Symptoms and treatment of chronic cor pulmonale. Cor pulmonale - causes and pathogenesis Cor pulmonale etiology pathogenesis classification

Along with other diseases, cor pulmonale is often found. This is a pathology in which the pressure of the blood flow in the pulmonary circulation rises as a result of an overload of the right heart.

Speaking in medical terms, there is hypertrophy (enlargement) of the right atrium and ventricle and thinning of their muscular structure, and the development of such an ailment is facilitated by pathological processes occurring in the bronchopulmonary system, in particular in the vessels of the lungs and respiratory tract.

At the same time, patients often complain of symptoms such as shortness of breath of varying degrees, pain that occurs suddenly in the thoracic region, tachycardia, cyanosis of the skin.

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During the diagnosis, a displacement of the borders of the heart to the right is often detected, an increased pulsation, which indicates an overload of the right heart. To make an accurate diagnosis, the patient is sent for an electrocardiogram, an ultrasound of the heart and an x-ray, although a visual examination of the patient by a doctor can provide a lot of information.

The mechanism of the occurrence of pathology

There may be many, but the main factor contributing to the development of cor pulmonale is a significant increase in blood pressure in the pulmonary circulation, otherwise this pathology is called pulmonary hypertension.

But in order for pulmonary hypertension to occur, other causes must also influence, which can be divided into three main groups:

Diseases associated with inflammation of the airways and lungs	Bronchial asthma, pneumonia, cystic lung hypoplasia, pneumosclerosis, as well as diseases in which a chronic suppurative process occurs in deformed bronchi.
Deviations from the norm of the structure of the chest	Deformation of the chest, various injuries of the thoracic region as a result of trauma, pleurofibrosis, complications after the operation, which consists in resection of the ribs.
Diseases caused by damage to the pulmonary vessels	Among such ailments, thromboembolism of the pulmonary artery, vasculitis, blockage of the pulmonary vessels with atherosclerotic formations, and primary pulmonary hypertension are most often distinguished.

In the process of development of the cor pulmonale, various ailments that complement each other can participate. But most often the founder in the occurrence of the disease is a disease of the bronchopulmonary system.

The fact is that an increase in blood pressure in small vessels and arteries of the lungs leads to blockage, the so-called obstruction, of the bronchi, as a result of which the vessels spasm and begin to deform.

Also, such bronchial obstruction can cause a decrease in the partial pressure of oxygen in the blood, and this, in turn, increases the amount of blood flow ejected per minute from the right ventricle. As a result of a lack of oxygen, certain biologically active substances are released that adversely affect the pulmonary arteries and small vessels, causing them to spasm.

Hypoxia affects not only the lungs, but the entire circulatory system. So, for example, with a sharp decrease in oxygen in the blood, the process of erythropoiesis intensifies, in which a large number of red blood cells are formed.

Getting into the blood, they contribute to its significant thickening. As a result, blood clots (blood clots) form in the veins and vessels, which can partially or completely block the vascular lumen in any part of the body.

But most often, thickening of the blood causes expansion of the bronchial vessels, which also leads to an increase in pressure in the pulmonary artery. Due to the high blood pressure resistance, the right ventricle is forced to work with redoubled force to push the blood flow out.

As a result, the right side of the heart is overloaded and enlarged, while losing the muscle mass of which it is composed. Such changes lead to stagnation of blood in the systemic circulation, which further exacerbates the effects of hypoxia.

Pathogenesis of different forms of cor pulmonale

Regardless of the reasons, at the root of the development of such a disease as cor pulmonale lies arterial hypertension that occurs in the lungs. Its formation is due to various pathological mechanisms.

However, the pathogenesis of cor pulmonale comes in two forms:

Acute

The pathogenesis of acute cor pulmonale is often formed in the presence of thromboembolism of the pulmonary artery. In this case, two pathological processes are involved: mechanical obstruction of the vascular bed and humoral changes.

Mechanical vascular obstruction occurs due to blockage of the arterial vessel of the lung, while small branches of the pulmonary artery are included in the pathological process, as a result, vascular resistance increases, which increases blood flow pressure.

Such resistance becomes an obstacle to the ejection of blood from the right ventricle, while the left ventricle is not filled with the necessary volume of blood, which leads to a decrease in blood pressure. As for humoral disorders, they usually occur in the first hours after the closure of the vascular bed.

This can lead to the release into the blood of such biologically active substances as serotonin, prostaglandins, convertase, histamine. At the same time, narrowing of the small branches of the pulmonary artery occurs.

When a pathology such as thromboembolism occurs, which is characterized by blockage of the pulmonary artery by a blood clot, the peak of pulmonary arterial hypertension occurs in the first hours. Due to the increase in blood pressure in the vessels of the lungs, the right ventricle overstrains and increases in size.

Chronic

In contrast to the acute form, the pathogenesis of chronic cor pulmonale develops in patients who already had any chronic respiratory diseases.

Let's look at the main causes leading to such an ailment using the example of chronic obstructive pulmonary disease, these include:

Hypoxic pulmonary vasoconstriction	This is a mechanism aimed at reducing blood flow in the area of the lungs, where there is a lack of oxygen.
Bronchial obstruction syndrome	Occurs in bronchial asthma, due to spasm of the smooth muscles of the bronchi or edema of the bronchial mucosa, also emit secondary bronchial obstruction, which leads to the formation of a tumor or the ingress of a foreign body into the bronchi, with infectious and inflammatory processes bronchitis, pneumonia, tuberculosis).
Acidosis	A condition in which there are changes in the acid-base balance in the body.
hyperviscose syndrome	A condition in which a large amount of protein is released into the blood, resulting in an increase in the viscosity of the blood, it becomes thick.
Increase in the volume of blood pumped out by the heart	Nerve stimulation or myocardial hypertrophy can lead to such changes.

Based on the above, we can conclude that the chronic form of the pathogenesis of the disease develops with bronchopulmonary pathology. With violations of the functionality of blood vessels and their resistance, persistent pulmonary hypertension occurs.

The main cause of such pathological changes is the organic narrowing of the vascular lumen of the pulmonary arteries.

However, pulmonary hypertension, which leads to the development of cor pulmonale, can also occur due to functional changes when the mechanics of breathing or ventilation of the alveoli is disturbed.

The development of cor pulmonale, regardless of the cause, is based on pulmonary arterial hypertension, the formation of which is due to several pathogenetic mechanisms.

Pathogenesis of acute cor pulmonale (for example, pulmonary embolism). Two pathogenic mechanisms are involved in the formation of ALS:

- "mechanical" obstruction of the vascular bed,
- humoral changes.

"Mechanical" obstruction of the vascular bed occurs due to extensive obstruction of the arterial bed of the lungs (by 40-50%, which corresponds to the inclusion of 2-3 branches of the pulmonary artery in the pathological process), which increases the total pulmonary vascular resistance (OLVR). An increase in OLSS is accompanied by an increase in pressure in the pulmonary artery, which prevents the ejection of blood from the right ventricle, a decrease in the filling of the left ventricle, which in total leads to a decrease in the minute volume of blood and a drop in blood pressure (BP).

Humoral disorders that occur in the first hours after obstruction of the vascular bed, as a result of the release of biologically active substances (serotonin, prostaglandins, catecholamines, the release of convertase, angiotensin-converting enzyme, histamine), lead to reflex narrowing of the small branches of the pulmonary artery (generalized hypertonic reaction of the pulmonary arteries), which further increases the OLSS.

The first hours after PE are characterized by particularly high pulmonary arterial hypertension, which quickly leads to right ventricular strain, dilatation and decompensation.

Pathogenesis of chronic cor pulmonale (on the example of COPD). The key links in the pathogenesis of CLS are:

- hypoxic pulmonary vasoconstriction,
- violations of bronchial patency,
- hypercapnia and acidosis,
- anatomical changes in the pulmonary vascular bed,
- hyperviscosity syndrome,
- an increase in cardiac output.

Hypoxic pulmonary vasoconstriction. The regulation of blood flow in the pulmonary circulation system is carried out due to the Euler-Liljestrand reflex, which provides an adequate ratio of ventilation and perfusion of the lung tissue. With a decrease in the oxygen concentration in the alveoli, due to the Euler-Liljestrand reflex, the precapillary sphincters reflexively close (vasoconstriction occurs), which leads to a restriction of blood flow in these areas of the lung. As a result, the local pulmonary blood flow adapts to the intensity of pulmonary ventilation, and there are no violations of ventilation-perfusion ratios.

In chronic lung diseases, prolonged alveolar hypoventilation causes a generalized increase in the tone of the pulmonary arterioles, leading to the development of stable pulmonary hypertension. In addition, there is an opinion that endothelial factors are involved in the mechanism of formation of hypoxic pulmonary vasoconstriction: endothelins and angiotensin II directly stimulate the contraction of the smooth muscles of the vascular wall, while a decrease in the synthesis of prostaglandin PgI2 and endothelial relaxing factor (NO) enhances vasoconstriction of the pulmonary arterioles.

Bronchial obstruction. Uneven lung ventilation causes alveolar hypoxia, causes disturbances in ventilation-perfusion ratios and leads to a generalized manifestation of the mechanism of hypoxic pulmonary vasoconstriction. The development of alveolar hypoxia and the formation of CLS are more susceptible to patients suffering from chronic obstructive bronchitis and bronchial asthma with a predominance of signs of respiratory failure ("blue puffiness"). In patients with a predominance of restrictive disorders and diffuse lung lesions (pink puffers), alveolar hypoxia is much less pronounced.

Hypercapnia does not directly but indirectly affect the occurrence of pulmonary hypertension by:

- the appearance of acidosis and, accordingly, reflex vasoconstriction,
- Decrease in the sensitivity of the respiratory center to CO2, which aggravates violations of lung ventilation.

Anatomical changes in the pulmonary vascular bed, causing an increase in OLSS, are the development of:

- hypertrophy of the media of the pulmonary arterioles (due to the proliferation of smooth muscles of the vascular wall),
- desolation of arterioles and capillaries,
- thrombosis of the microvasculature,
- development of bronchopulmonary anastomoses.

Hyperviscosity syndrome in patients with CHLS develops due to secondary erythrocytosis. This mechanism is involved in the formation of pulmonary arterial hypertension in any type of respiratory failure, manifested by severe cyanosis. In patients with CLS, an increase in the aggregation of blood cells and blood viscosity makes it difficult for blood flow through the vascular bed of the lungs. In turn, an increase in viscosity and a slowdown in blood flow contribute to the formation of parietal thrombi in the branches of the pulmonary artery. The whole set of hemostasiological disorders leads to an increase in OLSS.

An increase in cardiac output is due to:

- tachycardia (an increase in cardiac output with significant bronchial obstruction is achieved by an increase not in stroke volume, but in heart rate, since an increase in intrathoracic pressure prevents venous blood flow into the right ventricle);
- hypervolemia (one of the possible causes of hypervolemia is hypercapnia, which increases the concentration of aldosterone in the blood and, accordingly, the retention of Na + and water).

An indispensable part of the pathogenesis of cor pulmonale is the early development of right ventricular myocardial dystrophy and changes in hemodynamics.

The development of myocardial dystrophy is determined by the fact that shortening of diastole during tachycardia and an increase in intraventricular pressure leads to a decrease in blood flow in the muscle of the right ventricle and, accordingly, energy deficiency. In a number of patients, the development of myocardial dystrophy is associated with intoxication from foci of chronic infection in the respiratory tract or lung parenchyma.

Hemodynamic changes are most typical for patients with advanced clinical picture of CLS. The main ones are:

- right ventricular hypertrophy (HLS is characterized by a gradual and slow development, therefore, it is accompanied by the development of right ventricular myocardial hypertrophy. ALS develops as a result of a sudden and significant increase in pressure in the pulmonary artery, which leads to a sharp expansion of the right ventricle and thinning of its wall, therefore hypertrophy of the right parts of the heart does not have time to develop).
- decrease in systolic function of the right parts of the heart with the development of stagnation of blood in the venous bed of the systemic circulation,
- an increase in the volume of circulating blood,
- decrease in cardiac output and blood pressure.

Thus, in bronchopulmonary pathology, persistent pulmonary hypertension is formed due to organic narrowing of the lumen of the pulmonary vessels (due to obliteration, microthrombosis, vascular compression, reduced lung capacity to stretch) and functional changes (caused by violations of the mechanics of respiration, ventilation of the alveoli and hypoxia). And if in bronchopulmonary pathology the reduction in the total cross section of the pulmonary vessels is based on spasm of arterioles due to the development of the Euler-Liljestrand reflex, then in patients with the vascular form of the LS, organic changes (narrowing or blockage) of the vessel primarily occur due to thrombosis and embolism, necrotizing angiitis. Schematically, the pathogenesis can be represented as follows (Table 1)

Pulmonary heart- a complex of hemodynamic disorders in the pulmonary circulation, developing as a result of diseases of the bronchopulmonary apparatus, chest deformity or primary damage to the pulmonary arteries, manifested at the final stage by hypertrophy and dilatation of the right ventricle and progressive circulatory failure.

Etiology of cor pulmonale:

A) sharp(develops in minutes, hours or days): massive PE, valvular pneumothorax, severe asthma attack, widespread pneumonia

B) subacute(develops over weeks, months): repeated small PE, periarteritis nodosa, lung carcinomatosis, repeated attacks of severe asthma, botulism, myasthenia gravis, poliomyelitis

B) chronic(develops over several years):

1. diseases affecting the airways and alveoli: chronic obstructive bronchitis, pulmonary emphysema, bronchial asthma, pneumoconiosis, bronchiectasis, polycystic lung disease, sarcoidosis, pneumosclerosis, etc.

2. diseases affecting the chest with limited mobility: kyphoscoliosis and other deformities of the chest, ankylosing spondylitis, condition after thoracoplasty, pleural fibrosis, neuromuscular diseases (poliomyelitis), paresis of the diaphragm, Pickwickian syndrome in obesity, etc.

3. diseases affecting the pulmonary vessels: primary pulmonary hypertension, repeated thromboembolism in the pulmonary artery system, vasculitis (allergic, obliterating, nodular, lupus, etc.), atherosclerosis of the pulmonary artery, compression of the trunk of the pulmonary artery and pulmonary veins by tumors of the mediastinum, etc.

Pathogenesis of chronic cor pulmonale (CHP).

The main pathogenetic factor in the formation of CLS is pulmonary hypertension, which occurs due to a number of reasons:

1) in diseases with hypoventilation of the pulmonary alveoli in the alveolar air, the partial pressure of oxygen decreases, and the partial pressure of carbon dioxide increases; advancing alveolar hypoxia causes spasm of the pulmonary arterioles and an increase in pressure in the small circle (alveolo-capillary Euler-Liljestrand reflex)

2) hypoxia causes erythrocytosis with a subsequent increase in blood viscosity; increased blood viscosity contributes to increased platelet aggregation, the formation of microaggregates in the microcirculation system and an increase in pressure in the small branches of the pulmonary artery

3) a decrease in oxygen tension in the blood causes irritation of the chemoreceptors of the aortic-carotid zone, as a result, the minute volume of blood increases; its passage through spasmodic pulmonary arterioles leads to a further increase in pulmonary hypertension

4) during hypoxia, a number of biologically active substances (histamine, serotonin, etc.) are released in the tissues, which also contribute to spasm of the pulmonary arterioles

5) atrophy of the alveolar walls, their rupture with thrombosis and obliteration of part of the arterioles and capillaries due to various lung diseases leads to anatomical reduction of the vascular bed of the pulmonary artery, which also contributes to pulmonary hypertension.

Under the influence of all of the above factors, hypertrophy and dilatation of the right heart sections occur with the development of progressive circulatory failure.

Pathological signs of CHLS: expansion of the diameter of the trunk of the pulmonary artery and its large branches; hypertrophy of the muscular layer of the pulmonary artery wall; hypertrophy and dilatation of the right heart.

Cor pulmonale classification (according to Votchal):

1. Downstream: acute cor pulmonale, subacute cor pulmonale, chronic cor pulmonale

2. Depending on the level of compensation: compensated, decompensated

3. Depending on the genesis: vascular, bronchial, thoracophrenic

The main clinical manifestations of HLS.

1. Clinical manifestations of chronic obstructive and other lung diseases.

2. Complex of symptoms due to respiratory failure and significantly aggravated during the formation of chronic cor pulmonale:

- shortness of breath: worsens with physical exertion, orthopnea is not typical, decreases with the use of bronchodilators and oxygen inhalations

- severe weakness, persistent headaches, drowsiness during the day and insomnia at night, sweating, anorexia

- warm diffuse gray cyanosis

- palpitations, constant pain in the region of the heart (due to hypoxia and reflex narrowing of the coronary arteries - pulmocoronary reflex), decreasing after oxygen inhalation

3. Clinical signs of right ventricular hypertrophy:

- expansion of the right border of the heart (rare)

- displacement of the left border of the heart outward from the midclavicular line (due to displacement by an enlarged right ventricle)

- the presence of a cardiac impulse (pulsation) along the left border of the heart

– pulsation and better auscultation of heart sounds in the epigastric region

- systolic murmur in the area of the xiphoid process, aggravated on inspiration (Rivero-Corvallo symptom) - a sign of relative insufficiency of the tricuspid valve, which develops with an increase in the right ventricle

4. Clinical signs of pulmonary hypertension:

- an increase in the zone of vascular dullness in the II intercostal space due to the expansion of the pulmonary artery

- accent of the II tone and its splitting in the II intercostal space on the left

- the appearance of a venous network in the sternum

- the appearance of diastolic murmur in the pulmonary artery due to its dilatation (Graham-Still symptom)

5. Clinical signs of decompensated cor pulmonale:

– orthopnea

- cold acrocyanosis

- swelling of the jugular veins that does not decrease on inspiration

- liver enlargement

- Symptom Plesh (pressure on the enlarged painful liver causes swelling of the jugular veins);

- in severe heart failure, edema, ascites, hydrothorax may develop.

HLS diagnosis.

1. Echocardiography - signs of right ventricular hypertrophy: an increase in the thickness of its wall (normally 2-3 mm), expansion of its cavity (right ventricular index - the size of its cavity in terms of the body surface - normally 0.9 cm / m2); signs of pulmonary hypertension: an increase in the rate of opening of the pulmonary valve, its easy detection, W-shaped movement of the crescents of the pulmonary valve in systole, an increase in the diameter of the right branch of the pulmonary artery more than 17.9 mm; paradoxical movements of the interventricular septum and mitral valve, etc.

2. Electrocardiography - signs of right ventricular hypertrophy (increase in RIII, aVF, V1, V2; depression of the ST segment and changes in the T wave in leads V1, V2, aVF, III; rightogram; displacement of the transition zone in V4 / V5; complete or incomplete blockade of the right bundle branch of His; increase in the interval of internal deviation> 0.03 in V1, V2).

3. X-ray of the chest organs - an increase in the right ventricle and atrium; bulging of the cone and trunk of the pulmonary artery; a significant expansion of the basal vessels with a depleted peripheral vascular pattern; "chopping" of the roots of the lungs, etc.

4. Examination of the function of external respiration (to identify violations of the restrictive or obstructive type).

5. Laboratory data: KLA is characterized by erythrocytosis, high hemoglobin content, delayed ESR, and a tendency to hypercoagulability.

Principles of treatment of HLS.

1. Etiological treatment - aimed at treating the underlying disease that led to CLS (AB for bronchopulmonary infection, bronchodilators for broncho-obstructive processes, thrombolytics and anticoagulants for pulmonary embolism, etc.)

2. Pathogenetic treatment - aimed at reducing the severity of pulmonary hypertension:

A) long-term oxygen therapy - reduces pulmonary hypertension and significantly increases life expectancy

B) improvement of bronchial patency - xanthines: eufillin (2.4% solution 5-10 ml IV 2-3 times / day), theophylline (in tab. 0.3 g 2 times / day) repeated courses of 7-10 days, b2 - adrenomimetics: salbutamol (in tab. 8 mg 2 times / day)

C) decrease in vascular resistance - peripheral vasodilators: prolonged nitrates (sustac 2.6 mg 3 times a day), calcium channel blockers (nifedipine 10-20 mg 3 times a day, amlodipine, isradipine - have an increased affinity for SMC of pulmonary vessels ), endothelin receptor antagonists (bosentan), prostacyclin analogues (iloprost IV and inhalation up to 6-12 times / day, beraprost 40 mg orally up to 4 times / day, treprostinil), nitrous oxide and nitrous oxide donators (L- arginine, sodium nitroprusside - have a selective vasodilating effect, reduce the effects of pulmonary hypertension without affecting systemic blood pressure).

D) improvement of microcirculation - heparin courses of 5000 IU 2-3 times / day s / c until the increase in APTT by 1.5-1.7 times compared with the control, low molecular weight heparins (fraxiparin), with severe erythrocytosis - bloodletting followed by infusion solutions with low viscosity (rheopolyglucin).

3. Symptomatic treatment: to reduce the severity of right ventricular failure - loop diuretics: furosemide 20-40 mg / day (carefully, because they can cause hypovolemia, polycythemia and thrombosis), with a combination of heart failure with MA - cardiac glycosides, to improve myocardial function - metabolic agents (mildronate inside 0.25 g 2 times / day in combination with potassium orotate or panangin), etc.

4. Physiotherapy (breathing exercises, chest massage, hyperbaric oxygen therapy, exercise therapy)

5. In case of ineffective conservative treatment, transplantation of the lungs or the lung-heart complex is indicated.

ITU: Approximate terms of VN in decompensated cor pulmonale 30-60 days.

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

ICD-10

I27.9 Pulmonary heart failure, unspecified

General information

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

Reasons for the development of cor pulmonale

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

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

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

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

The mechanism of development of the cor pulmonale

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

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

Cor pulmonale classification

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

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

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

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

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

Cor pulmonale symptoms

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

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

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

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

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

Cor pulmonale diagnosis

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

Prognosis and prevention of cor pulmonale

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

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

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PULMONARY HEART (HR) is a clinical syndrome caused by hypertrophy and / or dilatation of the right ventricle resulting from hypertension in the pulmonary circulation, which in turn develops as a result of bronchial and lung disease, chest deformity or damage to the pulmonary vessels.

Classification

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B.E. Watchal (1964) proposes to classify cor pulmonale according to 4 main features:

1) the nature of the flow;
2) state of compensation;
3) predominant pathogenesis;
4) features of the clinical picture.

There are acute, subacute and chronic drugs, which is determined by the rate of development of pulmonary hypertension.

Table 7. Classification of cor pulmonale

With acute development of LS pulmonary hypertension occurs within a few hours or days, with subacute - a few weeks or months, with chronic - for several years.

Acute LS is most often (about 90% of cases) observed with pulmonary embolism or a sudden increase in intrathoracic pressure, subacute - with cancerous lymphangitis, thoracophrenic lesions.

Chronic drug in 80% of cases it occurs when the bronchopulmonary apparatus is damaged (moreover, in 90% of patients due to chronic nonspecific lung diseases); vascular and thoracophrenic forms of LS develop in 20% of cases.

Etiology

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All diseases that cause chronic LS, according to the classification of WHO experts (1960), are divided into 3 groups:

1) primarily affecting the passage of air in the lungs and alveoli;
2) primarily affecting the movement of the chest;
3) primarily affecting the pulmonary vessels.

The first group includes diseases, primarily affecting the bronchopulmonary apparatus (COPD, chronic bronchitis and pneumonia, pulmonary emphysema, fibrosis and granulomatosis of the lungs, tuberculosis, occupational lung diseases, etc.).

The second group consists of diseases leading to impaired ventilation due to pathological changes in the mobility of the chest (kyphoscoliosis, pathology of the ribs, diaphragm, ankylosing spondylitis, obesity, etc.).

The third group includes as etiological factors primarily affecting the pulmonary vessels, repeated pulmonary embolism, vasculitis and primary pulmonary hypertension, pulmonary artery atherosclerosis, etc.

Despite the fact that by now about 100 diseases leading to the development of chronic LS are known in the world literature, COPD remains the most common causes (primarily COPD and bronchial asthma).

Pathogenesis

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The main mechanism for the formation of drugs is an increase in pressure in the pulmonary artery system (pulmonary hypertension).

Among the mechanisms leading to the occurrence of pulmonary hypertension, there are anatomical and functional (Scheme 7).

Scheme 7. Pathogenesis of Chronic Cor pulmonale

To anatomical mechanisms include:

closure of the lumen of the vessels of the pulmonary artery system as a result of obliteration or embolization;
compression of the pulmonary artery from the outside;
a significant decrease in the bed of the pulmonary circulation as a result of pulmonectomy.

To functional mechanisms include:

narrowing of the pulmonary arterioles at low values of PaO 2 (alveolar hypoxia) and high values of PaCO 2 in the alveolar air;
increased pressure in the bronchioles and alveoli;
increase in blood levels of substances and metabolites of pressor action;
increase in cardiac output;
increase in blood viscosity.

The decisive role in the formation of pulmonary hypertension belongs to the functional mechanisms. Of primary importance is the narrowing of the pulmonary vessels (arterioles).

The most significant cause that causes narrowing of the pulmonary vessels is alveolar hypoxia, leading to a local release of biogenic amines (histamine, serotonin, etc., prostaglandins - vasoactive substances). Their release is accompanied by swelling of the capillary endothelium, accumulation of platelets (microthrombosis) and vasoconstriction. The Euler-Liljestrand reflex (spasm of the pulmonary arterioles with a decrease in PaO 2 in the alveoli) extends to vessels that have a muscular layer, including arterioles. The narrowing of the latter also leads to an increase in pressure in the pulmonary artery.

Alveolar hypoxia with varying degrees of severity develops in all COPD and ventilation disorders, accompanied by an increase in residual lung capacity. It is especially pronounced in violations of bronchial patency. In addition, alveolar hypoxia also occurs with hypoventilation of thoracophrenic origin.

Alveolar hypoxia contributes to an increase in pressure in the pulmonary artery and through arterial hypoxemia, which leads to:

a) to increase the minute volume of the heart through irritation of the chemoreceptors of the aortic-carotid zone;
b) to the development of polycythemia and an increase in blood viscosity;
c) to increase the level of lactic acid and other metabolites and biogenic amines (serotonin, etc.), which contribute to an increase in pressure in the pulmonary artery;
d) there is a sharp activation of the renin-angiotensin-aldosterone system (RAAS).

In addition, alveolar hypoxia leads to a decrease in the production of vasodilating substances (prostacyclin, endothelial hyperpolarizing factor, endothelial relaxing factor) produced by normal pulmonary vascular endothelial cells.

The pressure in the pulmonary artery increases with compression of the capillaries due to:

a) emphysema and increased pressure in the alveoli and bronchioles (with unproductive hacking cough, intense and physical activity);
b) a violation of the biomechanics of respiration and an increase in intrathoracic pressure in the phase of prolonged expiration (with broncho-obstructive syndrome).

Formed pulmonary hypertension leads to the development of hypertrophy of the right heart (first the right ventricle, then the right atrium). In the future, the existing arterial hypoxemia causes dystrophic changes in the myocardium of the right heart, which contributes to the more rapid development of heart failure. Its development is also facilitated by the toxic effect on the myocardium of infectious processes in the lungs, insufficient oxygen supply to the myocardium, existing coronary artery disease, arterial hypertension and other concomitant diseases.

Based on the identification of signs of persistent pulmonary hypertension, right ventricular hypertrophy in the absence of signs of heart failure, a diagnosis of compensated LS is made. If there are signs of right ventricular failure, decompensated LS is diagnosed.

Clinical picture (Symptoms)

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Manifestations of chronic LS consist of symptoms:

the underlying disease leading to the development of chronic LS;
respiratory (lung) insufficiency;
heart (right ventricular) failure.

The development of chronic LS (as well as the appearance of hypertension in the pulmonary circulation) is necessarily preceded by pulmonary (respiratory) insufficiency. Respiratory failure is a state of the body in which the normal gas composition of the blood is not maintained or it is achieved due to more intensive work of the external respiration apparatus and increased heart load, which leads to a decrease in the functional capabilities of the body.

There are three degrees of respiratory failure.

With respiratory failure I degree shortness of breath and tachycardia occur only with increased physical exertion; no cyanosis. Indicators of the function of external respiration (MOD, VC) at rest correspond to the proper values, but when the load is performed, they change; MVL decreases. The gas composition of the blood is not changed (there is no lack of oxygen in the body), the function of blood circulation and CBS is normal.

With respiratory failure II degree shortness of breath and tachycardia with little physical exertion. Indicators of MOD, VC deviated from the norm, MVL is significantly reduced. Pronounced cyanosis. In the alveolar air, the voltage of PaO 2 decreases and PaCO 2 increases

With respiratory failure III degree shortness of breath and tachycardia at rest; pronounced cyanosis. Significantly reduced indicators of VC, and MVL is impossible. Mandatory lack of oxygen in the body (hypoxemia) and excess carbon dioxide (hypercapnia); at research of KOS respiratory acidosis comes to light. Expressed manifestations of heart failure.

The concepts of "respiratory" and "pulmonary" insufficiency are close to each other, but the concept of "respiratory" insufficiency is wider than "pulmonary", since it includes not only the insufficiency of external respiration, but also the insufficiency of gas transport from the lungs to tissues and from tissues to the lungs, as well as insufficiency of tissue respiration, which develops with decompensated cor pulmonale.

HP develops against the background of respiratory failure II and more often III degree. The symptoms of respiratory failure are similar to those of heart failure, so the doctor faces the difficult task of differentiating them and determining the transition from compensated to decompensated drugs.

Cor pulmonale diagnosis

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When making a diagnosis of compensated LS, a decisive role belongs to the identification of hypertrophy of the right heart (ventricle and atrium) and pulmonary hypertension; in the diagnosis of decompensated LS, the identification of symptoms of right ventricular heart failure is of primary importance in the diagnosis of decompensated LS.

The formulation of a detailed clinical diagnosis takes into account:

the underlying disease that led to the formation of LS;
respiratory failure (severity);
cor pulmonale (stage):
- compensated;
- decompensated (indicates the severity of right ventricular failure, i.e. its stage).

Compensated and decompensated cor pulmonale
I, II and III stage of diagnostic search, X-ray methods and Electrocardiography

Cor pulmonale treatment

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The complex of therapeutic measures includes the impact of:

for a disease that is the cause of the development of drugs (since the most common cause is COPD, during the period of exacerbation of the inflammatory process in the bronchopulmonary system, antibiotics, sulfanilamide drugs, phytoncides are used - the tactics of treatment with antibacterial agents are described in the previous sections);
on the links of the pathogenesis of drugs (restoration of impaired ventilation and drainage function of the bronchi, improvement of bronchial patency, reduction of pulmonary hypertension, elimination of right ventricular failure).

The improvement of bronchial patency is facilitated by a decrease in inflammation and swelling of the bronchial mucosa (antibiotics, corticosteroids administered intratracheally) and the elimination of bronchospasm (sympathomimetic drugs; eufillin, especially its long-acting drugs; anticholinergics and calcium channel blockers).

Bronchial drainage is facilitated by sputum thinners, expectorants, as well as postural drainage and a special complex of physiotherapy exercises.

The restoration of bronchial ventilation and the improvement of bronchial patency lead to an improvement in alveolar ventilation and normalization of the oxygen transport system of the blood.

The main role in improving ventilation is played by gas therapy, including:

a) oxygen therapy (under the control of blood gases and indicators of the acid-base state), including long-term night therapy with 30% oxygen in the inhaled air; if necessary, a helium-oxygen mixture is used;
b) therapy with inhalation of CO 2 with its sharp decrease in the blood, which occurs with severe hyperventilation.

According to the indications, the patient breathes with positive end-expiratory pressure (auxiliary ventilation or artificial respiration regulator - Lyukevich's nebulizer). A special complex of respiratory gymnastics is used, aimed at improving pulmonary ventilation.

Currently, in the treatment of respiratory failure of the III degree, a new respiratory analeptic, armanor, is successfully used, which increases the oxygen tension in arterial blood by stimulating peripheral chemoreceptors.

Normalization of the oxygen transport system of the blood is achieved:

a) an increase in the supply of oxygen to the blood (hyperbaric oxygenation);
b) an increase in the oxygen function of erythrocytes using extracorporeal methods (hemosorption, erythrocytopheresis, etc.);
c) increased elimination of oxygen in tissues (nitrates).

Reducing pressure in the pulmonary artery is achieved in various ways:

the introduction of aminophylline,
saluretics,
aldosterone blockers,
a-adrenergic blockers,
angiotensin-converting enzyme blockers and especially angiotensin H receptor antagonists.

a role in reducing pulmonary artery pressure play drugs that replace the relaxing factor of endothelial origin (molsidamine, Corvaton).

An important role is played by the impact on the microcirculatory bed carried out with the help of xanthinol nicotinate, which acts on the vascular wall, as well as heparin, curantyl, rheopolyglucin, which have a beneficial effect on the intravascular link of hemostasis. Bloodletting is possible (in the presence of erythrocytosis and other manifestations of the plethoric syndrome).

The impact on right ventricular failure is carried out according to the basic principles of the treatment of heart failure:

diuretic,
aldosterone antagonists,
peripheral vasodilators (long-acting nitrates are effective).
The question of the use of cardiac glycosides is decided individually.