain, dyspeptic disorders appear - vomiting, nausea, diarrhea. In some cases, the temperature rises to 37.5 degrees. More rare signs of vasculitis include kidney damage in the form of glomerulonephritis and pulmonary syndrome, which is manifested by cough and shortness of breath.

When the disease occurs in a child, a functional systolic murmur may be heard in the heart. Also often due to inflammatory processes in the vessels of the brain, the central nervous system is affected. Children may complain of headache, weakness, dizziness, nausea and irritability. Sometimes boys experience testicular damage (mostly bilateral), which causes swelling and tenderness of the tissue.

Conservative treatment of hemorrhagic vasculitis

Treatment of hemorrhagic vasculitis begins with hospitalization, which lasts at least 20 days, and mandatory bed rest.

First of all, a strict diet is prescribed, which prevents the development of allergies in patients. The diet for hemorrhagic vasculitis excludes the consumption of chocolate, cocoa, citrus fruits, strong black tea and coffee, red fruits and berries. It is recommended to consume vegetable purees, olive oil, butter, low-fat dairy products, stewed or boiled meat and fish, cereal soups and stews, dry white bread, fruits, green tea with milk, jelly, juices, puddings. The duration of the diet for hemorrhagic vasculitis reaches 1-2 years to prevent relapse of the disease.

Drug treatment includes the use of the following drugs:

• antibiotics that do not cause an allergic reaction (rifampicin, ceporin) and are prescribed for acute forms of infectious diseases;
• enterosorbents (activated carbon) and gastric drops;
• antispasmodics to reduce pain (baralgin, no-shpa);
• vitamins A and E;
• infusion therapy for severe symptoms (heparin and glucocorticoids);
• pulse therapy with prednisone.

Since the disease is aggravated by emotional stress and anxiety, it is necessary to exclude stressful situations or use sedatives and tranquilizers that improve the result of complex treatment.

Treatment of hemorrhagic vasculitis in children is carried out over a long period of time - at least two years. It is imperative to register a sick child with a dispensary and visit a doctor every month for the first six months. Then once every 3 months or once every six months, depending on the condition. Preventive measures consist of treating foci of chronic infection, and systematically taking tests to detect helminth eggs. During treatment, it is forbidden to play sports, stay in the sun for a long time and do physical procedures.

According to most forums, hemorrhagic vasculitis has a positive prognosis, since 95 percent of sick children recover within 10-12 months.

Traditional methods of treatment

Treatment of hemorrhagic vasculitis with folk remedies consists of preparing infusions, ointments and teas based on plant materials. Folk remedies are used both externally and internally.

The most useful and effective remedies include the following recipes:

1. To prepare a medicinal ointment, you need to take dried rue leaves (50 g) and vegetable or butter (250 g). Chop the leaves thoroughly and mix with oil. Place the resulting mixture in a cold and dark room for at least 2 weeks. After this, you can use the ointment: apply to the surface of the skin or affected joints 3-4 times a day. Usually, skin rashes go away very quickly after using this product.
2. To prepare a medicinal tincture, take crushed herbs of yarrow, horsetail, mint, elderberry, string and calendula. All in equal proportions, 2 tbsp. Pour the resulting mixture with 200 ml of boiled water and leave in a cold and dark room for 2-4 hours. It is recommended to consume the strained tincture 100 ml 5 times a day.
3. Strong, freshly brewed green tea that can be consumed 2-3 times a day. Tea helps restore the elasticity of vascular walls and helps normalize blood circulation.

If the diagnosis of the disease is confirmed, then before using the above recipes you should carefully read the ingredients in order to exclude allergenic products or herbs to which individual intolerance occurs. It is also necessary to consult a doctor and not self-medicate.

Chronic cor pulmonale

• Causes
• What happens in the body
• Clinical course
• Clinical manifestations
• Diagnostics
• Functional classes
• Treatment
• Forecast

The term “chronic cor pulmonale” refers to changes in the heart muscle caused by lung diseases. This excludes cases of pathology complicating diseases of the heart and large vessels (mitral stenosis, cardiosclerosis after a heart attack, congenital defects, dilated cardiomyopathy).

In diagnosis, an indispensable condition must be a primary violation of the structure of the lung tissue and its functions. The prevalence of the recorded pathology among the adult population allows us to place it in third place after ischemic and hypertension diseases.

In the International Classification of Diseases (ICD-10), types of chronic pulmonary heart disease are included in the general class of cardiovascular diseases. Codes I26, I27, I28 differ in etiological factors. All cases are united by the gradual formation of overload of the right side of the heart due to the development of high blood pressure in the pulmonary circulation.

Causes

Depending on the causes, the WHO Expert Committee has developed a classification of chronic pulmonary heart disease. Diseases are divided into 3 groups:

• group 1 - diseases associated with impaired passage of air through the alveoli, these can be mechanical obstacles (bronchial asthma), inflammatory lesions (tuberculosis, chronic bronchitis, bronchiectasis, pneumoconiosis), replacement of lung tissue with fibrous tissue (systemic lupus erythematosus, sarcoidosis, eosinophilic infiltration ), a total of 21 nosologies are included;
• group 2 - diseases that impair ventilation of the lungs by affecting the auxiliary mechanisms of breathing (skeletal skeleton of the chest, ribs, muscles), this includes curvature of the spine, adhesions in the pleural cavity, chronic diseases associated with impaired neuromuscular conduction (poliomyelitis) , artificial hypoventilation after surgical interventions on the chest organs;
• group 3 - vascular lesions of the lungs (arteritis, thrombosis and embolism, compression of the main vessels by a tumor, aortic aneurysm and others).

All risk factors for underlying disease accelerate and negatively affect the heart.

What happens in the body

In patients of groups 1 and 2, all changes develop due to spasm of small arterioles in the lung tissue as a reaction to insufficient oxygen supply. In group 3, in addition to spasm, there is a narrowing or blockage of the vascular bed. The pathogenesis of the disease is associated with the following mechanisms.

1. Alveolar hypoxia (lack of oxygen in the alveoli) - scientists associate vascular spasm in response to hypoxia with disturbances in sympathoadrenal regulation. There is a contraction of vascular muscles, an increase in angiotensin-converting enzyme (ACE), calcium in the blood, and a decrease in relaxation factors of the pulmonary vessels.
2. Hypercapnia - an increase in the concentration of carbon dioxide in the blood does not directly affect the vascular wall, but through acidification of the environment and a decrease in the sensitivity of the respiratory center of the brain. This mechanism enhances the production of aldosterone (adrenal hormone), which retains water and sodium ions.
3. Changes in the vascular bed of the lungs - compression and emptying of capillaries due to developing fibrous tissue is important. Thickening of the muscular walls of the pulmonary vessels contributes to the narrowing of the lumen and the development of local thrombosis.
4. An important role is played by the development of anastomoses (connections) between the bronchial arteries, belonging to the systemic circulation, and the pulmonary vessels.
5. The pressure in the systemic circle is higher than in the lungs, so the redistribution goes towards the pulmonary vascular bed, which further increases the pressure in it.
6. In response to hypoxia, blood cells that carry hemoglobin and erythrocytes change. Their number increases simultaneously with platelets. Favorable conditions for thrombus formation are created and blood viscosity increases.

All taken together leads to increased load on the right ventricle, hypertrophy, and then failure of the right heart. An enlarged right atrioventricular orifice contributes to insufficient closure of the tricuspid valve.

Clinical course

Soviet pulmonologists B. Votchal and N. Palev proposed a clinical description of the stages of development of the pulmonary heart:

• in the initial (preclinical) stage - there are no symptoms of hypertension in the pulmonary circulation, hypertension is possible temporarily with an exacerbation of pulmonary disease;
• in the second stage - there is right ventricular hypertrophy, but all signs are compensated; instrumental examination reveals stable pulmonary hypertension;
• third stage - accompanied by decompensation (pulmonary heart failure), there are symptoms of right ventricular overload.

Clinical manifestations

At the early stage of the disease, the manifestations of chronic pulmonary heart disease do not differ from the typical symptoms of major pulmonary diseases. They intensify with exacerbation and are treatable.

Shortness of breath is a consequence of oxygen deficiency, but it also accompanies inflammation of the lung tissue, emphysema. The intensity does not always correspond to the degree of hypoxia.

Tachycardia is a nonspecific symptom; the heart rate increases in various diseases that are associated with an activated sympathetic nervous system and increased release of adrenaline.

Chest pain is not similar to angina. They are believed to be caused by insufficiency of the coronary vessels, which have to feed the thickened muscle of the right ventricle. Spasm of the arteries of the heart and intoxication of the myocardium with inflammatory products are also important.

Increased fatigue and weakness occur when the shock capacity of the heart decreases. Peripheral tissues of various organs, including the brain, lack blood supply.

Heaviness in the legs, swelling - in addition to myocardial weakness, an increase in the permeability of the vascular wall plays a role. Swelling occurs on the feet and legs. They intensify in the evening and subside during the night. In the third stage, they spread to the thighs.

The feeling of heaviness and pain in the right hypochondrium is caused by an enlarged liver and stretching of its capsule. In a severe form of the disease, ascites simultaneously appears and the abdomen “grows” rapidly. This symptom is more pronounced in elderly patients with concomitant atherosclerosis of the abdominal arteries.

A cough with a small amount of sputum is more associated with the underlying pathology of the lungs.

Manifestations of encephalopathy - chronic lack of oxygen and excess carbon dioxide cause pathological disorders in the brain, disrupt vascular permeability, and promote edema. Patients have 2 possible symptoms:

• increased excitability, aggressive behavior, euphoria, development of psychosis;
• lethargy, lethargy, indifference, drowsiness during the day, insomnia at night.

In severe cases, seizures occur with loss of consciousness or dizziness, cold sweat and decreased blood pressure.

Diagnostics

In people with chronic cor pulmonale, the diagnosis can be suspected by their appearance: in the compensation stage, dilated skin vessels appear in the cheek area (blush) and on the conjunctiva (“rabbit eyes”). Cyanosis is found on the lips, tip of the tongue, nose, and ears.

When examining the fingers, changes in the nail phalanges are visible: they become flat and widened (“drumsticks”). Unlike heart failure, the arms and legs remain warm to the touch.

When auscultating the heart, the doctor hears:

• characteristic changes in tones above the pulmonary artery;
• in the stage of decompensation - a murmur indicating insufficiency of the right atrioventricular valve;
• a lot of different types of wheezing in the lungs against the background of altered breathing.

The x-ray reveals a typical bulging of the contours of the pulmonary artery, an enhanced tissue pattern, and an expansion of the zone of lymphatic vessels. This indicates an increase in pressure in the pulmonary circle. In the decompensation stage, the heart shadow expands to the right.

Echocardiography assesses the strength of the right ventricle, the degree of dilatation, and overload. Due to increased pressure, the wall of the interventricular septum bends to the left.

Respiratory functions are measured with special devices, and the spirogram is deciphered by a doctor in the functional diagnostics office.

The study of pressure in the pulmonary artery is carried out in complex diagnostic cases. A reliable sign of hypertension in the pulmonary circle is considered to be a resting pressure of 25 mm Hg. Art. and higher, and with load - over 35.

Functional classes

During the examination, it is necessary to establish the functional class of manifestations of cor pulmonale.

• Class 1 - the main symptoms are diseases of the bronchi and lungs, pulmonary hypertension is detected only with instrumental examination and stress tests;
• Class 2 - in addition to the listed symptoms, there is respiratory failure due to narrowing of the bronchi;
• Class 3 - respiratory failure is severe, followed by cardiac failure. Constant shortness of breath, tachycardia, dilatation of the neck veins, cyanosis. Studies reveal persistent hypertension in the pulmonary circulation;
• Class 4 - decompensation, all clinical manifestations are pronounced, there are congestion, respiratory and heart failure of the third degree.

Treatment

Treatment of chronic pulmonary heart disease should begin with the prevention of exacerbations of respiratory diseases, especially colds and flu, with the timely use of antiviral and antibacterial treatment.

Mode Changes

Patients are advised to limit physical activity. Do not visit mountainous areas, since in high altitude conditions even a healthy person experiences oxygen deficiency. And in patients with pulmonary diseases, a reflex vascular spasm occurs and the degree of tissue hypoxia deepens.

Women should be aware of the negative effects of birth control pills.

It is necessary to stop smoking and even staying in a smoky room.

Directions of therapy

All treatment methods are aimed at eliminating or weakening the existing mechanisms of pathology, these include:

• treatment of the underlying pulmonary disease and compensation of lost respiratory function;
• decreased vascular resistance in the pulmonary circulation and unloading of the right ventricle;
• restoration of normal blood composition, antithrombotic therapy.

Oxygen treatment

Oxygen is supplied in a humidified form through a mask, cannulas in the nasal passages, and some clinics use oxygen tents with special air saturation conditions. For a therapeutic effect on chronic pulmonary heart disease, the oxygen level in the inhaled air must be at least 60%.

Therapy is carried out for an hour up to 5 times a day and more often.

How to lower pulmonary artery pressure

To reduce pressure in the pulmonary artery, medications of different groups are used:

• calcium antagonists (possible swelling and redness of the face, headache, feeling of heat, decreased blood pressure);
• α-adrenergic blockers - dilate blood vessels, reduce the ability of platelets to stick together (the side effects are the same, increased irritability and weakness are possible);
• inhaled nitric oxide (has no side effects);
• diuretics - medications with a diuretic effect unload the general bloodstream, facilitate the work of the heart (control of the potassium content in the blood is required);
• group of prostaglandins - selectively act on small blood vessels (side effects such as nasal congestion, increased cough, increased blood pressure, headache).

The drugs Heparin and Pentoxifylline are necessary to improve blood flow and antithrombotic action.

In case of severe heart failure, cardiac glycosides are prescribed very carefully.

Patients with symptoms of decompensation are treated in a hospital. Observation and clinical examination are carried out by a local therapist and pulmonologist.

Forecast

The mortality rate of patients from chronic pulmonary heart disease remains high: 45% of patients survive in the decompensation stage for about two years. Even with intensive therapy, their life expectancy is no more than four years.
Lung transplantation gives 60% of patients survival over the next two years.

The disease is very difficult to treat. Any person has the opportunity to rid himself of bad habits and take care of his health in a timely manner. The appearance of cough, shortness of breath and other symptoms requires immediate medical attention.

Causes

What happens in the body

Clinical course

Clinical manifestations

Changes in the phalanges occur due to impaired nutrition of the periosteum

Diagnostics

Swollen veins in the neck indicate the formation of stagnation at the level of the veins of the systemic circulation, more pronounced at the height of inspiration

Functional classes

Doppler examination allows you to quantify the pressure in the pulmonary artery, measure the reverse flow of blood (regurgitation) from the right ventricle into the atrium

Treatment

Mode Changes

Directions of therapy

Oxygen treatment

Oxygen supply can reduce all symptoms of the disease caused by hypoxia

Forecast

Other forms of pulmonary heart failure (I27)

To indicate the underlying disease, use an additional code, if necessary.

Excludes: Eisenmenger’s defect (Q21.8)

Chronic heart disease of pulmonary origin

Cor pulmonale (chronic) NOS

In Russia, the International Classification of Diseases, 10th revision (ICD-10) has been adopted as a single normative document for recording morbidity, reasons for the population's visits to medical institutions of all departments, and causes of death.

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. No. 170

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

With changes and additions from WHO.

Processing and translation of changes © mkb-10.com

Pulmonary heart failure code according to ICD 10

Classification of IHD according to the International Classification of Diseases

Coronary heart disease is a pathology of the heart muscle associated with a lack of blood supply and increasing hypoxia. The myocardium receives blood from the coronary (coronary) vessels of the heart. In diseases of the coronary vessels, the heart muscle lacks blood and the oxygen it carries. Cardiac ischemia occurs when oxygen demand exceeds oxygen availability. In this case, the heart vessels usually have atherosclerotic changes.

The diagnosis of IHD is common among people over 50 years of age. With increasing age, pathology occurs more often.

Species and subspecies

Ischemic disease is classified according to the degree of clinical manifestations, susceptibility to vasodilating (vasodilating) drugs, and resistance to physical exercise. Forms of IHD:

• Sudden coronary death is associated with disorders of the myocardial conduction system, that is, with sudden severe arrhythmia. In the absence of resuscitation measures or their failure, instantaneous cardiac arrest when confirmed by eyewitnesses, or death after an attack within six hours of its onset, a diagnosis of “primary cardiac arrest with fatal outcome” is made. If the patient is successfully resuscitated, the diagnosis is “sudden death with successful resuscitation.”
• Angina pectoris is a form of coronary artery disease in which a burning pain occurs in the middle of the chest, or more precisely, behind the sternum. According to ICD-10 (International Classification of Diseases, 10th revision), angina pectoris corresponds to code I20.

It also has several subspecies:

• Angina pectoris, or stable, in which the supply of oxygen to the heart muscle is reduced. In response to hypoxia (oxygen starvation), pain and spasm of the coronary arteries occurs. Stable angina, unlike unstable angina, occurs during physical activity of the same intensity, for example, walking 300 meters at a normal pace, and is relieved with nitroglycerin preparations.
• Unstable angina (ICD code - 20.0) is poorly controlled by nitroglycerin derivatives, attacks of pain become more frequent, and the patient's exercise tolerance decreases. This form is divided into types:
  • first appeared;
  • progressive;
  • early post-infarction or post-operative.
• Vasospastic angina caused by vascular spasm without atherosclerotic changes.
• Coronary syndrome (syndrome X).

  According to the international classification 10 (ICD-10), angiospastic angina (Prinzmetal's angina, variant) corresponds to 20.1 (Angina with confirmed spasm). Angina pectoris - ICD code 20.8. Unspecified angina was assigned code 20.9.

• Myocardial infarction. An attack of angina that lasts more than 30 minutes and is not relieved by nitroglycerin ends in a heart attack. Diagnosis of a heart attack includes ECG analysis, laboratory testing of the level of markers of damage to the heart muscle (fractions of the enzymes creatine phosphokinase and lactate dehydrogenase, tropomyosin, etc.). Based on the extent of the lesion, they are classified as:
  • transmural (large focal) infarction;
  • finely focal.

  According to the international classification of the 10th revision, acute infarction corresponds to code I21, its varieties are distinguished: acute extensive infarction of the lower wall, anterior wall and other localizations, unspecified localization. The diagnosis of “recurrent myocardial infarction” was assigned code I22.

• Post-infarction cardiosclerosis. Diagnosis of cardiosclerosis using an electrocardiogram is based on conduction disturbances due to cicatricial changes in the myocardium. This form of ischemic disease is indicated no earlier than 1 month from the moment of the heart attack. Cardiosclerosis is cicatricial changes that occur at the site of the heart muscle destroyed as a result of a heart attack. They are formed by rough connective tissue. Cardiosclerosis is dangerous due to the shutdown of a large part of the conduction system of the heart.

Other forms of IHD - codes I24-I25:

1. Painless form (according to the old classification of 1979).
2. Acute heart failure develops against the background of myocardial infarction or during shock conditions.
3. Heart rhythm disturbances. With ischemic damage, the blood supply to the conduction system of the heart is also disrupted.

ICD-10 code I24.0 is assigned to coronary thrombosis without infarction.

ICD code I24.1 - post-infarction Dressler syndrome.

Code I24.8 according to the 10th revision of the ICD - coronary insufficiency.

Code I25 according to ICD-10 - chronic ischemic disease; includes:

• atherosclerotic ischemic heart disease;
• previous heart attack and post-infarction cardiosclerosis;
• cardiac aneurysm;
• coronary arteriovenous fistula;
• asymptomatic ischemia of the heart muscle;
• chronic unspecified ischemic heart disease and other forms of chronic ischemic heart disease lasting more than 4 weeks.

Risk factors

The tendency to ischemia is increased with the following risk factors for ischemic heart disease:

1. Metabolic, or syndrome X, in which the metabolism of carbohydrates and fats is impaired, cholesterol levels are elevated, and insulin resistance occurs. People with type 2 diabetes are at risk for cardiovascular diseases, including angina and heart attack. If your waist circumference exceeds 80 cm, this is a reason to be more attentive to your health and nutrition. Timely diagnosis and treatment of diabetes mellitus will improve the prognosis of the disease.
2. Smoking. Nicotine constricts blood vessels, increases heart rate, and increases the heart muscle's need for blood and oxygen.
3. Liver diseases. With liver disease, cholesterol synthesis increases, this leads to increased deposition on the walls of blood vessels with further oxidation and inflammation of the arteries.
4. Drinking alcohol.
5. Physical inactivity.
6. Constantly exceeding the caloric intake of the diet.
7. Emotional stress. With anxiety, the body's need for oxygen increases, and the heart muscle is no exception. In addition, during prolonged stress, cortisol and catecholamines are released, which narrow the coronary vessels, and cholesterol production increases.
8. Lipid metabolism disorders and atherosclerosis of the coronary arteries. Diagnostics - study of the lipid spectrum of blood.
9. Syndrome of excessive colonization of the small intestine, which disrupts liver function and causes vitamin deficiency of folic acid and vitamin B12. This increases cholesterol and homocysteine ​​levels. The latter disrupts peripheral circulation and increases the load on the heart.
10. Itsenko-Cushing syndrome, which occurs with hyperfunction of the adrenal glands or with the use of steroid hormones.
11. Hormonal diseases of the thyroid gland, ovaries.

Men over 50 and women during menopause are most likely to suffer from angina and heart attacks.

Risk factors for coronary heart disease that aggravate the course of coronary heart disease: uremia, diabetes mellitus, pulmonary failure. IHD is aggravated by disturbances in the conduction system of the heart (blockade of the sinoatrial node, atrioventricular node, bundle branches).

The modern classification of coronary artery disease allows doctors to correctly assess the patient’s condition and take the right measures to treat it. For each form that has a code in the ICD, its own diagnostic and treatment algorithms have been developed. Only by freely navigating the varieties of this disease can the doctor effectively help the patient.

Hemorrhagic vasculitis

Hemorrhagic vasculitis is considered a disease that is a type of immune vasculitis of small vessels and is characterized by increased formation of immune complexes and increased permeability of vascular walls. This pathology can develop 2-3 weeks after acute tonsillitis, influenza or scarlet fever. Hemorrhagic vasculitis is more common in children than in adults. Children aged 4 to 12 years are especially susceptible to the disease. Boys get sick 2 times more often than girls.

Hemorrhagic vasculitis ICD 10 (according to the international classification of diseases, tenth revision) is included in the group of diseases under the code D69.0 Allergic purpura. Most photos of hemorrhagic vasculitis show that the main symptom of the disease is an allergic rash.

Etiology of the disease

The causes of hemorrhagic vasculitis in adults and children are divided into several types:

The most common causes of hemorrhagic vasculitis are associated with the influence of infectious agents.

The principle of the mechanism of formation of the disease is the formation of immune complexes, which, circulating through the bloodstream, can remain on the inner surface of the vascular walls. After this, immune complexes gradually destroy the walls of small vessels, which causes an inflammatory process of an aseptic nature and a decrease in the elasticity of the capillaries. As a result, this contributes to increased permeability of vessel walls and the formation of lumens, which lead to the formation of blood clots and fibrin deposits. Therefore, it is believed that the main symptom of vasculitis is hemorrhagic syndrome and microthrombosis.

Symptoms of the disease

Most photos of hemorrhagic vasculitis in children show that the disease begins with ordinary skin rashes. The rash is most often small-spotted in nature, located in a symmetrical order and does not disappear with pressure. The rash usually appears around the joint surfaces, in the area of ​​extension of the limbs and in the buttock area. A rash on the face, trunk, feet, or palms is quite rare. The intensity of the rash can vary - from rare and small elements to multiple ones that tend to merge. After the rashes disappear, pigmentation and severe peeling may remain in their place.

70 percent of patients exhibit symptoms of hemorrhagic vasculitis such as damage to the articular surfaces. This symptom often occurs along with rashes in the first week of the disease. Damage to joints can be minor and cause short-term pain, but it can also be more extensive, when not only large (ankle and knee) but also small articular surfaces are affected. Swelling occurs and the shape of the articular surface changes, and pain can last from 2 hours to 5 days. However, the disease does not cause severe deformation of the articular surfaces.

The third most common symptom is moderate abdominal pain, which may go away on its own within 24 hours. Typically, pain occurs at the very beginning of the disease, before rashes and joint disorders. For some, pain in the abdomen occurs suddenly in the form of intestinal colic, the location of which is difficult to determine. Painful sensations may appear several times throughout the day. In parallel with the pain, dyspeptic disorders appear - vomiting, nausea, diarrhea. In some cases, the temperature rises to 37.5 degrees. More rare signs of vasculitis include kidney damage in the form of glomerulonephritis and pulmonary syndrome, which is manifested by cough and shortness of breath.

When the disease occurs in a child, a functional systolic murmur may be heard in the heart. Also often due to inflammatory processes in the vessels of the brain, the central nervous system is affected. Children may complain of headache, weakness, dizziness, nausea and irritability. Sometimes boys experience testicular damage (mostly bilateral), which causes swelling and tenderness of the tissue.

Conservative treatment of hemorrhagic vasculitis

Treatment of hemorrhagic vasculitis begins with hospitalization, which lasts at least 20 days, and mandatory bed rest.

First of all, a strict diet is prescribed, which prevents the development of allergies in patients. The diet for hemorrhagic vasculitis excludes the consumption of chocolate, cocoa, citrus fruits, strong black tea and coffee, red fruits and berries. It is recommended to consume vegetable purees, olive oil, butter, low-fat dairy products, stewed or boiled meat and fish, cereal soups and stews, dry white bread, fruits, green tea with milk, jelly, juices, puddings. The duration of the diet for hemorrhagic vasculitis reaches 1-2 years to prevent relapse of the disease.

Drug treatment includes the use of the following drugs:

• antibiotics that do not cause an allergic reaction (rifampicin, ceporin) and are prescribed for acute forms of infectious diseases;
• enterosorbents (activated carbon) and gastric drops;
• antispasmodics to reduce pain (baralgin, no-shpa);
• vitamins A and E;
• infusion therapy for severe symptoms (heparin and glucocorticoids);
• pulse therapy with prednisone.

Since the disease is aggravated by emotional stress and anxiety, it is necessary to exclude stressful situations or use sedatives and tranquilizers that improve the result of complex treatment.

Treatment of hemorrhagic vasculitis in children is carried out over a long period of time - at least two years. It is imperative to register a sick child with a dispensary and visit a doctor every month for the first six months. Then once every 3 months or once every six months, depending on the condition. Preventive measures consist of treating foci of chronic infection, and systematically taking tests to detect helminth eggs. During treatment, it is forbidden to play sports, stay in the sun for a long time and do physical procedures.

According to most forums, hemorrhagic vasculitis has a positive prognosis, since 95 percent of sick children recover within months.

Traditional methods of treatment

Treatment of hemorrhagic vasculitis with folk remedies consists of preparing infusions, ointments and teas based on plant materials. Folk remedies are used both externally and internally.

The most useful and effective remedies include the following recipes:

1. To prepare a medicinal ointment, you need to take dried rue leaves (50 g) and vegetable or butter (250 g). Chop the leaves thoroughly and mix with oil. Place the resulting mixture in a cold and dark room for at least 2 weeks. After this, you can use the ointment: apply to the surface of the skin or affected joints 3-4 times a day. Usually, skin rashes go away very quickly after using this product.
2. To prepare a medicinal tincture, take crushed herbs of yarrow, horsetail, mint, elderberry, string and calendula. All in equal proportions, 2 tbsp. Pour the resulting mixture with 200 ml of boiled water and leave in a cold and dark room for 2-4 hours. It is recommended to consume the strained tincture 100 ml 5 times a day.
3. Strong, freshly brewed green tea that can be consumed 2-3 times a day. Tea helps restore the elasticity of vascular walls and helps normalize blood circulation.

If the diagnosis of the disease is confirmed, then before using the above recipes you should carefully read the ingredients in order to exclude allergenic products or herbs to which individual intolerance occurs. It is also necessary to consult a doctor and not self-medicate.

Chronic cor pulmonale

• Causes
• What happens in the body
• Clinical course
• Clinical manifestations
• Diagnostics
• Functional classes
• Treatment
• Forecast

The term “chronic cor pulmonale” refers to changes in the heart muscle caused by lung diseases. This excludes cases of pathology complicating diseases of the heart and large vessels (mitral stenosis, cardiosclerosis after a heart attack, congenital defects, dilated cardiomyopathy).

In diagnosis, an indispensable condition must be a primary violation of the structure of the lung tissue and its functions. The prevalence of the recorded pathology among the adult population allows us to place it in third place after ischemic and hypertension diseases.

In the International Classification of Diseases (ICD-10), types of chronic pulmonary heart disease are included in the general class of cardiovascular diseases. Codes I26, I27, I28 differ in etiological factors. All cases are united by the gradual formation of overload of the right side of the heart due to the development of high blood pressure in the pulmonary circulation.

Causes

Depending on the causes, the WHO Expert Committee has developed a classification of chronic pulmonary heart disease. Diseases are divided into 3 groups:

• group 1 - diseases associated with impaired passage of air through the alveoli, these can be mechanical obstacles (bronchial asthma), inflammatory lesions (tuberculosis, chronic bronchitis, bronchiectasis, pneumoconiosis), replacement of lung tissue with fibrous tissue (systemic lupus erythematosus, sarcoidosis, eosinophilic infiltration ), a total of 21 nosologies are included;
• group 2 - diseases that impair ventilation of the lungs by affecting the auxiliary mechanisms of breathing (skeletal skeleton of the chest, ribs, muscles), this includes curvature of the spine, adhesions in the pleural cavity, chronic diseases associated with impaired neuromuscular conduction (poliomyelitis) , artificial hypoventilation after surgical interventions on the chest organs;
• group 3 - vascular lesions of the lungs (arteritis, thrombosis and embolism, compression of the main vessels by a tumor, aortic aneurysm and others).

All risk factors for underlying disease accelerate and negatively affect the heart.

What happens in the body

In patients of groups 1 and 2, all changes develop due to spasm of small arterioles in the lung tissue as a reaction to insufficient oxygen supply. In group 3, in addition to spasm, there is a narrowing or blockage of the vascular bed. The pathogenesis of the disease is associated with the following mechanisms.

1. Alveolar hypoxia (lack of oxygen in the alveoli) - scientists associate vascular spasm in response to hypoxia with disturbances in sympathoadrenal regulation. There is a contraction of vascular muscles, an increase in angiotensin-converting enzyme (ACE), calcium in the blood, and a decrease in relaxation factors of the pulmonary vessels.
2. Hypercapnia - an increase in the concentration of carbon dioxide in the blood does not directly affect the vascular wall, but through acidification of the environment and a decrease in the sensitivity of the respiratory center of the brain. This mechanism enhances the production of aldosterone (adrenal hormone), which retains water and sodium ions.
3. Changes in the vascular bed of the lungs - compression and emptying of capillaries due to developing fibrous tissue is important. Thickening of the muscular walls of the pulmonary vessels contributes to the narrowing of the lumen and the development of local thrombosis.
4. An important role is played by the development of anastomoses (connections) between the bronchial arteries, belonging to the systemic circulation, and the pulmonary vessels.
5. The pressure in the systemic circle is higher than in the lungs, so the redistribution goes towards the pulmonary vascular bed, which further increases the pressure in it.
6. In response to hypoxia, blood cells that carry hemoglobin and erythrocytes change. Their number increases simultaneously with platelets. Favorable conditions for thrombus formation are created and blood viscosity increases.

All taken together leads to increased load on the right ventricle, hypertrophy, and then failure of the right heart. An enlarged right atrioventricular orifice contributes to insufficient closure of the tricuspid valve.

Clinical course

Soviet pulmonologists B. Votchal and N. Palev proposed a clinical description of the stages of development of the pulmonary heart:

• in the initial (preclinical) stage - there are no symptoms of hypertension in the pulmonary circulation, hypertension is possible temporarily with an exacerbation of pulmonary disease;
• in the second stage - there is right ventricular hypertrophy, but all signs are compensated; instrumental examination reveals stable pulmonary hypertension;
• third stage - accompanied by decompensation (pulmonary heart failure), there are symptoms of right ventricular overload.

Clinical manifestations

At the early stage of the disease, the manifestations of chronic pulmonary heart disease do not differ from the typical symptoms of major pulmonary diseases. They intensify with exacerbation and are treatable.

Shortness of breath is a consequence of oxygen deficiency, but it also accompanies inflammation of the lung tissue, emphysema. The intensity does not always correspond to the degree of hypoxia.

Tachycardia is a nonspecific symptom; the heart rate increases in various diseases that are associated with an activated sympathetic nervous system and increased release of adrenaline.

Chest pain is not similar to angina. They are believed to be caused by insufficiency of the coronary vessels, which have to feed the thickened muscle of the right ventricle. Spasm of the arteries of the heart and intoxication of the myocardium with inflammatory products are also important.

Increased fatigue and weakness occur when the shock capacity of the heart decreases. Peripheral tissues of various organs, including the brain, lack blood supply.

Heaviness in the legs, swelling - in addition to myocardial weakness, an increase in the permeability of the vascular wall plays a role. Swelling occurs on the feet and legs. They intensify in the evening and subside during the night. In the third stage, they spread to the thighs.

The feeling of heaviness and pain in the right hypochondrium is caused by an enlarged liver and stretching of its capsule. In a severe form of the disease, ascites simultaneously appears and the abdomen “grows” rapidly. This symptom is more pronounced in elderly patients with concomitant atherosclerosis of the abdominal arteries.

A cough with a small amount of sputum is more associated with the underlying pathology of the lungs.

Manifestations of encephalopathy - chronic lack of oxygen and excess carbon dioxide cause pathological disorders in the brain, disrupt vascular permeability, and promote edema. Patients have 2 possible symptoms:

• increased excitability, aggressive behavior, euphoria, development of psychosis;
• lethargy, lethargy, indifference, drowsiness during the day, insomnia at night.

In severe cases, seizures occur with loss of consciousness or dizziness, cold sweat and decreased blood pressure.

Diagnostics

In people with chronic cor pulmonale, the diagnosis can be suspected by their appearance: in the compensation stage, dilated skin vessels appear in the cheek area (blush) and on the conjunctiva (“rabbit eyes”). Cyanosis is found on the lips, tip of the tongue, nose, and ears.

When examining the fingers, changes in the nail phalanges are visible: they become flat and widened (“drumsticks”). Unlike heart failure, the arms and legs remain warm to the touch.

When auscultating the heart, the doctor hears:

• characteristic changes in tones above the pulmonary artery;
• in the stage of decompensation - a murmur indicating insufficiency of the right atrioventricular valve;
• a lot of different types of wheezing in the lungs against the background of altered breathing.

The x-ray reveals a typical bulging of the contours of the pulmonary artery, an enhanced tissue pattern, and an expansion of the zone of lymphatic vessels. This indicates an increase in pressure in the pulmonary circle. In the decompensation stage, the heart shadow expands to the right.

Echocardiography assesses the strength of the right ventricle, the degree of dilatation, and overload. Due to increased pressure, the wall of the interventricular septum bends to the left.

Respiratory functions are measured with special devices, and the spirogram is deciphered by a doctor in the functional diagnostics office.

The study of pressure in the pulmonary artery is carried out in complex diagnostic cases. A reliable sign of hypertension in the pulmonary circle is considered to be a resting pressure of 25 mm Hg. Art. and higher, and with load - over 35.

Functional classes

During the examination, it is necessary to establish the functional class of manifestations of cor pulmonale.

• Class 1 - the main symptoms are diseases of the bronchi and lungs, pulmonary hypertension is detected only with instrumental examination and stress tests;
• Class 2 - in addition to the listed symptoms, there is respiratory failure due to narrowing of the bronchi;
• Class 3 - respiratory failure is severe, followed by cardiac failure. Constant shortness of breath, tachycardia, dilatation of the neck veins, cyanosis. Studies reveal persistent hypertension in the pulmonary circulation;
• Class 4 - decompensation, all clinical manifestations are pronounced, there are congestion, respiratory and heart failure of the third degree.

Treatment

Treatment of chronic pulmonary heart disease should begin with the prevention of exacerbations of respiratory diseases, especially colds and flu, with the timely use of antiviral and antibacterial treatment.

Mode Changes

Patients are advised to limit physical activity. Do not visit mountainous areas, since in high altitude conditions even a healthy person experiences oxygen deficiency. And in patients with pulmonary diseases, a reflex vascular spasm occurs and the degree of tissue hypoxia deepens.

Women should be aware of the negative effects of birth control pills.

It is necessary to stop smoking and even staying in a smoky room.

Directions of therapy

All treatment methods are aimed at eliminating or weakening the existing mechanisms of pathology, these include:

• treatment of the underlying pulmonary disease and compensation of lost respiratory function;
• decreased vascular resistance in the pulmonary circulation and unloading of the right ventricle;
• restoration of normal blood composition, antithrombotic therapy.

Oxygen treatment

Oxygen is supplied in a humidified form through a mask, cannulas in the nasal passages, and some clinics use oxygen tents with special air saturation conditions. For a therapeutic effect on chronic pulmonary heart disease, the oxygen level in the inhaled air must be at least 60%.

Therapy is carried out for an hour up to 5 times a day and more often.

How to lower pulmonary artery pressure

To reduce pressure in the pulmonary artery, medications of different groups are used:

• calcium antagonists (possible swelling and redness of the face, headache, feeling of heat, decreased blood pressure);
• α-adrenergic blockers - dilate blood vessels, reduce the ability of platelets to stick together (the side effects are the same, increased irritability and weakness are possible);
• inhaled nitric oxide (has no side effects);
• diuretics - medications with a diuretic effect unload the general bloodstream, facilitate the work of the heart (control of the potassium content in the blood is required);
• group of prostaglandins - selectively act on small blood vessels (side effects such as nasal congestion, increased cough, increased blood pressure, headache).

The drugs Heparin and Pentoxifylline are necessary to improve blood flow and antithrombotic action.

In case of severe heart failure, cardiac glycosides are prescribed very carefully.

Patients with symptoms of decompensation are treated in a hospital. Observation and clinical examination are carried out by a local therapist and pulmonologist.

Forecast

The mortality rate of patients from chronic pulmonary heart disease remains high: 45% of patients survive in the decompensation stage for about two years. Even with intensive therapy, their life expectancy is no more than four years.

Lung transplantation gives 60% of patients survival over the next two years.

The disease is very difficult to treat. Any person has the opportunity to rid himself of bad habits and take care of his health in a timely manner. The appearance of cough, shortness of breath and other symptoms requires immediate medical attention.

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