Clinical recommendations: Lung hypertension. Chronic pulmonary heart: clinical signs and recommendations for the treatment of recommendation to diagnose the treatment of pulmonary hypertension

- this is a concept that includes a complex of violations of work of cardio-vascular systemcaused by the disease of the lungs. With insufficient work of the lungs and bronchi, the load on the heart increases, which begins to swing blood more active.

In this case, the connection between the heart and pulmonary disease is not traced immediately. Symptoms of violation of the cardiovascular system may be observed years after the start of the lung disease.

The appearance of a chronic pulmonary heart is usually caused by various ailments of the respiratory system. In contrast to the acute form, pathology can develop very slowly. It is possible to highlight 3 the most famous forms of HLS.

The most common is the bronchopal form, when the heartfelt disorders are caused by inflammatory processes of the lower respiratory tract. A vascular form is also observed (at which vessels are affected), thoracodiaphragmal form (pathological deformations of the spine and chest).Before prescribed clinical recommendationsChronic pulmonary heart must be examined and identified the cause of pathology.

The effectiveness of treatment depends on the correct definition of the cause, as the pulmonary heart is a secondary disease.

Based on the forms of the disease, the causes of the occurrence of pathology are divided into 3 large groups:

1. Diseases of bronchi and lungs. The occurrence of HLS can cause various acute and chronic inflammatory diseases of the respiratory organs. These include chronic bronchitis (inflammatory process in bronchi), bronchial asthma (often develops against the background of respiratory allergies, leads to a suffocation), pulmonary fibrosis (thickening of the lung tissues, leading to a partial loss of the organ functionality). All these diseases are accompanied by a respiratory impairment and gas exchange. This leads to the fact that the tissues are not sufficient oxygen. The heart begins to work more active, which provokes hypertrophy of its individual sections.
2. Pathologies associated with breast integrity impaired and spine. Various injuries of sternum, curvature and defects, removal of ribs, exhaustion lead to a violation of the ventilation of the lungs, because it is impossible to make a full breath and exhale it becomes impossible. This leads to heart pathologies.
3. Pathological processes in vessels. Pulmonary hypertension (high blood pressure in vessels and arteries pulmonary fabric), as well as vasculitis (inflammatory process directly by vessels).

After determining the cause of pathology, the doctor will prescribe a treatment that must necessarily be aimed at eliminating the main initial pathology and its consequences.

Signs and complications of the disease

The feature of the CHLS is that due to the violation of the work of the lungs, the right atrium and ventricles are increasing in volume. This is due to the increase in the load on the heart. Due to thickening of the walls of the right ventricle, the contractile function of the heart is significantly reduced.

Initially, only the symptoms associated with the initial disease appear to the fore, that is, with the pathology of the lungs. Gradually begin to show signs of cardiovascular diseases, but the manifestation of symptoms is inhomogeneously.

The main features of the chronic pulmonary heart include:

• Saddy and cough. These signs are accompanied by both diseases of the lungs and the pathology of the cardiovascular system. At the initial stages, shortness of breath appears only during physical exertion. With a further course of the disease, the feeling of the lack of air may appear and at rest. Also the patient torment the bouts of a dry cough at night, which is called a heart cough.
• Speakers on the neck. With chronic pulmonary heart, the patient often observes swelling of the veins on the neck. They do not come to the usual condition when inhaling or exhale.
• Skin skin. Due to the lack of oxygen in the blood and impaired circulation of the lips, feet, ears, the brush of the hands acquire the light blue shade.
• . Edems appear gradually and increase with the flow of illness. At a later stage, the liquid accumulates in the abdominal cavity and in the lungs, which causes the swelling of the entire body.
• Disorders of the nervous system. With chronic pulmonary heart, dizziness is observed, noise in the ears, which is also associated with oxygen fasting fabrics.
• Reinforced heartbeat, violation of heart rhythm. Since the heart is increased in size, it is not able to pump blood normally. The heart muscle begins to shrink more actively, causing attacks.

The consequences of chronic pulmonary heart can be serious enough. The most dangerous is the fatal outcome and a sudden stop of the heart. In the absence of treatment, the body exhaustion occurs due to the deterioration of blood supply and the lack of oxygen.

Death may occur within 2-5 years after the start of the disease.

The consequences of chronic pulmonary heart are chronic heart failure, various violations of the heart rhythm, which lead to a deterioration in the quality of the patient's life.

Diagnostics and methods of treatment

Diagnostic procedures are aimed at identifying the cause of the disease and diagnosis. The doctor collects anamnesis, clarifies the available symptoms and the frequency of their appearance. First of all, a general blood test is prescribed, a biochemical blood test, a common urine analysis and blood gas analysis. This will help reveal the decrease in blood oxygen levels.

In mandatory, electrocardiography is prescribed, and the radiography of the chest. As additional diagnostic procedures, spirometry recommended, CT.

Treatment is primarily aimed at improving the work of the lungs, a decrease in pulmonary hypertension and the normalization of the work of the right ventricle. Complex treatment of chronic pulmonary heart includes:

1. Inhalation. With violation of the operation of lungs and oxygen starvation, inhalation is prescribed with wet air with an increased amount of oxygen. Procedures are carried out using a mask or nasal catheter.
2. Diet. In the chronic pulmonary heart, the likelihood of edema formations increases, so it is recommended to reduce the use of a cook salt. Preferably use more protein, fiber in the form of vegetables and fruits, greenery, products rich in vitamins and microelements.
3. Moderate physical exertion. Violation of the work of the lungs and hearts do not allow large physical exertion, but hypodynamia can also be useful. With exacerbations, bedding is assigned. During remission, the doctor will recommend exercises to strengthen the body, therapeutic physical education.
4. Preparations to improve the work of the bronchi. To clear the bronchi and improve their work, mulitics are prescribed, expectorant means and bronchopholics. They help bring the bronchi wet.
5. Antibiotics. Antibacterial drugs prescribed in the event that the cause of the respiratory system is caused bacterial infection. For example, with tuberculosis, pneumonia antibacterial therapy is required.

Anticoagulants, heart glycosides, are also prescribed. If a medicia treatment It turns out ineffective, surgical treatment is appointed. For example, when visiting the chest, its correction is proposed using surgical methods.

Prediction and prevention

With severe disease, the forecast is disappointing. Chronic pulmonary heart can lead to disability and sudden death of the patient. Even on early stages The disease is noticeably affected by the patient's ability. The forecast is improved by timely formulation of the diagnosis and treatment of the disease in the initial stages.

Prevention measures are directed primarily to reduce the likelihood of respiratory disease. Since the most common cause of chronic pulmonary heart is infectious diseases of the lungs, it is necessary to strengthen the immunity and avoid contact with viruses and bacteria.

Prevention rules include:

• Compliance with the regime of labor and recreation. Overwork and constant stress lead to weakening the body, falling immunity. To maintain health, regular and long sleep is needed (at least 8 hours a day).
• Refusal from harmful habits. For lungs, it is a special danger of smoking, including passive. Chronical bronchitis Much more often occurs in smokers. To protect yourself from the development of lung diseases, it is necessary to abandon smoking.
• Proper nutrition. Balanced nutrition helps to normalize pressure, strengthen the immunity, to establish metabolism. The diet should include enough proteins, fats, vitamins, minerals and trace elements.
• Physical exercise. Training helps strengthen the heart muscle and increase the volume of the lungs. However, with existing diseases, caution should be exercised and consult with a doctor.
• Reception of vitamins. Reception multivitamin complexes Allows avoiding avitaminosis and strengthen the body in spring time.
• Hardening. Hardening is necessary to increase the protective function of the body. Pediatricians recommend teaching a child to hardening procedures from early childhood, but it is necessary to start gradually by catching the body to low temperatures.

more information about the causes of pain in the heart area can be found from the video:

Also important preventive measure is the timely visit of the doctor. All respiratory diseases need to be treated in time and prevent them in a chronic form.

The pulmonary heart (LS) is hypertrophy and / or pursuit of the right ventricle (PJ), 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 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 main disease caused by HLS (chronic obstructive bronchitis, bronchial asthma, etc.), elimination of alveolar hypoxia and hypoxhemia with a decrease in pulmonary hypertension (training of respiratory muscles, electrostimulation of the diaphragm, normalization of the oxygen-cycle blood function (heparin, erythrocytafferesis, Hemisorption), long oxygen therapy (DCT), almitrine), as well as 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- these are 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 defects Hearts.

The pulmonary heart (LS) is formed on the basis of pathological changes in the lighter, disorders of the extravalic mechanisms of respiration, ensuring the ventilation of the lung (damage to the respiratory muscles, the violation of the central regulation of the respiration, the elasticity of the bone-cartilage formations of the chest or the nervous impulse 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. The leading clinical symptom is the growing shortness of breath with a rapidly developing (for months) by referee. To other reasons, the PLS should include neuromuscular diseases (Miasthenia, polio, damage to the diaphragmal nerve), turning off from the respiratory act of a significant part of the respiratory lung (severe flow bronchial asthma, Miliary tuberculosis of the lung). A frequent cause of PLS \u200b\u200bis 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 CLN classification based on the presence of shortness of breath. 3 degrees of CLN are isolated: the appearance of shortness of shortness of breath with the previously available efforts - 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. At the beginning exercise (I Stage CLN), and then alone (III HLN Stage). 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. The presence of flicker arrhythmia, especially 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, it 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 heart turn around the longitudinal axis clockwise (shift of the transition zone to the left, to the V5-V6 leads and the appearance in leads V5, V6 qRS complex type RS; SV5-6 deep, and 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 COPD 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, so the ECG changes must be compared with the clinical picture of the disease and ECOCG 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. Tricespecial regurgitation of varying degrees, which in turn causes dilatation of the right atrium and the lower hollow vein, the decrease in the inspiratory collapse of which indicates high blood pressure In the right 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 pressure in the right atrium and PJ, pressure in the pulmonary artery, calculate the heart rate and pulmonary vascular resistance, determine the level of oxygenation of 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 acute viral respiratory diseases (vaccination) and smoking exclusion. 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 moderately pronounced respiration, which is not requiring use of O 2 or mechanical ventilation of the lungs (apnea syndrome in a dream, syndrome of obesity-hypoventilation), or if oxygen therapy is impossible. The number of few drugs that increase the oxygenation of arterial blood include nickelamide, acetosalamide, doxapram and medroxyprogesterone, but all these drugs with long-term use have a large number of 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 when long use 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 - powerful selective inhibitor TSGMF-dependent phosphodiesterase (type 5), preventing the degradation of CGMF, causes a decrease in pulmonary vascular resistance and overload 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 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 by-effect A diuretic therapy is a metabolic alkalosis, which in patients with cobc 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 last years Inhibitors of the angiotensin glittering enzyme (IAPF) appeared in the first place. The IAPF therapy in patients with HLS leads to a decrease in pulmonary hypertension and an increase in cardiac output. In order to select effective CHLS therapy in patients, the COPD is recommended to determine the 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.

Belarusian State Medical University

Trisvetova E.L.

Belarusian State Medical University, Minsk, Belarus

Pulmonary Hypertension In The New (2015)

Recommendations EUROPEAN SOCIETY OF CARDIOLOGY

Summary. In ESC / ERS 2015 Recommendations, based on the analysis of studies made from the date of publication of the previous publication, the main provisions of pulmonary hypertension are covered from the standpoint of evidence-based medicine: an improved classification of a doctor's strategy in a specific clinical situation, taking into account the disease of the disease in a patient, the risk ratio and the benefits of diagnostic procedures and the use of diagnostic procedures and Medical agents.

Keywords: pulmonary hypertension, pulmonary arterial hypertension, classification, diagnosis, treatment.

Summary. The recommendations of the ESC / ERS 2015 based on the analysis of studies carried out since the publication of the previous edition, highlights the key provisions of pulmonary hypertension with evidence-based medicine: an improved classification strategy physician in a particular clinical situation, taking into Account The Outcome of the Disease In A Patient, The Risks and Benefits of Diagnostic Procedures and Medical Means.

Keywords: pulmonary Hypertension, Pulmonary Arterial Hypertension, Classification, Diagnosis, Treatment.

Congress European society Cardiologists (ESC), held from August 29 to September 2, 2015 in London, saturated with events and reports on the results of scientific research, approved five new recommendations on clinical practice: prevention, diagnosis and treatment infectious endocarditis; ventricular arrhythmias and prevention of sudden cardiac death; Diagnosis and treatment of pericardium diseases; Treatment of patients with acute coronary syndrome without offset and lifting ST segment; Diagnosis and treatment of pulmonary hypertension.

In Recommendations (2015 ESC / Ers Guidelines for the Diagnosis and Treatment of Pulmonary Hypertension), illuminating the problems of pulmonary hypertension, based on the analysis of studies made from the moment of publicationgUIDELINES FOR THE DIAGNOSIS AND TREATMENT OF PULMONARY HYPERTENSION ESC, ERS, ISHLT, 2009), from the standpoint of evidence-based medicine presented a doctor's strategy in a specific clinical situation, taking into account the disease in the patient, the risk ratio and the benefits of diagnostic procedures and therapeutic agents.

Pulmonary hypertension (LH) refers to pathophysiological states complicating the course of many cardiovascular and respiratory diseases.

Definition and classification

LH is diagnosed with an increase in the averagepressure in the pulmonary artery (PAPM) ≥25 mm Hg. Art. Alone according to the results of catheterization of the right heads of the heart. Normal PAPM at rest is 14 ± 3 mm Hg. Art. With the upper limit of 20 mm Hg. Art. The clinical value of PAPM in the interval of 21-24 mm Hg. Art. undefined. In the absence of obvious clinical signs of diseases accompanied by LH, patients with PAPM values \u200b\u200bat the specified interval requires observation.

The term "pulmonary arterial hyperte niza "(PAh) is used to characterize patient groups with hemodynamic impairment in the form of preacpillary LS, for which the pressure of the junction (PAWP) ≤15 mm RT is characteristic. Art. and pulmonary vascular resistance (PVR)\u003e 3 units. Wood in the absence of other causes (lung disease, chronic thromboembolic LG, rare diseases, etc.).

In accordance with the combination of the values \u200b\u200bof the results of the study of PAP, PAWP, cardiac output, a gradient of diastolic pressure and PVR, estimated at rest, LH is classified by hemodynamic parameters (Table 1).

Table 1. Hemodynamic classification of pulmonary hypertension

NOTE: PAPM - average pressure in the pulmonary artery, PAWP - the pressure of the junction, PVR is the pulmonary vascular resistance, the DPG is a diastolic pressure gradient (the diastolic pressure in the pulmonary artery is the average pressure in the pulmonary artery).

The clinical classification of LH includes five groups of states combined by similar pathophysiological, clinical, hemodynamic characteristics and treatment strategy (Table 2).

Table 2. Clinical classification of pulmonary hypertension

NOTE: BMPR2 - Bone MorpHogenetic Protein Receptor, Type 2, receptors to bone morphogenetic protein; Eif2AK4 - Eukaryotic. Translation Initiation Factor-2-Alpha-KINASE-4 is a kinase family that phosphorylates the alpha subunit of eukaryotic initiation of translation factor-2.

Epidemiologyand risk factors LH

Data on the prevalence of LH is unconvincing. In the UK, 97 cases of LH are revealed to 1 million; Among women 1.8 times more than among men. In the USA standardized patient mortality with LG varies from 4.5 to 12.3 per 100 thousand population. Comparative epidemiological studies of various groups of patients with LH have shown that the disease is not widespread, the most commonly found 2rd group is the notifying LH, due to diseases of the left-wing hearts.

RAS (1st group) is rarely found: according to the results of research, in Europe 15-60 cases per million people, incidence during the year - 5-10 cases per million people. In registers, 50% of patients are diagnosed idiopathic, hereditary or drug wounds. Among the diseases of the connective tissue with associated wounds, the main reason is systemic sclerosis. The idiopathic wounds refers to sporadic diseases without family anamnesis of the LG or the famous trigger. It is more often diagnosed in old age, the average age of patients is 50-65 years (in the 1981 register, the average age of the diagnosis is 36 years). The predominance of women in old age, according to the results of research, doubtful.

Table 3. Risk factors for the development of pulmonary hypertension

NOTE: * - Increased risk of persisting LG in newborns from mothers, used selective selection inhibitors of serotonin reverse seizure; ** - Alkylating agents as a possible cause of pulmonary vein-compound disease.

The prevalence of LH in patients of the 2nd group increases with the appearance and progression of signs of heart failure. Increased pressure in the pulmonary artery is determined in 60% of patients with severe systolic dysfunction of the left ventricle and in 70% of patients with heart failure and stored left ventricular emission fraction.

With diseases of light and / or hypoxemia (3rd group), it is often mild, rarely heavy LH, mainly with a combination of emphysema and common fibrosis.

The prevalence of LH in chronic thromboembolism is 3.2 cases per million people. In survivors after the acute pulmonary embolism, the LG is diagnosed in 0.5-3.8% of cases.

Diagnosis of LG

The diagnosis of LH is based on clinical data, including history, the development of symptoms and physical research. An important role in confirming the diagnosis of LH is given by the results of instrumental research methods, interpreted by experienced specialists. The diagnostic algorithm is built on the results confirming or excluding diseases, accompanied by the development of LH (Groups 2-5).

Clinical signs

Clinical symptomylg non-councils and are due to the mainly progressive dysfunction of the right ventricle. Primary symptoms: shortness of breath, fatigue, weakness, angina painting pain in the heart, syncope - are associated with the load, there are still alone. An increase in abdomen, swelling of the ankles indicate the development of justifying heart failure.

Some patients appear symptoms (hemoptysis, votes, remote wheezing, angina) associated with mechanical complications arising from anomalous redistribution of blood flow in the pulmonary vascular bed.

Physical signs: pulsation to the left of the sternum in the parastinal line in the fourth intercostride, an increase in the right ventricle, with auscultation of the heart - the strengthening of the second tone in the second intercontalone on the left, the pantsistolic noise in the event of tricuspid deficiencies, the noise of the sin - style. The increase in venous pressure is manifested by the pulsation of the cervical veins, there are signs of the right-hand deficiency - hepatomegaly, peripheral edema, ascites. Clinical study will allow to identify the disease that caused LG: COPD - "Bochemy" chest, a change in the distal phalanx of the fingers - "drumsticks" and "hour glass"; with interstitial diseases of the lungs - "cellophane" wheezing at auscultation of the lungs; In hereditary hemorrhagic teleangioectasis and systemic sclerosis - TelangioEctasia on leather and mucous membranes, digital ulcers and / or sclerodctible; In case of diseases of the liver - palman erythema, testicular atrophy, teleangioectasia, etc.

Instrumental research methods

The results of electrocardiography confirm the diagnosis, but do not exclude it, in the absence of pathological changes on the ECG.With severe LH, the deviation of the electrical axis of the heart is to the right, the "pulmonal" p, signs of the hypertrophy of the right ventricle (sensitivity - 55%, specificity - 70%), the blockade of the right leg of the GISE beam, the elongation of the Qt interval. It is often noted by heart arrhythmias (sufficiently valuable extrasystolism, fluttering or atrial fibrillation), aggravating hemodynamic disorders and contributing to the progression of heart failure.

With an x-ray study of the chest in 90% of cases of idiopathic pulmonary arterial hypertension The characteristic changes are detected: the expansion of the main branches of the pulmonary artery contrasting with the depletion of the peripheral pulmonary pattern, an increase in the right heads of the heart (late stages). Radiographic research helps in differential diagnosis LG, as signs of lung diseases (3rd group) are detected, characteristic of arterial and venous hypertension. The degree of LH does not correlate with the degree of radiographic changes.

When studying the function of external an alia and gas composition of arterial blood determine the contribution of respiratory tract diseases and lung parenchyma in the development of LH. In patients with pulmonary arterial hypertension, there is a slight or moderate decrease in pulmonary volumes, depending on the severity of the disease, normal or slightly reduced indicators of the diffusion capacity of the lungs for carbon monoxide (DLCO). Low DLCO indicators (<45% от должного) свидетельствуют о плохом прогнозе. При ЛГ, обусловленной ХОБЛ, выявляют признаки необратимой обструкции, увеличение остаточного объема легких и снижение показателя DLCO.

When COPD, interstitial diseases of the lungs of changes in the gas composition of arterial blood include a decrease in PAO 2, raising RAS 2. With a combination of emphysema of light and pulmonary fibrosis, it is possible to obtain pseudonormal spirometry indicators, the decrease in DLCO indicators will indicate a violation of the functional state of the lungs.

Given the significant prevalence of LH (70-80%) during night hypoxemia and the central obstructive sleep apnea, in order to clarify the diagnosis, it is necessary to perform oximetry or polysomnography.

The method of transtorcal echocardio-Rartia estimate the state of the heart muscle and heart chambers to detect hypertrophy and dilatation of the right-hand heart departments, diagnostics of myocardial pathology and valve apparatus, hemodynamic disorders (Table 4). Evaluation of tricuspidal regurgitation and changes in the diameter of the lower hollow vein in respiratory maneuvers are carried out in the Doppler study to calculate the average systolic pressure in the pulmonary artery. Transtoracal echocardiography is not enough to judge the soft or low-power LG due to the methodological inaccuracies of the study and individual characteristics of patients. In a clinical context, the results of an echocardiographic study are necessary for making a decision on the performance of heart catheterization.

Table 4. Echocardiographic signs to assume LH (in addition to changing the speed of tricuspid regurgitation)

For obtaining a more detailed representation of structural changes in the heart and impairment of hemodynamics, perchivery echocardiography performs, occasionally with contrast.

In the case of the alleged thromboembolic LG, a ventilation and perfusion scanning of the lungs is required (sensitivity - 90-100%, specificity - 94-100%). In the case of RAS, the results of the ventilation and perfusion scanning can be normal or with small non-peripheral perfusion defects, which are also found at the pulmonary vein-compound disease. New research technologies appeared, such as three-dimensional magnetic resonance tomography, in which the study of perfusion is as informative as with a ventilation and perfusion scanning of the lungs.

Method computer tomography High resolution with contrasting of lung vessels allows you to get important information about the state of the parenchyma and the vascular bed of lungs, heart and mediastinum. The assumption of the LG will arise in the case of detection of highly specific features: expansion of the diameter of the pulmonary artery ≥29 mm, the ratio of the diameter of the pulmonary artery to the ascending aorta ≥1.0, the ratio of segmental bronchial arteries\u003e 1: 1 in three or four fractions. The method of informative in differential d ignostics of LH, developed during the damage to the pulmonary parenchyma, due to emphysemic lungs, with interstitial lung diseases, to select the surgical treatment tactics in chronic thromboembolism, during vasculitis and arteriovenous malformations.

The image of the heart with magnetic resonance imaging is accurate and well reproduced, is used for non-invasive assessment of the right ventricle, its morphology and functions, blood flow states, including the impact volume, the extensibility of the pulmonary arteries, the mass of the right ventricle. In patients with the alleged LH, the accumulation of gadolinium, a decrease in the extensibility of pulmonary arteries and retrograde blood flow have a high prognostic value in diagnosis.

To identify diseases, caused by the formation of LG, it is recommended to perform ultrasonic research Abdominal organs. The ultrasound results can confirm the presence of portal hypertension associated with LH.

Right heart catheterization is performed in specialized hospitals To confirm the diagnosis of pulmonary arterial hypertension, congenital heart shunts, diseases of the left sections of the heart, accompanied by LH, chronic thromboembolic LG, the gravity of hemodynamic disorders, conducting tests for vase absorption, to control the effectiveness of the treatment. The study is performed after receiving the results of routine methods indicating the estimated LH.

Samples for vase absorption during the catheterization of the right heart to identify patients capable of responding to high doses of calcium blockerschannels (BKK) are recommended for suspected idiopathic, hereditary or associated with the reception of the Russian Academy of Sciences. With other forms of the Russian Academy of Sciences and LH, the sample results are often dubious. To perform samples for vase absorption, nitrogen oxide or alternative means - epoprottenol, adenosine, iloprost are used. As a positive result is estimated in the case of a decrease in the average pulmonary blood pressure ≥10 mm Hg. Art., Before reaching the absolute value of the average pulmonary blood pressure ≤40 mm Hg. Art. With / without increasing cardiac output. Use oral or intravenous BKK when performing a dough for vase absorption is not recommended.

Laboratory research

The study of blood and urine is useful for verifying diseases in some forms of LH and status evaluation internal organs. Functional tests The liver may vary with high hepatic venous pressure, liver diseases, antagonists of endothelin receptor antagonists. Serological studies are performed for the diagnosis of viral diseases (including HIV). The study of the function of the thyroid gland, the violations of which are found at the RAS, are carried out with a deterioration in the course of the disease, immunological studies are necessary for the diagnosis of systemic sclerosis, antiphospholipid syndrome etc.

The study of the level of N-terminal blasting sodium-repeat peptide (NT-Promnip) is necessary because it is considered as an independent risk factor in patients with LG.

Molecular genetic diagnostics is carried out in suspected sporadic or family form of pulmonary arterial hypertension (Group 1).

The diagnostic LG algorithm (Figure) consists of several stages of the study, including methods confirming the assumption of LH (history, physical data, the results of an echocardiographic study), then follow the methods specifying the severity of LG and possible diseases that caused pressure in the pulmonary artery. In the absence of signs of diseases of 2-4 groups, diagnostic search for diseases of group 1 is carried out.

Clinical evaluation remains key in diagnosis of the patient's condition with LH. For an objective assessment of the functional ability of patients with LGs, a test with a 6-minute walk (MX) and evaluation of shortness of shortness of breath of G. borg (1982), as well as cardiopulmonal load tests with gas exchange estimate are used. The functional classification of the LH is carried out according to the modified version of the classification (NYHA) of heart failure (WHO, 1998). The deterioration of the functional class (FC) is an alarming indicator of the progression of the disease that encourages further research to clarify the causes of clinical worsening.

Risk assessment at pulmonary arterial hypertension (high, moderate, low) is carried out according to the results of a comprehensive patient survey (Table 5).

Table 5. Qualitative and quantitative clinical, instrumental and laboratory indicators for risk assessment at pulmonary arterial hypertension

NOTE: 6mx - Test 6-minute walk, PP - right atria, BNP - atrial sodium-weathetic peptide, NT-PROBNP - N-terminal protrusion sodium systemic peptide, VE / VCO 2 - Ventilation equivalent software 2, Rap - pressure in the right of atrium, Ci is the heart index, SVO 2 - the saturation of venous blood oxygen.

Thus, with pulmonary arterial hypertension, depending on the results of the recommended studies, a patient is possible low, moderate, high risk of clinical worsening or death. Undoubtedly, other factors not included in the table can affect the course and outcome of the disease. At the same time, at low risk (mortality for a year less than 5%) in patients, the patients define an unpressuring course of the disease with a low FC, 6mx test\u003e 440 m, without clinical significant signs of the dysfunction of the right ventricle. With a moderate (intermediate) risk (mortality for 1 year 5-10%), FC III and moderate disorders of tolerance to physical exertion, signs of dysfunction of the right ventricle are detected. At high risk (mortality\u003e 10%) diagnose the progression of the disease and signs of severe dysfunction and deficiency of the right ventricle with FC IV, the violation of the function of other organs.

Treatment

A modern strategy for treating patients with pulmonary arterial hypertension consists of three stages, including the following activities:

General (physical activity, controlled rehabilitation, planning and control during pregnancy, in postmenopausal period, prevention of infections, psychosocial support), supporting therapy (oral anticoagulants, oxygen therapy, digoxin, diuretics) (Table 6);

.? initial therapy of high doses of BKK in patients reacted positively to the test of vase absorption, or drugs recommended for the treatment of pulmonary arterial hypertension, with a negative test of vase absorption;

In the event of the ineffectiveness of treatment - a combination of recommended drugs, lung transplantation.

Oral anticoagulants are prescribed due to the high risk of development of vascular thrombotic complications in patients with RAS. Evidence of the effectiveness of the application was obtained in the same center. The place of new oral anticoagulants at the Russian Academy of Sciences is uncertain.

Diuretics are shown in decompensated heart failure with a fluid delay in the patient's body with wounds. Randomized clinical studies on the use of diuretics under the Russian Academy of Scientifications was not carried out, at the same time appointing drugs of the specified group, as well as aldosterone antagonists, are carried out according to recommendations for the treatment of heart failure.

Oxygen therapy is necessary for patients with arterial hypoxemia alone.

Digoxin increases cardiac selectionoS for bolus administration in patients with idiopathic wounds, its effectiveness during long-term intended purpose is unknown. Undoubtedly, to reduce the heart rate with sucanementaric tachyariums, digoxin is useful.

With regard to ACE inhibitors, sconce, beta-blockers and Ivabdin, there are no convincing data on the need for their appointment and safety at the Russian Academy of Sciences.

Iron deficiency occurs in 43% of patients with idiopathic wounds, 46% of patients with systemic sclerosis and wounds, 56% of patients with Eisenmenger syndrome. Preliminary results indicate that iron deficiency is conjugate with a decrease in physical activity tolerance, possibly with a higher mortality that does not depend on the availability and severity of anemia. An examination is recommended to identify the causes of iron deficiency and conducting substitution therapy (preferably intravenous) in patients with wounds.

Specific gear T.yerapia(Table 7)

In a small share of patients with idiopathic wounds with a positive vase absorption test during catheterization of the right heart, a favorable effect on BKK is observed during long-term treatment. In published works, used mainly nifedipine, diltiazene and, with a smaller clinical effect, amlodipine. The choice of the drug is focused on the initial frequency of the patient's heart abbreviations, in the case of relative brandcardia is used nifedipine or amlodipine, with tachycardia - diltiaze. Daily doses of BKK with idiopathic wounds High: nifedipine 120-240 mg, diltiam 240-720 mg, amlodipine 20 mg. Treatment starts with small doses, gradually titrating to the transferred maximum recommended dose of the drug, controlling the effectiveness of therapy after 3-4 months.

The vasodilating effect of the BACK does not have a favorable long-term effect under the Russian Academy of Sciences, due to the diseases of the connective tissue, HIV, portrait hypertension, a venoclusive disease.

Endothelin receptor blockers are prescribed due to the activation of the endothelin system in patients with RAS, despite the fact that it is still unknown, the cause or consequence of the disease is to increase the activity of endothelin. Preparations (AMBRISENTAN, BOSENTAN, MACITENTAN) have a vesseloring and mitogenic effect by binding with two receptor isoforms in smooth muscle cells of pulmonary vessels, type A and in endothelin receptors.

Phosphodiesterase-5 inhibitors (FDE-5) (Sildenafil, Tadalafil, Vardenafil) and guanillates (Riociguat) stimulants exhibit vazodilative and antiproliferative effects, have a positive effect on hemodynamics, increases tolerance to physical exertion with long-term treatment of patients with wounds.

The use of prostacyclin's analogues and prostacyclin receptor agonists (Beroprost, EpoproStenolol, Iloprost, Treprcentenil, Selexipag) is based on a modern idea of \u200b\u200bthe mechanisms of development of the Russian Academy of Sciences. Favorable effect Ana prostacyclin Logs are due to inhibition of platelet aggregation, cytoprotective and antiproliferative effect. Preparations of prostacycline analog groups improve exercise portability (BEROPROST); Improve the course of the disease, increase the tolerance to physical exertion, affect hemodynamics with idiopathic wounds and LH associated with systemic sclerosis, and reduce mortality in idiopodic wounds (EPOPROSTENOLOL, TREPROSTENIL).

In the event of ineffectiveness of monotherapy, the RAS simultaneously uses a combination of representatives of two or more classes of specific medicines affecting different pathogenetic illnesses of the disease. Combined therapy, depending on the state of the patient and the LG group, is used at the beginning of treatment or consistently, assigning drugs one by one.

In addition to general recommendations, supporting and specific therapy, treatment of patients with wounds in the ineffectiveness of drugs is carried out by surgical methods (balloon atrial septostomy, veno-arterial extracorporeal membrane oxygenation, lung transplantation or the "Heart-Light" complex).

Treatment of complications arising from the Russian Academy of Sciences are carried out in accordance with the recommendations developed for specific situations.

Summarizing a brief overview of new recommendations on the diagnosis and treatment of pulmonary hypertension, compared with the previous edition (2009), it is possible to note the simplification of the clinical classification, the introduction of new parameters of hemodynamics and pulmonary vascular resistance to the definition of post-cellular LG and RAS, achievements in genetic diagnostics of states proposed otherwise The systematization of risk factors is improved by the diagnostic algorithm, the development of gravity assessment and risk of RAS, new treatment algorithms are presented.

References

1. Gali. e. , N. 2015 ESC / Ers Guidelines for the Diagnosis and Treatment of Pulmonary Hypertension / N. Galie. , M. HUMBERT, J.-L. Vachiery. - Available at: http://dx.doi.org/10.1093/eurheartj/ehv317

International Reviews: Clinical Practice and Health. - 2016. - №2. - S.52-68.

Attention !The article is addressed to medical professionals. Reprinting this article or its fragments on the Internet without hyperlink to the original source is considered as a violation of copyright.

The pulmonary heart (LS) is hypertrophy and / or pursuit of the right ventricle (PJ), 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 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 main disease caused by HLS (chronic obstructive bronchitis, bronchial asthma, etc.), elimination of alveolar hypoxia and hypoxhemia with a decrease in pulmonary hypertension (training of respiratory muscles, electrostimulation of the diaphragm, normalization of the oxygen-cycle blood function (heparin, erythrocytafferesis, Hemisorption), long oxygen therapy (DCT), almitrine), as well as the correction of the right-hand heart failure (ACE inhibitors, diuretics, aldosterone blockers, angiothesine receptor antagonists). DCT is the most effective method of treating CHLN and HLS, 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 (LS) is formed on the basis of pathological changes in the lighter, disorders of the extravalic mechanisms of respiration, ensuring the ventilation of the lung (damage to the respiratory muscles, the violation of the central regulation of the respiration, the elasticity of the bone-cartilage formations of the chest or the nervous impulse 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. The leading clinical symptom is the growing shortness of breath with a rapidly developing (for months) by referee. 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). A frequent cause of PLS \u200b\u200bis 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 CLN classification 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. The presence of flicker arrhythmia, especially 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 >one; 8) Full blockade of the right leg of a beam of His 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 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 COPD 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. Tricespecial regurgitation of varying degrees, which in turn causes dilatation of the right atrium and the lower hollow vein, a decrease in the inspiratory collapse of which indicates an 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). With a high degree of LG, the MZHP becomes the wall of the PJ 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 pressure in the right atrium and PJ, pressure in the pulmonary artery, calculate the heart rate and pulmonary vascular resistance, determine the level of oxygenation of 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 acute viral respiratory diseases (vaccination) and smoking exclusion. 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 moderately pronounced respiration, which is not requiring use of O 2 or mechanical ventilation of the lungs (apnea syndrome in a dream, syndrome of obesity-hypoventilation), or if oxygen therapy is impossible. The number of few drugs that increase the oxygenation of arterial blood include nickelamide, acetosalamide, doxapram and medroxyprogesterone, but all these drugs with long-term use have a large number of 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. In order to select effective CHLS therapy in patients, the COPD is recommended to determine the 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.

- 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, the radiography of the chest organs, the ultrasound of the heart, the study of the FVD, the analysis of the gas composition of the blood is carried out.

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 chest (KIFoscoliosis, Bekhterev's disease, etc.), neuromuscular diseases (poliomyelitis), pathology of pleura, diaphragm (after thoracoplasty, with pneumosclerosis, diaphragm paresis, peebery 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, heavy attacks 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

By the rate of increasing clinical manifestations, there are several options for the flow of a pulmonary heart: acute (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. Characterized with reinforced pathological pulsations (precipitial and epigastric), expansion of the heart boundary to the right, rhythm of gallop in the zone mesia-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 during 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 with the exacerbation of the inflammatory process in the lungs. In the late stage, the edema increases, the increase in the liver (hepatomegaly) is progressing, appear neurological violations (dizziness, headaches, apathy, drowsiness) decreased 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. Early start complex therapy Allows you to significantly improve the labor forecast and increase lifespan.

For the prevention of a pulmonary heart, a warning is required, timely and efficient treatment of 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.