State educational institution of higher professional education "Moscow State Medical and Dental University of Roszdrav"

Medical Faculty

Martynov A.I., Maychuk E.Yu., Panchenkova L.A., Khamidova Kh.A.,

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

Chronic cor pulmonale

Teaching aid for conducting practical exercises in hospital therapy

Moscow 2012

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

d.m.s. Professor of the Department of Hospital Therapy No. 2 of GOU VPO MGMSU, Makoeva L.D.

Maychuk E.Yu., Martynov A.I., Panchenkova L.A., Khamidova Kh.A., Yurkova T.E., Pak L.S., Zavyalova A.I. Textbook for students of medical universities. Moscow: MGMSU, 2012, 25 p.

The textbook details modern concepts of 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 a lesson, an algorithm for substantiating a clinical diagnosis; included final test lessons, designed for self-assessment of knowledge by students, as well as situational tasks on the topic.

This study guide has been prepared in accordance with the working curriculum for the discipline "Hospital therapy", approved in 2008 at the Moscow State Medical and Dental University on the basis of model 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 No. 1

(Head of the Department - Doctor of Medical Sciences, Professor Maychuk E.Yu.)

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

MGMSU, 2012

Department of Hospital Therapy No. 1, 2012

Definition and theoretical basis of topic 4

Motivational characteristics of the topic 14

Diagnostic Search Steps 15

Clinical Objectives 18

Test items 23

Literature 28

DEFINITION AND THEORETICAL ISSUES OF THE TOPIC

Chronic cor pulmonale (CP) - hypertrophy and / or dilation of the right ventricle in combination with pulmonary hypertension, which occurs against the background of various diseases that disrupt the structure and / or function of the lungs, except for cases when changes in the lungs are themselves the result of primary lesions of the left heart or congenital heart defects and large 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, pulmonary resection and others);

diseases leading to limitation 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 thromboembolism of the pulmonary arteries).

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

CLASSIFICATION OF CHRONIC PULMONARY HEART:

By the degree of compensation:

compensated;

decompensated.

By origin:

vascular genesis;

bronchopulmonary genesis;

thoracodiaphragmatic genesis.

PATHOGENESIS OF CHRONIC PULMONARY HEART

There are 3 stages in the development of CLS:

precapillary hypertension in the pulmonary circulation;

hypertrophy of the right ventricle;

right ventricular heart failure.

The development of pulmonary hypertension lies at the heart of the pathogenesis of CLS.

Main pathogenetic mechanisms:

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

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

Hypertensive influence 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 intraalveolar pressure in obstructive bronchitis.

In the early stages of CLS formation, compensatory-adaptive reactions predominate, 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 failure of the right ventricle.

CLINICAL PICTURE

The clinical picture includes symptoms:

the underlying disease that led to the development of HLS;

respiratory failure;

heart (right ventricular) failure;

Complaints

Shortness of breath, aggravated by exertion. In contrast to patients with left ventricular failure with decompensated cor pulmonale, the position of the body does not affect the degree of dyspnea - patients can freely lie on their back or on their side. Orthopnea is not typical for them, since there is no congestion in the lungs, there is no "obstruction" of the small circle, as in the case of 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 organic diagnostic value.

Persistent tachycardia.

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

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

Neurological symptoms (cranialgia, dizziness, drowsiness, darkening and double vision, impaired speech, poor concentration of thoughts, loss of consciousness) are associated with a disorder of cerebral circulation.

Objective signs

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

Swelling of the cervical veins due to the 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 inhalation).

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

Swelling of the lower extremities, as a rule, is less pronounced and does not reach the same degree as in primary heart disease.

Enlarged liver, ascites, positive venous pulse, positive Plesha symptom (hepatojugular symptom - when pressing on the edge of the liver, swelling of the neck veins becomes obvious).

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 above the handle of the sternum with a tympanic shade, and above the xiphoid process becomes dull-tympanic or completely deaf.

Deafness of heart sounds.

The accent of the second tone over the pulmonary artery (with an increase in pressure in it 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 the clinical analysis of blood in patients with CLS, erythrocytosis, high hematocrit, and ESR slowdown are determined.

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

X-ray signs

Normal or enlarged lateral heart shadow

Relative increase in the RV arch in the left (second) oblique position.

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

Dilation of the main branch of the pulmonary artery more than 15 mm in the 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's lines (Kerley) - horizontal narrow darkening over the costal-phrenic sinus. It is believed that they arise due to the expansion of the lymphatic vessels at the thickening of the interlobular clefts. In the presence of the Curly line, pulmonary capillary pressure exceeds 20 mm Hg. Art. (normal - 5 - 7 mm Hg).

Electrocardiographic signs

Signs of hypertrophy and overload of the right heart are observed.

Direct signs of hypertrophy:

r wave in V1 more than 7 mm;

r / S ratio in V1 is more than 1;

own deviation V1 - 0.03 - 0.05 s;

qR form in V1;

incomplete right bundle branch block, if R is more than 10 mm;

complete blockade of the right bundle branch block, if R is more than 15 mm;

picture of overload of the right ventricle 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;

The R / S ratio in V5 is less than 1;

S-wave in V1 less than 2 mm;

Complete block of the right bundle branch block if R is less than 15 mm;

Incomplete right bundle branch block, if R is less than 10 mm;

standard leads:

P-pulmonale in II and III standard ECG leads;

deviation of EOS to the right;

type S1, S2, S3.

Echocardiographic signs

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

Dilation of the right heart (end diastolic size of the right ventricle more than 2.5 cm).

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

"D" -shaped shape of the right ventricle.

Tricuspid regurgitation.

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

I - 31 - 50 mm Hg;

II - 51 - 75 mm Hg;

III - 75 mm Hg. Art. and higher.

TREATMENT OF CHRONIC PULMONARY HEART

The basic principles of treatment of patients with HLS:

Prevention and treatment of underlying lung diseases.

Medication reduction 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 chronic pulmonary disease is a compensatory mechanism of ventilation-perfusion dysfunction.

Treatment of right ventricular failure.

The main goal of the treatment of patients with CLS is to improve the oxygen transport parameters 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 main 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 CLS flow pathogenetic treatment long-term oxygen therapy is used - inhalation of oxygen-enriched air (30 - 40% oxygen) through a nasal catheter. Oxygen flow rate - 2 - 3 liters per minute at rest and 5 liters per minute under load. Criteria for the appointment of long-term oxygen therapy: PAO2 less than 55 mm Hg. and oxygen saturation (saturation of the erythrocyte with oxygen, SAO2) less than 90%. Long-term oxygenation should be prescribed as early as possible in order to correct abnormalities in the blood gas composition, reduce arterial hypoxemia and prevent hemodynamic disturbances 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 pulmonary and systemic circulation, and therefore are referred to as direct vasodilators. Tactics of prescribing calcium antagonists: treatment begins with small doses of the drug, gradually increasing the daily dose, bringing it to the maximum tolerable; nifedipine is prescribed - 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 to 4 weeks to 3 to 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 the side effects that occur when prescribing calcium antagonists. An immediate effect should not be expected with calcium antagonists.

Nitrates cause dilatation of the arteries of the small circle of blood circulation; reduce the afterload on the right ventricle due to cardiodilation, reduce the afterload on the right ventricle due to a decrease in hypoxic vasoconstriction of the LA; reduce the 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 life prognosis in patients with congestive heart failure, including in patients with chronic heart failure, since the result of the use of an ACE inhibitor 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, increased cardiac output. Prescribe captopril (kapoten) in a daily dose of 75-100 mg, ramipril - 2.5-5 mg / day, etc., the dose depends on the initial level of blood pressure. With the development of side effects or intolerance to ACE inhibitors, antagonists of AT II receptors (losartan, valsartan, etc.) can be prescribed.

Prostaglandins - a group of drugs that can successfully reduce the pressure in the pulmonary artery with minimal effect on the 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 installed 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 endothelium relaxant factor. With the course of inhalation use of NO in patients with chronic pulmonary disease, 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, we must not forget about the toxic effect of NO on the human body, which requires compliance with a clear dosage regimen.

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

Diuretics prescribed when edema appears, combining them with limiting the intake of fluid and salt (furosemide, lasix, potassium-sparing diuretics - triamterene, combined 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 blood. At the initial stages of CLS development with fluid retention in the body due to hyperaldosteronism, caused by the stimulating effect of hypercapnia on the glomerular zone of the adrenal cortex, it is advisable to prescribe aldosterone antagonists in isolation (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 chronic pulmonary disease remains controversial. It is believed that cardiac glycosides, having a positive inotropic effect, lead to more complete emptying of the ventricles, increasing cardiac output. However, in this category of patients without concomitant cardiac pathology, cardiac glycosides do not increase hemodynamic parameters. Against the background of taking cardiac glycosides in patients with CLS, symptoms of digitalis intoxication are more often observed.

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

Use anticoagulants for the treatment and prevention of thrombosis, thromboembolic complications. In a hospital setting, heparin is mainly used in a daily dose of 5000 - 20,000 U 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 individual adjusted dose under INR control.

Also used antiplatelet agents (acetylsalicylic acid, courantil), hirudotherapy.

Preventive measures should be aimed at observing the work and rest regime. It is necessary to completely quit smoking (including passive smoking), avoid hypothermia, if possible, and prevent acute respiratory viral infections.

FORECAST

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

MOTIVATIVE CHARACTERISTIC OF THE TOPIC

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.

The purpose of the lesson: study the etiology, pathogenesis, clinical manifestations, diagnostic methods, approaches to the treatment of chronic pulmonary heart disease.

The student should know:

Questions to prepare for the lesson:

A) Definition of the concept "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 cor pulmonale.

F) Modern approaches to the therapy of chronic pulmonary heart disease

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LECTURE ON INTERNAL DISEASES.

THEME: PULMONARY HEART.

Relevance of the topic: Diseases of the bronchopulmonary system, chest are of great importance in heart damage. Most authors designate the defeat of the cardiovascular system in diseases of the bronchopulmonary system by the term cor pulmonale.

Chronic cor pulmonale develops in about 3% of patients suffering from chronic lung diseases, and in the general structure of mortality from congestive heart failure, chronic cor pulmonale accounts for 30% of cases.

Cor pulmonale is a hypertrophy and dilation or only dilation of the right ventricle resulting from hypertension of the pulmonary circulation, which developed as a result of diseases of the bronchi and lungs, chest deformities, or primary lesions of the pulmonary arteries. (WHO 1961).

Right ventricular hypertrophy and its dilatation with changes as a result of primary heart damage, or congenital defects do not belong to the concept of cor pulmonale.

Recently, clinicians have noticed that hypertrophy and dilation of the right ventricle are already late manifestations of cor pulmonale, when it is no longer possible to rationally treat such patients, so a new definition of cor pulmonale was proposed:

“Cor pulmonale is a complex of hemodynamic disorders in the pulmonary circulation, which develops as a result of diseases of the bronchopulmonary apparatus, chest deformities, and primary lesions of the pulmonary arteries, which at the final stage manifested by right ventricular hypertrophy and progressive circulatory failure ”.

ETIOLOGY OF THE PULMONARY HEART.

Cor pulmonale is a consequence of diseases of three groups:

Diseases of the bronchi and lungs, primarily affecting the passage of air and alveoli. This group includes approximately 69 diseases. They cause the development of cor pulmonale in 80% of cases.

chronic obstructive bronchitis

pneumosclerosis of any etiology

pneumoconiosis

tuberculosis, not by itself, like post-tuberculosis outcomes

SLE, Boeck's sarcoidosis, fibrosing alveolitis (endogenous and exogenous)

Diseases primarily affecting the chest, diaphragm with limited mobility:

kyphoscoliosis

multiple rib injuries

obesity Pickwick syndrome

ankylosing spondylitis

pleural suppuration after suffering pleurisy

Diseases primarily affecting the pulmonary vessels

primary arterial hypertension (Ayerza`s disease)

recurrent pulmonary embolism (PE)

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

Diseases of the second and third groups are the cause of the development of cor pulmonale in 20% of cases. That is why they say that, depending on the etiological factor, three forms of cor pulmonale are distinguished:

bronchopulmonary

thoracodiaphragmatic

vascular

Standards for values \u200b\u200bcharacterizing the hemodynamics of the pulmonary circulation.

The systolic pressure in the pulmonary artery is approximately five times less than the systolic pressure in the systemic circulation.

Pulmonary hypertension is said to be if the systolic pressure in the pulmonary artery at rest is more than 30 mm Hg, the diastolic pressure is more than 15, and the mean pressure is more than 22 mm Hg.

PATHOGENESIS.

Pulmonary hypertension is the cornerstone of the pathogenesis of cor pulmonale. Since cor pulmonale most often develops in bronchopulmonary diseases, we will start with this. All diseases, and in particular chronic obstructive bronchitis, will primarily lead to respiratory (pulmonary) failure. Pulmonary insufficiency is a condition in which the normal gas composition of the blood is disrupted.

This is a state of the body in which either the maintenance of the normal blood gas composition is not ensured, or the latter is achieved by abnormal operation of the external respiration apparatus, leading to a decrease in the functional capabilities of the body.

There are 3 stages of pulmonary failure.

Arterial hypoxemia underlies the pathogenesis underlies in chronic heart disease, especially in chronic obstructive bronchitis.

All of these diseases lead to respiratory failure. Arterial hypoxemia will lead to alveolar hypoxia at the same time due to the development of pneumofibrosis, pulmonary emphysema, and intraalveolar pressure increases. In conditions of arterial hypoxemia, the non-respiratory function of the lungs is disturbed - biological active substances begin to be produced, which have not only bronchospastic, but also vasospastic effect. At the same time, with this, a violation of the vascular architectonics of the lungs occurs - some of the vessels die, some expand, etc. Arterial hypoxemia leads to tissue hypoxia.

The second stage of pathogenesis: arterial hypoxemia will lead to a restructuring of central hemodynamics - in particular, an increase in the amount of circulating blood, polycythemia, polyglobulia, an increase in blood viscosity. Alveolar hypoxia will lead to hypoxemic vasoconstriction by a reflex pathway called the Euler-Liestrand reflex. Alveolar hypoxia led to hypoxemic vasoconstriction, an increase in intra-arterial pressure, which leads to an increase in hydrostatic pressure in the capillaries. Impaired non-respiratory function of the lungs leads to the release of serotonin, histamine, prostaglandins, catecholamines, but the most important thing is that in conditions of tissue and alveolar hypoxia, the interstitium begins to produce more angiotensin-converting enzyme. The lungs are the main organ where this enzyme is produced. It converts angiotensin 1 into angiotensin 2. Hypoxemic vasoconstriction, release of biologically active substances under conditions of restructuring of central hemodynamics will lead not only to an increase in pressure in the pulmonary artery, but to a persistent increase in it (above 30 mm Hg), that is, to the development of pulmonary hypertension. If the processes continue further, if the underlying disease is not treated, then naturally some of the vessels in the pulmonary artery system die due to pneumosclerosis, and the pressure steadily increases in the pulmonary artery. At the same time, persistent secondary pulmonary hypertension will lead to the opening of shunts between the pulmonary artery and bronchial arteries and unoxygenated blood enters the systemic circulation through the bronchial veins and also contributes to an increase in the work of the right ventricle.

So, the third stage is persistent pulmonary hypertension, the development of venous shunts, which enhance the work of the right ventricle. The right ventricle is not powerful by itself, and hypertrophy with dilatation elements rapidly develops in it.

The fourth stage is hypertrophy or dilation of the right ventricle. Dystrophy of the right ventricular myocardium will contribute as well as tissue hypoxia.

So, arterial hypoxemia led to secondary pulmonary hypertension and hypertrophy of the right ventricle, to its dilation and the development of predominantly right ventricular circulatory failure.

Pathogenesis of the development of cor pulmonale in the thoracodiaphragmatic form: in this form, the leading is hypoventilation of the lungs due to kyphoscoliosis, pleural suppuration, spinal deformities, or obesity in which the diaphragm rises high. Hypoventilation of the lungs will primarily lead to a restrictive type of respiratory failure, as opposed to obstructive which is caused in chronic cor pulmonale. And then the mechanism is the same - a restrictive type of respiratory failure will lead to arterial hypoxemia, alveolar hypoxemia, etc.

The pathogenesis of the development of pulmonary heart in vascular form is that with thrombosis of the main branches of the pulmonary arteries, the blood supply to the lung tissue sharply decreases, since along with thrombosis of the main branches, there is a friendly reflex narrowing of small branches. In addition, in the vascular form, in particular in primary pulmonary hypertension, the development of cor pulmonale is facilitated by pronounced humoral changes, that is, a noticeable increase in the amount of sertonin, prostaglandins, catecholamines, the release of convertase, an angiotensin-converting enzyme.

The pathogenesis of cor pulmonale is multi-stage, multi-stage, in some cases not completely clear.

PULMONARY HEART CLASSIFICATION.

There is no single classification of cor pulmonale, but the first international classification is mainly etiological (WHO, 1960):

bronchopulmonary heart

thoracodiaphragmatic

vascular

A domestic classification of cor pulmonale is proposed, which provides for the division of cor pulmonale according to the rate of development:

• subacute

  chronic

Acute cor pulmonale develops within a few hours, minutes, maximum days. Subacute cor pulmonale develops over several weeks or months. Chronic cor pulmonale develops over several years (5-20 years).

This classification provides for compensation, but acute cor pulmonale is always decompensated, that is, requires immediate assistance. Subacute can be compensated and decompensated mainly by the right ventricular type. Chronic cor pulmonale can be compensated, subcompensated, decompensated.

By its genesis, acute cor pulmonale develops in vascular and bronchopulmonary forms. Subacute and chronic cor pulmonale can be vascular, bronchopulmonary, thoracodiaphragmatic.

Acute cor pulmonale develops primarily:

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

with pneumothorax (especially valve),

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

with acute drainage pneumonia

right-sided total pleurisy

A practical example of a subacute pulmonary heart disease is recurrent thrombolism of small branches of the pulmonary arteries, with an attack of bronchial asthma. A classic example is cancerous lymphangitis, especially with chorionepitheliomas, with peripheral lung cancer. The thoracodiphragmatic form develops with hypoventilation of central or peripheral origin - myasthenia gravis, botulism, poliomyelitis, etc.

To distinguish at what stage the cor pulmonale passes from the stage of respiratory failure to the stage of heart failure, another classification was proposed. Cor pulmonale is divided into three stages:

latent latent insufficiency - there is a violation of the function of external respiration - the VC / FVC decreases to 40%, but there are no changes in the gas composition of the blood, that is, this stage characterizes respiratory failure of the 1-2 stage.

stage of severe pulmonary failure - the development of hypoxemia, hypercapnia, but without signs of heart failure in the periphery. There is dyspnea at rest, which cannot be attributed to heart damage.

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

Chronic cor pulmonale in terms of pulmonary insufficiency, arterial oxygen saturation, right ventricular hypertrophy and circulatory failure is divided into 4 stages:

the first stage - pulmonary insufficiency of the 1st degree - VC / CZHL decreases to 20%, the gas composition is not disturbed. Right ventricular hypertrophy is absent on the ECG, but there is hypertrophy on the echocardiogram. There is no circulatory insufficiency at this stage.

pulmonary insufficiency 2 - VC / VC up to 40%, oxygen saturation up to 80%, the first indirect signs of right ventricular hypertrophy appear, circulatory failure +/-, that is, only shortness of breath at rest.

the third stage - pulmonary insufficiency 3 - VC / FVC less than 40%, arterial blood saturation up to 50%, signs of right ventricular hypertrophy appear on the ECG in the form of direct signs. Circulatory insufficiency 2A.

fourth stage - pulmonary insufficiency 3. Blood oxygen saturation less than 50%, right ventricular hypertrophy with dilation, circulatory insufficiency 2B (dystrophic, refractory).

CLINIC OF ACUTE PULMONARY HEART.

The most common cause of development is PE, an acute increase in intrathoracic pressure due to an attack of bronchial asthma. Arterial precapillary hypertension in acute cor pulmonale, as in the vascular form of chronic cor pulmonale, is accompanied by an increase in pulmonary resistance. Next comes the rapid development of right ventricular dilatation. Acute right ventricular failure is manifested by pronounced shortness of breath turning into an inspiratory dyspnea, rapidly growing cyanosis, pain behind the breastbone of a different nature, shock or collapse, rapidly increasing liver size, edema on the legs, ascites, epigastric pulsation, tachycardia (120-140), breathing hard , in some places weakened vesicular; wet, variegated rales are heard especially in the lower parts of the lungs. Of great importance in the development of acute pulmonary heart are additional research methods, especially ECG: a sharp deviation of the electrical axis to the right (R 3\u003e R 2\u003e R 1, S 1\u003e S 2\u003e S 3), P-pulmonale appears - a pointed tooth P, in the second , the third standard leads. The right bundle branch block is complete or incomplete, ST inversion (often ascending), S in the first lead is deep, Q in the third lead is deep. Negative S wave in the second and third leads. The same symptoms may occur in acute myocardial infarction of the posterior wall.

Emergency care depends on the cause of the acute cor pulmonale. If there was PE, then painkillers, fibrinolytic and anticoagulant drugs (heparin, fibrinolysin), streptodecase, streptokinase) are prescribed, up to surgical treatment.

In case of status asthmaticus - large doses of intravenous glucocorticoids, bronchodilators through a bronchoscope, transfer to mechanical ventilation and bronchial lavage. If this is not done, the patient dies.

With valvular pneumothorax - surgical treatment. With drainage pneumonia, along with antibiotic treatment, diuretics and cardiac glycosides are necessarily prescribed.

CLINIC OF CHRONIC PULMONARY HEART.

Patients are worried about shortness of breath, the nature of which depends on the pathological process in the lungs, the type of respiratory failure (obstructive, restrictive, mixed). With obstructive processes, dyspnea of \u200b\u200ban expiratory nature with an unchanged breathing rate, with restrictive processes, the duration of exhalation decreases, and the respiratory rate increases. In an objective study, along with signs of the underlying disease, cyanosis appears, most often diffuse, warm due to the preservation of peripheral blood flow, in contrast to patients with heart failure. In some patients, cyanosis is so pronounced that the skin acquires a cast-iron color. Swollen neck veins, swelling of the lower extremities, ascites. The pulse is speeded up, the borders of the heart expand to the right, and then to the left, the tones are muffled due to emphysema, the accent of the second tone over the pulmonary artery. Systolic murmur at the xiphoid process due to dilation of the right ventricle and relative insufficiency of the right tricuspid valve. In some cases, with severe heart failure, you can listen to a diastolic murmur on the pulmonary artery - the Graham-Still murmur, which is associated with the relative insufficiency of the pulmonary valve. Above the lungs, percussion sound is boxy, vesicular breathing, hard. In the lower parts of the lungs, stagnant, non-sounding moist rales. On palpation of the abdomen - an enlarged liver (one of the reliable, but not early signs of cor pulmonale, since the liver can be displaced due to emphysema). The severity of symptoms depends on the stage.

The first stage: against the background of the underlying disease, shortness of breath increases, cyanosis appears in the form of acrocyanosis, but the right border of the heart is not enlarged, the liver is not enlarged, physical data in the lungs depend on the underlying disease.

The second stage - shortness of breath turns into attacks of suffocation, with difficulty breathing, cyanosis becomes diffuse, from the data of objective research: pulsation appears in the epigastric region, the tones are muffled, the accent of the second tone over the pulmonary artery is not constant. The liver is not enlarged, it can be omitted.

The third stage - signs of right ventricular failure join - an increase in the right border of cardiac dullness, an increase in the size of the liver. Constant edema in the lower limbs.

The fourth stage - shortness of breath at rest, forced position, often accompanied by respiratory rhythm disorders such as Cheyne-Stokes and Biota. Edema is constant, not amenable to treatment, the pulse is weak, fast, bovine heart, muffled tones, systolic murmur at the xiphoid process. There is a mass of moist wheezing in the lungs. The liver is of considerable size, does not contract under the influence of glycosides and diuretics, as fibrosis develops. Patients are constantly asleep.

Diagnostics of the thoracodiaphragmatic heart is often difficult, one must always remember about the possibility of its development in kyphoscoliosis, ankylosing spondylitis, etc. The most important symptom is the early appearance of cyanosis, and a noticeable increase in shortness of breath without asthma attacks. Pickwick's syndrome is characterized by a triad of symptoms - obesity, drowsiness, severe cyanosis. This syndrome was first described by Dickens in the Posthumous Papers of the Pickwick Club. It is associated with traumatic brain injury, obesity is accompanied by thirst, bulimia, arterial hypertension. Diabetes mellitus often develops.

Chronic cor pulmonale in primary pulmonary hypertension is called Aerza's disease (described in 1901). A polyetiological disease, of unknown origin, mainly affects women from 20 to 40 years old. Pathomorphological studies have established that in primary pulmonary hypertension, the intima of the precapillary arteries thickens, that is, thickening of the media is noted in the arteries of the muscle type, and fibrinoid necrosis develops, followed by sclerosis and the rapid development of pulmonary hypertension. Symptoms are varied, usually complaints of weakness, fatigue, pain in the heart or in the joints, 1/3 of patients may experience fainting, dizziness, Raynaud's syndrome. And in the future, shortness of breath increases, which is the sign that indicates that primary pulmonary hypertension passes into a stable final stage. Cyanosis rapidly grows, which is expressed to the degree of a cast-iron shade, becomes permanent, swelling rapidly increases. The diagnosis of primary pulmonary hypertension is established by exclusion. Most often, this diagnosis is pathological. In these patients, the entire clinic progresses without a background in the form of obstructive or restrictive breathing disorders. With echocardiography, the pressure in the pulmonary artery reaches its maximum values. Treatment is ineffective, death occurs from thromboembolism.

Additional research methods for pulmonary heart: in a chronic process in the lungs - leukocytosis, an increase in the number of red blood cells (polycythemia associated with increased erythropoiesis due to arterial hypoxemia). X-ray data: appear very late. One of the early symptoms is a bulging of the pulmonary artery trunk on radiographs. The pulmonary artery is bulging, often flattening the waist of the heart, and many doctors mistake this heart for a mitral configuration of the heart.

ECG: there are indirect and direct signs of right ventricular hypertrophy:

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

direct signs - blockade of the right bundle of His bundle, the amplitude of the R wave in V 1 more than 10 mm with complete blockade of the right bundle of His bundle. The appearance of a negative T wave with a displacement of the wave below the isoline in the third, second standard lead, V1-V3.

Of great importance is spirography, which reveals the type and degree of respiratory failure. On ECG, signs of right ventricular hypertrophy appear very late, and if only deviations of the electrical axis to the right appear, then they already speak of pronounced hypertrophy. The most basic diagnostics is Doppler cardiography, echocardiography - an increase in the right heart, increased pressure in the pulmonary artery.

PRINCIPLES OF PULMONARY HEART TREATMENT.

Treatment of cor pulmonale consists in treating the underlying disease. With exacerbation of obstructive diseases, bronchodilators, expectorants are prescribed. With Pickwick's syndrome - obesity treatment, etc.

Reduce the pressure in the pulmonary artery with calcium antagonists (nifedipine, verapamil), peripheral vasodilators that reduce preload (nitrates, corvaton, sodium nitroprusside). Of greatest importance is sodium nitroprusside in combination with angiotensin-converting enzyme inhibitors. Nitroprusside 50-100 mg intravenously, kapoten 25 mg 2-3 times a day, or enalapril (second generation, 10 mg per day). They also use treatment with prostaglandin E, antiserotonin drugs, etc. But all these drugs are effective only at the very beginning of the disease.

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

Anticoagulant, antiaggregant therapy - heparin, trental, etc. Due to tissue hypoxia, myocardial dystrophy develops rapidly, so cardioprotectors (potassium orotate, panangin, riboxin) are prescribed. Cardiac glycosides are prescribed very carefully.

PREVENTION.

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

Today, cardiac pathologies are quite common. This negatively affects the state of human health. When heart disease occurs against the background of damage to the lungs and their vessels, it is customary to talk about pulmonary heart.

What is this anomaly, what are its causes, development and symptoms? How is the abnormality classified and also treated depending on the diagnostic results? In this article we will try to figure it out.

Cor pulmonale is not an independent disease. This is a symptom complex that occurs due to pulmonary thromboembolism, diseases of the cardiovascular system or respiratory system. It is characterized by:

• significant increase and expansion of the right atrium and ventricle;
• deterioration in the supply of blood to the heart due to increased pressure in the pulmonary circulation.

Another feature of the pathology is that it is always associated with anomalies of the respiratory system (lungs, bronchi, pulmonary arteries). Also, its occurrence is observed against the background of deformation of the chest, which affects pulmonary activity.

Pathology is acute or chronic. The acute course is characterized by the development of symptoms in a matter of hours. The chronic form begins imperceptibly and develops over several months or years. Such an anomaly significantly aggravates diseases of the cardiovascular system. This increases the risk of death.

Why and how is it developing?

The causes of pathology are different. Depending on which group of diseases provoked the deviation, the following forms of deviation are distinguished:

The most common cause of the abnormality is thromboembolism. This causes a blood clot to block the artery that feeds the lungs. Thromboembolism develops when:

Cor pulmonale develops, usually due to an increase in blood pressure in the lungs. In this case, there is a narrowing of the pulmonary vessels, which provokes bronchospasm. There is a sharp decrease in pressure in the systemic circulation and, as a result, a deterioration in gas exchange and ventilation.

Cardiac departments are overloaded and gradually increase due to stagnation of blood in them. The vessels begin to become sclerosed, small blood clots appear in them. This leads to dystrophy of the muscles of the heart and necrotic processes. In severe cases, the blood begins to press on the surrounding tissues and vessels, which allow fluid to pass into the alveoli, which provokes pulmonary edema.

Deviation classification

The classification of the deviation is related to the rate of occurrence of clinical signs. At the same time, the following types of flow are distinguished:

• chronic;
• subacute;
• spicy.

The acute form of pathology occurs against the background of severe lesions of the respiratory organs. It is developing very rapidly. The first signs are observed within a few minutes or hours after lung damage (for example, a severe attack of bronchial asthma). This form is quite difficult, since the patient's well-being is constantly deteriorating.

The subacute course is a transitional phase when the symptoms of the acute form subside. The subacute form often turns into a chronic one, which develops over many months and even years. It has the following stages:

In addition to the described forms, according to the intensity of development of the clinic, types are distinguished depending on the etiology. These are bronchopulmonary, thoraco-diaphragmatic and vascular. We examined them in detail in the previous section.

Symptoms

The manifestations of pathology largely depend on the stage of its development and etiological form. So for the acute phase it is characteristic:

With pulmonary embolism, pulmonary edema and severe disruption of the cardiovascular system also occur. In this case, the patient may be in a state of shock. If he is not helped in time, then necrosis (infarction) of the lungs develops, which often leads to death. How do you recognize this anomaly? Pulmonary infarction has specific symptoms:

• sensation of pain when inhaling;
• cyanosis (blue discoloration) of the skin;
• dry cough, sometimes with hemoptysis;
• high body temperature (it cannot be brought down with antibiotics);
• weak breathing.

Subacute course of drugs

Symptomatic manifestations of the chronic form of pulmonary heart disease depend on the stage of the disorder. For a compensated one, the prevalence of signs of the pathology that provoked the anomaly is characteristic. Symptoms of an enlarged right ventricle (heart pain, cyanosis of the skin, high blood pressure) develop much later.

With the decompensated stage, cardiopulmonary failure develops. In this case, there is:

Also, this stage is characterized by the addition of disturbances in the activity of the central nervous system. This is manifested by headaches, fainting, drowsiness, apathy, loss of working capacity.

Diagnostic manipulations

If unpleasant symptoms appear, you should seek the advice of a cardiologist or pulmonologist. First of all, the patient is examined and interviewed, as well as anamnesis is collected. To make a diagnosis and identify the cause of the pathology, additional research methods may be prescribed:

After the diagnosis is made and the severity of the pathology is determined, appropriate treatment is prescribed. As a rule, it is carried out in a hospital setting.

Therapeutic manipulations and prognosis

First of all, pathology therapy should eliminate the underlying disease. For this purpose, the following medications may be prescribed:

Also, treatment includes getting rid of the patient from unpleasant symptoms - cough, high fever, thrombus formation, pain. In this case, the following medications are taken:

• anticoagulants (Clopidogrel, Plavix);
• mucolytics (to thin phlegm when coughing): Mukaltin, Bromhexin;
• antipyretic (Paracetamol, Nimid);
• diuretics (to relieve edema): Spironolactone, Furosemide;
• inotropes (to improve the contractile activity of the heart muscle): Adrenaline, Dopamine;
• painkillers and other drugs (Analgin, Solpadein).

It is important to remember that an acute phase or an advanced course of deviation can cause cardiac arrest and breathing problems.

Therefore, if there are clear signs of deterioration, an ambulance should be called. Before her arrival, the patient undergoes resuscitation actions - indirect heart massage and artificial respiration.

The prognosis depends on the severity of the underlying disease, as well as on the course of the pathology. As a rule, complete recovery does not occur, even if treatment is started in a timely manner. But with the right lifestyle and constant observation, with this anomaly they live for 5 years, and sometimes more.

Prevention

Prevention consists in treating the disease that can provoke the development of the anomaly. It is also important to lead a healthy lifestyle:

Such beneficial actions contribute to the overall strengthening of the body. This improves respiratory and cardiac functionality.

Pulmonary heart syndrome is a symptom complex, which is characterized by the presence of heart problems against the background of damage to the respiratory system. It can occur in acute, subacute and chronic forms. Therapy is aimed at eliminating the underlying disease and reducing symptomatic manifestations and allows you to completely cope with the pathology.

Increased pressure in the pulmonary capillary system (pulmonary hypertension, hypertension) is most often a secondary disease that is not directly related to vascular lesions. The primary conditions are not well understood, but the role of the vasoconstrictor mechanism, thickening of the arterial wall, fibrosis (tissue compaction) has been proven.

In accordance with ICD-10 (International Classification of Diseases), only the primary form of pathology is coded as I27.0. All secondary signs are attached as complications to the underlying chronic disease.

Some features of the blood supply to the lungs

The lungs have a doubled blood supply: a system of arterioles, capillaries and venules is included in the gas exchange. And the tissue itself receives nutrition from the bronchial arteries.

The pulmonary artery is divided into the right and left trunks, then into branches and lobar vessels of large, medium and small caliber. The smallest arterioles (part of the capillary network) have a diameter 6–7 times larger than in the systemic circulation. Their powerful muscles are capable of narrowing, completely closing or expanding the arterial bed.

With constriction, resistance to blood flow increases and internal pressure in the vessels increases, expansion reduces pressure, reduces the force of resistance. The occurrence of pulmonary hypertension depends on this mechanism. The total network of pulmonary capillaries covers an area of \u200b\u200b140 m2.

The veins of the pulmonary circle are wider and shorter than in the peripheral circulation. But they also have a strong muscle layer, capable of influencing the pumping of blood towards the left atrium.

How is the pressure in the pulmonary vessels regulated?

The value of blood pressure in the pulmonary vessels is regulated:

• pressor receptors in the vascular wall;
• branches of the vagus nerve;
• sympathetic nerve.

Extensive receptor zones are located in large and medium arteries, in places of branching, in veins. Spasm of the arteries leads to impaired blood oxygen saturation. And tissue hypoxia promotes the release into the blood of substances that increase tone and cause pulmonary hypertension.

Irritation of the vagus nerve fibers increases blood flow through the lung tissue. The sympathetic nerve, on the other hand, causes a vasoconstrictor effect. Under normal conditions, their interaction is balanced.

The indicators of pressure in the pulmonary artery are taken as the norm:

• systolic (upper level) - from 23 to 26 mm Hg;
• diastolic - from 7 to 9.

Pulmonary arterial hypertension, according to international experts, starts from the upper level - 30 mm Hg. Art.

Factors causing hypertension in a small circle

The main factors of pathology, according to the classification of V. Parin, are divided into 2 subspecies. Functional factors include:

• constriction of arterioles in response to low oxygen and high concentration of carbon dioxide in the inhaled air;
• an increase in the minute volume of passing blood;
• increased intrabronchial pressure;
• increased blood viscosity;
• failure of the left ventricle.

Anatomical factors include:

• complete obliteration (overlap of the lumen) of the vessels with a thrombus or embolus;
• impaired outflow from the zonal veins due to their compression in aneurysm, tumor, mitral stenosis;
• changes in blood circulation after removal of the lung by surgery.

What are the causes of secondary pulmonary hypertension?

Secondary pulmonary hypertension occurs due to known chronic diseases of the lungs and heart. These include:

• chronic inflammatory diseases of the bronchi and lung tissue (pneumosclerosis, emphysema, tuberculosis, sarcoidosis);
• thoracogenic pathology in violation of the structure of the chest and spine (ankylosing spondylitis, consequences of thoracoplasty, kyphoscoliosis, Pickwick's syndrome in obese people);
• mitral stenosis;
• congenital heart defects (for example, non-closure of the Botallov's duct, “windows” in the atrial and interventricular septum);
• tumors of the heart and lungs;
• diseases accompanied by thromboembolism;
• vasculitis in the area of \u200b\u200bthe pulmonary artery.

What causes primary hypertension?

Primary pulmonary hypertension is also called idiopathic, isolated. The prevalence of pathology is 2 people per 1 million inhabitants. The final reasons remain unclear.

It has been established that women make up 60% of patients. Pathology is found both in childhood and in old age, but the average age of the identified patients is 35 years.

In the development of pathology, 4 factors are important:

• primary atherosclerotic process in the pulmonary artery;
• congenital inferiority of the wall of small vessels;
• increased tone of the sympathetic nerve;
• vasculitis of the pulmonary vessels.

The role of the mutating gene of bone protein, angioproteins, their influence on the synthesis of serotonin, increased blood clotting due to the blocking of anticoagulant factors has been established.

A special role is given to infection with the herpes simplex virus of the eighth type, which causes metabolic changes leading to the destruction of the walls of the arteries.

The result is hypertrophy, then expansion of the cavity, loss of tone of the right ventricle and the development of failure.

Other causes and factors of hypertension

There are many causes and lesions that can cause hypertension in the pulmonary circle. Some of them need to be highlighted.

Among acute diseases:

• respiratory distress syndrome in adults and newborns (toxic or autoimmune damage to the membranes of the respiratory lobules of the lung tissue, causing a lack of a surfactant substance on its surface);
• severe diffuse inflammation (pneumonitis) associated with the development of a massive allergic reaction to inhaled odors of paint, perfume, flowers.

In this case, pulmonary hypertension can be caused by food, drugs and folk remedies.

Pulmonary hypertension in newborns can be caused by:

• persistent fetal circulation;
• aspiration of meconium;
• diaphragmatic hernia;
• general hypoxia.

In children, enlarged palatine tonsils contribute to hypertension.

Classification by the nature of the flow

It is convenient for clinicians to divide hypertension in the pulmonary vessels by the timing of development into acute and chronic forms. This classification helps to "combine" the most common causes and clinical course.

Acute hypertension occurs due to:

• pulmonary embolism;
• pronounced asthmatic status;
• respiratory distress syndrome;
• sudden left ventricular failure (due to myocardial infarction, hypertensive crisis).

The chronic course of pulmonary hypertension is caused by:

• increased pulmonary blood flow;
• increased resistance in small vessels;
• increased pressure in the left atrium.

A similar development mechanism is typical for:

• defects of the interventricular and interatrial septum;
• patent ductus arteriosus;
• mitral valve disease;
• overgrowth of myxoma or thrombus in the left atrium;
• gradual decompensation of chronic left ventricular failure, for example, with ischemic disease or cardiomyopathies.

Diseases lead to chronic pulmonary hypertension:

• hypoxic nature - all obstructive diseases of the bronchi and lungs, prolonged oxygen deficiency at altitude, hypoventilation syndrome associated with chest wounds, apparatus breathing;
• mechanical (obstructive) origin, associated with narrowing of the arteries - a reaction to drugs, all variants of primary pulmonary hypertension, recurrent thromboembolism, connective tissue diseases, vasculitis.

Clinical picture

Symptoms of pulmonary hypertension appear if the pressure in the pulmonary artery is increased by 2 times or more. Patients with hypertension in the pulmonary circle notice:

• shortness of breath, aggravated by physical exertion (may develop paroxysmal);
• general weakness;
• rarely loss of consciousness (in contrast to neurological causes without convulsions and involuntary urination);
• paroxysmal chest pain, similar to angina pectoris, but accompanied by an increase in shortness of breath (scientists explain them by a reflex connection of the pulmonary and coronary vessels);
• an admixture of blood in sputum when coughing is characteristic of a significantly increased pressure (associated with the release of erythrocytes into the interstitial space);
• hoarseness of the voice is determined in 8% of patients (caused by mechanical compression of the dilated pulmonary artery of the recurrent nerve on the left).

The development of decompensation as a result of pulmonary heart failure is accompanied by pain in the right hypochondrium (stretching of the liver), edema in the feet and legs.

When examining a patient, the doctor pays attention to the following:

• blue tint of the lips, fingers, ears, which increases as the shortness of breath worsens;
• the symptom of "drum" fingers is detected only with prolonged inflammatory diseases, defects;
• the pulse is weak, arrhythmias are rare;
• blood pressure is normal, with a tendency to decrease;
• palpation in the epigastric zone allows you to determine the increased tremors of the hypertrophied right ventricle;
• an accentuating second tone on the pulmonary artery is auscultated, diastolic murmur is possible.

The connection of pulmonary hypertension with permanent causes and certain diseases makes it possible to identify variants in the clinical course.

Portopulmonary hypertension

Pulmonary hypertension leads to a simultaneous increase in pressure in the portal vein. In this case, the patient may have cirrhosis of the liver or not. It accompanies chronic liver disease in 3–12% of cases. The symptoms are the same as those listed. Swelling and heaviness in the hypochondrium on the right are more pronounced.

Pulmonary hypertension with mitral stenosis and atherosclerosis

The disease is characterized by the severity of the course. Mitral stenosis contributes to the occurrence of atherosclerotic lesions of the pulmonary artery in 40% of patients due to increased pressure on the vessel wall. The functional and organic mechanisms of hypertension are combined.

The narrowed left atrioventricular passage in the heart is the “first barrier” to blood flow. In the presence of narrowing or blockage of small vessels, a "second barrier" is formed. This explains the ineffectiveness of surgery to eliminate stenosis in the treatment of heart disease.

By catheterization of the heart chambers, high pressure inside the pulmonary artery (150 mm Hg and above) is detected.

Vascular changes progress and become irreversible. Atherosclerotic plaques do not grow to large sizes, but they are sufficient for narrowing of small branches.

Pulmonary heart

The term cor pulmonale includes a symptom complex caused by damage to the lung tissue (pulmonary form) or pulmonary artery (vascular form).

There are flow options:

1. acute - typical for pulmonary embolization;
2. subacute - develops with bronchial asthma, lung carcinomatosis;
3. chronic - caused by emphysema, functional spasm of the arteries, turning into an organic narrowing of the bed, characteristic of chronic bronchitis, pulmonary tuberculosis, bronchiectasis, frequent pneumonia.

The increase in resistance in the vessels gives a pronounced load on the right heart. The general lack of oxygen also affects the myocardium. The thickness of the right ventricle increases with the transition to dystrophy and dilatation (persistent expansion of the cavity). The clinical signs of pulmonary hypertension gradually increase.

Hypertensive crises in the vessels of the "small circle"

The crisis course often accompanies pulmonary hypertension associated with heart defects. A sharp deterioration in the condition due to a sudden increase in pressure in the pulmonary vessels is possible once a month or more often.

Patients note:

• increased shortness of breath in the evening;
• a feeling of external compression of the chest;
• severe cough, sometimes with hemoptysis;
• pain in the interscapular region with irradiation to the anterior sections and sternum;
• cardiopalmus.

The examination reveals:

• agitated state of the patient;
• inability to lie in bed due to shortness of breath;
• severe cyanosis;
• weak, fast pulse;
• visible pulsation in the pulmonary artery;
• swollen and throbbing neck veins;
• the release of copious amounts of light urine;
• involuntary defecation is possible.

Diagnostics

Diagnosis of hypertension in the pulmonary circulation is based on the identification of its signs. These include:

• hypertrophy of the right heart;
• determination of increased pressure in the pulmonary artery according to the results of measurements using catheterization.

Russian scientists F. Uglov and A. Popov proposed to distinguish between 4 elevated levels of hypertension in the pulmonary artery:

• I degree (mild) - from 25 to 40 mm Hg. Art .;
• II degree (moderate) - from 42 to 65;
• III - from 76 to 110;
• IV - above 110.

Examination methods used in the diagnosis of right heart chambers hypertrophy:

1. Radiography - indicates the expansion of the right borders of the heart shadow, an increase in the arch of the pulmonary artery, reveals its aneurysm.
2. Ultrasound methods (ultrasound) - allow you to accurately determine the size of the heart chambers, the thickness of the walls. A type of ultrasound - Doppler ultrasound - shows a violation of blood flow, flow rate, the presence of obstacles.
3. Electrocardiography - reveals early signs of right ventricular and atrial hypertrophy by characteristic deviation of the electrical axis to the right, enlarged atrial "P" wave.
4. Spirography is a method for studying the possibility of breathing, establishes the degree and type of respiratory failure.
5. In order to detect the causes of pulmonary hypertension, pulmonary tomography is performed using X-ray sections of different depths or, in a more modern way, computed tomography.

More complex methods (radionuclide scintigraphy, angiopulmonography). Biopsy to study the condition of the lung tissue and vascular changes is used only in specialized clinics.

When catheterizing the cavities of the heart, not only the pressure is measured, but also the blood oxygen saturation is measured. This helps in identifying the causes of secondary hypertension. During the procedure, they resort to the introduction of vasodilators and check the reaction of the arteries, which is necessary in the choice of treatment.

How is the treatment carried out?

Treatment of pulmonary hypertension is aimed at excluding the underlying pathology that caused the increase in pressure.

At the initial stage, anti-asthma drugs, vasodilator drugs provide help. Folk remedies can further enhance the allergic mood of the body.

If the patient is diagnosed with chronic embolization, then the only remedy is the surgical removal of the thrombus (embolectomy) by excising it from the pulmonary trunk. The operation is carried out in specialized centers, it is necessary to switch to artificial circulation. The mortality rate reaches 10%.

Primary pulmonary hypertension is treated with calcium channel blockers. Their effectiveness leads to a decrease in pressure in the pulmonary arteries in 10-15% of patients, accompanied by a good response from critically ill patients. This is considered an auspicious sign.

An analogue of Prostacyclin - Epoprostenol is injected intravenously through a subclavian catheter. Inhalation forms of medicines (Iloprost), Beraprost tablets inside are used. The effect of subcutaneous administration of a drug such as Treprostinil is being studied.

Bosentan is used to block receptors that cause vasospasm.

At the same time, patients need drugs to compensate for heart failure, diuretics, anticoagulants.

A temporary effect is provided by the use of solutions of Euphyllin, No-shpy.

Are there folk remedies?

It is impossible to cure pulmonary hypertension with folk remedies. Recommendations on the use of diuretic preparations, agents for soothing coughs are very carefully applied.

Do not get involved in healing with this pathology. Lost time in diagnostics and initiation of therapy can be lost forever.

Forecast

Without treatment, the average survival of patients is 2.5 years. Epoprostenol treatment extends the period to five years in 54% of patients. The prognosis of pulmonary hypertension is poor. Patients die from progressive right ventricular failure or thromboembolism.

Patients with pulmonary hypertension associated with heart disease and arterial sclerosis live up to 32–35 years of age. The crisis course aggravates the patient's condition, is regarded as a poor prognosis.

The complexity of the pathology requires maximum attention to cases of frequent pneumonia, bronchitis. Prevention of pulmonary hypertension consists in preventing the development of pneumosclerosis, emphysema, early detection and surgical treatment of congenital defects.

Clinical picture, diagnosis and treatment of rheumatic heart disease

Rheumatic heart disease is an acquired pathology. It is usually classified as a vascular disease in which damage is directed against the tissues of the heart, causing malformations. At the same time, the joints and nerve fibers are affected in the body.

The inflammatory response is triggered predominantly by group A hemolytic streptococcus, which causes upper respiratory tract disease (angina). Mortality and hemodynamic disturbances occur due to damage to the heart valves. Most often, chronic rheumatic processes cause damage to the mitral valve, less often to the aortic valve.

Mitral valve lesions

Acute rheumatic fever leads to the development of mitral stenosis 3 years after the development of the disease. It has been established that every fourth patient with rheumatic heart disease has isolated mitral stenosis. In 40% of cases, a combined valve lesion develops. According to statistics, mitral stenosis is more common in women.

Inflammation leads to damage to the edge of the valve leaflets. After an acute period, thickening and fibrosis of the edges of the valves occurs. When the tendon cords and muscles are involved in the inflammatory process, their shortening and scarring occurs. As a result, fibrosis and calcification lead to changes in the structure of the valve, which becomes rigid and immobile.

Rheumatic lesions lead to a halving of the valve opening. Now, in order to push blood through the narrow opening from the left atrium into the left ventricle, a higher pressure is needed. Increased pressure in the left atrium leads to "jamming" in the pulmonary capillaries. Clinically, this process is manifested by dyspnea on exertion.

Patients with such a pathology very poorly tolerate increased heart rate. Functional mitral valve failure can cause fibrillation and pulmonary edema. This development of events can occur in patients who have never noticed the symptoms of the disease.

Clinical features

Rheumatic heart disease with mitral valve damage manifests itself in patients with symptoms:

• dyspnea;
• cough and wheezing during an attack.

At the beginning of the disease, the patient may not pay attention to the symptoms, since they do not have a pronounced manifestation. Only during stress are pathological processes exacerbated. As the disease progresses, the patient is unable to breathe normally while lying down (orthopnea). Only by taking a forced sitting position, the patient breathes. In some cases, severe shortness of breath occurs at night with attacks of suffocation, which forces the patient to sit in a sitting position.

Patients can withstand moderate stress. However, they have a risk of pulmonary edema, which can be triggered by:

• pneumonia;
• stress;
• pregnancy;
• sexual intercourse;
• atrial fibrillation.

With a coughing fit, hemoptysis may occur. The causes of complications are associated with the rupture of the bronchial veins. Such profuse bleeding is rarely life-threatening. Blood-stained phlegm may appear during suffocation. With a long course of the disease, against the background of heart failure, a lung infarction may occur.

Thromboembolism is life threatening. During atrial fibrillation, a detached blood clot can enter the kidneys, arteries of the heart, the area of \u200b\u200bthe aortic bifurcation, or the brain with blood flow.

Symptoms include:

• chest pain;
• hoarseness (with compression of the laryngeal nerve);
• ascites;
• enlarged liver;
• swelling.

Diagnostics

In order to make a diagnosis, a number of examinations are carried out. The doctor examines the pulse, pressure, interrogates the patient. In the case when pulmonary hypertension has not yet developed, the pulse and pressure are normal. In severe pulmonary hypertension, the heart rate changes. During auscultation, changes in heart sounds are detected, and the severity of stenosis is assessed.

Instrumental survey methods include:

1. Chest X-ray.
2. Echocardiography.
3. Doppler ultrasonography.
4. Cardiac catheterization.
5. Coronary angiography.

ECG is one of the least sensitive research methods, which allows to detect signs only in the presence of a severe degree of stenosis. Radiography allows you to assess the degree of enlargement of the left atrium. Echocardiography confirms the diagnosis. The method evaluates the thickening, calcification and mobility of the valve leaflets.

Doppler ultrasonography detects the severity of stenosis and blood flow velocity. If the patient is planning to undergo surgery for valve replacement, cardiac catheterization is included in the examination.

Treatment

Chronic rheumatic heart disease is treated conservatively and promptly. Conservative treatment includes:

• Lifestyle changes.
• Prevention of recurrence of rheumatic fever.
• Antibiotic therapy for endocarditis (if any).
• Anticoagulant administration (Warfarin).
• Diuretics (Furosemide, Lasix, etc.).
• Nitrates (when there is chronic valve failure).
• Beta blockers.

The choice of surgery depends on the severity of the patient's condition. To alleviate the condition, carry out:

• closed or open mitral commissurotomy (separation of the valve leaflets, cleansing them from calcifications and blood clots during surgery);
• mitral valve replacement;
• percutaneous balloon valvuloplasty.

Balloon repair is performed on patients whose valve cusps are flexible and mobile enough. The catheter is inserted through the femoral vein into the atrial septum. Place the balloon at the site of the hole stenosis and inflate. Thanks to this procedure, stenosis is reduced. The operation allows you to delay valve replacement. The risk of balloon plastic surgery is minimal, which allows women who are expecting a baby to be operated on.

If the patient has a severe degree of calcification, pronounced valve changes, valve replacement surgery is indicated. It should be borne in mind that rheumatic processes in the heart will sooner or later lead to serious consequences. Medicines only provide temporary relief. After valve replacement, anticoagulant therapy (warfarin) under clotting control is important. With inadequate therapy after prosthetics, the risk of thromboembolism is possible.

Doctors cannot predict the exact time of development of stenosis. With successful prevention of rheumatic fever and commissurotomy, patients can live for a long time without signs of valve stenosis.

Rheumatic aortic valve disease

In rare cases, rheumatic heart disease can lead to aortic stenosis. Rarely is this pathology isolated. In most cases, a combined lesion of the valves is detected. Damage to the leaflets leads to fibrosis, rigidity and severe stenosis.

With attacks of rheumatism, valvulitis (inflammation of the valves) develops. This leads to adhesion of the edges of the valve leaflets, scarring, thickening and shortening of the leaflets. As a result, the normal tricuspid valve becomes fused, with a small opening.

In patients with chronic processes, adaptation to pathological changes occurs. Myocardial hypertrophy maintains cardiac output for a long time without the onset of symptoms and valve dilatation. The disease is characterized by a prolonged asymptomatic period. The patient may complain of angina attacks after exertion.

Rheumatic inflammation of the valve can lead to sagging of the leaflets. As a result of prolapse, blood from the aorta is pumped into the left ventricle. The patient develops heart failure. Complete exhaustion of the heart occurs 15 years after the development of the disease.

The development of pathology leads to shortness of breath, dizziness, suffocation when lying down (orthopnea). During the examination, the doctor reveals a pulse of low filling, a violation of heart sounds, a rough systolic ejection murmur into the aorta. Additionally, the doctor prescribes an EchoCG.

Treatment includes:

• prevention of infective endocarditis;
• prevention of rheumatic attacks;
• lifestyle change;
• correction of physical activity.

To stop the attacks of angina pectoris, patients are prescribed long-acting nitrates. Treatment includes the appointment of cardiac glycosides and diuretics. The progression of the disease worsens the prognosis, therefore, valve replacement is indicated for patients at a late stage of valvular stenosis, since treatment with drugs does not provide improvement.

Prevention

Chronic rheumatic pathology is prevented by timely treatment of laryngitis, pharyngitis caused by hemolytic streptococcus A. Diseases are treated with antibiotics of the penicillin series or erythromycin in case of allergy to penicillins.

Secondary prevention is to prevent rheumatic attacks and fever. Patients are prescribed antibiotics on an individual basis. With signs of carditis, patients continue to receive a course of antibiotic treatment for ten years after rheumatic fever. It should be noted that neglect of primary prevention leads to the risk of developing malformations after rheumatism. Conservative treatment of defects helps to slow down the progression of pathology and increases patient survival.

Signs, degrees and treatment of pulmonary hypertension

Pulmonary hypertension is a pathology in which a persistent increase in blood pressure is observed in the vascular bed of an artery. This disease is considered progressive, and eventually leads to the death of a person. The symptoms of pulmonary hypertension manifest themselves depending on the severity of the disease. It is very important to identify it in time and start timely treatment.

• Causes
• Classification
• Primary pulmonary hypertension
• Secondary hypertension
• Symptoms
• Diagnostics
• Treatment
• Effects
• Prevention

This ailment sometimes occurs in children. With pulmonary hypertension in newborns, there is no possibility of pulmonary circulation to maintain or reduce the already reduced vascular resistance of the lungs at birth. Usually this condition is observed in post-term or premature babies.

Causes

There are many reasons and risk factors leading to the disease. The main ailments against which the syndrome develops are lung diseases. Most often, they are bronchopulmonary diseases, in which the structure of the lung tissue is disturbed and alveolar hypoxia occurs. In addition, the disease can develop against the background of other diseases of the pulmonary system:

• Bronchiectasis. The main symptom of this disease is considered to be the formation of cavities in the lower part of the lungs and suppuration.
• Obstructive chronic bronchitis. In this case, the lung tissue gradually changes, and the airways are closed.
• Fibrosis of the lung tissue. This condition is characterized by a change in lung tissue when connective tissue replaces normal cells.

Normal lung and bronchiectasis

The causes of pulmonary hypertension can also lie in heart disease. Among them, importance is attached to congenital malformations, such as open ductus botalis, septal defects and an open oval window. A prerequisite may be diseases in which the functional capabilities of the heart muscle are disturbed, contributing to blood stasis in the small circle of blood circulation. Such ailments include cardiomyopathy, coronary artery disease and hypertension.

There are several ways in which pulmonary arterial hypertension develops:

1. Alveolar hypoxia is the main cause of the development of the disease. With it, the alveoli receive an insufficient amount of oxygen. This is observed with uneven pulmonary ventilation, which gradually increases. If a reduced amount of oxygen enters the lung tissue, the vessels of the bloodstream of the pulmonary system narrow.
2. Changes in the structure of lung tissue when connective tissue grows.
3. An increase in the number of red blood cells. This condition is due to constant hypoxia and tachycardia. Microthrombi appear as a result of vasospasm and increased adhesion of blood cells. They block the lumen of the pulmonary vessels.

Primary pulmonary hypertension in children develops for unknown reasons. Diagnostics of children showed that the basis of the disease is neurohumoral instability, hereditary predisposition, pathology of the homeostasis system and vascular lesions of the pulmonary circulation of an autoimmune nature.

Several other factors may contribute to the development of pulmonary hypertension. This can be the intake of certain drugs that affect the lung tissue: antidepressants, cocaine, amphetamines, anorexigens. Toxins can also affect the development of the disease. These include poisons of biological origin. There are certain demographic and medical factors that can lead to the onset of hypertension. These include pregnancy, female sex, hypertension. Liver cirrhosis, HIV infections, blood diseases, hyperthyroidism, hereditary ailments, portal hypertension, and other rare diseases can help develop pulmonary hypertension. Compression of the pulmonary vessels by a tumor, the consequences of obesity and a deformed chest cell, as well as rise in the highlands, can have an effect.

Classification

There are two important forms of the disease, primary and secondary.

Primary pulmonary hypertension

With this form, a persistent increase in pressure in the artery is observed, however, not against the background of diseases of the cardiovascular and respiratory systems. There is no thoraco-diaphragmatic pathology. This type of disease is considered hereditary. It is usually transmitted in an autosomal recessive manner. Sometimes development occurs in a dominant manner.

A prerequisite for the development of this form can be a strong platelet aggregation activity. This leads to the fact that a large number of small vessels located in the circulatory pulmonary system are clogged with blood clots. Because of this, there is a sharp increase in the intravascular pressure in the system, which acts on the walls of the artery of the lungs. In order to cope with this and push the required amount of blood further, the muscular part of the arterial wall is enlarged. This is how her compensatory hypertrophy develops.

Primary hypertension can develop against a background of concentric pulmonary artery fibrosis. This leads to a narrowing of its lumen and an increase in the pressure of the blood flow. As a result of this, and also due to the inability of healthy pulmonary vessels to support the advancement of blood with high pressure or the inability of altered vessels to maintain the advancement of blood with normal pressure, a compensatory mechanism develops. It is based on the emergence of detours, which are open arteriovenous shunts. The body tries to lower the high pressure level by transferring blood through them. However, the muscle wall in arterioles is weak, so shunts quickly fail. This creates areas that also increase the pressure value. Shunts disrupt the correct blood flow, which leads to disruption of the processes of blood oxygenation and oxygen supply to tissues. Despite the knowledge of all these factors, primary pulmonary hypertension is still poorly understood.

Secondary hypertension

The course of this type of disease is slightly different. It is caused by many diseases - hypoxic conditions, congenital heart defects, and so on. Cardiac diseases that contribute to the development of the secondary form:

• Diseases that cause LV failure. The ailments that are the root cause of hypertension and accompany the diseases of this group include: ischemic myocardial damage, aortic valve defects, myocardial and cardiomyopathic LV injuries.
• Diseases leading to an increase in pressure in the left atrial chamber: developmental abnormalities, tumor lesions of the atrium and mitral stenosis.

The development of pulmonary hypertension can be divided into two links:

• Functional mechanisms. Their development is due to the violation of normal and or the formation of new functional pathological features. Drug therapy is aimed specifically at their correction and elimination. The functional links include an increase in blood volume per minute, an increase in blood viscosity, Savitsky's pathological reflex, the effect of frequent infections of a bronchopulmonary nature and the effect of biologically active elements on the artery.
• Anatomical mechanisms. Their occurrence is preceded by certain anatomical defects in the artery of the lungs or the pulmonary circulatory system. In this case, drug therapy does not bring almost any benefit. Some defects can be repaired with surgery.

Depending on the severity of hypertension, four degrees are distinguished.

1. Pulmonary hypertension 1 degree. This form proceeds without disturbing the activity of the physical plane. Normal exercise does not lead to shortness of breath, dizziness, weakness, or chest pain.
2. 2nd degree. The disease causes a slight disruption of activity. The habitual exercise is accompanied by shortness of breath, weakness, chest pain and dizziness. At rest, there are no such symptoms.
3. Grade 3 is characterized by significant impairment of physical activity. Light exercise can cause shortness of breath and other of the above symptoms.
4. Grade 4 is accompanied by the mentioned signs at the slightest load and at rest.

There are two more forms of the disease:

1. Chronic thromboembolic hypertension. It develops rapidly as a result of thromboembolism of the trunk and large branches of the artery. Characteristic features are acute onset, rapid progression, development of pancreatic insufficiency, hypoxia, and a drop in blood pressure.
2. Pulmonary hypertension due to unclear mechanisms. Presumptive causes include sarcoidosis, tumors, and fibrosing mediastitis.

Depending on the pressure, three more three types of the disease are distinguished:

1. Mild form, when the pressure is from 25 to 36 mm Hg;
2. Moderate pulmonary hypertension, pressure from 35 to 45 mm Hg;
3. Severe form with a pressure greater than 45 mm Hg.

Symptoms

The disease can be asymptomatic and compensated. In this regard, it is most often found when a severe form begins to develop. The initial manifestations are noted when the pressure in the artery system of the lungs is increased by two or more times compared with the norm. As the disease progresses, symptoms such as weight loss, shortness of breath, fatigue, hoarseness, coughing and palpitations appear. A person cannot explain them. At an early stage of the disease, fainting may appear due to acute cerebral hypoxia and heart rhythm disturbances, as well as dizziness.

Since the signs of pulmonary hypertension are not very specific, it is difficult to make an accurate diagnosis based on subjective complaints. Therefore, it is very important to conduct a thorough diagnosis and pay attention to all symptoms, at least somehow indicating problems with the pulmonary artery or other systems in the body, a failure in which can lead to the development of hypertension.

Diagnostics

Since a disease of a secondary nature is a complication of other diseases, it is important to identify the underlying ailment during diagnosis. This is possible thanks to the following measures:

• Study of the history of the disease. This includes collecting information about when shortness of breath, chest pain and other symptoms appeared, with which the patient himself associates such conditions, and how they were treated.
• Lifestyle analysis. This is information about the patient's bad habits, similar diseases in relatives, working and living conditions, the presence of congenital pathological conditions and previous operations.
• Visual examination of the patient. The doctor should pay attention to the presence of such external signs as blue skin, changes in the shape of the fingers, enlargement of the liver, edema of the lower extremities, pulsation of the veins of the neck. The lungs and heart are also listened to with a phonendoscope.
• ECG. Allows you to see signs of an increase in the right heart sections.
• An x-ray of the chest organs can help detect an enlarged heart.
• Ultrasound of the heart. Helps to estimate the size of the heart and indirectly determine the pressure in the artery of the lungs.
• Artery catheterization. Using this method, you can determine the pressure in it.

Such data will help determine whether primary pulmonary hypertension in humans or secondary, treatment tactics and prognosis. In order to establish the class and type of the disease, as well as to assess the tolerance of physical activity, spirometry, CT of the chest, assessment of diffuse pulmonary capacity, ultrasound of the abdominal cavity, blood tests, and so on are performed.

Treatment

The treatment of pulmonary hypertension is based on several methods.

1. Drug-free treatment. It includes drinking no more than 1.5 liters of liquid per day, as well as reducing the amount of table salt used. Oxygen therapy is effective, as it helps to eliminate acidosis and restore the functions of the nervous central system. It is important for patients to avoid situations that cause shortness of breath and other symptoms, so avoiding physical exertion is a good recommendation.
2. Drug therapy: diuretics, calcium antagonists, nitrates, ACE inhibitors, antiplatelet agents, antibiotics, prostaglandins, and so on.
3. Surgical treatment of pulmonary hypertension: thrombendarectomy, atrial septostomy.
4. Traditional methods. Alternative treatment can be used only on the recommendation of a doctor.

Effects

A common complication of the disease is pancreatic heart failure. It is accompanied by a disturbance in the rhythm of the heart, which is manifested by atrial fibrillation. For severe stages of hypertension, the development of thrombosis of pulmonary arterioles is characteristic. In addition, hypertensive crises can develop in the bed of blood vessels, which are manifested by attacks of pulmonary edema. The most dangerous complication of hypertension is death, which usually occurs due to the development of arterial thromboembolism or cardiopulmonary failure.

In a severe stage of the disease, thrombosis of pulmonary arterioles is possible

In order to avoid such complications, it is necessary to start treatment of the disease as early as possible. Therefore, at the first sign, you need to rush to the doctor and undergo a full examination. In the course of treatment, you must adhere to the doctor's recommendations.

Prevention

You can prevent this terrible disease with the help of some measures that are aimed at improving the quality of life. It is necessary to give up bad habits and avoid psycho-emotional stress. Any diseases must be treated promptly, especially those that can lead to the development of pulmonary hypertension.

By taking good care of yourself, you can avoid many diseases that shorten your life span. Let's remember that our health often depends on ourselves!

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Is a concept that includes a complex of disorders of the cardiovascular system caused by lung disease. With insufficient work of the lungs and bronchi, the load on the heart increases, which begins to pump blood more actively.

However, the link between heart and lung disease is not immediately apparent. Symptoms of a disorder of the cardiovascular system can be observed years after the onset of lung disease.

The appearance of chronic cor pulmonale, as a rule, is caused by various ailments of the respiratory system. Unlike the acute form, pathology can develop very slowly. There are 3 most famous forms of CLS.

The most common is the bronchopulmonary form, when violations of cardiac function are caused by inflammatory processes of the lower respiratory tract. There is also a vascular form (in which the vessels are affected), a thoracodiaphragmatic form (pathological deformities of the spine and chest).Before clinical guidelines are prescribed, chronic cor pulmonale must be examined and the cause of the pathology identified.

The effectiveness of treatment largely depends on the correct determination of the cause, since cor pulmonale is a secondary disease.

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

1. Diseases of the bronchi and lungs. Various acute and chronic inflammatory diseases of the respiratory system can lead to the onset of chronic pulmonary disease. These include chronic bronchitis (inflammation in the bronchi), bronchial asthma (often developing against the background of respiratory allergies, leading to suffocation), pulmonary fibrosis (thickening of the lung tissue, leading to a partial loss of organ functionality). All these diseases are accompanied by impaired breathing and gas exchange. This leads to the fact that the tissues lack oxygen. The heart begins to work more actively, which provokes hypertrophy of its individual parts.
2. Pathologies associated with violation of the integrity of the chest and spine. Various injuries of the sternum, curvatures and defects, removal of ribs, exhaustion lead to impaired ventilation of the lungs, since it becomes impossible to make a full inhalation and exhalation. This also leads to heart pathologies.
3. Pathological processes in the vessels. Pulmonary hypertension (high blood pressure in the vessels and arteries of the lung tissue), as well as vasculitis (an inflammatory process of the vessels directly), can lead to the appearance of the disease.

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

Signs and complications of the disease

A feature of HLS is that due to disruption of the lungs, the right atrium and ventricle increase in volume. This is associated with increased stress on the heart. Due to the thickening of the walls of the right ventricle, the contractile function of the heart is significantly reduced.

Initially, only the symptoms associated with the initial disease, that is, with the pathology of the lungs, come to the fore. Gradually, signs of cardiovascular disease begin to appear, but the manifestation of symptoms is not uniform.

The main signs of chronic pulmonary heart disease include:

• Shortness of breath and cough. These signs accompany both lung disease and pathology of the cardiovascular system. In the initial stages, shortness of breath appears only with physical exertion. With the further course of the disease, a feeling of lack of air may appear at rest. Also, the patient is tormented by bouts of dry cough at night, which is called a heart cough.
• Protruding veins in the neck. In chronic pulmonary heart disease, the patient often has swelling of the veins in the neck. They do not return to their normal state when inhaling or exhaling.
• Bluish skin color. Due to the lack of oxygen in the blood and impaired blood circulation, the lips, feet, ears, hands acquire a light blue tint.
• ... Swelling appears gradually and increases with the course of the disease. At a later stage, fluid builds up in the abdomen and lungs, causing the entire body to swell.
• Nervous system disorders. In chronic cor pulmonale, dizziness and tinnitus are observed, which is also associated with oxygen starvation of tissues.
• Increased heart rate, abnormal heart rhythm. Because the heart is enlarged, it cannot pump blood normally. The heart muscle begins to contract more actively, causing seizures.

The consequences of chronic cor pulmonale can be quite serious. The most dangerous is death and sudden cardiac arrest. If untreated, the body is depleted due to deterioration of blood supply and lack of oxygen.

Death can occur within 2-5 years after the onset of the disease.

Also, the consequences of chronic cor pulmonale are chronic heart failure, various heart rhythm disturbances, which lead to a deterioration in the patient's quality of life.

Diagnostics and treatment methods

Diagnostic procedures are aimed at identifying the cause of the disease and making a diagnosis. The doctor collects an anamnesis, specifies the existing symptoms and the frequency of their occurrence. First of all, a general blood test, a biochemical blood test, a general urine test and a blood gas analysis are prescribed. This will help detect a decrease in blood oxygen levels.

Electrocardiography and chest x-ray are mandatory. Spirometry and CT are recommended as additional diagnostic procedures.

Treatment is primarily aimed at improving lung function, reducing pulmonary hypertension, and normalizing the right ventricle. Complex treatment of chronic cor pulmonale includes:

1. Inhalation. In case of disruption of the lungs and oxygen starvation, inhalations with moist air with an increased amount of oxygen are prescribed. The procedures are performed using a mask or nasal catheter.
2. Diet. With chronic cor pulmonale, the likelihood of edema increases, so it is recommended to reduce the use of table salt. It is advisable to consume more protein, fiber in the form of vegetables and fruits, herbs, foods rich in vitamins and microelements.
3. Moderate physical activity. Disruption of the lungs and heart does not allow for great physical exertion, but physical inactivity also cannot be useful. In case of exacerbations, bed rest is prescribed. During remission, the doctor will recommend exercises to strengthen the body, physical therapy.
4. Preparations for improving the functioning of the bronchi. To cleanse the bronchi and improve their work, mucolytics, expectorants and bronchodilators are prescribed. They help remove phlegm from the bronchi.
5. Antibiotics. Antibacterial drugs are prescribed if a bacterial infection is the cause of the respiratory system malfunction. For example, with tuberculosis, pneumonia, antibiotic therapy is required.

Anticoagulants, cardiac glycosides, can also be prescribed. If drug treatment is ineffective, surgical treatment is prescribed. For example, in case of a curvature of the chest, it is proposed to correct it using surgical methods.

Forecast and prevention

With severe development of the disease, the prognosis is disappointing. Chronic cor pulmonale can lead to disability and sudden death of the patient. Even in the early stages of the disease, the patient's ability to work is noticeably affected. The prognosis improves with timely diagnosis and treatment of the disease at the initial stages.

Prevention measures are primarily aimed at reducing the likelihood of respiratory illness. Since infectious lung diseases are the most common cause of chronic cor pulmonale, it is necessary to strengthen the immune system and avoid contact with viruses and bacteria.

Prevention rules include:

• Compliance with the regime of work and rest. Overwork and constant stress lead to a weakening of the body, a drop in immunity. To maintain health, regular and prolonged sleep is necessary (at least 8 hours a day).
• Rejection of bad habits. For the lungs, smoking, including passive smoking, is especially dangerous. Chronic bronchitis is much more common in smokers. To protect yourself from developing lung disease, you must quit smoking.
• Proper nutrition. A balanced diet helps to normalize blood pressure, strengthen immunity, and improve metabolism. The diet should include enough proteins, fats, vitamins, minerals and trace elements.
• Physical exercise. Exercise helps to strengthen the heart muscle and increase lung capacity. However, with pre-existing medical conditions, caution should be exercised and a doctor should be consulted.
• Taking vitamins. Taking multivitamin complexes allows you to avoid vitamin deficiency and strengthen the body in the spring.
• Hardening. Hardening is necessary to increase the protective function of the body. Pediatricians recommend teaching a child to hardening procedures from early childhood, but you need to start gradually, accustoming the body to low temperatures.

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

Also an important preventive measure is a timely visit to the doctor. All diseases of the respiratory tract must be treated in time and prevented from becoming chronic.