Clinical guidelines: Pulmonary hypertension. Chronic cor pulmonale Drug, route of administration

State Educational Institution of Higher Professional Education "Moscow State Medical and Dental University of Roszdrav"

Medical Faculty

Martynov A.I., Maichuk E.Yu., Panchenkova L.A., Khamidova H.A.,

Yurkova T.E., Pak L.S., Zavyalova A.I.

Chronic cor pulmonale

Educational and methodological manual for conducting practical classes in hospital therapy

Moscow 2012

Reviewers: d.m.s. Professor of the Department of Emergency Conditions at the Clinic of Internal Diseases of the FPPO PMSMU named after N.M. Sechenova Shilov A.M.

MD Professor of the Department of Hospital Therapy No. 2 of the State Educational Institution of Higher Professional Education MGMSU, Makoeva L.D.

Maichuk E.Yu., Martynov A.I., Panchenkova L.A., Khamidova Kh.A., Yurkova T.E., Pak L.S., Zavyalova A.I. Tutorial for medical students. M.: MGMSU, 2012.25 p.

The training manual details modern ideas about the classification, clinical picture, principles of diagnosis and treatment of chronic cor pulmonale. The manual contains a work plan for a practical lesson, questions for preparing for the lesson, an algorithm for substantiating a clinical diagnosis; includes final test classes designed for self-assessment of knowledge by students, as well as situational tasks on the topic.

This textbook has been prepared in accordance with the working curriculum for the discipline "Hospital Therapy", approved in 2008 at the Moscow State University of Medicine and Dentistry on the basis of exemplary curricula of the Ministry of Health and Social Development of the Russian Federation and the State Educational Standard of Higher Professional Education in the specialty "060101-General Medicine ".

The manual is intended for teachers and students of medical universities, as well as clinical residents and interns.

Department of Hospital Therapy №1

(head of the department - d.m.s., professor Maychuk E.Yu.)

Authors: professor, d.m.s. Maychuk E.Yu., Academician, Doctor of Medical Sciences Martynov A.I., Professor, MD Panchenkova L.A., assistant, Ph.D. Khamidova Kh.A., assistant, Ph.D. Yurkova T.E., professor, MD Pak L.S., Associate Professor, Candidate of Medical Sciences, Zavyalova A.I.

MGMSU, 2012

Department of Hospital Therapy №1, 2012

Definition and theoretical foundations of topic 4

Motivational characteristics of topic 14

Diagnostic search steps 15

Clinical tasks 18

Test items 23

Literature 28

DEFINITION AND THEORETICAL QUESTIONS OF THE TOPIC

Chronic cor pulmonale (CHLS)- right ventricular hypertrophy and/or dilatation in combination with pulmonary hypertension occurring against the background of various diseases that disrupt the structure and/or function of the lungs, except in cases where the changes in the lungs are themselves the result of a primary lesion of the left heart or congenital heart defects and major blood vessels.

ETIOLOGY

According to the etiological classification developed by the WHO committee (1961), there are 3 groups of pathological processes leading to the formation of CLS:

diseases leading to a primary violation of the passage of air in the bronchi and alveoli (chronic obstructive pulmonary disease, bronchial asthma, pulmonary emphysema, bronchiectasis, pulmonary tuberculosis, silicosis, pulmonary fibrosis, pulmonary granulomatosis of various etiologies, lung resection, and others);

diseases leading to restriction of the movement of the chest (kyphoscoliosis, obesity, pleural fibrosis, ossification of the costal joints, the consequences of thoracoplasty, myasthenia gravis, etc.);

diseases accompanied by damage to the pulmonary vessels (primary pulmonary hypertension, vasculitis in systemic diseases, recurrent pulmonary embolism).

The main cause is chronic obstructive pulmonary disease (COPD), which accounts for 70-80% of all cases of CPS.

CLASSIFICATION OF CHRONIC PULMONARY HEART:

Compensation level:

compensated;

decompensated.

Origin:

vascular genesis;

bronchopulmonary genesis;

thoracodiaphragmatic genesis.

PATHOGENESIS OF CHRONIC PULMONARY HEART

There are 3 stages in the development of HLS:

precapillary hypertension in the pulmonary circulation;

right ventricular hypertrophy;

right ventricular heart failure.

At the heart of the pathogenesis of CLS is the development of pulmonary hypertension.

Main pathogenetic mechanisms:

Lung disease, damage to the chest, spine, diaphragm. Violations of ventilation and respiratory mechanics. Violation of bronchial conduction (obstruction). Reducing the respiratory surface (restriction).

Generalized hypoxic vasoconstriction due to alveolar hypoventilation (generalized Euler-Liljestrand reflex), i.e. a generalized increase in the tone of small pulmonary vessels occurs and pulmonary arterial hypertension develops.

Hypertensive effect of humoral factors (leukotrienes, PgF 2 α, thromboxane, serotonin, lactic acid).

Reduction of the vascular bed, sclerotic and atherosclerotic changes in the branches of the pulmonary artery and the pulmonary trunk.

An increase in blood viscosity due to erythrocytosis, which develops in response to chronic hypoxemia.

Development of bronchopulmonary anastomoses.

Increased intra-alveolar pressure in obstructive bronchitis.

Compensatory-adaptive reactions predominate in the early stages of HLS formation, however, a prolonged increase in pressure in the pulmonary artery leads to hypertrophy over time, with repeated exacerbations of bronchopulmonary infection, an increase in obstruction - to dilatation and right ventricular failure.

CLINICAL PICTURE

The clinical picture includes symptoms:

the underlying disease that led to the development of CHLS;

respiratory failure;

heart (right ventricular) failure;

Complaints

Shortness of breath, aggravated by physical activity. Unlike patients with left ventricular failure with decompensated cor pulmonale, the position of the body does not affect the degree of shortness of breath - patients can freely lie on their back or side. Orthopnea is not typical for them, since there is no stagnation in the lungs, there is no "obstruction" of the small circle, as with insufficiency of the left heart. Shortness of breath for a long time is mainly due to respiratory failure, it is not affected by the use of cardiac glycosides, it decreases with the use of bronchodilators, oxygen. The severity of shortness of breath (tachypnea) is often not associated with the degree of arterial hypoxemia, therefore it has an organic diagnostic value.

Persistent tachycardia.

Cardialgia, the development of which is associated with metabolic disorders (hypoxia, infectious-toxic effect), insufficient development of collaterals, reflex narrowing of the right coronary artery (pulmonary coronary reflex), a decrease in the filling of the coronary arteries with an increase in end-diastolic pressure in the cavity of the right ventricle.

Arrhythmias are more common during exacerbation of COPD, in the presence of cor pulmonale decompensation in patients suffering from concomitant coronary heart disease, arterial hypertension, and obesity.

Neurological symptoms (cranialgia, dizziness, drowsiness, darkening and double vision, speech disturbance, poor concentration of thoughts, loss of consciousness) are associated with cerebral circulatory disorders.

Objective signs

Diffuse "warm" cyanosis (the distal extremities are warm due to the vasodilating effect of carbon dioxide accumulating in the blood);

Swelling of the cervical veins due to obstructed outflow of blood to the right atrium (the cervical veins swell only on exhalation, especially in patients with obstructive pulmonary lesions; when heart failure is attached, they remain swollen on inspiration).

Thickening of the terminal phalanges ("drumsticks") and nails ("watch glasses").

Edema lower extremities, as a rule, are less pronounced and do not reach the same degree as in primary heart diseases.

Enlargement of the liver, ascites, positive venous pulse, positive symptom of Plesh (hepatojugular symptom - when pressing on the edge of the liver, swelling of the veins of the neck becomes apparent).

Systolic precordial and epigastric pulsation (due to right ventricular hypertrophy).

Percussion is determined by the expansion of the absolute and relative cardiac dullness of the right border of the heart; percussion sound over the handle of the sternum with a tympanic tinge, and over the xiphoid process it becomes bluntly tympanic or completely deaf.

Deafness of heart sounds.

Emphasis of the second tone over the pulmonary artery (with an increase in pressure in it by more than 2 times).

Increased systolic murmur above the xiphoid process or to the left of the sternum with the development of relative valve insufficiency.

DIAGNOSTICS OF CHRONIC PULMONARY HEART

Laboratory data

In a clinical blood test in patients with CLS, erythrocytosis, high hematocrit, and a slowdown in ESR are determined.

In the biochemical analysis of blood with the development of decompensation according to the right ventricular type, increases in residual nitrogen, bilirubin, hypoalbuminemia, hyperglobulinemia are possible.

X-ray signs

Normal or enlarged shadow of the heart in lateral projection

Relative increase in the arc of the pancreas in the left (second) oblique position.

Dilatation of the common trunk of the pulmonary artery in the right (first) oblique position.

Expansion of the main branch of the pulmonary artery more than 15 mm in lateral projection.

An increase in the difference between the width of the shadow of the main segmental and subsegmental branches of the pulmonary artery.

Kerley lines (Kerley) - horizontal narrow darkening over the costophrenic sinus. It is believed that they arise due to the expansion of the lymphatic vessels at the thickening of the interlobular fissures. In the presence of the Kerley line, pulmonary capillary pressure exceeds 20 mm Hg. Art. (normal - 5 - 7 mm Hg).

Electrocardiographic signs

Observe signs of hypertrophy and overload of the right heart.

Direct signs of hypertrophy:

R wave in V1 more than 7 mm;

R/S ratio in V1 is greater than 1;

own deviation V1 - 0.03 - 0.05 s;

form qR in V1;

incomplete blockade of the right leg of the bundle of His, if R is more than 10 mm;

complete blockade of the right leg of the bundle of His, if R is more than 15 mm;

picture of right ventricular overload in V1 - V2.

Indirect signs of hypertrophy:

chest leads:

R wave in V5 less than 5 mm;

S wave in V5 more than 7 mm;

R/S ratio in V5 less than 1;

S wave in V1 less than 2 mm;

Complete blockade of the right leg of the bundle of His, if R is less than 15 mm;

Not complete blockade the right leg of the bundle of His, if R is less than 10 mm;

standard leads:

P-pulmonale in II and III standard ECG leads;

EOS deviation to the right;

type S1, S2, S3.

Echocardiographic features

Hypertrophy of the right ventricle (the thickness of its anterior wall exceeds 0.5 cm).

Dilatation of the right heart (final diastolic size of the right ventricle more than 2.5 cm).

Paradoxical movement of the interventricular septum in diastole towards the left departments.

"D"-shaped form of the right ventricle.

Tricuspid regurgitation.

Systolic pressure in the pulmonary artery, determined by echocardiography, is normally 26 - 30 mm Hg. There are degrees of pulmonary hypertension:

I - 31 - 50 mm Hg;

II - 51 - 75 mm Hg;

III - 75 mm Hg. Art. and higher.

TREATMENT OF CHRONIC PULMONARY HEART

Basic principles of treatment of patients with CHLS:

Prevention and treatment of underlying lung diseases.

Medical management of pulmonary hypertension. However, a sharp drug-induced decrease in pulmonary hypertension can lead to a deterioration in the gas exchange function of the lungs and an increase in the venous blood shunt, since moderate pulmonary hypertension in patients with CPS is a compensatory mechanism for ventilation-perfusion dysfunction.

Treatment of right ventricular failure.

The main goal of the treatment of patients with chronic respiratory disease is to improve the parameters of oxygen transport to reduce the level of hypoxemia and improve the contractile ability of the myocardium of the right heart, which is achieved by reducing the resistance and vasoconstriction of the pulmonary vessels.

Treatment and prevention the underlying disease, for example, anticholinergics, bronchodilators - anticholinergic drugs (atrovent, berodual), selective β2 - antagonists (berotek, salbutomol), methylxanthines, mucolytics. With an exacerbation of the process - antibacterial drugs, if necessary - corticosteroids.

At all stages of the course of HLS pathogenetic method of treatment long-term oxygen therapy is used - inhalation of air enriched with oxygen (30 - 40% oxygen) through a nasal catheter. The oxygen flow rate is 2-3 liters per minute at rest and 5 liters per minute during exercise. Criteria for the appointment of long-term oxygen therapy: PAO2 less than 55 mm Hg. and oxygen saturation (erythrocyte oxygen saturation, SAO2) less than 90%. Long-term oxygenation should be prescribed as early as possible in order to correct blood gas disorders, reduce arterial hypoxemia and prevent hemodynamic disorders in the pulmonary circulation, which allows to stop the progression of pulmonary hypertension and remodeling of pulmonary vessels, increase survival and improve the quality of life of patients.

calcium antagonists cause dilatation of the vessels of the small and large circles of blood circulation, and therefore they are referred to as direct vasodilators. The tactics of prescribing calcium antagonists: treatment begins with small doses of the drug, gradually increasing the daily dose, bringing it to the maximum tolerated; prescribe nifedipine - 20 - 40 mg / day, adalat - 30 mg / day, diltiazem from 30 - 60 mg / day to 120 - 180 mg / day, Isradin - 2.5 5.0 mg / day, verapamil - from 80 to 120 - 240 mg / day, etc. The course of therapy ranges from 3 - 4 weeks to 3 - 12 months. The dose of the drug is selected taking into account the level of pressure in the pulmonary artery and a differentiated approach to side effects that occur when prescribing calcium antagonists. An immediate effect should not be expected when prescribing calcium antagonists.

Nitrates cause dilatation of the arteries of the pulmonary circulation; reduce afterload on the right ventricle due to cardiodilatation, reduce afterload on the right ventricle due to a decrease in hypoxic LA vasoconstriction; reduce pressure in the left atrium, reduce postcapillary pulmonary hypertension by reducing the end-diastolic pressure in the left ventricle. Average therapeutic dose: nitrosorbide - 20 mg 2 times a day.

ACE inhibitors (ACE inhibitors) significantly improve the survival and prognosis of life in patients with congestive heart failure, including in patients with chronic heart failure, since the result of the use of ACE inhibitors is a decrease in arterial and venous tone, a decrease in venous return of blood to the heart, a decrease in diastolic pressure in the pulmonary artery and right atrium, increase in cardiac output. Assign captopril (kapoten) in daily dose 75 - 100 mg, ramipril - 2.5 - 5 mg / day, etc., the dose depends on the initial level of blood pressure. With the development side effects or intolerance to ACE inhibitors, AT II receptor antagonists (losartan, valsartan, etc.) can be prescribed.

Prostaglandins- a group of drugs that can successfully reduce pressure in the pulmonary artery with minimal effect on systemic blood flow. A limitation to their use is the duration of intravenous administration, since prostaglandin E1 has a short half-life. For long-term infusion, a special portable pump is used, connected to a Hickman catheter, which is placed in the jugular or subclavian vein. The dose of the drug varies from 5 ng / kg per minute to 100 ng / kg per minute.

Nitric oxide acts similarly to the endothelial relaxing factor. With the course inhalation use of NO in patients with CLS, a decrease in pressure in the pulmonary artery, an increase in the partial pressure of oxygen in the blood, and a decrease in pulmonary vascular resistance are observed. However, one should not forget about the toxic effect of NO on the human body, which requires adherence to a clear dosing regimen.

Prostacyclin(or its analogue - iloprost) is used as a vasodilator.

Diuretics prescribed for the appearance of edema, combining them with restriction of fluid and salt intake (furosemide, lasix, potassium-sparing diuretics - triamterene, combination drugs). It should be borne in mind that diuretics can cause dryness of the bronchial mucosa, reduce the mucosal index of the lungs and worsen the rheological properties of the blood. At the initial stages of the development of CLS with fluid retention in the body due to hyperaldosteronism, due to the stimulating effect of hypercapnia on the glomerular zone of the adrenal cortex, it is advisable to use isolated aldosterone antagonists (veroshpiron - 50 - 100 in the morning daily or every other day).

The question of the appropriateness of the application cardiac glycosides in the treatment of patients with CHLS remains controversial. It is believed that cardiac glycosides, having a positive inotropic effect, lead to a more complete emptying of the ventricles, increasing cardiac output. However, in this category of patients without concomitant heart disease, cardiac glycosides do not increase hemodynamic parameters. Against the background of taking cardiac glycosides in patients with chronic respiratory disease, symptoms of digitalis intoxication are more often observed.

An important component of the treatment is the correction of hemorheological disorders.

use anticoagulants for the treatment and prevention of thrombosis, thromboembolic complications. In a hospital, heparin is mainly used in a daily dose of 5000 - 20000 IU subcutaneously under the control of laboratory parameters (blood clotting time, activated partial thromboplastin time). Of the oral anticoagulants, preference is given to warfarin, which is prescribed in an individually selected dose under the control of INR.

Antiplatelet agents (acetylsalicylic acid, chimes), hirudotherapy are also used.

Preventive measures should be aimed at observing the regime of work and rest. A complete cessation of smoking (including passive smoking), avoiding hypothermia and prevention of acute respiratory viral infections is necessary.

FORECAST

The duration of pulmonary hypertension (from its onset to death) is approximately 8 to 10 years or more. 30 - 37% of patients with circulatory failure and 12.6% of all patients with cardiovascular diseases die from decompensation of HLS.

MOTIVATIONAL CHARACTERISTIC OF THE THEME

Knowledge of the topic is necessary for the formation of students' skills and abilities in the diagnosis and treatment of chronic cor pulmonale. To study the topic, it is necessary to repeat the sections of the course of normal anatomy and physiology of the respiratory system, the course of pathology of the respiratory system, propaedeutics of internal diseases, and clinical pharmacology.

Purpose of the lesson: to study the etiology, pathogenesis, clinical manifestations, diagnostic methods, approaches to the treatment of chronic cor pulmonale.

The student must know:

Questions to prepare for the lesson:

A) Definition of the concept of "Chronic cor pulmonale".

B) Etiological factors of chronic cor pulmonale.

C) The main pathophysiological mechanisms of the development of chronic cor pulmonale.

D) Classification of chronic cor pulmonale.

E) Laboratory and instrumental diagnostics of chronic pulmonary heart.

E) Modern approaches for the treatment of chronic cor pulmonale

- pathology of the right heart, characterized by an increase (hypertrophy) and expansion (dilatation) of the right atrium and ventricle, as well as circulatory failure, which develops as a result of hypertension of the pulmonary circulation. The formation of the cor pulmonale is promoted by pathological processes of the bronchopulmonary system, the vessels of the lungs, and the chest. The clinical manifestations of acute cor pulmonale include shortness of breath, retrosternal pain, increased skin cyanosis and tachycardia, psychomotor agitation, hepatomegaly. The examination reveals an increase in the borders of the heart to the right, gallop rhythm, pathological pulsation, signs of overload of the right heart on the ECG. Additionally, chest X-ray, ultrasound of the heart, respiratory function examination, blood gas analysis are performed.

ICD-10

I27.9 Pulmonary heart failure, unspecified

General information

- pathology of the right heart, characterized by an increase (hypertrophy) and expansion (dilatation) of the right atrium and ventricle, as well as circulatory failure, which develops as a result of hypertension of the pulmonary circulation. The formation of the cor pulmonale is promoted by pathological processes of the bronchopulmonary system, the vessels of the lungs, and the chest.

The acute form of cor pulmonale develops quickly, in a few minutes, hours or days; chronic - for several months or years. Almost 3% of patients with chronic bronchopulmonary diseases gradually develop cor pulmonale. Cor pulmonale significantly aggravates the course of cardiopathologies, occupying the 4th place among the causes of mortality in cardiovascular diseases.

Reasons for the development of cor pulmonale

The bronchopulmonary form of the pulmonary heart develops with primary lesions of the bronchi and lungs as a result of chronic obstructive bronchitis, bronchial asthma, bronchiolitis, pulmonary emphysema, diffuse pneumosclerosis of various origins, polycystic lung disease, bronchiectasis, tuberculosis, sarcoidosis, pneumoconiosis, Hamman-Rich syndrome, etc. This form can cause about 70 bronchopulmonary diseases, contributing to the formation of cor pulmonale in 80% of cases.

The emergence of the thoracophrenic form of the pulmonary heart is promoted by primary lesions of the chest, diaphragm, limitation of their mobility, significantly disrupting ventilation and hemodynamics in the lungs. These include diseases that deform the chest (kyphoscoliosis, Bechterew's disease, etc.), neuromuscular diseases (poliomyelitis), pathologies of the pleura, diaphragm (after thoracoplasty, with pneumosclerosis, paresis of the diaphragm, Pickwick's syndrome with obesity, etc.). ).

The vascular form of the pulmonary heart develops with primary lesions of the pulmonary vessels: primary pulmonary hypertension, pulmonary vasculitis, thromboembolism of the branches of the pulmonary artery (PE), compression of the pulmonary trunk by an aortic aneurysm, atherosclerosis of the pulmonary artery, tumors of the mediastinum.

The main causes of acute cor pulmonale are massive pulmonary embolism, severe attacks of bronchial asthma, valvular pneumothorax, acute pneumonia. Subacute cor pulmonale develops with repeated pulmonary embolism, cancerous lymphangitis of the lungs, in cases of chronic hypoventilation associated with poliomyelitis, botulism, myasthenia gravis.

The mechanism of development of the cor pulmonale

Arterial pulmonary hypertension plays a leading role in the development of cor pulmonale. On the initial stage it is also associated with a reflex increase in cardiac output in response to increased respiratory function and resulting in respiratory failure tissue hypoxia. With a vascular form of the pulmonary heart, resistance to blood flow in the arteries of the pulmonary circulation increases mainly due to the organic narrowing of the lumen of the pulmonary vessels when they are blocked by emboli (in the case of thromboembolism), with inflammatory or tumor infiltration of the walls, closure of their lumen (in the case of systemic vasculitis). With bronchopulmonary and thoracophrenic forms of the pulmonary heart, the narrowing of the lumen of the pulmonary vessels occurs due to their microthrombosis, fusion connective tissue or compression in areas of inflammation, tumor or sclerosis, as well as weakening the ability of the lungs to stretch and collapse of blood vessels in the altered segments of the lungs. But in most cases, the leading role is played by the functional mechanisms of the development of pulmonary arterial hypertension, which are associated with impaired respiratory function, lung ventilation and hypoxia.

Arterial hypertension of the pulmonary circulation leads to an overload of the right heart. As the disease develops, a shift in acid-base balance occurs, which may initially be compensated, but later decompensation of disorders may occur. With cor pulmonale, there is an increase in the size of the right ventricle and hypertrophy of the muscular membrane of large vessels of the pulmonary circulation, narrowing of their lumen with further sclerosis. Small vessels are often affected by multiple blood clots. Gradually, dystrophy and necrotic processes develop in the heart muscle.

Cor pulmonale classification

By rate of rise clinical manifestations there are several variants of the course of cor pulmonale: acute (develops in a few hours or days), subacute (develops over weeks and months) and chronic (occurs gradually, over a number of months or years against the background of prolonged respiratory failure).

The process of formation of chronic pulmonary heart goes through the following stages:

• preclinical - manifested by transient pulmonary hypertension and signs of hard work of the right ventricle; are detected only during instrumental research;
• compensated - characterized by right ventricular hypertrophy and stable pulmonary hypertension without signs of circulatory failure;
• decompensated (cardiopulmonary failure) - symptoms of right ventricular failure appear.

There are three etiological forms of cor pulmonale: bronchopulmonary, thoracophrenic and vascular.

On the basis of compensation, chronic cor pulmonale can be compensated or decompensated.

Cor pulmonale symptoms

The clinical picture of cor pulmonale is characterized by the development of heart failure on the background of pulmonary hypertension. The development of acute pulmonary heart is characterized by the appearance of sudden chest pain, severe shortness of breath; a decrease in blood pressure, up to the development of collapse, cyanosis of the skin, swelling of the cervical veins, increasing tachycardia; progressive enlargement of the liver with pain in the right hypochondrium, psychomotor agitation. Characterized by enhanced pathological pulsations (precordial and epigastric), expansion of the border of the heart to the right, gallop rhythm in the zone of the xiphoid process, ECG signs overload of the right atrium.

With massive PE, a state of shock develops in a few minutes, pulmonary edema. Acute coronary insufficiency is often associated, accompanied by rhythm disturbance, pain syndrome. In 30-35% of cases, there is sudden death. Subacute cor pulmonale presents with sudden moderate painful sensations, shortness of breath and tachycardia, short syncope, hemoptysis, signs of pleuropneumonia.

In the compensation phase of chronic cor pulmonale, symptoms of the underlying disease are observed with gradual manifestations of hyperfunction, and then hypertrophy of the right heart, which are usually mild. Some patients have a pulsation in the upper abdomen caused by an enlarged right ventricle.

In the stage of decompensation, right ventricular failure develops. The main manifestation is shortness of breath, aggravated by physical exertion, inhalation of cold air, in the supine position. There are pains in the region of the heart, cyanosis (warm and cold cyanosis), palpitations, swelling of the jugular veins that persist on inspiration, liver enlargement, peripheral edema, resistant to treatment.

Examination of the heart reveals muffled heart sounds. Blood pressure is normal or low arterial hypertension characteristic of congestive heart failure. The symptoms of cor pulmonale become more pronounced with an exacerbation of the inflammatory process in the lungs. In the late stage, edema increases, liver enlargement (hepatomegaly) progresses, neurological disorders appear (dizziness, headaches, apathy, drowsiness), diuresis decreases.

Cor pulmonale diagnosis

Diagnostic criteria for cor pulmonale consider the presence of diseases - causative factors of cor pulmonale, pulmonary hypertension, enlargement and expansion of the right ventricle, right ventricular heart failure. Such patients need to consult a pulmonologist and a cardiologist. When examining a patient, attention is paid to signs of respiratory failure, cyanosis of the skin, pain in the region of the heart, etc. Direct and indirect signs of right ventricular hypertrophy are determined on the ECG.

Prognosis and prevention of cor pulmonale

In cases of development of cor pulmonale decompensation, the prognosis for working capacity, quality and life expectancy is unsatisfactory. Usually, the ability to work in patients with cor pulmonale suffers already in the early stages of the disease, which dictates the need for rational employment and addressing the issue of assigning a disability group. The early start of complex therapy can significantly improve the labor prognosis and increase life expectancy.

Prevention of cor pulmonale requires warning, timely and effective treatment diseases leading to it. First of all, this concerns chronic bronchopulmonary processes, the need to prevent their exacerbations and the development of respiratory failure. To prevent the processes of cor pulmonale decompensation, it is recommended to adhere to moderate physical activity.

Cor pulmonale (PC) is hypertrophy and/or dilatation of the right ventricle (RV) resulting from pulmonary arterial hypertension caused by diseases that affect the function and / or structure of the lungs, and are not associated with a primary pathology of the left heart or congenital heart defects. LS is formed due to diseases of the bronchi and lungs, thoracophrenic lesions or pathology of the pulmonary vessels. The development of chronic cor pulmonale (CHP) is most often due to chronic pulmonary insufficiency (CLF), and the main cause of the formation of CLP is alveolar hypoxia, which causes spasm of the pulmonary arterioles.

Diagnostic search is aimed at identifying the underlying disease that led to the development of CHL, as well as assessing CRF, pulmonary hypertension, and the condition of the pancreas.

The treatment of CHLS is the treatment of the underlying disease that causes CHLS (chronic obstructive bronchitis, bronchial asthma, etc.), elimination of alveolar hypoxia and hypoxemia with a decrease in pulmonary arterial hypertension (training of the respiratory muscles, electrical stimulation of the diaphragm, normalization of the oxygen transport function of the blood (heparin, erythrocytapheresis, hemosorption), long-term oxygen therapy (VCT), almitrin), as well as correction right ventricular heart failure (ACE inhibitors, diuretics, aldosterone blockers, angiothesin II receptor antagonists). VCT is the most effective method treatment of CLN and HLS, which can increase the life expectancy of patients.

Keywords: cor pulmonale, pulmonary hypertension, chronic pulmonary insufficiency, chronic cor pulmonale, right ventricular heart failure.

DEFINITION

Pulmonary heart- this is hypertrophy and / or dilatation of the right ventricle, resulting from pulmonary arterial hypertension caused by diseases that affect the function and / or structure of the lungs and are not associated with a primary pathology of the left heart or congenital heart defects.

Pulmonary heart (PC) is formed on the basis of pathological changes of the lung itself, violations of extrapulmonary respiratory mechanisms that provide ventilation of the lung (damage to the respiratory muscles, violation of the central regulation of respiration, elasticity of the bone and cartilage formations of the chest or conduction of a nerve impulse along n. diaphragmicus, obesity), as well as damage to the pulmonary vessels.

CLASSIFICATION

In our country, the classification of cor pulmonale proposed by B.E. Votchalom in 1964 (Table 7.1).

Acute LS is associated with a sharp increase in pulmonary arterial pressure (PAP) with the development of right ventricular failure and is most often caused by thromboembolism of the main trunk or large branches of the pulmonary artery (PE). However, the doctor sometimes encounters a similar condition when large areas of lung tissue are turned off from the circulation (bilateral extensive pneumonia, status asthmaticus, valve pneumothorax).

Subacute cor pulmonale (PLC) is most often the result of recurrent thromboembolism of small branches of the pulmonary artery. Leading clinical symptom is the increasing shortness of breath with rapidly developing (within months) right ventricular failure. Other causes of PLS ​​include neuromuscular diseases (myasthenia gravis, poliomyelitis, damage to the phrenic nerve), exclusion of a significant part of the respiratory section of the lung from the act of breathing (severe bronchial asthma, miliary pulmonary tuberculosis). A common cause of PLS ​​are oncological diseases of the lungs, gastrointestinal tract, breast and other localization, due to lung carcinomatosis, as well as compression of the lung vessels by a germinating tumor, followed by thrombosis.

Chronic cor pulmonale (CHP) in 80% of cases occurs with damage to the bronchopulmonary apparatus (most often with COPD) and is associated with a slow and gradual increase in pressure in the pulmonary artery over many years.

The development of CLS is directly related to chronic pulmonary insufficiency (CLF). In clinical practice, the classification of CRF based on the presence of dyspnea is used. There are 3 degrees of CLN: the appearance of shortness of breath with previously available efforts - I degree, shortness of breath during normal exertion - II degree, shortness of breath at rest - III degree. It is sometimes appropriate to supplement the above classification with data on the gas composition of the blood and pathophysiological mechanisms for the development of pulmonary insufficiency (Table 7.2), which makes it possible to select pathogenetically substantiated therapeutic measures.

Classification of cor pulmonale (according to Votchal B.E., 1964)

Table 7.1.

The end of the table. 7.1.

Note. The diagnosis of cor pulmonale is made after the diagnosis of the underlying disease: when formulating the diagnosis, only the first two columns of the classification are used. Columns 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 insufficiency

(Aleksandrov O.V., 1986)

In the presented classification of CLN, the diagnosis of CLN with a high probability can be made at stages II and III of the process. In stage I CLN (latent), rises in PAP are detected, usually in response to physical activity and during an exacerbation of the disease in the absence of signs of RV hypertrophy. This circumstance made it possible to express the opinion (N.R. Paleev) that for the diagnosis of the initial manifestations of CLS, it is necessary to use not the presence or absence of RV myocardial hypertrophy, but an increase in LBP. However, in clinical practice, direct measurement of PAP in this group of patients is not sufficiently substantiated.

Over time, the development of decompensated HLS is possible. In the absence of a special classification of RV failure, the well-known classification of heart failure (HF) according to V.Kh. Vasilenko and N.D. Strazhesko, which is usually used for heart failure, which has developed as a result of damage to the left ventricle (LV) or both ventricles. The presence of left ventricular HF in patients with CLS is most often due to two reasons: 1) CHL in people over 50 years of age is often combined with coronary artery disease, 2) systemic arterial hypoxemia in patients with CLS leads to dystrophic processes in the LV myocardium, to its moderate hypertrophy and contractile insufficiency.

Chronic obstructive pulmonary disease is the main cause of chronic cor pulmonale.

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 PH in patients with bronchopulmonary and thoracophrenic forms of CLS is alveolar hypoxia, the role of which in the development of pulmonary vasoconstriction was first shown in 1946 by U. Von Euler and G. Lijestrand. The development of the Euler-Liljestrand reflex is explained by several mechanisms: the effect of hypoxia is associated with the development of depolarization of vascular smooth muscle cells and their contraction due to changes in the function of potassium channels of cell membranes.

wounds, exposure to the vascular wall of endogenous vasoconstrictor mediators, such as leukotrienes, histamine, serotonin, angiotensin II and catecholamines, the production of which increases significantly under hypoxic conditions.

Hypercapnia also contributes to the development of pulmonary hypertension. However, a high concentration of CO 2, apparently, does not act directly on the tone of the pulmonary vessels, but indirectly - mainly through the acidosis caused by it. In addition, CO 2 retention contributes to a decrease in the sensitivity of the respiratory center to CO 2, which further reduces lung ventilation and contributes to pulmonary vasoconstriction.

Of particular importance in the genesis of PH is endothelial dysfunction, manifested by a decrease in the synthesis of vasodilating antiproliferative mediators (NO, prostacyclin, prostaglandin E 2) and an increase in the level of vasoconstrictors (angiotensin, endothelin-1). Pulmonary endothelial dysfunction in COPD patients is associated with hypoxemia, inflammation, and exposure to cigarette smoke.

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

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

In patients with severe obesity, Pickwick's syndrome (named after the work of Charles Dickens) develops, 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 impaired ventilation due to mechanical limitation by adipose tissue with dysfunction (fatigue) respiratory muscles.

Elevated blood pressure in the pulmonary artery may initially contribute to an increase in the volume of perfusion of the pulmonary capillaries, however, over time, hypertrophy of the myocardium of the pancreas develops, followed by its contractile insufficiency. Indicators of pressure in the pulmonary circulation are presented in table. 7.3.

Table 7.3

Indicators of pulmonary hemodynamics

The criterion for pulmonary hypertension is the level of mean pressure in the pulmonary artery at rest, exceeding 20 mm Hg.

CLINIC

The clinical picture consists of the manifestations of the underlying disease, leading to the development of CHLS and damage to the pancreas. In clinical practice, chronic obstructive pulmonary disease (COPD) is most often found among the causative pulmonary diseases, i.e. bronchial asthma or chronic obstructive bronchitis and emphysema. The CLS clinic is inextricably linked with the manifestation of CHLN itself.

A characteristic complaint of patients is shortness of breath. Initially, during exercise (stage I of CRF), and then at rest (stage III of CRF). It has an expiratory or mixed character. A long course (years) of COPD dulls the patient's attention and forces him to consult a doctor when shortness of breath appears during mild physical exertion or at rest, that is, already in stage II-III CRF, when the presence of CHL is indisputable.

Unlike dyspnea associated with left ventricular failure and venous stasis of blood in the lungs, dyspnea in pulmonary hypertension does not increase in the horizontal position of the patient and does not

decreases in the sitting position. Patients may even prefer a horizontal position of the body, in which the diaphragm takes a greater part in intrathoracic hemodynamics than facilitates the breathing process.

Tachycardia is a frequent complaint of patients with CHL and appears even at the stage of development of CRF in response to arterial hypoxemia. Disorder heart rate occurs infrequently. The presence of atrial fibrillation, especially in people over 50 years of age, is usually associated with concomitant coronary artery disease.

Half of the patients with CLS experience pain in the region of the heart, often of an indeterminate nature, without irradiation, as a rule, not associated with physical activity and not relieved by nitroglycerin. The most common view on the mechanism of pain is relative coronary insufficiency due to a significant increase in the muscle mass of the pancreas, as well as a decrease in the filling of the coronary arteries with an increase in end-diastolic pressure in the pancreatic cavity, myocardial hypoxia against the background of general arterial hypoxemia (“blue angina pectoris”) and reflex narrowing right coronary artery (pulmocoronary reflex). A possible cause of cardialgia may be stretching of the pulmonary artery with a sharp increase in pressure in it.

With decompensation of the pulmonary heart, edema may appear on the legs, which first occur most often during an exacerbation of a bronchopulmonary disease and are first localized in the area of ​​the feet and ankles. As right ventricular failure progresses, edema spreads to the area of ​​the legs and thighs, and rarely, in severe cases of right ventricular failure, there is an increase in the abdomen in volume due to emerging ascites.

A less specific symptom of cor pulmonale is loss of voice, which is associated with compression of the recurrent nerve by a dilated trunk of the pulmonary artery.

Patients with CRF and CLS may develop encephalopathy due to chronic hypercapnia and hypoxia of the brain, as well as impaired vascular permeability. With severe encephalopathy, some patients experience increased excitability, aggressiveness, euphoria, and even psychosis, while other patients experience lethargy, depression, drowsiness during the day and insomnia at night, and headaches. Rarely, syncope occurs during physical exertion as a result of severe hypoxia.

A common symptom of CLN is a diffuse "grayish-blue", warm cyanosis. When right ventricular failure occurs in patients with CLS, cyanosis often acquires a mixed character: against the background of diffuse bluish staining of the skin, cyanosis of the lips, tip of the nose, chin, ears, fingertips and toes appears, and the limbs in most cases remain warm, possibly due to peripheral vasodilation due to hypercapnia. Swelling of the cervical veins is characteristic (including on inspiration - Kussmaul's symptom). Some patients may develop a painful blush on the cheeks and an increase in the number of vessels on the skin and conjunctiva (“rabbit or frog eyes” due to hypercapnia), Plesh’s symptom (swelling of the neck veins when pressing the palm of the hand on the enlarged liver), Corvisar’s face, cardiac cachexia, signs of the main diseases (emphysematous chest, kyphoscoliosis of the thoracic spine, etc.).

On palpation of the region of the heart, a pronounced diffuse cardiac impulse, epigastric pulsation (due to hypertrophy and dilatation of the pancreas) can be detected, and with percussion, an expansion of the right border of the heart to the right. However, these symptoms lose their diagnostic value due to the often developing pulmonary emphysema, in which the percussion dimensions of the heart can even be reduced (“drip heart”). The most common auscultatory symptom in CHLS is the emphasis of the second tone over the pulmonary artery, which can be combined with splitting of the second tone, right ventricular IV heart sound, diastolic murmur of pulmonary valve insufficiency (Graham-Still murmur) and systolic murmur of tricuspid insufficiency, with the intensity of both murmurs increasing by inspiratory height (Rivero-Corvalho symptom).

Arterial pressure in patients with compensated CHLS is often increased, and in decompensated patients it is reduced.

Hepatomegaly is detected in almost all patients with decompensated LS. The liver is enlarged, compacted on palpation, painful, the edge of the liver is rounded. With severe heart failure, ascites appears. In general, such severe manifestations of right ventricular heart failure in CHL are rare, because the very presence of severe CRF or the addition of an infectious process in the lung leads to a tragic ending for the patient earlier than it occurs due to heart failure.

The clinic of chronic cor pulmonale is determined by the severity of pulmonary pathology, as well as pulmonary and right ventricular heart failure.

INSTRUMENTAL DIAGNOSIS

The X-ray picture of CLS depends on the stage of CRF. Against the background of radiological manifestations of a pulmonary disease (pneumosclerosis, emphysema, increased vascular pattern, etc.), at first there is only a slight decrease in the shadow of the heart, then a moderate bulging of the cone of the pulmonary artery appears in the direct and right oblique projection. Normally, in direct projection, the right heart contour is formed by the right atrium, and in CHLS with an increase in the RV, it becomes edge-forming, and with significant hypertrophy of the RV, it can form both the right and left edges of the heart, pushing the left ventricle back. In the final decompensated stage of HLS, the right edge of the heart can be formed by a significantly dilated right atrium. Nevertheless, this "evolution" takes place against the background of a relatively small shadow of the heart ("drip" or "hanging").

Electrocardiographic diagnosis of CLS is reduced to the detection of pancreatic hypertrophy. The main (“direct”) ECG criteria for RV hypertrophy include: 1) R in V1>7mm; 2) S in V5-6 > 7 mm; 3) RV1 + SV5 or RV1 + SV6 > 10.5 mm; 4) RaVR > 4 mm; 5) SV1,V2 =s2 mm; 6) RV5,V6<5 мм; 7) отношение R/SV1 >one; 8) complete blockade of the right leg of the bundle of His with RV1>15 mm; 9) incomplete blockade of the right leg of the bundle of His with RV1>10 mm; 10) negative TVl and decrease in STVl, V2 with RVl>5 mm and no coronary insufficiency. In the presence of 2 or more "direct" ECG signs, the diagnosis of RV hypertrophy is considered reliable.

Indirect ECG signs of RV hypertrophy suggest RV hypertrophy: 1) rotation of the heart around the longitudinal axis clockwise (shift of the transition zone to the left, to leads V5-V6 and the appearance in leads V5, V6 of the QRS type RS complex; SV5-6 is deep, and RV1-2 - normal amplitude); 2) SV5-6 > RV5-6; 3) RaVR > Q(S)aVR; 4) deviation electrical axis hearts to the right, especially if α>110; 5) electric axis heart type

SI-SII-SIII; 6) complete or incomplete blockade right leg of the bundle of His; 7) electrocardiographic signs of right atrial hypertrophy (P-pulmonale in leads II, III, aVF); 8) an increase in the activation time of the right ventricle in V1 by more than 0.03 s. There are three types of ECG changes in CHLS:

1. rSR "-type ECG is characterized by the presence of a split QRS complex of the rSR type in lead V1 and is usually detected with severe RV hypertrophy;

2. The R-type ECG is characterized by the presence of a QRS complex of the Rs or qR type in lead V1 and is usually detected with severe RV hypertrophy (Fig. 7.1).

3. S-type ECG is often detected in COPD patients with emphysema. It is associated with a posterior displacement of the hypertrophied heart, which is caused by pulmonary emphysema. The ECG looks like rS, RS or Rs with a pronounced S wave in both the right and left chest leads

Rice. 7.1. ECG of a patient with COPD and CHLS. Sinus tachycardia. Pronounced hypertrophy of the right ventricle (RV1 = 10 mm, SV1 is absent, SV5-6 = 12 mm, a sharp EOS deviation to the right (α = +155°), negative TV1-2 and a decrease in the STV1-2 segment). Right atrial hypertrophy (P-pulmonale in V2-4)

Electrocardiographic criteria for RV hypertrophy are not sufficiently specific. They are less clear-cut than in LV hypertrophy and can lead to false positive and false negative diagnoses. Normal ECG does not exclude the presence of CHLS, especially in patients with COPD, therefore ECG changes should be compared with the clinical picture of the disease and echocardiography data.

Echocardiography (EchoCG) is the leading non-invasive method for assessing pulmonary hemodynamics and diagnosing LS. Ultrasound diagnostics LS is based on the identification of signs of damage to the myocardium of the pancreas, which are given below.

1. Change in the size of the right ventricle, which is assessed in two positions: in the parasternal position along the long axis (normally less than 30 mm) and in the apical four-chamber position. To detect dilatation of the pancreas, measurement of its diameter (normally less than 36 mm) and area at the end of diastole along the long axis in the apical four-chamber position is more often used. In order to more accurately assess the severity of RV dilatation, it is recommended to use the ratio of the RV end-diastolic area to the LV end-diastolic area, thereby excluding individual differences in heart size. An increase in this indicator of more than 0.6 indicates a significant dilatation of the pancreas, and if it becomes equal to or greater than 1.0, then a conclusion is made about a pronounced dilatation of the pancreas. With dilatation of the RV in the apical four-chamber position, the shape of the RV changes from crescent-shaped to oval, and the apex of the heart may be occupied not by the LV, as is normal, but by the RV. Dilatation of the pancreas may be accompanied by dilatation of the trunk (more than 30 mm) and branches of the pulmonary artery. With massive thrombosis of the pulmonary artery, its significant dilatation (up to 50-80 mm) can be determined, and the lumen of the artery becomes oval.

2. With hypertrophy of the pancreas, the thickness of its anterior wall, measured in diastole in the subcostal four-chamber position in the B- or M-mode, exceeds 5 mm. In patients with CHLS, as a rule, not only the anterior wall of the pancreas is hypertrophied, but also the interventricular septum.

3. Tricuspid regurgitation of varying degrees, which in turn causes dilatation of the right atrium and inferior vena cava, the decrease in inspiratory collapse of which indicates increased pressure in the right atrium.

4. Evaluation of the diastolic function of the pancreas is performed on the basis of the transtricuspid diastolic flow in the mode of pulsed

wave Doppler and color M-modal Doppler. In patients with CHLS, a decrease in the diastolic function of the pancreas is found, which is manifested by a decrease in the ratio of peaks E and A.

5. Reduced contractility of the pancreas in patients with LS is manifested by hypokinesia of the pancreas with a decrease in its ejection fraction. An echocardiographic study determines such indicators of RV function as end-diastolic and end-systolic volumes, ejection fraction, which normally is at least 50%.

These changes have different severity depending on the severity of the development of drugs. So, in acute LS, dilatation of the pancreas will be detected, and in chronic LS, signs of hypertrophy, diastolic and systolic dysfunction of the pancreas will be added to it.

Another group of signs is associated with the development of pulmonary hypertension in LS. The degree of their severity is most significant in acute and subacute LS, as well as in patients with primary pulmonary hypertension. CHLS is characterized by a moderate increase in systolic pressure in the pulmonary artery, which rarely reaches 50 mm Hg. Assessment of the pulmonary trunk and flow in the outflow tract of the pancreas is performed from the left parasternal and subcostal short-axis approach. In patients with pulmonary pathology, due to the limitation of the ultrasound window, the subcostal position may be the only possible access to visualize the outflow tract of the pancreas. Using pulsed wave Doppler, you can measure the average pressure in the pulmonary artery (Ppa), for which the formula proposed by A. Kitabatake et al. is usually used. (1983): Log10(Pra) = - 2.8 (AT/ET) + 2.4, where AT is the acceleration time of the flow in the outflow tract of the pancreas, ET is the ejection time (or the time of expulsion of blood from the pancreas). The Ppa value obtained using this method in COPD patients correlates well with the data of an invasive examination, and the possibility of obtaining a reliable signal from the pulmonary valve exceeds 90%.

The most important for the detection of pulmonary hypertension is the severity of tricuspid regurgitation. The use of a jet of tricuspid regurgitation is the basis of the most accurate non-invasive method for determining systolic pressure in the pulmonary artery. Measurements are carried out in the continuous-wave Doppler mode in the apical four-chamber or subcostal position, preferably with the simultaneous use of color Doppler

whom mapping. To calculate the pressure in the pulmonary artery, it is necessary to add the pressure in the right atrium to the pressure gradient across the tricuspid valve. Measurement of the transtricuspid gradient can be performed in more than 75% of patients with COPD. There are qualitative signs of pulmonary hypertension:

1. With PH, the nature of the movement of the posterior cusp of the pulmonary valve changes, which is determined in the M-mode: a characteristic indicator of PH is the presence of an average systolic tooth due to partial overlap of the valve, which forms a W-shaped movement of the valve in systole.

2. In patients with pulmonary hypertension, due to increased pressure in the right ventricle, the interventricular septum (IVS) flattens, and the left ventricle resembles the letter D (D-shaped left ventricle) along the short axis. At high degree LH IVS becomes like a wall of the pancreas and moves into 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 volume, is compressed by the dilated right ventricle and takes on the shape of a crescent.

3. Possible regurgitation on the pulmonary valve (regurgitation of the first degree is normal in young people). With a constant-wave Doppler study, it is possible to measure the rate of pulmonary regurgitation with a further calculation of the magnitude of the end-diastolic pressure gradient of the LA-RV.

4. Change in the shape of the blood flow in the outflow tract of the pancreas and at the mouth of the LA valve. At normal pressure in the LA, the flow has an isosceles shape, the peak of the flow is located in the middle of systole; in pulmonary hypertension, the peak flow shifts to the first half of systole.

However, in patients with COPD, their pulmonary emphysema often makes it difficult to clearly visualize the structures of the heart and narrows the echocardiogram window, making the study informative in no more than 60-80% of patients. In recent years, a more accurate and informative method of ultrasound examination of the heart has appeared - transesophageal echocardiography (TEE). TEE in COPD patients is the preferred method for accurate measurements and direct visual assessment of the structures of the pancreas, due to the higher resolution of the transesophageal probe and the stability of the ultrasound window, and is of particular importance in emphysema and pneumosclerosis.

Catheterization of the right heart and pulmonary arteries

Right heart and pulmonary artery catheterization is the gold standard for diagnosing PH. This procedure allows you to directly measure the pressure in the right atrium and RV, pressure in the pulmonary artery, calculate cardiac output and pulmonary vascular resistance, determine the level of oxygenation of mixed venous blood. Catheterization of the right heart due to its invasiveness cannot be recommended for widespread use in the diagnosis of CHL. Indications are: severe pulmonary hypertension, frequent episodes of decompensated right ventricular failure, and selection of candidates for lung transplantation.

Radionuclide ventriculography (RVG)

RVG measures the right ventricular ejection fraction (REF). EFVC is considered abnormal below 40-45%, but the EFVC itself is not a good indicator of right ventricular function. It allows you to evaluate the systolic function of the right ventricle, which is highly dependent on afterload, decreasing with an increase in the latter. Therefore, a decrease in EFVC is recorded in many patients with COPD, and is not an indicator of true right ventricular dysfunction.

Magnetic resonance imaging (MRI)

MRI is a promising method for assessing pulmonary hypertension and changes in the structure and function of the right ventricle. An MRI-measured right pulmonary artery diameter greater than 28 mm is a highly specific sign of PH. However, the MRI method is quite expensive and is available only in specialized centers.

The presence of a chronic lung disease (as a cause of CLS) requires a special study of the function of external respiration. The doctor is faced with the task of clarifying the type of ventilation insufficiency: obstructive (impaired passage of air through the bronchi) or restrictive (decrease in the area of ​​gas exchange). In the first case, chronic obstructive bronchitis, bronchial asthma can be cited as an example, and in the second - pneumosclerosis, lung resection, etc.

TREATMENT

CLS occurs most often after the onset of CLN. Therapeutic measures are complex in nature and are aimed mainly at correcting these two syndromes, which can be represented as follows:

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

2) treatment of CLN and PH;

3) treatment of right ventricular heart failure. Basic therapeutic and preventive measures include

prevention of acute viral respiratory diseases (vaccination) and exclusion of smoking. With the development of chronic pulmonary pathology of an inflammatory nature, it is necessary to treat exacerbations with antibiotics, mucoregulatory drugs and immunocorrectors.

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

The most common cause of CLN is broncho-obstructive syndrome, the cause of which is the reduction smooth muscle bronchi, accumulation of viscous inflammatory secretion, swelling of the bronchial mucosa. These changes require the use of beta-2-agonists (fenoterol, formoterol, salbutamol), M-anticholinergics (ipratropium bromide, tiotropium bromide), and in some cases inhaled glucocorticosteroid drugs in the form of inhalations using a nebulizer or an individual inhaler. It is possible to use methylxanthines (eufillin and prolonged theophyllines (teolong, teotard, etc.)). Therapy with expectorants is very individual and requires various combinations and selection of herbal remedies (coltsfoot, wild rosemary, thyme, etc.), and chemical production (acetylcysteine, ambroxol, etc.).

If necessary, exercise therapy and postural drainage of the lungs are prescribed. Breathing with positive expiratory pressure (no more than 20 cm of water column) is shown using both simple devices

in the form of "whistles" with a movable diaphragm, and complex devices that control the pressure on exhalation and inhalation. This method reduces the air flow inside the bronchus (which has a bronchodilator effect) and increases the pressure inside the bronchi in relation to the surrounding lung tissue.

The extrapulmonary mechanisms of CRF development include a decrease in the contractile function of the respiratory muscles and diaphragm. The possibilities for correcting these disorders are still limited: exercise therapy or electrical stimulation of the diaphragm in stage II. HLN.

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

Due to the increase in the aggregation properties of erythrocytes, blood viscosity increases, which requires the appointment of antiplatelet agents (chimes, reopoliglyukin) and heparin (preferably the use of low molecular weight heparins - fraxiparin, etc.).

In patients with hypoventilation associated with reduced activity of the respiratory center, drugs that increase central inspiratory activity - respiratory stimulants - can be used as auxiliary methods of therapy. They should be used for moderate respiratory depression that does not require the use of O 2 or mechanical ventilation (sleep apnea syndrome, obesity-hypoventilation syndrome), or when oxygen therapy is not possible. The few drugs that increase arterial blood oxygenation include nikethamide, acetosalamide, doxapram, and medroxyprogesterone, but all of these drugs have a large number of side effects with long-term use and therefore can only be used for a short time, such as during an exacerbation of the disease.

Almitrina bismesylate is currently among the drugs capable of correcting hypoxemia in patients with COPD for a long time. Almitrin is a specific ago-

nistome of peripheral chemoreceptors of the carotid node, the stimulation of which leads to an increase in hypoxic vasoconstriction in poorly ventilated regions of the lungs with an improvement in ventilation-perfusion ratios. The ability of almitrin at a dose of 100 mg / day has been proven. in patients with COPD lead to significant increase pa0 2 (by 5-12 mm Hg) and a decrease in paCO 2 (by 3-7 mm Hg) with an improvement in clinical symptoms and a decrease in the frequency of exacerbations of the disease, which can delay the appointment of long-term 0 2 therapy for several years . Unfortunately, 20-30% of COPD patients do not respond to therapy, and widespread use is limited by the possibility of developing peripheral neuropathy and other side effects. Currently, the main indication for the appointment of almitrin is moderate hypoxemia in patients with COPD (pa0 2 56-70 mm Hg or Sa0 2 89-93%), as well as its use in combination with VCT, especially against the background of hypercapnia.

Vasodilators

In order to reduce the degree of PAH in complex therapy cor pulmonale patients include peripheral vasodilators. The most commonly used calcium channel antagonists and nitrates. Two calcium antagonists currently recommended are nifedipine and diltiazem. The choice in favor of one of them depends on the initial heart rate. Patients with relative bradycardia should be recommended nifedipine, with relative tachycardia - diltiazem. The daily doses of these drugs, which have proven effective, are quite high: for nifedipine 120-240 mg, for diltiazem 240-720 mg. Favorable clinical and prognostic effects of calcium antagonists used in high doses in patients with primary PH (especially those with a previous positive acute test) have been shown. III generation dihydropyridine calcium antagonists - amlodipine, felodipine, etc. - are also effective in this group of patients with LS.

However, calcium channel antagonists are not recommended for COPD-associated pulmonary hypertension, despite their ability to reduce Ppa and increase cardiac output in this group of patients. This is due to the aggravation of arterial hypoxemia caused by dilatation of the pulmonary vessels in

poorly ventilated areas of the lungs with deterioration in ventilation-perfusion ratios. In addition, with long-term therapy with calcium antagonists (more than 6 months), the beneficial effect on the parameters of pulmonary hemodynamics is leveled.

A similar situation in patients with COPD occurs with the appointment of nitrates: acute samples demonstrate a deterioration in gas exchange, and long-term studies show the absence of a positive effect of drugs on pulmonary hemodynamics.

Synthetic prostacyclin and its analogues. Prostacyclin is a powerful endogenous vasodilator with antiaggregatory, antiproliferative and cytoprotective effects that are aimed at preventing pulmonary vascular remodeling (reducing endothelial cell damage and hypercoagulability). The mechanism of action of prostacyclin is associated with relaxation of smooth muscle cells, inhibition of platelet aggregation, improvement of endothelial function, inhibition of vascular cell proliferation, as well as a direct inotropic effect, positive changes in hemodynamics, and an increase in oxygen utilization in skeletal muscles. The clinical use of prostacyclin in patients with PH is associated with the synthesis of its stable analogues. To date, the greatest experience in the world has been accumulated for epoprostenol.

Epoprostenol is a form of intravenous prostacyclin (prostaglandin I 2). Favorable results were obtained in patients with vascular form of LS - with primary PH in systemic connective tissue diseases. The drug increases cardiac output and reduces pulmonary vascular resistance, and with long-term use improves the quality of life of patients with LS, increasing exercise tolerance. The optimal dose for most patients is 20-40 ng/kg/min. An analog of epoprostenol, treprostinil, is also used.

Oral formulations of a prostacyclin analogue have now been developed. (beraprost, iloprost) and clinical trials are being conducted in the treatment of patients with a vascular form of LS developed as a result of pulmonary embolism, primary pulmonary hypertension, and systemic connective tissue diseases.

In Russia, from the group of prostanoids for the treatment of patients with LS, only prostaglandin E 1 (vazaprostan) is currently available, which is prescribed intravenously

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

Endothelin receptor antagonists

Activation of the endothelin system in patients with PH was the rationale for the use of endothelin receptor antagonists. The effectiveness of two drugs of this class (bosentan and sitaczentan) in the treatment of patients with CPS, which developed against the background of primary PH or against the background of systemic connective tissue diseases, has been proven.

Phosphodiesterase type 5 inhibitors

Sildenafil is a powerful selective inhibitor of cGMP-dependent phosphodiesterase (type 5), preventing the degradation of cGMP, causes a decrease in pulmonary vascular resistance and right ventricular overload. To date, there are data on the effectiveness of sildenafil in patients with LS of various etiologies. When using sildenafil in doses of 25-100 mg 2-3 times a day, it caused an improvement in hemodynamics and exercise tolerance in patients with LS. Its use is recommended when other drug therapy is ineffective.

Long-term oxygen therapy

In patients with bronchopulmonary and thoracophrenic form of CLS, the main role in the development and progression of the disease belongs to alveolar hypoxia, therefore, oxygen therapy is the most pathogenetically substantiated method of treating these patients. The use of oxygen in patients with chronic hypoxemia is critical and must be continuous, long-term, and usually administered at home, hence this form of therapy is called long-term oxygen therapy (LTOT). The task of VCT is to correct hypoxemia with the achievement of pO 2 values ​​>60 mm Hg. and Sa0 2 >90%. It is considered optimal to maintain paO 2 within 60-65 mm Hg, and exceeding these values ​​leads only to a slight increase in Sa0 2 and oxygen content in arterial blood, however, it may be accompanied by CO 2 retention, especially during sleep, which has negative

effects on the function of the heart, brain and respiratory muscles. Therefore, VCT is not indicated for patients with moderate hypoxemia. Indications for VCT: raO 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%). For most patients with COPD, an O 2 flow of 1–2 l/min is sufficient, and in the most severe patients, the flow can be increased to 4–5 l/min. The oxygen concentration should be 28-34% vol. VCT is recommended for at least 15 hours per day (15-19 hours per day). The maximum breaks between oxygen therapy sessions should not exceed 2 hours in a row, because. breaks of more than 2-3 hours significantly increase pulmonary hypertension. Oxygen concentrators, liquid oxygen tanks and compressed gas cylinders can be used for VCT. The most commonly used concentrators (permeators) that release oxygen from the air by removing nitrogen. VCT increases the life expectancy of patients with CRF and CLS by an average of 5 years.

Thus, despite the presence of a large arsenal of modern pharmacological agents, VCT is the most effective method of treating most forms of CLS, so the treatment of patients with CLS is primarily the task of a pulmonologist.

Long-term oxygen therapy is the most effective method of treating CLN and HLS, increasing the life expectancy of patients by an average of 5 years.

Long-term home ventilation

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

NO inhalation therapy

Inhalation therapy with NO, whose action is similar to the endothelium-relaxing factor, has a positive effect in patients with CHD. Its vasodilating effect is based on the activation of guanylate cyclase in the smooth muscle cells of the pulmonary vessels, which leads to an increase in the level of cyclo-GMP and a decrease in the intracellular calcium content. Inhalation N0 region

gives a selective effect on the vessels of the lungs, and it causes vasodilation mainly in well-ventilated regions of the lungs, improving gas exchange. With the course application of NO in patients with chronic respiratory disease, there is a decrease in pressure in the pulmonary artery, an increase in the partial pressure of oxygen in the blood. In addition to its hemodynamic effects, NO prevents and reverses pulmonary vascular and pancreatic remodeling. The optimal doses of inhaled NO are concentrations of 2-10 ppm, and high concentrations of NO (more than 20 ppm) can cause excessive vasodilation of the pulmonary vessels and lead to a deterioration in the ventilation-perfusion balance with increased hypoxemia. The addition of NO inhalations to VCT in patients with COPD enhances the positive effect on gas exchange, reducing the level of pulmonary hypertension and increasing cardiac output.

CPAP therapy

Continuous Positive Airway Pressure Therapy (continuous positive airway pressure- CPAP) is used as a method of treatment for CRF and CLS in patients with obstructive sleep apnea syndrome, preventing the development of airway collapse. The proven effects of CPAP are the prevention and resolution of atelectasis, an increase in lung volumes, a decrease in ventilation-perfusion imbalance, an increase in oxygenation, lung compliance, and redistribution of fluid in lung tissue.

cardiac glycosides

Cardiac glycosides in patients with COPD and cor pulmonale are effective only in the presence of left ventricular heart failure, and may also be useful in the development of atrial fibrillation. Moreover, it has been shown that cardiac glycosides can induce pulmonary vasoconstriction, and the presence of hypercapnia and acidosis increases the likelihood of glycoside intoxication.

Diuretics

In the treatment of patients with decompensated CHLS with edematous syndrome, diuretic therapy, including antagonists, is used.

aldosterone (aldactone). Diuretics should be administered cautiously, with small doses, since in the development of RV failure, cardiac output is more dependent on preload, and, therefore, an excessive reduction in intravascular fluid volume can lead to a decrease in RV filling volume and a decrease in cardiac output, as well as an increase in 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 COPD patients with respiratory failure can lead to inhibition of the activity of the respiratory center and deterioration of gas exchange.

Angiotensin-converting enzyme inhibitors

In the treatment of patients with decompensated cor pulmonale in recent years, angiotensin-converting enzyme inhibitors (ACE inhibitors) have come to the fore. ACE inhibitor therapy in patients with CHLS leads to a decrease in pulmonary hypertension and an increase in cardiac output. For the purpose of selection effective therapy ChLS in patients with COPD is recommended to determine the polymorphism of the ACE gene, because. only in patients with subtypes of the ACE II and ID gene, a pronounced positive hemodynamic effect of ACE inhibitors is observed. The use of ACE inhibitors in minimal therapeutic doses is recommended. In addition to the hemodynamic effect, there is a positive effect of ACE inhibitors on the size of the heart chambers, remodeling processes, exercise tolerance and increased life expectancy in patients with heart failure.

Angiotensin II receptor antagonists

In recent years, data have been obtained on the successful use of this group of drugs in the treatment of CLS in patients with COPD, which was manifested by an improvement in hemodynamics and gas exchange. The appointment of these drugs is most indicated in patients with CLS with intolerance to ACE inhibitors (due to dry cough).

Atrial septostomy

Recently, in the treatment of patients with right ventricular heart failure that developed against the background of primary PH, there have been

use an atrial septostomy, i.e. creation of a small perforation in the interatrial septum. Creating a right-to-left shunt allows you to reduce the average pressure in the right atrium, unload the right ventricle, increase the left ventricular preload and cardiac output. Atrial septostomy is indicated when all types of medical treatment of right ventricular heart failure are ineffective, especially in combination with frequent syncope, or as a preparatory stage before lung transplantation. As a result of the intervention, there is a decrease in syncope, an increase in exercise tolerance, but the risk of developing life-threatening arterial hypoxemia increases. The mortality rate of patients during atrial septostomy is 5-15%.

Lung or heart-lung transplant

From the end of the 80s. In the 20th century, after the introduction of the immunosuppressive drug cyclosporine A, lung transplantation began to be successfully used in the treatment of end-stage pulmonary insufficiency. In patients with CLN and LS, transplantation of one or both lungs, the heart-lung complex is performed. It was shown that 3 and 5-year survival after transplantation of one or both lungs, heart-lung complex in patients with LS was 55 and 45%, respectively. Most centers prefer to perform bilateral lung transplantation due to fewer postoperative complications.

Given guidelines dedicated to the clinic, diagnosis and treatment of cor pulmonale. Recommendations are addressed to students of 4-6 courses. The electronic version of the publication is available on the SPbGMU website (http://www.spb-gmu.ru).

Guidelines are addressed to students of 4-6 courses Chronic cor pulmonale Under chronic cor pulmonale

Ministry of Health and Social Development

Russian Federation

G OU HPE "SAINT PETERSBURG STATE

MEDICAL UNIVERSITY

NAMED AFTER ACADEMICIAN I.P. PAVLOV»

Associate Professor V.N. Yablonskaya

Associate Professor O.A. Ivanova

assistant Zh.A. Mironova

Editor: Head Department of Hospital Therapy, St. Petersburg State Medical University. acad. I.P. Pavlova Professor V.I. Trofimov

Reviewer: Professor of the Department of Propaedeutics of Internal Diseases

SPbGMU im. acad. I.P. Pavlova B.G. Lukichev

Chronic cor pulmonale

Under chronic cor pulmonale (HLS) understand right ventricular (RV) hypertrophy, or a combination of hypertrophy with dilatation and/or right ventricular heart failure (RVF) due to diseases that primarily affect lung function or structure, or both, and not associated with primary left heart failure or congenital or acquired heart defects.

This definition of the WHO expert committee (1961), according to a number of experts, currently needs to be corrected due to the introduction into practice modern methods diagnostics and accumulation of new knowledge about the pathogenesis of CLS. In particular, CHLS is proposed to be considered as pulmonary hypertension in combination with hypertrophy. dilatation of the right ventricle, dysfunction of both ventricles of the heart associated with primary structural and functional changes in the lungs.

Pulmonary hypertension (PH) is said to be when the pressure in the pulmonary artery (PA) exceeds established normal values:

Systolic - 26 - 30 mm Hg.

Diastolic - 8 - 9 mm Hg.

Average - 13 - 20 mm Hg.St.

Chronic cor pulmonale is not an independent nosological form, but it complicates many diseases that affect the airways and alveoli, the chest with limited mobility, and pulmonary vessels. Essentially all diseases that can lead to the development of respiratory failure and pulmonary hypertension (there are more than 100 of them) can cause chronic cor pulmonale. At the same time, in 70-80% of cases, chronic obstructive pulmonary disease (COPD) accounts for CLS. Currently, chronic cor pulmonale is observed in 10-30% of pulmonological patients hospitalized in a hospital. It is 4-6 times more common in men. Being a severe complication of chronic obstructive pulmonary disease (COPD), CLS determines the clinic, course and prognosis of this disease, leads to early disability of patients and often causes death. Moreover, the mortality rate in patients with CLS over the past 20 years has increased by 2 times.

ETIOLOGY AND PATHOGENESIS OF CHRONIC PULMONARY HEART.

Since chronic cor pulmonale is a condition that occurs secondarily and is essentially a complication of a number of respiratory diseases, the following types of CHLS are usually distinguished in accordance with the primary causes:

1. Bronchopulmonary:

The reason is diseases that affect the airways and alveoli:

Obstructive diseases (chronic obstructive pulmonary disease (COPD), primary pulmonary emphysema, severe bronchial asthma with significant irreversible obstruction)

Diseases that occur with severe pulmonary fibrosis (tuberculosis, bronchiectasis, pneumoconiosis, repeated pneumonia, radiation injury)

Interstitial lung diseases (idiopathic fibrosing alveolitis, lung sarcoidosis, etc.), collagenosis, lung carcinomatosis

2. Thoracodiaphragmatic:

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

Chronic cor pulmonale: the view of cardiologists

Prepared by Maxim Gvozdyk | 03/27/2015

The prevalence of chronic obstructive pulmonary disease (COPD) is rapidly increasing worldwide: if

in 1990 they were in twelfth place in the structure of morbidity, then according to WHO experts, by 2020 they will move into the top five after such pathologies as coronary heart disease (CHD), depression, injuries due to traffic accidents and cerebrovascular disease. It is also predicted that by 2020 COPD will take the third place in the structure of causes of death. Coronary artery disease, arterial hypertension and obstructive pulmonary disease are often combined, which gives rise to a number of problems in both pulmonology and cardiology. November 30, 2006

at the Institute of Phthisiology and Pulmonology named after F.G. Yanovsky of the Academy of Medical Sciences of Ukraine, a scientific-practical conference “Peculiarities of diagnosis and treatment of obstructive pulmonary diseases with concomitant pathology” was held

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

and pulmonology.

The report "Heart failure in chronic cor pulmonale: a cardiologist's point of view" was presented by

Corresponding Member of the Academy of Medical Sciences of Ukraine, Doctor of Medical Sciences, Professor Ekaterina Nikolaevna Amosova .

- In modern cardiology and pulmonology, there are a number of common problems in respect of which it is necessary to reach a consensus and unify approaches. One of them is chronic cor pulmonale. Suffice it to say that dissertations on this topic are equally often defended both in cardiological and pulmonological councils, it is included in the list of problems dealt with by both branches of medicine, but unfortunately, a unified approach to this pathology has not yet been developed. Let's not forget general practitioners and family doctors who find it difficult to understand the conflicting information and information printed in the pulmonological and cardiology literature.

The definition of chronic cor pulmonale in a WHO document dates back to 1963. Unfortunately, since that time, WHO recommendations on this important issue have not been clarified or reaffirmed, which, in fact, led to discussions and contradictions. Today, there are practically no publications on chronic cor pulmonale in the foreign cardiological literature, although there is a lot of talk about pulmonary hypertension, moreover, the recommendations of the European Society of Cardiology regarding pulmonary hypertension have recently been revised and approved.

The concept of "cor pulmonale" includes extremely heterogeneous diseases, they differ in etiology, the mechanism of development of myocardial dysfunction, its severity, and have different approaches to treatment. Chronic cor pulmonale is based on both hypertrophy, dilatation, and dysfunction of the right ventricle, which, by definition, are associated with pulmonary hypertension. The heterogeneity of these diseases is even more obvious if we consider the degree of increase in pressure in the pulmonary artery in pulmonary hypertension. In addition, its very presence has absolutely different meaning with various etiological factors of chronic cor pulmonale. So, for example, in vascular forms of pulmonary hypertension, this is the basis that requires treatment, and only a decrease in pulmonary hypertension can improve the patient's condition; in COPD - pulmonary hypertension is not so pronounced and does not need treatment, as evidenced by Western sources. Moreover, a decrease in pressure in the pulmonary artery in COPD does not lead to relief, but worsens the patient's condition, as there is a decrease in blood oxygenation. Thus, pulmonary hypertension is an important condition for the development of chronic cor pulmonale, but its importance should not be absolute.

Often this pathology becomes the cause of chronic heart failure. And if we talk about it with cor pulmonale, then it is worth recalling the criteria for diagnosing heart failure (HF), which are reflected in the recommendations of the European Society of Cardiology. To make a diagnosis, there must be: firstly, the symptoms and clinical signs of heart failure, and secondly, objective signs of systolic or diastolic myocardial dysfunction. That is, the presence of dysfunction (changes in myocardial function at rest) is mandatory for diagnosis.

The second question is the clinical symptoms of chronic cor pulmonale. In the cardiology audience, it is necessary to say that edema does not correspond to the fact of the presence of right ventricular failure. Unfortunately, cardiologists are very little aware of the role of non-cardiac factors in the origin of clinical signs of venous congestion in big circle circulation. Edema in such patients is often perceived as a manifestation of heart failure, it is actively treated, but to no avail. This situation is well known to pulmonologists.

The pathogenetic mechanisms of the development of chronic cor pulmonale also include non-cardiac factors of blood deposition. Of course, these factors are important, but you should not overestimate them and associate everything only with them. And finally, we talk little, in essence, just started, about the role of hyperactivation of the renin-angiotensin-aldosterone system and its significance in the development of edema and hypervolemia.

In addition to these factors, it is worth mentioning the role of myocardiopathy. In the development of chronic pulmonary heart, a large role is played by myocardial damage not only of the right ventricle, but also of the left, which occurs under the influence of a complex of factors, including toxic, which is associated with bacterial agents, in addition, it is a hypoxic factor that causes dystrophy of the myocardium of the ventricles of the heart .

In the course of our studies, it was found that there is practically no correlation between systolic pressure in the pulmonary artery and the size of the right ventricle in patients with chronic cor pulmonale. There is some correlation between the severity of COPD and impaired right ventricular function, with respect to the left ventricle, these differences are less pronounced. When analyzing the systolic function of the left ventricle, its deterioration was noted in patients with severe COPD. The contractility of the myocardium, even of the left ventricle, is extremely difficult to correctly assess, because the indices that we use in clinical practice are very rough and depend on pre- and afterload.

As for the indicators of diastolic function of the right ventricle, all patients were diagnosed with a hypertrophic type of diastolic dysfunction. The indicators from the right ventricle are expected, but from the left side, we somewhat unexpectedly received signs of impaired diastolic relaxation, which increased depending on the severity of COPD.

Indicators of ventricular systolic function in patients with COPD and idiopathic pulmonary hypertension are different. Of course, changes in the right ventricle are more pronounced in idiopathic pulmonary hypertension, while the systolic function of the left ventricle is more changed in COPD, which is associated with the effect of adverse factors of infection and hypoxemia on the myocardium of the left ventricle, and then it makes sense to talk about cardiopathy in that broad sense. understanding that is present in cardiology today.

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

Echocardiography of all patients measured the diameter of the inferior vena cava and determined the degree of its collapse during inspiration. It was found that in moderate COPD, the diameter of the inferior vena cava is not increased, it increased only in severe COPD, when FEV1 is less than 50%. This allows us to raise the question that the role of extracardiac factors should not be absolutized. At the same time, the collapse of the inferior vena cava on inspiration was already disturbed in moderate COPD (this indicator reflects an increase in pressure in the left atrium).

We also analyzed heart rate variability. It should be noted that cardiologists consider a decrease in heart rate variability to be a marker of activation of the sympathoadrenal system, the presence of heart failure, that is, a poor prognostic indicator. We found a decrease in variability in moderate COPD, the severity of which increased in accordance with obstructive disorders of the ventilation function of the lungs. Moreover, we found a significant correlation between the severity of heart rate variability disorder and right ventricular systolic function. This suggests that heart rate variability in COPD appears quite early and can serve as a marker of myocardial damage.

When diagnosing chronic cor pulmonale, especially in pulmonary patients, it is necessary to pay great attention to the instrumental study of myocardial dysfunction. In this regard, echocardiography is the most convenient study in clinical practice, although there are limitations for its use in patients with COPD, in which, ideally, radionuclide ventriculography of the right ventricle should be used, which combines relatively low invasiveness and very high accuracy.

Of course, it is not news to anyone that chronic cor pulmonale in COPD and idiopathic pulmonary hypertension is very heterogeneous in terms of the morphofunctional state of the ventricles, prognosis and a number of other reasons. The existing European classification of heart failure, which was included in the document of the Ukrainian Society of Cardiology almost unchanged, does not reflect the difference in the mechanisms of development of this disease. If these classifications were convenient in clinical practice, we would not be discussing this topic. It seems logical to us to leave the term "chronic pulmonary heart" for bronchopulmonary pathology, to emphasize - decompensated, subcompensated and compensated. This approach will avoid the use of the terms FK and CH. In vascular forms of chronic pulmonary heart (idiopathic, post-thromboembolic pulmonary hypertension), it is advisable to use the approved HF gradation. However, it seems to us appropriate, by analogy with cardiology practice, to indicate the presence of right ventricular systolic dysfunction in the diagnosis, because this is important for chronic cor pulmonale associated with COPD. If the patient does not have dysfunction, this is one situation in the prognostic and treatment plans, if there is, the situation is significantly different.

Cardiologists of Ukraine have been using the Strazhesko-Vasilenko classification when making a diagnosis of chronic heart failure for several years, necessarily indicating whether the systolic function of the left ventricle is preserved or reduced. So why not use it for chronic cor pulmonale?

Doctor of Medical Sciences, Professor Yuri Nikolaevich Sirenko devoted his speech to the peculiarities of the treatment of patients with coronary artery disease and arterial hypertension in combination with COPD.

– In preparation for the conference, I tried to find on the Internet references over the past 10 years to pulmonogenic arterial hypertension, a nosology that often appeared in the USSR. I managed to find about 5 thousand references to arterial hypertension in chronic obstructive pulmonary diseases, but the problem of pulmonogenic arterial hypertension does not exist anywhere in the world, except for the post-Soviet countries. To date, there are several positions regarding the diagnosis of the so-called pulmonogenic arterial hypertension. They were developed in the early 1980s, when more or less reliable functional research methods appeared.

The first position is the development of pulmonary arterial hypertension 5-7 years after the onset of chronic lung disease; the second is the relationship between an increase in blood pressure and an exacerbation of COPD; the third is an increase in blood pressure due to increased bronchial obstruction; fourth - with daily monitoring, a relationship is revealed between an increase in blood pressure and inhalation of sympathomimetics; fifth - high variability of blood pressure during the day with a relatively low average level.

I managed to find a very serious work by the Moscow Academician E.M. Tareeva "Does pulmonary arterial hypertension exist?", in which the author makes a mathematical assessment of the possible relationship of the above factors in patients with arterial hypertension and COPD. And no dependency found! The results of the studies did not confirm the existence of independent pulmonogenic arterial hypertension. Moreover, E.M. Tareev believes that systemic arterial hypertension in patients with COPD should be considered as hypertension.

After such a categorical conclusion, I looked at the world's recommendations. In the modern recommendations of the European Society of Cardiology there is not a single line about COPD, the American ones (seven recommendations of the National Joint Committee) also say nothing on this topic. It was possible to find only in the American recommendations of 1996 (in six editions) information that non-selective beta-blockers should not be used in patients with COPD, and if there is a cough, ACE inhibitors should be replaced with angiotensin receptor blockers. That is, there really is no such problem in the world!

Then I reviewed the statistics. It turned out that they started talking about pulmonary arterial hypertension after it was established that approximately 35% of patients with COPD have high blood pressure. Today, Ukrainian epidemiology gives the following figures: among the adult rural population, blood pressure is increased in 35%, in urban - in 32%. We cannot say that COPD increases the incidence of arterial hypertension, so we should not talk about pulmonogenic arterial hypertension, but about some specifics of the treatment of arterial hypertension in COPD.

Unfortunately, in our country, sleep apnea syndrome, in addition to the Institute of Phthisiology and Pulmonology named after. F.G. Yanovsky of the Academy of Medical Sciences of Ukraine, practically nowhere are they engaged. This is due to the lack of equipment, money and the desire of specialists. And this question is very important and represents another problem where cardiac pathology intersects with the pathology of the respiratory tract and there is a very high percentage of the risk of developing cardiovascular complications and death. Pulmonary hypertension, heart and respiratory failure complicate and worsen the course of arterial hypertension and, most importantly, worsen the ability to treat patients.

I would like to start a conversation about the treatment of arterial hypertension with a simple algorithm, which is the basis for cardiologists and therapists. Before a doctor who meets a patient with hypertension, questions arise: what form of arterial hypertension does the patient have - primary or secondary - and are there signs of target organ damage and cardiovascular risk factors? By answering these questions, the doctor knows the tactics of treating the patient.

To date, there is not a single randomized clinical trial that was specifically designed to clarify the tactics of treating arterial hypertension in COPD, so current recommendations are based on three very unreliable factors: retrospective analysis, expert opinion and the doctor's own experience.

Where should treatment begin? Of course, with first-line antihypertensive drugs. The first and main group of them is beta-blockers. Many questions arise regarding their selectivity, but there are already drugs with a fairly high selectivity, confirmed in the experiment and the clinic, which are safer than the drugs that we used before.

When assessing the airway patency in healthy people after taking atenolol, a deterioration in the response to salbutamol and minor changes when taking more modern drugs were established. Although, unfortunately, such studies have not been conducted with the participation of patients, nevertheless, the categorical ban on the use of beta-blockers in patients with COPD should be lifted. They should be prescribed if the patient tolerates them well, it is advisable to use them in the treatment of arterial hypertension, especially in combination with coronary artery disease.

The next group of drugs is calcium antagonists, they are almost ideal for the treatment of such patients, but it must be remembered that drugs of the non-dihydropyridine series (diltiazem, verapamil) should not be used with increased blood pressure in the pulmonary artery system. They have been shown to worsen the course of pulmonary hypertension. The remaining dihydropyridines are known to improve bronchial patency and thus may reduce the need for bronchodilators.

Today, all experts agree that ACE inhibitors do not impair airway patency, do not cause cough in patients with COPD, and if it occurs, patients should be transferred to angiotensin receptor blockers. We did not conduct special studies, but based on the literature data and our own observations, it can be argued that the experts are a little cunning, since a certain number of patients with COPD react with a dry cough to ACE inhibitors, and there is a serious pathogenetic reason for this.

Unfortunately, very often one can observe the following picture: a patient with high blood pressure goes to a cardiologist, he is prescribed ACE inhibitors; after some time, the patient begins to cough, goes to a pulmonologist, who cancels ACE inhibitors, but does not prescribe angiotensin receptor blockers. The patient again gets to the cardiologist, and everything starts all over again. The reason for this situation is the lack of control over appointments. It is necessary to move away from this practice, therapists and cardiologists should take a comprehensive approach to treating the patient.

Another very important point in the treatment of patients, which allows to reduce the possibility of side effects, is the use of lower doses. Modern European recommendations give the choice between low doses of one or two drugs. Today, the great effectiveness of a combination of different drugs has been proven, which affects various links in pathogenesis, mutually reinforcing the effect medicines. I believe that combination therapy for patients with COPD is the choice in the treatment of arterial hypertension.

For citation: Vertkin A.L., Topolyansky A.V. Cor pulmonale: diagnosis and treatment // BC. 2005. No. 19. S. 1272

Cor pulmonale - an increase in the right ventricle of the heart in diseases that disrupt the structure and (or) function of the lungs (with the exception of cases of primary damage to the left heart, congenital heart defects).

The following diseases lead to its development:
- Primarily affecting the passage of air in the lungs and alveoli (chronic bronchitis, bronchial asthma, pulmonary emphysema, tuberculosis, pneumoconiosis, bronchiectasis, sarcoidosis, etc.);
- primarily affecting the mobility of the chest (kyphoscoliosis and other deformities of the chest, neuromuscular diseases - for example, polio, obesity - Pickwick's syndrome, sleep apnea);
- Primarily affecting the vessels of the lungs (primary pulmonary hypertension, arteritis, thrombosis and embolism of the vessels of the lungs, compression of the trunk of the pulmonary artery and pulmonary veins by a tumor, aneurysm, etc.).
In the pathogenesis of cor pulmonale, the main role is played by a decrease in the total cross section of the vessels of the lungs. In diseases that primarily affect the passage of air in the lungs and the mobility of the chest, alveolar hypoxia leads to spasm of the small pulmonary arteries; in diseases affecting the vessels of the lungs, an increase in resistance to blood flow is due to narrowing or blockage of the lumen of the pulmonary arteries. An increase in pressure in the pulmonary circulation leads to hypertrophy of the smooth muscles of the pulmonary arteries, which become more rigid. Overloading the right ventricle with pressure causes its hypertrophy, dilatation, and later - right ventricular heart failure.
Acute cor pulmonale develops with pulmonary embolism, spontaneous pneumothorax, a severe attack of bronchial asthma, severe pneumonia in a few hours or days. Manifested by sudden pressing pain behind the sternum, severe shortness of breath, cyanosis, arterial hypotension, tachycardia, amplification and accent of the II heart sound over the pulmonary trunk; deviation of the electrical axis of the heart to the right and electrocardiographic signs of overload of the right atrium; rapidly increasing signs of right ventricular failure - swelling of the cervical veins, enlargement and tenderness of the liver.
Chronic cor pulmonale is formed over a number of years in chronic obstructive pulmonary disease, kyphoscoliosis, obesity, recurrent pulmonary embolism, primary pulmonary hypertension. There are three stages in its development: I (preclinical) - diagnosed only with instrumental examination; II - with the development of right ventricular hypertrophy and pulmonary hypertension without signs of heart failure; III (decompensated cor pulmonale) - when symptoms of right ventricular failure appear.
Clinical signs of chronic cor pulmonale - shortness of breath, aggravated by exertion, fatigue, palpitations, pain in chest, fainting. When the recurrent nerve is compressed by the dilated trunk of the pulmonary artery, hoarseness occurs. On examination, objective signs of pulmonary hypertension can be detected - accent II tone on the pulmonary artery, Graham-Still diastolic murmur (noise of relative insufficiency of pulmonary artery valves). An increase in the right ventricle may be evidenced by a pulsation behind the xiphoid process, which increases on inspiration, an expansion of the boundaries of the relative dullness of the heart to the right. With significant dilatation of the right ventricle, relative tricuspid insufficiency develops, manifested by systolic murmur at the base of the xiphoid process, pulsation of the cervical veins and liver. In the stage of decompensation, signs of right ventricular failure appear: liver enlargement, peripheral edema.
The ECG reveals hypertrophy of the right atrium (spiky high P waves in leads II, III, aVF) and the right ventricle (deviation of the electrical axis of the heart to the right, an increase in the amplitude of the R wave in the right chest leads, blockade of the right leg of the His bundle, the appearance of a deep S wave in I and Q wave in III standard leads).
Radiologically acute and subacute pulmonary heart is manifested by an increase in the right ventricle, expansion of the arch of the pulmonary artery, expansion of the lung root; chronic cor pulmonale - hypertrophy of the right ventricle, signs of hypertension in the pulmonary circulation, expansion of the superior vena cava.
Echocardiography may show hypertrophy of the right ventricular wall, dilatation of the right chambers of the heart, dilation of the pulmonary artery and superior vena cava, pulmonary hypertension, and tricuspid insufficiency.
In a blood test in patients with chronic cor pulmonale, polycythemia is usually detected.
With the development of acute pulmonary heart, treatment of the underlying disease is indicated (elimination of pneumothorax; heparin therapy, thrombolysis or surgical intervention for pulmonary embolism; adequate therapy of bronchial asthma, etc.).
Treatment of cor pulmonale proper is mainly aimed at reducing pulmonary hypertension, and with the development of decompensation, it includes correction of heart failure (Table 1). Pulmonary hypertension decreases with the use of calcium antagonists - nifedipine at a dose of 40–180 mg per day (preferably the use of long-acting forms of the drug), diltiazem at a dose of 120–360 mg per day [Chazova I.E., 2000], and amlodipine (Amlovas ) at a dose of 10 mg per day. So, according to Franz I.W. et al. (2002), during therapy with amlodipine at a dose of 10 mg per day for 18 days in 20 COPD patients with pulmonary hypertension, a significant decrease in pulmonary vascular resistance and pressure in the pulmonary artery was noted, while changes in gas exchange parameters in the lungs were not observed. According to the results of a crossover randomized study conducted by Sajkov D. et al. (1997), equivalent doses of amlodipine and felodipine equally reduced pulmonary artery pressure, but side effects ( headache and edematous syndrome) developed less frequently during amlodipine therapy.
The effect of therapy with calcium antagonists usually appears after 3-4 weeks. It has been shown that a decrease in pulmonary pressure during calcium antagonist therapy significantly improves the prognosis of these patients, however, only a third of patients respond to calcium antagonist therapy in this way. Patients with severe right ventricular failure usually respond poorly to calcium antagonist therapy.
In clinical practice, in patients with signs of cor pulmonale, theophylline preparations (intravenous drip, prolonged oral preparations) are widely used, which reduce pulmonary vascular resistance, increase cardiac output and improve the well-being of these patients. At the same time, there appears to be no evidence base for the use of theophylline preparations in pulmonary hypertension.
Effectively reduces pressure in the pulmonary artery by intravenous infusion of prostacyclin (PGI2), which has antiproliferative and antiplatelet effects; the drug increases exercise tolerance, improves the quality of life and reduces mortality in these patients. Its disadvantages include often developing side effects (dizziness, arterial hypotension, cardialgia, nausea, abdominalgia, diarrhea, rash, pain in the extremities), the need for constant (long-term) intravenous infusions, as well as the high cost of treatment. The efficacy and safety of prostacyclin analogues, iloprost, used in the form of inhalation and beraprost, used orally, as well as treprostinil, administered both intravenously and subcutaneously, are being studied.
The possibility of using the endothelin receptor antagonist bosentan, which effectively reduces pressure in the pulmonary artery, is being studied, but severe systemic side effects are limited intravenous use this group of drugs.
Inhalation of nitric oxide (NO) for several weeks also reduces pulmonary hypertension, but this therapy is not available to all medical institutions. In recent years, attempts have been made to use PDE5 inhibitors in pulmonary hypertension, in particular, sildenafil citrate. Charan N.B. in 2001, described two patients who noted an improvement in the course of COPD while taking sildenafil, which they took for erectile dysfunction. Today, the bronchodilatory, anti-inflammatory effect of sildenafil and its ability to reduce pressure in the pulmonary artery has been shown both in experimental and clinical studies. According to the data obtained, PDE5 inhibitors in pulmonary hypertension significantly improve exercise tolerance, increase the cardiac index, improve the quality of life of patients with pulmonary hypertension, including primary. Long-term multicentre studies are needed to definitively resolve the issue of the effectiveness of this class of drugs in COPD. In addition, the high cost of treatment certainly hinders the widespread introduction of these drugs into clinical practice.
In the formation of chronic cor pulmonale in patients with chronic obstructive pulmonary diseases ( bronchial asthma, chronic bronchitis, emphysema) in order to correct hypoxia, long-term oxygen therapy is indicated. With polycythemia (in the case of an increase in hematocrit above 65–70%), bloodletting is used (usually a single one), which allows to reduce pressure in the pulmonary artery, increase the patient's tolerance to physical activity and improve his well-being. The amount of blood removed is 200-300 ml (depending on the level of blood pressure and the patient's well-being).
With the development of right ventricular failure, diuretics are indicated, incl. spironolactone; it should be borne in mind that diuretics do not always help to reduce shortness of breath in pulmonary hypertension. ACE inhibitors (captopril, enalapril, etc.) are also used. The use of digoxin in the absence of left ventricular failure is ineffective and unsafe, since hypoxemia and hypokalemia developing against the background of diuretic therapy increase the risk of developing glycoside intoxication.
Considering the high probability of thromboembolic complications in heart failure and the need for active diuretic therapy, prolonged bed rest, the appearance of signs of phlebothrombosis, preventive anticoagulant therapy is indicated (usually subcutaneous administration of heparin 5000 IU 2 times a day or low molecular weight heparin 1 time per day). In patients with primary pulmonary hypertension, indirect anticoagulants (warfarin) are used under the control of INR. Warfarin increases the survival of patients, but does not affect their general condition.
Thus, in modern clinical practice drug treatment cor pulmonale is reduced to the treatment of heart failure (diuretics, ACE inhibitors), as well as the use of calcium antagonists and theophylline drugs to reduce pulmonary hypertension. A good effect on calcium antagonist therapy significantly improves the prognosis of these patients, and the lack of an effect requires the use of drugs of other classes, which is limited by the complexity of their use, the high likelihood of side effects, the high cost of treatment, and in some cases - insufficient knowledge question.

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