Pulmonary heart.

The relevance of the topic: diseases of the bronchopulmonary system, chest are of great importance in the defeat of the heart. The damage to the cardiovascular system with diseases of the bronchopulmonary apparatus Most authors refers to the term pulmonary heart.

Chronic pulmonary heart develops approximately 3% of patients with chronic lung diseases, and in the overall structure of mortality from stagnant heart failure to the share of chronic pulmonary heart accounts for 30% of cases.

Lonantic Heart - These are hypertrophy and dilatation or only the pursuit of the right ventricle arising from hypertension of a small circle of blood circulation, developed due to diseases of the bronchi and lungs, deformity of the chest, or the primary lesion of the pulmonary arteries. (WHO 1961).

Hypertrophy of the right ventricle and its dialation in changes as a result of the primary damage of the heart, or congenital defects do not belong to the concept of a pulmonary heart.

Recently, clinicians have been noticed that hypertrophy and pursuit of the right ventricle are already late manifestations of a pulmonary heart when it is already impossible to rationally treat such patients, so there was a proposal for a new definition of a pulmonary heart:

"The pulmonary heart is a complex of hemodynamic disorders in a small circulation of blood circulation, developing due to diseases of the bronchopile apparatus, chest deformities, and primary lesions of pulmonary arteries, which at the final stage It is manifested by hypertrophy of the right ventricle and progressive insufficiency of blood circulation. "

Etiology of the pulmonary heart.

The pulmonary heart is a consequence of diseases of three groups:

Diseases of bronchi and lungs that primarily affect the passage of air and Alveol. This group has about 69 diseases. The cause of the development of a pulmonary heart in 80% of cases.

chronic obstructive bronchitis

pneumosclerosis of any etiology

pneumoconiosis

tuberculosis, not by itself, as posttuberculosis outcomes

SLE, Sarcoidoism Beck (BOECK), FIBrosters alveolites (endo- and exogenous)

Diseases primarily affecting the chest, a diaphragm with limiting their mobility:

kifoscoliosis

multiple damage to ribs

syndrome Pickwick in obesity

bekhtereva's disease

pleural suppuration after transferred pleuritic

Diseases primaryly affecting pulmonary vessels

primary arterial hypertension (Aerza disease, Disease Ayerza`s)

recurrent thromboembolia pulmonary artery (TEL)

compression of the pulmonary artery from the veins (aneurysm, tumors, etc.).

The diseases of the second and third group are the cause of the development of the pulmonary heart in 20% of cases. That is why they say that, depending on the etiological factor, three forms of the pulmonary heart are distinguished:

bronchildo

thoracodiaphragmal

vascular

Standards of values \u200b\u200bcharacterizing hemodynamics of a small circle of blood circulation.

Systolic pressure in the pulmonary artery less systolic pressure in a large circulation of blood circulation is about five times.

The pulmonary hypertension speaks if the systolic pressure in the pulmonary artery in the peace is greater than 30 mm.rt. The diastolic pressure is greater than 15, and the average pressure is more than 22 mm.rt.

PATHOGENESIS.

The pathogenesis of the pulmonary heart is based on pulmonary hypertension. Since the most often pulmonary heart develops with bronchopal diseases, then with this and begin. All diseases, and in particular, chronic obstructive bronchitis will primarily lead to respiratory (pulmonary) failure. Pulmonary failure is such a state in which the normal gas composition of the blood is disturbed.

This is such a state of the body in which it is either no maintenance of a normal gas composition of blood, or the latter is achieved by an abnormal operation of an external respiratory unit, leading to a decrease in the functionality of the body.

There are 3 stages of pulmonary failure.

The arterial hypoxemia underlies pathogenesis underly under chronic heart diseases, especially in chronic obstructive bronchitis.

All these diseases lead to respiratory failure. Arterial hypoxemia will lead to alveolar hypoxia at the same time as a result of the development of pneumophybosis, the emphysema of the lungs increases intrastoleolar pressure. In the conditions of arterial hypoxemia, the irregular function of the lungs is disturbed - biological active substances begin to produce, which have not only bronchospastic, but also a vasospast effect. At the same time, at this, there is a violation of the vascular architectoectonics of the lungs - part of the vessels is dying, part expands, etc. Arterial hypoxemia leads to tissue hypoxia.

The second stage of pathogenesis: arterial hypoxemia will lead to the restructuring of central hemodynamics - in particular an increase in the amount of circulating blood, polycythemia, polyglobulia, an increase in blood viscosity. Alveolar hypoxia will lead to hypoxmic vasoconstriction by reflex, using reflex which is called the reflex Euler-Lesrand. Alveolar hypoxia led to hypoxcemic vasoconstrictions, an increase in intraarterial pressure, which leads to an increase in hydrostatic pressure in capillaries. The absorption of the non-spiratory function of the lungs leads to the release of serotonin, histamine, forebanding, catecholamines, but the most basic thing is that in the conditions of fabric and alveolar hypoxia of interstics begins to produce an enzyme angiotensin in a larger number of angiotensin. Lightweight is the main body where this enzyme is formed. It turns angiotensin 1 to angiotensin 2. Hypoxmic vasoconstriction, the release of Bav in the conditions of rebuilding of central hemodynamics will be given not just to increase the pressure in the pulmonary artery, but to a resistant increase in it (above 30 mm.T.st.), that is, to the development of pulmonary hypertension. If the processes continue further if the main disease is not treated, then naturally part of the vessels in the pulmonary artery system die, due to pneumosclerosis, and the pressure is raised in the pulmonary artery. At the same time, persistent secondary pulmonary hypertension will lead to the fact that shunts are revealed between the pulmonary artery and bronchial arteries and the neoxygenated blood enters a large circle of blood circulation through the bronchial veins and also contributes to an increase in the work of the right ventricle.

So, the third stage is a persistent pulmonary hypertension, the development of venous shunts that strengthen the work of the right ventricle. The right ventricle is not powerful by itself, and hypertrophy with elements of dialing quickly develops.

The fourth stage is hypertrophy or pushing the right ventricle. The myocardial dystrophy of the right ventricle will also contribute as tissue hypoxia.

So, arterial hypoxemia led to secondary pulmonary hypertension and hypertrophy of the right ventricle, to its dilatation and development of mainly the right-hand deficiency of blood circulation.

The pathogenesis of the pulmonary heart development during thoracodiaphragmal form: in this form, the leading is the leading of the lungs due to kifoscoliosis, pleural suppurations, spinal deformations, or obesity at which the diaphragm rises high. Hypotentilation of the lungs will primarily lead to the restrictive type of respiratory failure, in contrast to obstructive, which is caused by chronic pulmonary heart. And then the mechanism is the same - restrictive type of respiratory failure will lead to arterial hypoxemia, alveolar hypoxemia, etc.

The pathogenesis of the pulmonary heart disease is that during thrombosis of the main branches of pulmonary arteries, the blood supply of pulmonary tissue sharply decreases, since along with thrombosis of the main branches, there are friendly reflex narrowings of small branches. In addition, with vascular form, in particular, pronounced humoral shifts contribute to the development of the pulmonary heart, the development of a pulmonary heart, that is, a noticeable increase in the number of solenone, foremeadyness, catecholamines, isolating the conversion, angiotensin-shift enzyme.

The pathogenesis of the pulmonary heart is a multi-step, multistage, in some cases not to the end of a clear one.

Classification of the pulmonary heart.

The uniform classification of the pulmonary heart does not exist, but the first international Classification Mainly etiological (WHO, 1960):

bronchopulmonary heart

thoracodiaphragmal

vascular

A domestic classification of the pulmonary heart is proposed, which provides for the division of a pulmonary heart at the pace of development:

• subacute

  chronic

The sharp pulmonary heart develops within a few hours, minutes for a maximum of days. Subacute pulmonary heart develops for several weeks, months. Chronic pulmonary heart develops for several years (5-20 years).

This classification provides compensation, but the sharp pulmonary heart is always decompensated, that is, it requires immediate assistance. The subacute can be compensated and decompensated mainly by the right-hand type. Chronic pulmonary heart can be compensated, subcompensated, decompensated.

In Genesis, the sharp pulmonary heart is developing with vascular and bronchopulmonary forms. The subacute and chronic pulmonary heart can be vascular, bronchopile, thoracodiaphragmal.

The sharp pulmonary heart develops primarily:

with embolism - not only with thromboembolism, but also with gas, tumor, fat, etc.,

at pneumothoraksk (especially valvable),

with an attack of bronchial asthma (especially with asthmatic status - a qualitatively new state of patients with bronchial asthma, with a complete blockade of beta2-adrenoreceptors, and with a sharp pulmonary heart);

with acute drain pneumonia

right-sided Total Pleurrites

The practical example of a subacute pulmonary heart is a recurrent thrombolbolia of small branches of pulmonary arteries, with an attack of bronchial asthma. A classic example is cancer lymphanget, especially when chorioneepitheloma, with peripheral lung cancer. The thoracodifragmal form develops in hypoventilation of central or peripheral origin - Miastic, botulism, poliomyelitis, etc.

To delimit at what stage, the pulmonary heart from the stage of respiratory failure passes into the stage of heart failure another classification was proposed. The pulmonary heart is divided into three stages:

hidden latent insufficiency - the violation of the external respiratory function is - the drum / zel is reduced to 40%, but there are no changes in the gas composition of blood, that is, this stage characterizes respiratory failure of 1-2 stages.

stage of pronounced pulmonary failure - the development of hypoxemia, hyperkapin, but without signs of heart failure on the periphery. There are shortness of breath at rest, which cannot be attributed to the strike of the heart.

stage of pulmonary heart failure of varying degrees (swelling on the limbs, an increase in abdomen, etc.).

Chronic pulmonary heart in terms of pulmonary failure, saturation of arterial blood oxygen, right ventricular hypertrophy and blood circulation deficiency is divided into 4 stages:

the first stage is the pulmonary failure of the 1st degree / Zel decreased to 20%, the gas composition is not broken. Hypertrophy of the right ventricle is absent on the ECG, but on the echocardiogram hypertrophy there is. There are no blood circulation in this stage.

pulmonary failure 2 - jerks / kerity up to 40%, saturacy of oxygen up to 80%, first appear indirect signs Hypertrophy of the right ventricle, insufficiency of blood circulation +/-, that is, only shortness of breath alone.

the third stage is the pulmonary failure of 3 - jerks / жel less than 40%, the saturation of arterial blood is up to 50%, there are signs of hypertrophy of the right ventricle to the ECG in the form of direct signs. Insufficiency of blood circulation 2a.

the fourth stage is pulmonary failure 3. Blood saturation with oxygen less than 50%, hypertrophy of the right ventricle with a dialation, the lack of blood circulation 2b (dystrophic, refractory).

Clinic of acute pulmonary heart.

The most common cause of development is TEL, an acute increase in intragenic pressure due to the attack of bronchial asthma. Arterial prokapillary hypertension with an acute pulmonary heart, as in the vascular form of a chronic pulmonary heart is accompanied by an increase in pulmonary resistance. Next is the rapid development of the right ventricular duty. Outragia right-hand deficiency is manifested by a pronounced shortness of an inspiratory switch, rapidly increasing cyanosis, sternum pain, shock or collapse, quickly increase liver dimensions, edema on legs, ascites, epigastric pulsation, tachycardia (120-140), breathing hard , in some places weakened vesicular; Wet wet, single-caliber wheezing especially in the lower lungs. Of great importance in the development of the acute pulmonary heart, additional research methods are especially ECG: a sharp deviation of the electric axis to the right (R 3\u003e R 2\u003e R 1, S 1\u003e S 2\u003e S 3), the P-Pulmonale appears - a pointed teeth of P, in the second , Third standard leads. The blockade of the right leg of the Gis beam is complete or incomplete, Inversion ST (more often asylum), s in the first definition of deep, q in the third assignment deep. Negative teeth S in the second and third assignment. The same signs can also with acute myocardial infarction of the rear wall.

Emergency care depends on the cause of the sharp pulmonary heart. If there was a TELE, they prescribe painkillers, fibrinolytic and anticoagulant drugs (heparin, fibrinolysin), streptodecase, streptocinase), up to surgical treatment.

With asthmatic status - large doses of glucocorticoids intravenously, bronchological preparations through the bronchoscope, translation to IVL and lavage of the bronchi. If this is not done, the patient dies.

With valve pneumothorax - surgical treatment. Under the drain pneumonia, along with treatment with antibiotics, diuretic and heart glycosides are prescribed.

Clinic chronic pulmonary heart.

The patients are bothering shortness of breath, the character of which depends on the pathological process in the lungs, such as respiratory failure (obstructive, restrictive, mixed). With obstructive processes, shortness of expiratory character with an unchanged respiratory frequency, during restrictive processes, the duration of the exhalation is reduced, and the respiratory rate increases. With an objective study, along with signs of the underlying disease, cyanosis appears, most often diffuse, warm due to the preservation of peripheral blood flow, in contrast to patients with heart failure. In some patients, cyanosis is expressed so much that the skin covers acquire a cast-iron color. Nobukh cervical veins, swelling of the lower extremities, ascites. The pulse is rapidly, the boundaries of the heart are expanding to the right, and then a deep tone of the deaf due to emphysema, the accent of the second tone above the pulmonary artery. Systolic noise at the Meso-shaped process due to the pursuit of the right ventricle and relative deficiency of the right three-risk valve. In some cases, with severe heart failure, a diastolic noise on the pulmonary artery can be heard - the noise of sin-style, which is associated with the relative failure of the pulmonary artery valve. Over light percussion sound box, breathing vesicular, rigid. In the lower parts of the lungs are stagnant, unailwaters. When the belly palpation is an increase in the liver (one of the reliable, but not early signs of the pulmonary heart, as the liver can shift due to emphysema). The severity of symptoms depends on the stage.

The first stage: Against the background of the main disease, shortness of breath is enhanced, cyanosis appears to acrocyanosis, but the right boundary of the heart is not expanded, the liver is not increased, in the lungs, physical data depend on the underlying disease.

The second stage - shortness of breath goes into the attacks of suffocation, with a difficult breath, cyanosis becomes diffuse, from the data of an objective study: a pulsation appears in the epigastric region, the tones of the deaf, the accent of the second tone above the pulmonary artery is not permanent. The liver is not increased, can be omitted.

The third stage is joined by signs of destroying deficiency - an increase in the right boundary of cardiac dullness, an increase in the size of the liver. Permanent swelling on the lower limbs.

Fourth stage - shortness of breath at rest, forced position, often join the respiratory rhythm disorders of the Chein Stokes type and biota. Edems are permanent, do not succumb to treatment, the pulse is weak frequent, the bullish heart, the tones of the deaf, systolic noise of the mild-shaped process. In the lungs mass of wet wheezing. The liver of significant sizes is not reduced by the action of glycosides and diuretic as fibrosis develops. Patients are constantly dormant.

The diagnosis of the thoracodiaphragmal heart is often complex, it is always necessary to remember the possibility of its development during kifoscolyosis, diseases of Bekhtereva, etc. The most important feature is the early appearance of cyanosis, and a noticeable increase in shortness of shortness of scratch. Pickwick syndrome is characterized by triad symptoms - obesity, drowsiness, pronounced cyanosis. For the first time, this syndrome was described by Dickens in the "posthumous notes of the Pickwick Club". It is associated with the cranopy and brain injury, obesity is accompanied by thirst, bulimia, arterial hypertension. Sugar diabetes is often developing.

Chronic pulmonary heart with primary pulmonary hypertension is called Aerza (described in 1901). The polyethological disease, not clear genesis, mostly sick women from 20 to 40 years. Patomorphological studies have been established that with primary pulmonary hypertension, the intima of the prepillary arteries is thickening, that is, the media thickening is noted in the arteries of the muscular type, and fibrino-shaped necrosis develops with subsequent sclerosis and the rapid development of pulmonary hypertension. The symptoms are varied, usually complaints about weakness, fatigue, heart pain, or in the joints, fainting, dizziness, Reyno syndrome can appear in 1/3 of patients. And in the future, shortness of breath is growing, which is the sign, which indicates that the primary pulmonary hypertension goes into a stable final stage. Cyanosis is rapidly growing, which is expressed to the degree of cast-iron shade, becomes constant, sweeping rapidly. The diagnosis of primary pulmonary hypertension is set by the exclusion method. Most often, this diagnosis is pathologist. In these patients, the entire clinic progresses without a background in the form of obstructive or restrictive respiratory disruption. With echocardiography, the pressure in the pulmonary artery reaches the maximum digits. The treatment is ineffective, death comes from thromboembolism.

Additional methods of research at a pulmonary heart: in the chronic process in the lungs - leukocytosis, an increase in the amount of erythrocytes (polycythemia associated with the enhancement of erythropoese, due to the arterial hypoxemia). Radiological data: appear very late. One of the earliest symptoms is to escape the trunk of the pulmonary artery on the radiograph. Pulmonary artery scattering, often smoothing the waist of the heart, and this heart many doctors take for a mitral heart configuration.

ECG: indirect and direct signs of hypertrophy of the right ventricle appear:

deviation of the electrical axis of the heart to the right - R 3\u003e R 2\u003e R 1, S 1\u003e S 2\u003e S 3, an angle is greater than 120 degrees. The most important indirect sign is an increase in the cluster interval R in V 1 more than 7 mm.

direct signs - blockade of the right leg of a beam of Gis, the amplitude of the R in V 1 more than 10 mm with a full blockade of the right leg of the GIS beam. The appearance of a negative teeth with the displacement of the teeth below is an isolated in the third, second standard assignment, V1-V3.

Of great importance is spirography, which reveals the type and degree of respiratory failure. On the ECG signs of hypertrophy of the right ventricle appear very late, and if only deviations of the electric axis appear to the right, they already talk about pronounced hypertrophy. The most basic diagnosis is dopplerocardiography, echocardiography - an increase in the right heads of the heart, an increase in pressure in the pulmonary artery.

Principles of treatment of the pulmonary heart.

The treatment of the pulmonary heart is the treatment of the main disease. In the exacerbation of obstructive diseases, bronchyolitic agents are prescribed, expectorant means. In the Syndrome of Piviquia - treatment of obesity, etc.

Lower the pressure in the pulmonary artery calcium antagonists (nifedipine, verapamil), peripheral vasodilators reducing preload (nitrates, Corvaton, nitroprusside sodium). Sodium nitroprusside in combination with an angiotensional enzyme inhibitors has an impaired value. Nitroprusside at 50-100 mg intravenously, drotted 25 mg 2-3 times a day, or enalapril (second generation, 10 mg per day). We also use the treatment of forebanding E, antiserotonin drugs, etc. But all these drugs are effective only at the very beginning of the disease.

Treatment of heart failure: diuretic, glycosides, oxygen therapy.

Anticoagulant, anti-aggregative therapy - heparin, Trental, et al. Due to the tissue hypoxia, myocardiodistrophy is rapidly developing, therefore, cardioprotectors are prescribed (potassium orotat, Panangin, Riboxin). Very carefully prescribed heart glycosides.

Prevention.

Primary - prevention of chronic bronchitis. Secondary - treatment of chronic bronchitis.

- The pathology of the right sections of the heart, characterized by an increase (hypertrophy) and an expansion (dilatation) of the right atrium and ventricle, as well as the insufficiency of blood circulation, developing due to hypertension of a small circle of blood circulation. The formation of the pulmonary heart is promoted by the pathological processes of the bronchology system, vessels of the lungs, chest. The clinical manifestations of the acute pulmonary heart include shortness of breath, stipulated pain, the growth of skin cyanosis and tachycardia, psychomotor excitement, hepatomegaly. The survey reveals an increase in the boundaries of the heart to the right, the rhythm of gallop, pathological pulsation, signs of overloading of the right heads of the heart on the ECG. Additionally conduct radiography of the organs of the chest, ultrasound of the heart, the study of FVD, analysis gas composition blood.

MKB-10.

I27.9. Elementary heart failure unspecified

General

- The pathology of the right sections of the heart, characterized by an increase (hypertrophy) and an expansion (dilatation) of the right atrium and ventricle, as well as the insufficiency of blood circulation, developing due to hypertension of a small circle of blood circulation. The formation of the pulmonary heart is promoted by the pathological processes of the bronchology system, vessels of the lungs, chest.

The acute shape of the pulmonary heart is developing quickly, in a few minutes, hours or days; Chronic - for several months or years. Almost 3% of patients with chronic bronchopulmonary diseases are gradually developing a pulmonary heart. The pulmonary heart significantly aggregates the Cardiopathology during the 4th place among the causes of mortality in cardiovascular diseases.

Causes of the development of the pulmonary heart

The bronchouselet shape of the pulmonary heart develops with primary lesions of the bronchi and lungs as a result of chronic obstructive bronchitis, bronchial asthma, bronchiolite, emphysema, diffuse pneumosclerosis of various genesis, polycystic, bronchoctasis, tuberculosis, sarcoidosis, pneumoconiosis, Hamman's syndrome - Richa, etc. This form. About 70 bronchopulmonary diseases that contribute to the formation of a pulmonary heart in 80% of cases can cause.

The appearance of the thoracodiaphraggmal shape of the pulmonary heart contributes to primary damage to the chest, the diaphragm, the limitation of their mobility, significantly disturbing ventilation and hemodynamics in the lungs. These include diseases deforming the chest (kifoscoliosis, behterev's disease, etc.), neuromuscular diseases (poliomyelitis), the pathology of the pleura, the diaphragm (after thoracoplasty, with pneumosclerosis, the diaphragm paresis, the peeper syndrome during obesity, etc. ).

The vascular shape of the pulmonary heart is developing with primary lesions of pulmonary vessels: primary pulmonary hypertension, pulmonary vasculitis, thromboembolism of the branches of the pulmonary artery (TEL), squeezing the pulmonary aneurysm of the aorta, atherosclerosis of the pulmonary artery, mediastinal tumors.

The main causes of the acute pulmonary heart are massive tel, severe bouts of bronchial asthma, valve pneumothorax, acute pneumonia. The pulmonary heart of a subacute flow develops at repeated TEL, cancer lymphangee of the lungs, in cases of chronic hypoventilation associated with polio, botulism, myasthenia.

Mechanism for the development of a pulmonary heart

The leading importance in the development of the pulmonary heart is arterial pulmonary hypertension. On the initial stage It is also associated with a reflex increase in cardiac output in response to the amplification of the respiratory function and the hypoxia of tissues occurs during respiratory failure. With vascular shape of a pulmonary heart, the resistance of blood flow in the arteries of a small circle of blood circulation increases mainly due to the organic narrowing of the lumen of the pulmonary vessels in the blockage of their embols (in the case of thromboembolism), with inflammatory or tumor infiltration of the walls, and their lumen (in the case of systemic vasculites). With bronchopulmonary and thoracodiaphragmal forms of the pulmonary heart, the narrowing of the lumen of pulmonary vessels occurs due to their microcurrent, in connective tissue or compression in the zones of inflammation, tumor process or sclerosis, as well as when weakening the ability of the lungs to stretch and decay the vessels in the modified light segments. But in most cases, the leading role is played by the functional mechanisms for the development of pulmonary arterial hypertension, which are associated with impaired respiratory function, ventilation of lungs and hypoxia.

Arterial hypertension of a small circle of blood circulation leads to overloading of the right heart departments. As the disease develops, an acid-alkaline equilibrium shift occurs, which initially be compensated, but in the future, decompensation of violations can occur. With a pulmonary heart there is an increase in the size of the right ventricle and the muscle hypertrophy of the muscular shell of large vessels of the small circle of blood circulation, narrowing their lumen with further sclerization. Small vessels are often amazed by multiple thrombami. Gradually, dystrophy and necrotic processes are developing in the heart muscle.

Classification of the pulmonary heart

At the rate of increment clinical manifestations There are several options for the flow of a pulmonary heart: sharp (develops in a few hours or days), subacute (develops for weeks and months) and chronic (emerging gradually, for a number of months or years on the background of long respiratory failure).

The process of forming a chronic pulmonary heart takes place the following stages:

• preclinical - manifests itself by transient pulmonary hypertension and signs of hard work of the right ventricle; detected only with the instrumental study;
• compensated - characterized by hypertrophy of the right ventricle and stable pulmonary hypertension without phenomena of blood circulation deficiency;
• decompensated (cardiovary lack of failure) - symptoms of deficiency of right ventricle appear.

Three etiological forms of pulmonary heart are isolated: bronchopulmonary, thoracodiaphragmal and vascular.

By sign of compensation, chronic pulmonary heart can be compensated or decompensated.

Symptoms of the pulmonary heart

The clinical picture of the pulmonary heart is characterized by the development of heart failure phenomena on the background of pulmonary hypertension. The development of an acute pulmonary heart is characterized by the appearance of sudden pain behind the sternum, cutting shortness; reduced arterial pressure, up to the development of collapse, sinusiness of the skin, swelling of the cervical veins, increasing tachycardia; Progressive increase in liver with pain in the right hypochondrium, psychomotor excitation. Increased pathological pulsations (precipitial and epigastric), expansion of the heart boundary to the right, the rhythm of the gallop in the zone of the sword-shaped process, EcG-signs Overload of the right atrium.

With a massive tel in a few minutes, a shock state develops, pulmonary edema. It is often joined by sharp coronary failure, accompanied by a rhythm impairment, painful syndrome. In 30-35% of cases, a sudden death is observed. The subacute pulmonary heart is manifested by sudden moderate painful sensations, shortness of breath and tachycardia, a short faint, hemoprod, signs of pleuropneumonia.

In the compensation phase of the chronic pulmonary heart, symptomatics of the main disease is observed with gradual manifestations of hyperfunction, and then hypertrophy of the right departments of the heart, which are usually neuroprically expressed. In some patients, ripples in the upper part of the abdomen caused by an increase in the right ventricle.

In the stage of decompensation, destroying failure is developing. The main manifestation is shortness of breath, increasing with exercise, inhalation of cold air, in a lying position. Pains in the heart pain appear, sinushesity (warm and cold cyanosis), rapid heartbeat, swelling of the cervical veins, which persists on inhale, increase the liver, peripheral swelling, resistant to treatment.

During the examination of the heart, the deafness of the heart tones is detected. Arterial pressure is normal or lowered, arterial hypertension is characteristic of stagnant heart failure. More pronounced symptoms of the pulmonary heart become in exacerbation inflammatory process In the lungs. In the late stage, the edema increases, the increase in the liver (hepatomegaly) is progressing, neurological disorders appear (dizziness, headaches, apathy, drowsiness) decreases diuresis.

Diagnosis of the pulmonary heart

The diagnostic criteria of the pulmonary heart is considered the presence of diseases - causal factors of the pulmonary heart, pulmonary hypertension, increasing and expanding the right ventricle, refereeless heart failure. Such patients need consultation of the pulmonologist and cardiologist. When examining the patient, pay attention to the signs of respiratory impairment, skin sinusiness, heart pain, etc. The ECG is defined by direct and indirect signs of the right ventricle hypertrophy.

Prediction and prevention of the pulmonary heart

In cases of decompensation of pulmonary heart, the forecast for working capacity, quality and life expectancy is unsatisfactory. Usually, patients with a pulmonary heart suffers already in the early stages of the disease, which dictates the need for rational employment and to solve the issue of the assignment group. The early start of complex therapy makes it possible to significantly improve the labor forecast and increase the life expectancy.

For the prevention of a pulmonary heart, a warning is required, timely and effective treatment Diseases leading to it. First of all, this concerns chronic bronchopulmonary processes, the need to prevent their exacerbations and develop respiratory failure. For the prevention of pulmonary heart decompression processes, it is recommended to adhere to moderate physical activity.

The pulmonary heart (LS) is hypertrophy and / or the pursuit of the right ventricle (PJ), which arose as a result of the pulmonary arterial hypertension, due to diseases affecting the function and / or the structure of the lungs, and not related to the primary pathology of the left hearts or congenital heart defects. LS is formed due to diseases of the bronchi and light, thoracodiaphraggmal lesions or pathology of pulmonary vessels. The development of chronic pulmonary heart (HLS) is most often due to chronic pulmonary failure (CLN), and the main reason for the formation of HLS is alveolar hypoxia, which causes the spasm of pulmonary arterioles.

The diagnostic search is aimed at identifying the underlying disease that led to the development of HLS, as well as the estimate of CLN, pulmonary hypertension and the state of the PJ.

CHLS treatment is therapy of the underlying disease, which is the cause of HLS (chronic obstructive bronchitis, bronchial asthma etc.), elimination of alveolar hypoxia and hypoxemia with a decrease in pulmonary arterial hypertension (training of respiratory muscles, electrostimulation of the diaphragm, normalization of the oxygen-cycle blood function (hemosorbing), long-term oxygen and therapy (DCT), almitrine), and the correction of the right-hand heart failure (ACE inhibitors, diuretics, aldosterone blockers, angiothesine receptor antagonists). DCT - very effective method CHL and HLS treatment capable of increasing the life expectancy of patients.

Keywords: pulmonary heart, pulmonary hypertension, chronic pulmonary failure, chronic pulmonary heart, justifying heart failure.

Definition

Lonantic Heart- It is hypertrophy and / or dilatation of the right ventricle, resulting from pulmonary arterial hypertension due to diseases affecting the function and / or the structure of the lungs and non-primary pathology of the left heap or congenital heart defects.

The pulmonary heart (PLS) is formed on the basis of pathological changes in the lighter, disorders of the extrapilence mechanisms of respiration, providing ventilation of the lung (damage to the respiratory muscles, violation of the central regulation of respiration, the elasticity of bone-cartilage formations of the chest or conduct nervous impulse by n. Diaphragmicus,obesity), as well as lesions of pulmonary vessels.

CLASSIFICATION

In our country, the classification of a pulmonary heart, proposed by B.E. received the greatest distribution Voted in 1964 (Table 7.1).

The acute LS is associated with a sharp increase in the pulmonary blood pressure (LAD) with the development of the right-handed failure and is due to the most often thromboembolism of the main trunk or large branches of the pulmonary artery (TEL). However, the doctor is sometimes faced with a similar condition and, when it is turned off from the blood circulation of large parts of the pulmonary fabric (bilateral extensive pneumonia, asthmatic status, valve pneumothorax).

The subacute pulmonary heart (PLS) is most often a consequence of a recurrent thromboembolism of small branches of the pulmonary artery. Lead clinical symptom It is an increasing shortness of breath with a rapidly developing (for months) by worldwide failure. To other reasons, the PLS should include neuromuscular diseases (Miasthenia, polio, damage to the diaphragmal nerve), turning off from the act of breathing a significant part of the respiratory lung respiratory department (severe heavily of bronchial asthma, miliar tuberculosis of the lung). Frequent cause PLS are oncological diseases of the lungs, gastrointestinal tract, breast and other localization, due to carcinomateness of the lungs, as well as the compression of the vessels of the lungs by germinating tumor with subsequent thrombosis.

Chronic pulmonary heart (HLS) in 80% of cases occurs during the damage to the bronchopile apparatus (most often when COPD) and is associated with slow and gradual increase in pressure in the pulmonary artery for many years.

The development of CHLS is directly interconnected with chronic pulmonary failure (CLN). IN clinical practice Use the classification of CLN based on the presence of shortness of breath. There are 3 degrees of CHLD: the appearance of shortness of shortness of breath with the previously available forces - I degree, shortness of breath with conventional loads - II degree, shortness of breath alone - III degree. The above classification is sometimes appropriate to be supplemented with data on gas composition and pathophysiological mechanisms for the development of pulmonary failure (Table 7.2), which allows you to choose pathogenetically substantiated therapeutic measures.

Classification of the pulmonary heart (according to V. B.E., 1964)

Table 7.1.

Ending table. 7.1.

Note.The diagnosis of the pulmonary heart is raised after the diagnosis of the main disease: with the formulation of the diagnosis, only the first two classification graphs are used. Graphs 3 and 4 contribute to an in-depth understanding of the essence of the process and the choice of therapeutic tactics

Table 7.2.

Clinical and pathophysiological classification of chronic pulmonary failure

(Alexandrov O.V., 1986)

In the presented CLN classification, the diagnosis of HLS is highly likely to be put on the II and III stage of the process. At the I stage of CLN (latent), the lifts of the PLA are usually detected in response to the physical activity and when the disease is exacerbated in the absence of signs of PJ hypertrophy. This circumstance made it possible to express an opinion (N.R. Paleyev), which for the diagnosis of initial manifestations of HLS, it is necessary to use the presence or absence of hypertrophy of myocardial PJ, but an increase in the way. However, in clinical practice, the direct measurement of the way in this group of patients is not fairly reasonable.

Over time, the Decompensation of HLS is possible. In the absence of a special classification of PZ insufficiency, a well-known classification of heart failure (CH) in V.K. Vasilenko and N.D. Straightened, which is usually applied with CH, developed due to the lesion of the left ventricle (LV) or both ventricles. The presence in patients with HLS left vehicles are most often due to two reasons: 1) CHLS in persons over 50 years often combined with IBS, 2) systemic arterial hypoxemia in patients with HLS leads to dystrophic processes in the myocardium of LVE, to its moderate hypertrophy and contractile failure.

The main reason for the development of chronic pulmonary heart are chronic obstructive lung diseases.

PATHOGENESIS

The development of chronic LS is based on the gradual formation of pulmonary arterial hypertension due to several pathogenetic mechanisms. The main cause of LH in patients with the broncho-pulmonary and thoracodiaphragmal forms of HLS is alveolar hypoxia, the role of which in the development of pulmonary vasoconstriction was first shown in 1946. U. Von Euler and G. Lijestrand. The development of the Euler-Liestrand reflex is explained by several mechanisms: the effect of hypoxia is associated with the development of depolarization of smooth muscle cells of vessels and their reduction due to the change in the function of potassium channels of cell memb

wound, exposure to the wall of vessels of endogenous vasoconstrictor mediators, such as leukotreines, histamine, serotonin, angiotensin II and catecholamines, the products of which in hypoxia increase significantly.

Hypercapnia also contributes to the development of pulmonary hypertension. However, the high concentration of CO 2, apparently, acts not directly on the tone of pulmonary vessels, and indirectly - preferably through the acidosis determined by it. In addition, the delay of CO 2 contributes to a decrease in the sensitivity of the respiratory center to CO 2, which further reduces the ventilation of the lungs and promotes the pulmonary vasoconstriction.

Endothelium dysfunction that manifests the reduction in the synthesis of vasodilative antiproliferative mediators (NO, Prostaziklin, Prostaglandin E 2) and an increase in vasoconstrictors (angiotensin, endothelin-1) is given in particular importance in the genesis of LG. Dysfunction of the endothelium of pulmonary vessels in patients with COPD is associated with hypoxemia, inflammation, as well as the effects of cigarette smoke.

In patients with HLS, structural changes of the vascular channel occur - remodeling of pulmonary vessels, characterized by the thickening of the intima due to the proliferation of smooth muscle cells, the deposition of elastic and collagen fibers, the hyperrophy of the muscular layer of arteries with a decrease in the inner diameter of the vessels. In patients with COPD due to emphysema, the reduction of the capillary channel, the compression of the pulmonary vessels.

In addition to chronic hypoxia, along with structural changes in lung vessels, a number of other factors affect the increase in pulmonary pressure: polycythemia with a change in the rheological properties of blood, violation of the metabolism of vasoactive substances in the lungs, an increase in the minute volume of blood, which is due to tachycardia and hypervolemia. One of the possible causes of hypervolemia are hypercapnia and hypoxemia, contributing to an increase in the concentration of aldosterone in the blood and, accordingly, the delay of Na + and water.

In patients with a severe obesity, the Picklise syndrome (named for the work of Charles Dickens) is developing, which is manifested by hypoventilation with hypercapnia, which is associated with a decrease in the sensitivity of the respiratory center to CO 2, as well as violation of ventilation due to mechanical restriction with fatty tissue with dysfunction (fatter) respiratory muscles.

Increased blood pressure in the pulmonary artery at first can contribute to an increase in the volume of perfusion of pulmonary capillaries, but over time, the hypertrophy of the Miocardium PJ is developing with subsequent contractile failure. Pressure indicators in a small circulation circle are presented in Table. 7.3.

Table 7.3.

Indicators of pulmonary hemodynamics

The criterion of pulmonary hypertension is the level of average pressure in the pulmonary artery in peace, exceeding 20 mm Hg.

CLINIC

The clinical picture is developing from the manifestations of the main disease, leading to the development of HLS and the lesion of the PJ. In clinical practice, chronic obstructive pulmonary disease (COPD) are most often found among the causal pulmonary diseases. Bronchial asthma or chronic obstructive bronchitis and lung emphysema. The CHLS clinic is inextricably linked with the manifestation of the actual CLN.

The characteristic complaint of patients is shortness of breath. Initially, during exercise (I, the stage of CLN), and then alone (III stage of CLN). It has expiratory or mixed character. For a long time (years) COPD dults the attention of the patient and makes you turn to the doctor when the shortness of breath appears with a light physical activity or alone, that is, already at the CLN II-III stage, when the presence of HLS is indisputable.

In contrast to shortness of breath, associated with the left-detecting deficiency and venous stagnation of blood in the lungs, shortness of breath at pulmonary hypertension is not intensified in the horizontal position of the patient and not

it decreases in the sitting position. Patients may even prefer the horizontal position of the body, in which the diaphragm takes greater participation in intrathoracic hemodynamics, which is facilitated by the respiratory process.

Tachycardia is a frequent complaint with HLS patients and appears at the stage of development of CLN in response to arterial hypoxemia. Heart rhythm disorder occurs infrequently. Availability clear arrhythmiaEspecially in persons over 50 years, as a rule, is associated with the concomitant IBS.

In half of the housing patients, pain in the heart pain occurs, more often than an indefinite nature, without irradiation, as a rule, not related to physical activity and non-nitroglycerin not bordering. The most common look at the pain mechanism is the relative coronary insufficiency due to a significant increase in the muscle mass of the PJ, as well as a decrease in the filling of the coronary arteries with an increase in the finite-diastolic pressure in the PJ cavity, hypoxia of myocardium amid the general arterial hypoxemia ("blue angina) and a reflex narrowing The right coronary artery (bulk-level reflex). Possible cause of cardialgia can be a stretching of the pulmonary artery with a sharp increase in pressure in it.

During the decomptionation of the pulmonary heart, swelling on the legs may appear, which for the first time occur most often when the bronchopile disease is exacerbated and first localized in the field of stop and ankles. As the proceedings are progressing, the edema is distributed to the area of \u200b\u200bthe legs and the hips, and rarely, in severe cases of referenceless failure, there is an increase in abdomen in the amount due to the formative ascites.

The less specific symptom of the pulmonary heart is the loss of votes, which is associated with the recurrent nerve compression by a dilated pulmonary artery trunk.

In patients with CLN and HLS, encephalopathy may develop due to chronic hyperkapin and hypoxia of the brain, as well as violations of vascular permeability. With severe encephalopathy, part of patients has increased excitability, aggressiveness, euphoria, and even psychosis, and other patients - lethargy, depression, drowsiness during the day and insomnia at night, headaches. Rarely fainting during exercise as a result of pronounced hypoxia.

The frequent symptom of CLN is the diffuse "grayish blue", warm cyanosis. In the event of a justifying deficiency in patients with HLS, cyanosis often acquires a mixed nature: against the background of diffuse blue skin coloring, the tip of the nose, chin, ears, finger tips, and the fingertips, and the limbs in most cases remain warm, possibly due to peripheral vasodilation caused by hypercaps. Characteristic is the swelling of the cervical veins (including in the breath - symptom of Kussmouul). In some patients, a painful blush on the cheeks can appear and an increase in the number of vessels on the skin and conjunctivans ("rabbit or frogs" due to hypercapnia), the symptom of the Shoulder (swelling of the cervical veins when pressing the palm to the enlarged liver), the face of Corvisar, cardiac cachexia, signs of the main Diseases (emphysematous chest, kifoscolosis of the thoracic spine, etc.).

With palpation of the heart area, a pronounced spilled heart impetus can be detected, epigastric pulsation (due to hypertrophy and dilatation of PJ), and at percussion - expansion of the right border of the heart to the right. However, these symptoms lose their diagnostic significance due to frequently developing lung emphysema, in which the percussion dimensions of the heart can even be reduced ("drip heart"). The most frequent auscultative symptom for the CHLS is the focus of the second tone above the pulmonary artery, which can be combined with the splitting of the second tone, the right-handed IV tone of the heart, the diastolic noise of the lack of pulp (Graham-style noise) and systolic noise of tricuspid deficiency, and the intensity of both noises is enhanced by Inhalation altitude (symptom of River Corvalo).

Arterial pressure in patients with compensated HLS is more frequent, and with decomposed - reduced.

Hepatomegaly is detected from almost all patients with decompensated drugs. The liver is enlarged in size, when palpation is sealed, painful, the edge of the liver is rounded. With severe heart failure, ascites appears. In general, such severe manifestations of the right-hand heart failure at the CHLS are rare, for the very presence of severe CLN or the attachment of the infectious process in light leads to the tragic patient's final earlier than it comes due to heart failure.

The chronic pulmonary heart clinic is determined by the severity of pulmonary pathology, as well as pulmonary and rightful heart failure.

Instrumental diagnostics

The X-ray picture of the CHLS depends on the stage of CLN. Against the background of radiological manifestations of the pulmonary disease (pneumosclerosis, emphysema, amplification of vascular pattern, etc.), only a certain decrease in the shade of the heart is noted first, then a moderate emplessness of the pulmonary artery cone appears in the direct and right oblique projection. Normally, in a direct projection, the right side of the heart is formed by the right atrium, and with an increase in the PJ, it becomes corrupting, and with significant PJ hypertrophy, it can form both the right and the left edge of the heart, the left ventricle back. In the final decompensated stage of the HLS, the right edge of the heart can be formed by a significantly expanded right atrium. Nevertheless, this "evolution" occurs on the background of a relatively small shadow of the heart ("drip" or "hanging").

Electrocardiographic diagnosis of hls comes down to the detection of PJ hypertrophy. To the main ("direct") ECG criteria for PJ hypertrophy include: 1) R in V1\u003e 7mm; 2) S in V5-6\u003e 7 mm; 3) RV1 + SV5 or RV1 + SV6\u003e 10.5 mm; 4) RAVR\u003e 4 mm; 5) sv1, v2 \u003d s2 mm; 6) RV5, V6<5 мм; 7) отношение R/SV1 >1; 8) full blockade right legs of the Gis beam at rv1\u003e 15 mm; 9) incomplete blockade of the right leg of a beam of His at RV1\u003e 10 mm; 10) Negative TVL and reduction of STVL, V2 with RVL\u003e 5 mm and the absence of coronary failure. If there are 2 and more "direct" ECG signs, the diagnosis of PJ hypertrophy is considered reliable.

Indirect ECG signs of PJ hypertrophy allow you to assume pzh hypertrophy: 1) a turn of the heart around the longitudinal axis clockwise (the shift of the transition zone to the left, to the V5-V6 leads and the appearance of the QRS type RS complex V5, V6, and the appearance of the QRS type RS; SV5-6 RV1-2 - normal amplitude); 2) SV5-6\u003e RV5-6; 3) RAVR\u003e Q (S) AVR; 4) deviation of the electrical axis of the heart to the right, especially if α\u003e 110; 5) electric axis of the heart type

Si-Sii - Siii; 6) Complete or incomplete blockade of the right leg of a beam of Gis; 7) electrocardiographic signs of hypertrophy of the right atrium (P-Pulmonale in leads II, III, AVF); 8) an increase in the activation time of the right ventricle in V1 more than 0.03 s. There are three types of ECG changes at hls:

1. RSR "STIP ECG is characterized by the presence of a RSR type QRS split complex in the V1 assignment and is usually detected with expressed PJ hypertrophy;

2. R-type ECG is characterized by the presence of a QRs type RS or QR in the V1 assignment and is usually detected with the pronounced PJ hypertrophy (Fig. 7.1).

3. S-type ECG is often detected in patients with COPD with emphysema lungs. It is binding to the displacement of the hypertrophied heart by the POST, which is due to emphysemic lungs. ECG has the form of RS, RS or RS with pronounced teeth S and in the right, and in the left chest leads

Fig. 7.1.ECG patient Cobl and hls. Sinus tachycardia. The pronounced hypertrophy of the right ventricle (RV1 \u003d 10 mm, Sv1 is missing, Sv5-6 \u003d 12 mm, the sharp deviation of the EOS to the right (α \u003d + 155 °), negative TV1-2 and the decrease in the STV1-2 segment). Right atrium hypertrophy (P-Pulmonale in v2-4)

Electrocardiographic criteria for hypertrophy of PJ are not sufficiently specific. They are less clear than with LV hypertrophy, and can lead to false-positive and false negative diagnosis. Normal ECG does not exclude the presence of HLS, especially in patients with COPD, therefore, the ECG changes must be compared with the clinical picture of the disease and ECOG data.

Echocardiography (ECCG) is a leading non-invasive method for assessing pulmonary hemodynamics and diagnostics of drugs. Ultrasonic diagnosis of drugs is based on identifying signs of lesion of the Myocardial of the PJ, which are given below.

1. Changing the size of the right ventricle, which is estimated in two positions: in a parastinal position along the long axis (normally less than 30 mm) and in the apical four-chamber position. To identify the dilatation of PJ more often uses the measurement of its diameter (normally less than 36 mm) and the area at the end of the diastole along the long axis in the apical four-chamber position. In order to more accurately estimate the severity of Dilation of the PJ, it is recommended to use the ratio of the finite-diastolic area of \u200b\u200bthe PJ to the finite-diastolic area of \u200b\u200bLV, thereby eliminating individual differences in the sizes of the heart. Increasing this indicator more than 0.6 indicates a significant dilatation of PJ, and if it becomes equal to or more than 1.0, then there is a conclusion about the sharply pronounced dilatation of the PJ. With dilatation of the PJ in the apical four-chamber position, the PJ shape changes with the sickle on oval, and the top of the heart can be occupied not LV, as normal, and pzh. The dilatation of the PJ may be accompanied by the dilatation of the trunk (more than 30 mm) and the branches of the pulmonary artery. In massive pulmonary artery thrombosis, its significant dilatation may be determined (up to 50-80 mm), and the clearance of the arteries becomes oval.

2. With the hypertrophy of the PJ, the thickness of its front wall, measured in the diastole in the subcosteal four-chamber position in V- or M-mode, exceeds 5 mm. In patients with HLS, as a rule, not only the front wall of the PJ, but also the interventricular partition is also hypertrophy.

3. Trickspecial regurgitation various degreesIn turn, it causes the dilatation of the right atrium and the lower hollow vein, a decrease in the inspiratory collapse of which indicates increased pressure in the right of atrium.

4. Evaluation of the diastolic function of the PJ is made according to the transcispical diastolic flow in the mode of impulse

wave Doppler and Color M-MODAL Doppler. In patients with HLS, the decrease in the diastolic function of the PJ, which is manifested by a decrease in the ratio of peaks E and A.

5. Reducing the contractile ability of the PJ in patients with drugs is manifested by PJ hypokinesia with a decrease in its emission fraction. In case of echocardiographic examination, such indicators of the PJ function are determined, as a finite-diastolic and finite systolic volumes, the emission fraction, which is normally at least 50%.

These changes have a different severity depending on the development of drug development. Thus, during acute drugs, the dilatation of the PJ will be detected, and the signs of hypertrophy, diastolic and systolic dysfunction of the PJ will be added to it.

Another group of features is associated with the development of pulmonary hypertension at LS. The degree of their severity is most significant in acute and subacute LS, as well as in patients with primary pulmonary hypertension. For hls, a moderate increase in systolic pressure in a pulmonary artery, which rarely reaches 50 mm Hg.st. The assessment of the pulmonary trunk and the flow in the outlet path of the PJ is carried out from the left parastinal and sub-staple access on the short axis. In patients with pulmonary pathology due to restriction of the ultrasound window, the sub-staple position may be the only possible access to visualize the PJ output tract. With the help of pulse-wave doppler, the average pressure in the pulmonary artery (PRI) can be measured, for which the formula proposed by A. Kitabatake et al. (1983): LOG10 (PRA) \u003d - 2.8 (AT / ET) + 2.4, where AT is the flux acceleration time in the PJ, ET - emission time (or time of blood exile from PJ). The magnitude of the PRR, obtained using this method, in patients with COPD correlates well with the data of an invasive examination, and the possibility of obtaining a reliable signal from the pulmonary artery valve exceeds 90%.

The most important value for the detection of pulmonary hypertension is the severity of tricuspid regurgitation. The use of a jet of tricuspid regurgitation underlies the most accurate non-invasive method of determining systolic pressure in the pulmonary artery.Measurements are carried out in the mode of continuous-wave doppler in the apical four-chamber or subcosteal position, it is desirable to simultaneously use the color doppler

who mapping. To calculate the pressure in the pulmonary artery, it is necessary to add pressure in the right atrium to the pressure gradient on the tricuspid valve. Measurement of the transstickspecial gradient can be made more than 75% of COPD patients. There are high-quality signs of pulmonary hypertension:

1. In LH, the nature of the motion of the rear wave of the pulmonary artery valve changes, which is determined in the M-mode: the characteristic indicator of the LG is the presence of an average systemic teeth due to partial overlap of the valve, which forms a W-shaped valve movement in systole.

2. In patients with pulmonary hypertension due to an increase in pressure in the right ventricle, the interventricular partition (MZHP) is compacting, and the left ventricle resembles the short axis letter D (D-shaped left ventricle). For high degree LG MZP becomes like a PZ wall and moves to the diastole paradoxically towards the left ventricle. When the pressure in the pulmonary artery and the right ventricle becomes more than 80 mm Hg, the left ventricle decreases in the volume, is squeezed with a dilated right ventricle and acquires the shape of a crescent.

3. Possible regurgitation on the pulmonary valve (the first degree is possible in the norm in young people). With a constantly wave doppler study, a measurement of pulmonary regurgitation rate is possible with a further calculation of the magnitude of the finite-diastolic gradient of La PZh.

4. Changing the flow of blood flow in the PG rail and in the mouth of the latch. Under normal pressure in La, the flow has an equilibried form, the flow peak is located in the middle of systole; With pulmonary hypertension, the flow of the flow shifts in the first half of the systole.

However, in patients with COPD, they have lung emphysema, it often makes it difficult to clearly visualize the structures of the heart and narrows the "Window" of EchoCg, making a study with informative no more than 60-80% of patients. In recent years, a more accurate and informative method of ultrasound examination of the heart appeared - perchive echocardiography (CPE). The CPE in patients with COPD is a more preferred method for accurate measurements and direct visual assessment of the PJ structures, which is due to a higher resolution of the percussion sensor and the stability of the ultrasonic window, and is of particular importance in the emphysema of the lungs and pneumosclerosis.

Catheterization of the right heart and pulmonary artery

The catheterization of the right sections of the heart and pulmonary artery is the "Gold Standard" method in the diagnosis of LG. This procedure allows you to directly measure the pressure in the right atrium and PJ, the pressure in the pulmonary artery, calculate the heart discharge and pulmonary vascular resistance, determine the level of oxygenation mixed venous blood. The catheterization of the right heart departments due to its invasiveness cannot be recommended for widespread use in the diagnosis of HLS. Indications are: severe pulmonary hypertension, frequent episodes of decompensation of worldwide failure, as well as the selection of candidates for lung pervasure.

Radionuclide Ventriaculture (RVG)

RVG allows you to measure the outer ventricle emission fraction (FVPZ). The FVPG is considered to be abnormal at a value below 40-4 45%, but the FVPG indicator itself is not a good indicator to evaluate the function of the right ventricle. It allows you to evaluate the systolic function of the right ventricle, which strongly depends on the post-load load, decreases with increasing the latter. Therefore, the decrease in the FVPG is registered in many patients with COPD, without being an indicator of true dysfunction of the right ventricle.

Magnetic resonance Tomography (MRI)

MRI is a promising method that allows to evaluate the pulmonary hypertension and changes in the structure and function of the right ventricle. The diameter of the right pulmonary artery, measured at MRI, more than 28 mm is a highly specific feature of LH. However, the MRI method is quite expensive and is available only in specialized centers.

The presence of chronic pulmonary disease (as the causes of HLS) requires a special study of the function of external respiration. The doctor has a task to clarify the type of ventilation failure: obstructive (violation of air passage by bronchoms) or restrictive (reduction of gas exchange area). In the first case, chronic obstructive bronchitis, bronchial asthma, and pneumosclerosis, light resection, etc. can be brought as an example.

TREATMENT

HLS occurs most often after the advent of CLN. Thera-pectic measures are complex and are directed mainly on the correction of these two syndromes, which can be submitted in the following form:

1) Treatment and prevention of the main disease - most often exacerbations of chronic pulmonary pathology (basic therapy);

2) CHL and LH treatment;

3) Treatment of right-hand heart failure. Basis Medical and Preventive Events include

prevention of sharp viral diseases respiratory tract (vaccination) and the exclusion of smoking. In the development of chronic pulmonary pathology of an inflammatory nature, treatment of exacerbations with the help of antibiotics, mucoculating drugs and immunocorrectors is necessary.

The main thing in the therapy of the chronic pulmonary heart is the improvement of the function of external respiration (elimination of inflammation, broncho-prestructive syndrome, improving the condition of respiratory muscles).

The most common cause of CLN is the broncho-abstructive syndrome, the cause of which in the reduction of the smooth muscles of the bronchi, the accumulation of a viscous inflammatory secret, swelling of the mucous membranes. These changes require the use of beta-2-ages (phenoterol, formoterol, salbutamol), M-cholinolithics (bromide, bromide tiotropia), and in some cases inhaled glucocorticosteroid drugs in the form of inhalations using a nebulizer or an individual inhaler. It is possible to use methylxantine (Eufillin and prolonged theophyllins (Teolong, Teotard, etc.)). Therapy by expectorant means is very individual and requires various combinations and selection of plant in plant origin (mother-and-stepmother, a richness, a chabret, etc.), and chemical production (acetylcisteine, ambroxol, etc.).

If necessary, prescribe LFCs and postural lung drainage. Showing a breath with positive pressure on exhalation (no more than 20 cm of water column) using as simple devices

in the form of "whistles" with mobile diaphragm and complex devices controlling pressure on exhalation and inhale. This method reduces the flow rate inside the bronchi (which has a bronchhalytic effect) and increases the pressure inside the bronchi with respect to the surrounding lung tissue.

The extralegal mechanisms for the development of CLN refers to a decrease in the contractile function of respiratory muscles and the diaphragm. The ability to correct these violations is still limited: the leaf or electrostimulation of the diaphragm at II of Art. CLN.

In CLH, the erythrocytes undergo significant functional and morphological restructuring (echinocytosis, stomatocytosis, etc.), which significantly reduces their oxygen transport function. In this situation, it is desirable to bring erythrocytes from the blood flow with lost function and stimulate the release of young (functionally more capable). For this purpose, the use of erythrocytacherresis, extracorporeal blood oxygenation, hemosorption is possible.

Due to the increase in the aggregation properties of the erythrocytes, the viscosity of blood increases, which requires the purpose of the antiagregant (chief, refooliglukin) and heparin (preferably the use of low molecular weight heparins - fractioniparin, etc.).

In patients with hypoventilation associated with a reduced activity of the respiratory center, drugs that increase central inspiratory activity can be used as auxiliary treatment methods - respiratory stimulants. They should be used with a moderately pronounced inhibition of respiration that does not require use of 2 or mechanical ventilation of the lungs ( syndrome apnea In a dream, obesity syndrome-hypoventilation), or at the impossibility of oxygen therapy. To the number of few drugs that increase oxygenation arterial bloodThese include nickelamide, acetosalamamide, doxapram and medroxiprogesterone, but all these drugs with long-term use have a lot of quantities side Effects And therefore can be used only for a short time, for example, during the exacerbation of the disease.

Currently, drugsmith in patients with COPDs is currently in preparations for long-term time, almitrine bisme. Almitrine is a specific ago-

a nicer of peripheral chemoreceptors of a carotid node, whose stimulation leads to increased hypoxic vasoconstrictions in poorly ventilated regions of the lungs with an improvement in ventilation and perfusion ratios. The ability of almitrine in a dose of 100 mg / day is proved. In patients with COPD, lead to a significant increase in RA0 2 (by 5-12 mm Hg) and a decrease in RA10 2 (by 3-7 mm Hg) with improved clinical symptoms and a decrease in the frequency of disease exacerbations, which is capable of several Years to delay the appointment of long-term 0 2-lap. Unfortunately, 20-30% of patients with COPD are not responding to therapy, and widespread use is limited to the possibility of developing peripheral neuropathy and other side effects. Currently, the main indication for the purpose of almitrin is moderate hypoxemia in patients with COPD (RA0 2 56-70 mm Hg or SA0 2 89-93%), as well as its use in the complex to the DCT, especially against the background of hypercap.

Vasodilators

In order to reduce the degree of lag into complex therapy of patients with a pulmonary heart include peripheral vasodilators. The most commonly used antagonists of calcium channels and nitrates. The currently recommended calcium antagonists include two drugs - nifedipine and diltiazem. The choice in favor of one of them depends on the initial cardiac frequency. Patients with relative bradycardia should be recommended by nifedipine, with relative tachycardia - diltiaze. Daily doses of these drugs that have proven efficacy rather high: for nifedipine 120-240 mg, for diltiazem 240-720 mg. The favorable clinical and prognostic effects of calcium antagonists used in high doses in patients with primary LH (especially with preceding positive acute breakdown) were shown. Calcium antagonists of dihydropyridine series III generation - amlodipine, feelodipine, etc. - are also effective in this group of patients with HP.

However, with pulmonary hypertension, due to COPD, calcium channel antagonists are not recommended for use, despite their ability to reduce the RRA and increase the heart emission from this group of patients. This is due to the aggravation of arterial hypoxemia caused by the dilatation of pulmonary vessels in

poorly ventilated light zones with a deterioration of ventilation-fusion ratios. In addition, with long-term therapy with calcium antagonists (more than 6 months), a favorable effect on the parameters of pulmonary hemodynamics is leveled.

A similar situation in patients with COPD takes place in the appointment of nitrates: sharp samples demonstrate the deterioration of gas exchange, and long-term studies are the lack of a positive effect of drugs on pulmonary hemodynamics.

Synthetic prostacycline and its counterparts.Prostacyclinlin is a powerful endogenous vasodilator with anti-aggregation, antiproliferative and cytoprotective effects, which are aimed at preventing remodeling of pulmonary vessels (reducing damage to endothelial cells and hypercoagulation). The mechanism of action of prostacyclin is associated with the relaxation of smooth muscle cells, inhibition of platelet aggregation, improvement of endothelial function, inhibition of the proliferation of vascular cells, as well as a direct inotropic effect, positive changes in hemodynamics, an increase in oxygen disposal in skeletal muscles. The clinical use of prostacyclin in patients with LG is associated with the synthesis of its stable analogues. To date, the greatest experience in the world has accumulated for Epoprostolenol.

Epoprostolen is a form of intravenous prostacyclin (prostaglandin I 2). Favorable results were obtained in patients with vascular form LS - with primary LH in systemic diseases of the connective tissue. The drug increases cardiac output and reduces pulmonary vascular resistance, and with long-term use, it improves the quality of life of LS patients, increasing tolerance to physical exertion. The dose optimal for most patients is 20-40 ng / kg / min. The analogue of epoprottenol is also used - treprostinyl.

Currently developed oral forms of prostacyclin analog (Beradrost, Iloprost)and clinical trials are carried out in the treatment of patients with a vascular form of drugs, which developed due to TEL, primary pulmonary hypertension, systemic diseases of the connective tissue.

In Russia, only prostaglandin E 1 (Vasaporgan), which is prescribed from intravenously drip, to the treatment of patients with drugs, is currently affordable.

5-30 ng / kg / min. Currency treatment with the drug is carried out in a daily dose of 60-80 μg for 2-3 weeks against the background of long-term therapy with calcium antagonists.

Receptor antagonists for endothelin

The activation of the endothelin system in patients LG served as a justification for the use of receptor antagonists to endothelin. The effectiveness of two drugs of this class (bosentan and sintuntane) in the treatment of housing patients, developed against the background of primary LH or against the background of systemic connecting tissue diseases, is proved.

Phosphodiesterase type 5 inhibitors

Sildenafil is a powerful selective inhibitor of CGMF-dependent phosphodiesterase (type 5), preventing the degradation of CGMF, causes a decrease in pulmonary vascular resistance and overloading of the right ventricle. To date, there are data on the effectiveness of sildenafil in patients with LS of various etiology. When using Sildenafil in doses of 25-100 mg 2-3 times a day, it caused the improvement of hemodynamics and tolerance to physical stress in patients with HP. It is recommended for use in the ineffectiveness of other drug therapy.

Long oxygenaterapy

In patients with bronchopulmonary and thoracodiaphragmal form of HLS, the main role in the development and progression of the disease belongs to alveolar hypoxia, so oxygen therapy is the most pathogenetically substantiated method of treating these patients. The use of oxygen in patients with chronic hypoxhemia is decisive and must be permanent, long, and usually carried out at home, therefore such a form of therapy is called long oxygen and therapy (DCT). The task of the DCT is the correction of hypoxemia with the achievement of RAO 2\u003e 60 mm Hg values. and sa0 2\u003e 90%. It is considered the optimal maintenance of RAO 2 in the range of 60-65 mm Hg, and the exceeding of these values \u200b\u200bleads only to a minor increase in SA0 2 and the content of oxygen in arterial blood, but may be accompanied by a delay from 2, especially during sleep, which has a negative

consequences for the function of the heart, brain and respiratory muscles. Therefore, the DCT is not shown in patients with moderate hypoxemia. Discount testimony: RA 2<55 мм рт.ст. или Sa0 2 < 88% в покое, а также раО 2 56-59 мм рт.ст. или Sa0 2 89% при наличии легочного сердца или полицитемии (гематокрит >55%). Most patients with COPDs are quite a stream of 2 1-2 l / min., And in the most severe patients the flow can be increased to 4-5 l / min. Oxygen concentration should be 28-34% vol. An account was recommended for at least 15 hours per day (15-19 h / day). Maximum breaks between oxygen sessions should not exceed 2 h in a row, because Breaks of more than 2-3 h significantly enhance the pulmonary hypertension. Oxygen concentrators, liquid oxygen tanks and compressed gas cylinders can be used. Most often hubs (permeators), separating oxygen from the air due to removal of nitrogen. The DCT increases the life expectancy of patients with CLN and HLS on average for 5 years.

Thus, despite the presence of a large arsenal of modern pharmacological funds, the DCT is the most effective method for the treatment of most forms of CHLS, therefore the treatment of patients with HLS is primarily the task of a pulmonologist.

Long-term hydrocerapy is the most efficient method of treating CHL and HLS, which increases the life expectancy of patients on average for 5 years.

Long home ventilation of the lungs

In the terminal stages of pulmonary diseases due to the reduction of the ventilation reserve, hypercupinia may develop, requiring respiratory support, which should be carried out for a long time on an ongoing basis at home.

Inhalation Therapy No.

Inhalation therapy N0, the action of which is similar to the endothelium-relaxing factor, has a positive effect in patients with HLS. Its vazodilative effect is based on activation of guanillates in smooth muscle cells of pulmonary vessels, which leads to an increase in the level of cyclo-GMF and a decrease in intracellular calcium content. Inhalation N0

gives selective effect on the vessels of the lungs, and it causes vasodilatia mainly in well ventilated regions of the lungs, improving gas exchange. During the course use of N0 in patients with hls, a decrease in pressure in the pulmonary artery is observed, increasing the partial pressure of oxygen in the blood. In addition to its hemodynamic effects, N0 helps to prevent and reverse the development of remodeling of pulmonary vessels and PJ. Optimal doses of inhalation N0 are concentrations 2-10 ppm, and high concentrations N0 (more than 20 ppm) are able to cause excessive vasodilation of pulmonary vessels and lead to a deterioration of the ventilation and perfusion balance with hypoxemia enhancement. Adding Inhalations N0 to the DCT in patients with COPDs enhance the positive effect on gas exchange, reducing the level of pulmonary hypertension and increasing cardiac output.

CPAP therapy

Method of therapy with constant positive pressure in respiratory tract CONTINUUS POSITIVE AIRWAY PRESSURE- CPAP) Finds use as a method of treatment with CLN and HLS in patients with obstructive night apnea syndrome, preventing the development of the collapse of the respiratory tract. The proven spectacles are the prevention and dissection of atelectasis, an increase in pulmonary volumes, a decrease in the ventilation and perfusion imbalance, an increase in oxygenation, lung complens, the redistribution of fluid in the lung tissue.

Cardiac glycosides

Cardiac glycosides in patients with COPD and a pulmonary heart are effective only in the presence of left ventricular heart failure, and can also be useful in the development of fliccular arrhythmia. Moreover, it is shown that cardiac glycosides can induce pulp vasoconstriction, and the presence of hypercaps and acidosis increases the likelihood of glycoside intoxication.

Diuretics

In the treatment of patients with decompensated hls with enemy syndrome use the therapy with diuretics, including antagonists

aldosterone (Aldakton). Diuretics should be prescribed carefully, from small doses, since the development of PJ insufficiency, the cardiac emission depends more on the preload, and, consequently, an excessive reduction in the intravascular volume of the fluid may lead to a decrease in the volume of filling of the PJ and reduce heart emissions, as well as to increase blood viscosity and a sharp decrease in pressure in the pulmonary artery, thereby worsening the diffusion of gases. Another serious side effect of diuretic therapy is metabolic alkalosis, which in patients with COPD with respiratory failure can lead to the oppression of the activity of the respiratory center and the deterioration of gas exchange indicators.

Inhibitors of angiotensin glossy enzyme

In the treatment of patients with a decompensated pulmonary heart in recent years, inhibitors of an angiotensin glider enzyme (IAPF) were published. The IAPF therapy in patients with HLS leads to a decrease in pulmonary hypertension and an increase in cardiac output. For the purpose of selection effective therapy HLS in patients COPD recommended the definition of polymorphism of the ACE gene, because Only in patients with subtypes of the APE II and ID gene and ID, a pronounced positive hemodynamic effect of the IAPF is observed. The use of IAPP in minimal therapeutic doses is recommended. In addition to the hemodynamic effect, there is a positive effect of the IAPF on the dimensions of the heart chambers, the processes of remodeling, tolerance to physical exertion and improving the life expectancy of patients with heart failure.

Angiotensin II receptor antagonists

In recent years, data has been obtained about the successful use of this group of drugs in the treatment of HLS in patients with COPD, which was manifested by improving hemodynamics and gas exchange. The most shown the appointment of these drugs in patients with HLS in the intolerance to the IAPF (due to dry cough).

Atrial septostomy

Recently, in the treatment of patients with destroyed heart failure, developed against the background of primary LG, steel

use atrial septomomy, i.e. Creating a small perforation in the interpresentation partition. The creation of a shunt on the right left allows to reduce the average pressure in the right atrium, unload the right ventricle, increase the preload of the left ventricle and the cardiac output. The atrial septostomy is shown in the ineffectiveness of all types of drug treatment of the right-hand heartless heart failure, especially in combination with frequent syncope, or as a preparatory stage before the lung transplantation. As a result of the intervention, there is a decrease in the syncope, an increase in load tolerance, however, the risk of developing vital arterial hypoxemia increases. Mortality of patients during atrial septostomy 5-15%.

Lungs or Heart-Light Transplantation

From the late 80s. The XX century after the start of the application of the immunosuppressive drug of cyclosporine, and in the treatment of terminal stages of pulmonary failure, the lung transplantation was successfully used. In patients with CLN and LS carry out transplantation operations of one or both lungs, the heart-lung complex. It was shown that 3 and 5-year survival after the transplantations of one or both lungs, the heart-lung complex in patients with HP was 55 and 45%, respectively. Most centers are preferred to perform bilateral lung transplant due to a smaller number of postoperative complications.

Citation:Vertkin A.L., Topolyansky A.V. Pulmonary heart: diagnosis and treatment // RMW. 2005. №19. P. 1272.

The pulmonary heart is an increase in the right ventricle of the heart in diseases that violate the structure and (or) the function of the lungs (except in cases of primary damage to the left hearts, congenital heart defects).

The following diseases lead to its development:
- primarily affecting the passage of air in the lungs and alveoli (chronic bronchitis, bronchial asthma, lung emphysema, tuberculosis, pneumoconiosis, bronchiectatic disease, sarcoidosis, etc.);
- primarily affecting the mobility of the chest (kifoscolyosis and other thoracic deformations, neuromuscular diseases - for example, polio, obesity - Pickwick syndrome, apnea in a dream);
- primary lung vessels (primary pulmonary hypertension, arteries, thrombosis and embolism of lung vessels, compression of a pulmonary artery trunk and pulmonary veins by tumor, aneurysm, etc.).
In the pathogenesis of the pulmonary heart, the main role plays a decrease in the total cross section of the lung veses. In diseases that primarily affect the passage of air in the lungs and on the mobility of the chest, alveolar hypoxia leads to the spasm of small pulmonary arteries; For diseases affecting the vessels of the lungs, the increase in resistance to blood flow is due to the narrowing or blockage of the lumen of the pulmonary arteries. Increased pressure in a small circulation circle leads to hypertrophy of smooth muscles of pulmonary arteries, which become more rigid. The overload of the right ventricular pressure determines its hypertrophy, dilatation, in the future - the right-hand heartless deficiency.
The acute pulmonary heart is developing with pulmonary arterial thromboembolism, spontaneous pneumothorax, heavy attack of bronchial asthma, heavy pneumonia in a few hours or days. It is manifested by suddenly emerging grace of sternum, cutting shortness of breath, cyanosis, arterial hypotension, tachycardia, amplification and accent II of the heart of the heart over the pulmonary barrel; deviation of the electrical axis of the heart to the right and electrocardiographic signs of the overload of the right atrium; Fastly increasing signs of destroying deficiency - swelling of the cervical veins, increasing and soreness of the liver.
Chronic pulmonary heart is formed for a number of years in chronic obstructive diseases of the lungs, kifoscoliosis, obesity, recurrent thromboembolism of pulmonary arteries, primary pulmonary hypertension. In its development, three stages are distinguished: I (preclinical) - diagnosed only in the instrumental study; II - with the development of hypertrophy of the right ventricle and pulmonary hypertension without signs of heart failure; III (decompensated pulmonary heart) - with the appearance of symptoms of worldwide failure.
Clinical signs of chronic pulmonary heart - shortness of breath, increasing during exercise, fast fatigue, patience attacks, chest pain, fainting. When squeezing a return nerve, an expanded pulmonary artery trunk arises of voice hoarse. In case of inspection, objective signs of pulmonary hypertension can be detected - focus of the second tones on the pulmonary artery, the diastolic noise of the sin-style (the noise of relative insufficiency of the pulmonary artery valves). The increase in the right ventricle may indicate the pulsation for a sword-shaped process, increasing on the breath, expanding the boundaries of the relative dullness of the heart to the right. With significant dilatation of the right ventricle, relative tricuspid failure develops, manifested by systolic noise at the base of the sword-shaped process, the pulsation of the cervical veins and the liver. In the decompensation stage there are signs of destroying failure: an increase in liver, peripheral edema.
The ECG is revealed by hypertrophy of the right atrium (pointed high teeth r in leads II, III, AVF) and right ventricle (deviation of the electrical axis of the heart to the right, increasing the amplitude of the priest R in the right infants, the blockade of the right leg of the GISE beam, the appearance of deep teeth S in I and q teeth in III standard leads).
Radiologically sharp and subacute pulmonary heart is manifested by an increase in the right ventricle, the expansion of the lung artery arc, the expansion of the root of the lung; Chronic pulmonary heart - hypertrophy of the right ventricle, signs of hypertension in a small circulation circle, expansion of the upper hollow vein.
At echocardiography, hypertrophy of the wall of the right ventricle can be detected, the dilatation of the right chambers of the heart, the expansion of the pulmonary artery and the upper hollow vein, pulmonary hypertension and tricuspid failure.
In the analysis of blood in patients with chronic pulmonary heart, polycythemia is usually identified.
When developing an acute pulmonary heart, the treatment of the main disease is shown (the liquidation of the pneumothorax; heparinotherapy, thrombolysis, or surgery during thromboembolism of pulmonary arteries; adequate therapy of bronchial asthma, etc.).
The treatment of the pulmonary heart actually is directed mainly on the decrease in pulmonary hypertension, and in the development of decompensation, it includes the correction of heart failure (Table 1). Pulmonary hypertension decreases using calcium antagonists - nifedipine at a dose of 40-180 mg per day (preferably the use of long-acting forms of the drug), diltiazem at a dose of 120-360 mg per day [Chazov I.E., 2000], as well as amlodipine (AMLOVAS ) In a dose of 10 mg per day. So, according to Franz I.W. et al. (2002), on the background of amlodipine therapy at a dose of 10 mg per day for 18 days in 20 patients with COPDs with pulmonary hypertension, a significant decrease in the resistance of pulmonary vessels and pressure in the pulmonary artery was noted, with changes in the parameters of gas exchange in the lungs. According to the results of the cross-randomized study conducted by SAJKOV D. et al. (1997), amlodipine and feelodipine in equivalent doses equally reduced pressure in the pulmonary artery, but side effects ( headache And the sweeping syndrome) less often developed against the background of amlodipine therapy.
The effect of calcium antagonists is usually manifested in 3-4 weeks. It is shown that the decrease in pulmonary pressure on the background of therapy with calcium antagonists significantly improves the forecast of these patients, but only a third of the patients responds to the treatment of calcium antagonists in a similar way. Patients with severe right-hand deficiency are usually poorly reacting to calcium antagonists.
In clinical practice, theophylline preparations (intravenously drip, prolonged drugs for intake intake) are widely used in patients with signs of the pulmonary heart, which reduce the pulmonary vascular resistance, which increase the heart rate and improving the well-being of these patients. At the same time, the evidence base for the use of theophylline preparations at pulmonary hypertension, it seems that there is no.
Effectively reduces the pressure in the pulmonary artery intravenous prostacyclin (PGI2) infusion (PGI2), which has antiproliferative and antiagregative effect; The drug increases tolerance to physical exertion, improves the quality of life and reduces the mortality of these patients. Its deficiencies include developing side effects (dizziness, arterial hypotension, cardialgia, nausea, abdomalgia, diarrhea, rash, pain in the limbs), the need for constant (perennial) intravenous infusions, as well as the high cost of treatment. The effectiveness and safety of the use of analogs of prostacyclin - Iloprost used in the form of inhalation and beraprost used inside, as well as treprostinyl, introduced both intravenously and subcutaneously is carried out.
The possibility of using an endothelin receptor antagonist of bosentane receptor, which effectively reduces the pressure in the pulmonary artery, but the pronounced side system effects limits intravenous application This group of drugs.
Inhalation of nitrogen oxide (NO) for several weeks also allows to reduce pulmonary hypertension, but such therapy is available not to all therapeutic institutions. In recent years, attempts are undertaken to use PDE5 inhibitors with pulmonary hypertension, in particular - siltenafil citrate. Charan N.B. In 2001, described two patients who marked the improvement of the COPD flow against the background of Sildenafil's reception, which they took about erectile dysfunction. Today, the browillating, anti-inflammatory effect of sildenafil and its ability to reduce the pressure in the pulmonary artery is shown both in experimental and clinical studies. According to the data obtained, the PDE5 inhibitors at pulmonary hypertension significantly improves physical exhaust tolerance, increase the heart index, improve the quality of life of patients with pulmonary hypertension, including primary. For the final decision on the effectiveness of this class of drugs during COPD, long-term multicenter studies are needed. In addition, the widespread introduction of these drugs in clinical practice is certainly preventing the high cost of treatment.
In the formation of a chronic pulmonary heart in patients with chronic obstructive pulmonary diseases (bronchial asthma, chronic bronchitis, Emified lungs) In order to correct hypoxia, long oxygen therapy is shown. With polycythemia (in the case of increasing hematocrit above 65-70%), blood consumption is used (usually one-time), which allows to reduce the pressure in the pulmonary artery, increase the tolerance of the patient to physical exertion and improve its well-being. The amount of blood removed is 200-300 ml (depending on the level of blood pressure and well-being of the patient).
Diuretics are shown in the development of right-hand deficiencies, incl. spironolactone; It should be borne in mind that with pulmonary hypertension, diuretics do not always help reduce shortness of breath. ACE inhibitors are also used (captopril, enalapril, etc.). The use of digoxin in the absence of left ventricular insufficiency is ineffective and unsafe, since hypoxemia and developing against the background of diuretic therapy hypocalemia increase the risk of glyconidation intoxication.
Given the high probability of thromboembolic complications in the heart failure and the need for active diuretic therapy, long-term bed mode, the appearance of phlebotommability features is shown preventive anticoagulant therapy (usually - subcutaneous administration of heparin at 5000 users 2 times a day or low molecular weight heparin 1 times a day). Patients with primary pulmonary hypertension use indirect anticoagulants (warfarin) under the control of many. Warfarin increases the survival of patients, but does not affect their overall state.
Thus, in modern clinical practice medicia treatment The pulmonary heart is reduced to the therapy of heart failure (diuretics, ACE inhibitors), as well as to the use of calcium antagonists and theophylline drugs to reduce pulmonary hypertension. The good effect on the therapy with calcium antagonists significantly improves the forecast of these patients, and the lack of effect requires the use of drugs of other classes, which is limited by the complexity of their use, the high probability of developing side effects, the high cost of treatment, and in some cases, the insufficient issue of the issue.

Literature
1. Chazov I.E. Modern approaches To the treatment of a pulmonary heart. Rus Med Journal, 2000; 8 (2): 83-6.
2. BARST R., RUBIN L., LONG W. ET AL. A Comparison of Continuous Intravenous EpoproStenol (Prostacyclin) with Conventional Therapy for Primary Pulmonary Hypertension. N ENGL J ME.D 1996; 334: 296-301.
3. BARST R.J., Rubin L.J., McGoon M.d. et al. SURVIVAL IN PRIMARY PULMONARY HYPERTENSION WITH LONG-TERM CONTINUUS INTRAVENOUS PROSTACYCLIN. Ann Intern Med. 1994; 121: 409-415.
4. Charan N.B. Does Sildenafil Also Improve Breathing? Crested. 2001; 120 (1): 305-6.
5. FISNMAN A.P. Pulmonary Hypertension - Beyond Vasodiator Therapy. The New ENG J Med. 1998; 5: 338.
6. Franz I.W., Van der Meyden J., Schaupp S., Tonnesmann U. The Effect of Amlodipine On Exercise-InduCed Pulmonary Hypertension and Right Heart Function in Pulmonary Disease. Z Kardiol. 2002; 91 (10): 833-839.
7. Galie N., Hinderliter A.L., Torbicki A. et al. Effects of the Oral Endothelin Receptor Antagonist Bosentan on Echocardiographic and Doppler Measures in Patients with Pulmonary Arterial Hypertension. American Congress of Cardiology, Atlanta, USA; 17-20 March 2002. ABSTRACT # 2179.
8. GALIE N., HUMBERT M., WACHIERY J.L. et al. Effects of Beraprost Sodium, An Oral Prostacyclin Analogue, in Patients with Pulmonary Arterial Hypertension: A Randomized, Double-Blind, Placebo-Controlled Trial. J am Coll Cardiol. 2002; 39: 1496-1502.
9. Groechenig E. Cor Pulmonale. Treatment of Pulmonary Hypertension. Blackwell Science, Berlin-Vienna, 1999; 146.
10. McLaughlin V., Shillington A., Rich S. Survival in Primary Pulmonary Hypertension: The Impact of Epoprounol Therapy. Circulation. 2002; 106: 1477-1482.
11. Olchewski H., Ghofrani H., Schmehl T. et al. INHALED ILOPROST TO TREAT SEVERE PULMONARY HYPERTENSION: AN UNCONTROLLED TRIAL. Ann Intern Med. 2000; 132: 435-443.
12. Rich S., Kaufmann E., Levy P.S. The Effect of High Doses of Calcium Channel Blockers on Survival in Primary Pulmonary Hypertension. N engl j med. 1992; 327: 76-81.
13. Rubin L.J., Badesch D.B., BARST R.J. et al. BOSENTAN THERAPY FOR PULMONARY ARTERIAL HYPERTENSION. N engl j med. 2002; 346: 896-903.
14. Sajkov D., Wang T., Frith P.A. et al. A Comparison of Two Long-Acting Vasoselective Calcium Antagonists in Pulmonary Hypertension Secondary to Copd. Crested. 1997; 111 (6): 1622-1630.
15. Sastry B., Narasimhan C., REDDY N. ET AL. A Study of Clinical Efficacy of Sildenafil Inpatients with Primary Pulmonary Hypertension. INDIAN HEART J. 2002; 54: 410-414.
16. Sastry B.K., Narasimhan C., Reddy N.K., Raju BS. Clinical Efficacy of Sildenafil in Primary Pulmonary Hypertension: A Randomized, Placebo-Controlled, Double-Blind, Crossover Study. J am Coll Cardiol. 2004; 43 (7): 1149-53.
17. SEBKHI A., Strange J.W., Phillips S.C. et al. PHOSPHODIESTERASE TYPE 5 AS A TARGET FOR THE TREATMENT OF HYPOXIA-INDUCED PULMONARY HYPERTENSION. Circulation. 2003; 107 (25): 3230-5.
18. Simmoneau G., Barst R., Galie N. et al. Continuous Subcutaneous Infusion Of Treprostinil, a Prostacyclin Analogue, in Patients with Pulmonary Arterial Hypertension. Am j Respit Crit Care MED 2002; 165: 800-804.
19. Toward T.j., Smith N., Broadley K.J. Effect of Phosphodiesterase-5 Inhibitor, Sildenafil (Viagra), in Animal Models of Airways Disease. Am J Respir Crit Care Med. 2004; 169 (2): 227-34.
20. Wilkens H., Guth A., Konig J. et al. Effect of Inhaled Iloprost Plus Oral Sildenafil in Patients with Primary Pulmonary Hypertension. Circulation 2001; 104: 1218-1222.
21. Woodmansey P.A., O'Toole L., Channer K.S., Morice A.H. Acute Pulmonary Vasodilatory Properties of Amlodipine In Humans with Pulmonary Hypertension. Heart. 1996; 75 (2): 171-173.

Posted guidelinesdedicated to the clinic, diagnosis and treatment of the pulmonary heart. Recommendations are addressed to students of 4-6 courses. Electronic version The publication is posted on the SPbGMU website (http://www.spb-gmu.ru).

Methodical recommendations are addressed to students of 4-6 courses Chronic pulmonary heart under a chronic pulmonary heart

Ministry of Health and Social Development

Russian Federation

G. OU VPO "St. Petersburg State

MEDICAL UNIVERSITY

Named academician I.P.Pavlova

associate Professor V.N. Yablonskaya

associate Professor O.A.Ivanova

assistant J.A.Mironova

Editor: Head Department of Hospital Therapy SPbGMU. Acad. I.P.Pavlova professor V.I.Trefimov

Reviewer: Professor of the Department of Propedeutics of Internal Diseases

SPBGMU them. Acad. I.P.Pavlova B.G. Lukichev

Chronic pulmonary heart

Under a chronic pulmonary heart (HLS) Understand Hypertrophy of the right ventricle (PJ), or a combination of hypertrophy with dilatation and / or right-hand heartless heart failure (PJN) due to diseases, primaryly affecting the functions or the structure of the lungs, or both at the same time, and not related to the primary failure of the left and innocent and acquired Pulks of the heart.

This definition of the WHO Expert Committee (1961), according to a number of specialists, is currently needing correction due to the implementation of modern methods diagnostics and accumulation of new knowledge about the pathogenesis of HLS. In particular, CHLS is proposed to be considered as a pulmonary hypertension in combination with hypertrophy. dilatation of the right ventricle, dysfunction of both ventricles of the heart associated with primary structural and functional changes in the lungs.

On pulmonary hypertension (LH) say when pressure in the pulmonary artery (la) exceeds the established normal values:

Systolic - 26 - 30 mm Hg.

Diastolytic - 8 - 9 mm Hg.

Average - 13 - 20 mm Hg.

Chronic pulmonary heart is not an independent nosological form, but it complicates many diseases affecting the air and the alveoli, the chest with limiting its mobility, as well as pulmonary vessels. In essence, all diseases that can lead to the development of respiratory failure and pulmonary hypertension (more than 100 them) may cause chronic pulmonary heart. At the same time, in 70-80% of cases, HLS accounts for chronic obstructive pulmonary disease (COPD). Currently, chronic pulmonary heart is observed in 10-30% of pulmonary patients hospitalized in the hospital. It is 4-6 times more common in men. Being a severe complication of chronic obstructive pulmonary disease (COPD), HLS determines the clinic, the course and forecast of this disease leads to early disability of patients and is often the cause of deaths. Moreover, mortality in patients with HLS over the past 20 years increased by 2 times.

Etiology and pathogenesis of chronic pulmonary heart.

Since the chronic pulmonary heart is a state that occurs again and is essentially a complication of a number of respiratory diseases, in accordance with primary reasons It is customary to allocate the following types of HLS:

1.Bronholegling:

The reason is the diseases affecting the air pathways and Alveolas:

Obstructive diseases (chronic obstructive pulmonary disease (COPD), primary lung emphysema, bronchial asthma of severe flow with significantly expressed irreversible obstruction)

Diseases leaking with severe fibrosis of the lungs (tuberculosis, bronchiectatic disease, pneumoconiosis, repeated pneumonia, radiation damage)

Interstitial lung diseases (idiopathic fibrosis alveolo, sarcoidosis of the lungs, etc.), collagenoses, lung carcinomatosis

2. Thoracodiaphragmal:

The reason is the diseases affecting the chest (bones, muscles, pleura) and affecting the mobility of the chest:

Chronic pulmonary heart: Cardiology view

Prepared Maxim carnations | 03/27/2015

The prevalence of chronic obstructive diseases of the lungs (Hose) is growing rapidly around the world: if

in 1990, they were at a twelfth place in the incidence structure, according to the forecasts of WHO experts, by 2020 will go out to the top five after such pathologies as coronary heart disease (IBS), depression, injuries due to an accident and disease of the brain vessels. It is also predicted that by 2020 the CHOOL will take the third place in the cause of mortality. IHD, arterial hypertension and obstructive lung diseases are quite often combined, which breeds a number of problems both in pulmonology and in cardiology. November 30, 2006

at the Institute of Phthisiology and Pulmonology, the scientific and practical conference "Features of the diagnosis and treatment of obstructive diseases of the lungs in concomitant pathology took place.

cardiovascular system ", during which much attention was paid to the general problems of cardiology

and pulmonology.

With a report "Heart deficiency in chronic pulmonary heart: the view of the cardiologist" spoke

corresponding Member of the AMN of Ukraine, Doctor of Medical Sciences, Professor Ekaterina Nikolaevna Amosova .

- In modern cardiology and pulmonology there are a number of common problems in respect of which one needs to be achieved and unify approaches. One of them is a chronic pulmonary heart. It is sufficient to say that the dissertation work on this topic is equally protected both in the cardiological and pulmonological councils, it is included in the list of problems that are engaged in both sectors of medicine, but unfortunately not yet developed a single approach to this pathology. Do not forget about the therapists of a wide profile and family doctors who are difficult to understand disordering information and information printed in pulmonary and cardiac literature.

The definition of a chronic pulmonary heart in WHO document is dated 1963. Unfortunately, since that time, on this important issue, WHO recommendations were not specified and not reaffected, which, in fact, led to discussions and contradictions. Today, in foreign cardiology literature, there are practically no publications about the chronic pulmonary heart, although there are a lot of talk about pulmonary hypertension, moreover, the recommendations of the European Cardiology Society concerning pulmonary hypertension were recently revised and approved.

The concept of "pulmonary heart" includes extremely heterogeneous diseases, they differ in etiology, the mechanism for the development of myocardial dysfunction, its severity, have different approaches to treatment. At the heart of the chronic pulmonary heart is also hypertrophy, and dilatation, and the dysfunction of the right ventricle, which, by definition, are associated with pulmonary hypertension. The heterogeneity of these diseases is even more obvious if we consider the degree of increase in pressure in the pulmonary artery at pulmonary hypertension. In addition, its very presence is absolutely different in various etiological factors of the chronic pulmonary heart. For example, with vascular forms of pulmonary hypertension, this is the basis requiring treatment, and only a decrease in pulmonary hypertension allows to improve the patient's condition; In the CHOOL - pulmonary hypertension is not so pronounced and does not need treatment, as evidenced by Western sources. Moreover, the reduction in pressure in the pulmonary artery at the CHOOL does not lead to relief, but worsens the patient's condition, as the blood oxygenation decreases. Thus, pulmonary hypertension is important condition For the development of a chronic pulmonary heart, but its value should not be absoluting.

Often, this pathology becomes the cause of chronic heart failure. And if we talk about it at a pulmonary heart, then it is necessary to remind the criteria for diagnosing heart failure (CH), which are reflected in the recommendations of the European Cardiology Society. To form a diagnosis, there must be: firstly, the symptoms and clinical signs of heart failure, secondly, objective signs of systolic or diastolic dysfunction of myocardium. That is, the presence of dysfunction (changes in the function of myocardium alone) is mandatory for the diagnosis.

The second question is the clinical symptoms of the chronic pulmonary heart. In the cardiology audience, it is necessary to say that swelling does not correspond to the fact of the availability of worldwide failure. Unfortunately, cardiologists are very little aware of the role of extraordinary factors in the origin of clinical signs venous stagnation in big Circle blood circulation. Edems in such patients are often perceived as a manifestation of heart failure, it is started to be actively treated, but to no avail. This situation is well known to pulmonologists.

The pathogenetic mechanisms for the development of chronic pulmonary heart are also the extraordinary factors of blood depositing. Of course, these factors matter, but should not overestimate them and associate everything with them. Finally, we are little talking, in essence, only began, about the role of hyperactivation of the renin-angiotensin-aldosterone system and its meaning in the development of edema and hypervolemia.

In addition to listed factors, it is worth mentioning about the role of myocardiopathy. In the development of a chronic pulmonary heart, a large role is distinguished by the damage to myocardium not only the right ventricle, but also the left, which is influenced by the complex of factors, including toxic, which is associated with bacterial agents, in addition, it is a hypoxic factor causing the dystrophy of myocardial myocardials of the heart .

In the course of our studies, it was established that the correlation between systolic pressure in the pulmonary artery and the dimensions of the right ventricle in patients with chronic pulmonary heart are practically absent. There is some correlation between the severity of the COP and the violations of the function of the right ventricle, with respect to the left ventricle, these differences are less pronounced. When analyzing the systolic function of the left ventricle, its deterioration is noted in patients with severe Hose. The contractile ability of myocardium even the left ventricle correctly evaluated extremely difficult, because the indices that we use in clinical practice are very coarse and depend on pre-loading.

As for the indicators of the diastolic function of the right ventricle, the hypertrophic type of diastolic dysfunction is diagnosed in all patients. Indicators on the part of the right ventricle are expected, but by the left of the left, we suddenly suddenly received signs of a diastolic relaxation violation, which increased depending on the severity of the Hoze.

Indicators of the systolic function of the ventricles in patients with colers and idiopathic pulmonary hypertension are different. Of course, changes in the right ventricle under idiopathic pulmonary hypertension are more pronounced, while at the same time the systolic function of the left ventricle is more changed in the COP, which is associated with the action of adverse factors of infection and hypoxemia on myocardium left ventricle, and then it makes sense to talk about cardiopathy in that wide Understanding, which is present today in Cardiology.

In our study, all patients are registered I type of disorders of the diastolic function of the left ventricle, peak indicators were more pronounced in the right ventricle in patients with idiopathic pulmonary hypertension, diastolic disorders - in patients with Hozle. It is worth emphasizing that this is relative indicators, because we took into account different ages of patients.

With all patients with echoch, the diameter of the lower hollow vein was measured and determined the degree of falling on it on the breath. It was found that at moderate colers, the diameter of the lower vein should not be increased, it increased only with pronounced COcls when the FEV1 is less than 50%. This allows you to raise the question that you should not absolutize the role of incomographic factors. At the same time, the falling of the lower hollow vein on the breath was violated already with moderate COcl (this indicator reflects an increase in pressure in the left atrium).

We also analyzed the cardiac rhythm variability. It should be noted that cardiologists consider a decrease in the cardiac rhythm variability with a sympathetic system of activation marker, the presence of heart failure, that is, prognostically unfavorable. We revealed a decrease in variability with moderate COCL, the severity of which increased in accordance with obstructive violations of the ventilation function of the lungs. Moreover, we revealed a reliable correlation between the severity of the violation of the heart rate variability and the systolic function of the right ventricle. This suggests that the cardiac rhythm variability in the COP appears pretty early and can serve as a marker of myocardial damage.

In the diagnosis of chronic pulmonary heart, especially in pulmonial patients, it is necessary to pay great attention to the instrumental study of myocardial dysfunction. In this regard, the most convenient study in clinical practice is EchoCG, although there are restrictions for its use in patients with Hose, in which ideally need to use radionuclide ventriculography of the right ventricle, which combines relatively low invasiveness and very high accuracy.

Of course, none of any news that the chronic pulmonary heart with the COP and idiopathic pulmonary hypertension is very heterogeneously on the morphofunctional state of the ventricles, according to the forecast and a number of other reasons. In the existing European classification of CH, which has been practically unchanged in the document of the Ukrainian Society of Cardiologists, does not reflect the difference in the development mechanisms of this disease. If these classifications were comfortable in clinical practice, we would not be a discussion on this topic. It seems to us a logical term "chronic pulmonary heart" to leave for bronchopulmonary pathology, emphasize - decompensated, subcompensated and compensated. This approach will avoid the use of FC and CH terms. With vascular forms of chronic pulmonary heart (idiopathic, post-terro-human pulmonary hypertension), it is advisable to use the approved gradation of CH. However, it seems appropriate to us, by analogy with cardiological practice, to indicate in the diagnosis of systolic dysfunction of the right ventricle, because it matters for the chronic pulmonary heart associated with the Hose. If the patient has no dysfunction - this is one situation in predictive and therapeutic plans, if any - the situation is essentially different.

Cardiologists of Ukraine have been used for several years during the formulation of the diagnosis of chronic heart failure, the classification of storage-vasilenko, necessarily indicating, preserved or reduced systolic function of the left ventricle. So why not use in relation to chronic pulmonary heart?

Doctor of Medical Sciences, Professor Yuri Nikolaevich Sirenko He dedicated his speech to the peculiarities of the treatment of patients with IHD and arterial hypertension in combination with the Hose.

- When preparing for the conference, I tried to find references on the Internet for the last 10 years on the pulmongenic arterial hypertension - nosology, which often appeared in the USSR. I managed to find approximately 5 thousand references to arterial hypertension in chronic obstructive diseases of the lungs, however, the problems of the pulmongenic arterial hypertension in the world, except the countries of the post-Soviet space, does not exist. To date, there are several positions regarding the diagnosis of the so-called pulmongenic arterial hypertension. They developed in the early 1980s, when more or less reliable functional research methods appeared.

The first position is the development of pulmongenic arterial hypertension in 5-7 years after the occurrence of chronic lung disease; The second is the connection of increasing blood pressure with the exacerbation of COLS; The third is an increase in blood pressure in connection with the enhancement of the bronchorate; The fourth - in daily monitoring, the connection is revealed between the increase in blood pressure and inhalation of sympathomimetics; The fifth is the high variability of blood pressure during the day with a relatively low average level.

I managed to find a very serious work of the Moscow Academician E.M. Tareeva "Is there a pulmongenic arterial hypertension?" In which the author conducts a mathematical assessment of the possible connection of the above factors in patients with arterial hypertension and colers. And no dependence found! The results of the research did not confirm the existence of independent pulmongenic arterial hypertension. Moreover, E.M. Tareev believes that the systemic arterial hypertension in patients with COP should be considered as a hypertensive disease.

After such a categorical output, I viewed the global recommendations. In modern recommendations of the European Society of Cardiologists, there is not a single line about COZL, US (seven recommendations of the National Joint Committee) also do not speak anything on this topic. It was possible to find only in the American Recommendations of 1996 (in six editions) information on what should not be used in patients with Noselylective beta adrenoblays, and if there is a cough, ACE inhibitors replace on angiotensin receptor blockers. That is, in the world such a problem does not really exist!

Then I revised the statistics. It turned out that the pulmongenic arterial hypertension began to speak after it was established that approximately 35% of the hose patients had increased blood pressure. Today, Ukrainian epidemiology gives the following figures: among adult rural population, blood pressure is increased in 35%, urban - in 32%. We cannot say that the CHOOL increases the frequency of the occurrence of arterial hypertension, so it should be not about the pulmongenic arterial hypertension, but about some specificity of the treatment of arterial hypertension at the CHOOL.

Unfortunately, in our country, the night apnea syndrome, except for the Institute of Phtisiology and Pulmonology. F.G. Yanovsky AMN of Ukraine, practically do not do anywhere. This is due to the lack of equipment, money and the desire of specialists. And this question is very important and represents another problem, where cardiac pathology with the pathology of the respiratory tract is crossed and a very large percentage of the risk of developing cardiovascular complications and death is observed. Pulmonary hypertension, cardiac and respiratory failure complicate and worsen the course of arterial hypertension and the most important thing - worsen the possibility of treating patients.

I would like to start a conversation about the treatment of arterial hypertension from a simple algorithm, which for cardiologists and therapists is the basis. Before the doctor who meets a patient with hypertension, questions arise: what form of arterial hypertension in the patient is primary or secondary - and is there signs of defeat of target organs and cardiovascular risk factors? Having answered these questions, the doctor knows the tactics of the patient's treatment.

Today there is no single randomized clinical researchwhich was specially organized to clarify the tactics of the treatment of arterial hypertension at the COLD, therefore modern recommendations They are based on three very unreliable factors: a retrospective analysis, the opinion of experts and their own experience of the Doctor.

How do you need to start treatment? Of course, with antihypertensive preparations of the first row. The first and basic group are beta-adrenoblays. Many questions arise regarding their selectivity, but already there are preparations with quite high selectivity confirmed in the experiment and clinic that are safer than the drugs that we used before.

In assessing the airways of the respiratory tract in healthy people after receiving the atenolol, the deterioration of the reaction to salbutamol and minor changes when receiving more modern drugs. Although, unfortunately, with the participation of patients, such studies were not carried out, after all, a categorical ban on the use of beta-adrenoblockers in patients with Hosl should be removed. They cost them to be prescribed if the patient is well tolerated, it is desirable to apply in the treatment of arterial hypertension, especially in combination with IBS.

The following group of drugs - calcium antagonists, are almost ideal for the treatment of such patients, but it should be remembered that the drugs of the Nedigidropyridine row (diltiazene, verapamil) should not be used with elevated arterial pressure In the pulmonary artery system. It is proved that they worsen the flow of pulmonary hypertension. Digidropyridines remain, it is known that they improve the permeability of the bronchi, and due to this they can reduce the need to use bronchodulators.

For today, all experts agree that the ACE inhibitors do not worsen the patency of the respiratory tract, do not cause cough in patients with colel, and if it occurs, patients should be translated into angiotensin receptor blockers. We did not conduct special research, but based on these literature and our own observations, it can be argued that experts are slightly cursed, because a certain number of patients with COPs react to dry cough on ACE inhibitors, and there is a serious pathogenetic basis.

Unfortunately, it is very often possible to observe the following picture: Patient with increased pressure goes to the cardiologist, he is prescribed ACE inhibitors; After some time, the patient begins to cough, goes to a pulmonologist, which cancels the ACE inhibitors, but does not prescribe an angiotensin receptor blockers. The patient gets to the cardiologist again, and it all starts first. The reason for such a position in the absence of assignment control. It is necessary to move away from such practices, therapists and cardiologists must comprehensively approach the treatment of the patient.

Another very important point in the treatment of patients, which reduces the possibility of side effects, is the use of lower doses. Modern european recommendations They give the right to choose between low doses of one or two drugs. Today, the greater efficiency of the combination of different drugs has been proven, which affects the various tracks of pathogenesis, mutually resides the effect medicines. I believe that it is the combination therapy for patients with CHOOLs is a choice in the treatment of arterial hypertension.