National guidelines for chronic pulmonary heart disease. Pulmonary heart

For quotation: Vertkin A.L., Topolyansky A.V. Pulmonary heart: diagnosis and treatment // Breast cancer. 2005. No. 19. S. 1272

Cor pulmonale is an enlargement of the right ventricle of the heart in diseases that impair the structure and (or) function of the lungs (except for cases of primary damage to the left side of the heart, congenital heart defects).

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

Literature
1. Chazova I.E. Modern approaches for the treatment of cor pulmonale. Rus Med Journal, 2000; 8(2): 83–6.
2. Barst R., Rubin L., Long W. et al. A comparison of continuous intravenous epoprostenol (prostacyclin) with conventional therapy for primary pulmonary hypertension. N Engl J Me.d 1996; 334:296–301.
3. Barst R.J., Rubin L.J., McGoon M.D. et al. Survival in primary pulmonary hypertension with long–term continuous intravenous prostacyclin. Ann Intern Med. 1994; 121:409–415.
4. Charan N.B. Does sildenafil also improve breathing? Chest. 2001; 120(1):305–6.
5. Fisnman A.P. Pulmonary hypertension – beyond vasodiator therapy. The New Eng J Med. 1998; 5:338.
6. Franz I.W., Van Der Meyden J., Schaupp S., Tonnesmann U. The effect of amlodipine on exercise–induced pulmonary hypertension and right heart function in patients with chronic obstructive pulmonary disease. Z Cardiol. 2002; 91(10):833–839.
7. Galie N., Hinderliter A.L., Torbicki A. et al. Effects of the oral endothelin receptor antagonist bosentan on echocardiographic and Doppler measures in patients with pulmonary arterial hypertension. American Congress of Cardiology, Atlanta, USA; 17–20 March 2002. Abstract #2179.
8. Galie N., Humbert M., Wachiery J.L. et al. Effects of beraprost sodium, an oral prostacyclin analogue, in patients with pulmonary arterial hypertension: a randomized, double-blind, placebo-controlled trial. J Am Coll Cardiol. 2002; 39:1496–1502.
9. Groechenig E. Cor pulmonale. Treatment of pulmonary hypertension. Blackwell Science, Berlin–Vienna, 1999; 146.
10. McLaughlin V., Shillington A., Rich S. Survival in primary pulmonary hypertension: the impact of epoprostenol therapy. Circulation. 2002; 106:1477–1482.
11. Olchewski H., Ghofrani H., Schmehl T. et al. Inhaled iloprost to treat severe pulmonary hypertension: an uncontrolled trial. Ann Intern Med. 2000; 132:435–443.
12. Rich S., Kaufmann E., Levy P.S. The effect of high doses of calcium channel blockers on survival in pulmonary primary hypertension. N Engl J Med. 1992; 327:76–81.
13. Rubin L.J., Badesch D.B., Barst R.J. et al. Bosentan therapy for pulmonary arterial hypertension. N Engl J Med. 2002; 346:896–903.
14. Sajkov D., Wang T., Frith P.A. et al. A comparison of two long-acting vasoselective calcium antagonists in pulmonary hypertension secondary to COPD. Chest. 1997; 111(6):1622–1630.
15. Sastry B., Narasimhan C., Reddy N. et al. A study of clinical efficacy of sildenafil in patients with primary pulmonary hypertension. Indian Heart J 2002; 54:410–414.
16. Sastry B.K., Narasimhan C., Reddy N.K., Raju B.S. Clinical efficacy of sildenafil in primary pulmonary hypertension: a randomized, placebo-controlled, double-blind, crossover study. J Am Coll Cardiol. 2004; 43(7):1149–53.
17. Sebkhi A., Strange J.W., Phillips S.C. et al. Phosphodiesterase type 5 as a target for the treatment of hypoxia–induced pulmonary hypertension. Circulation. 2003; 107(25):3230–5.
18. Simmoneau G., Barst R., Galie N. et al. Continuous subcutaneous infusion of treprostinil, a prostacyclin analogue, in patients with pulmonary arterial hypertension. Am J Respit Crit Care Med 2002; 165:800–804.
19. Toward T.J., Smith N., Broadley K.J. Effect of phosphodiesterase–5 inhibitor, sildenafil (Viagra), in animal models of airways disease. Am J Respir Crit Care Med. 2004; 169(2):227–34.
20. Wilkens H., Guth A., Konig J. et al. Effect of inhaled iloprost plus oral sildenafil in patients with primary pulmonary hypertension. Circulation 2001; 104:1218–1222.
21. Woodmansey P.A., O’Toole L., Channer K.S., Morice A.H. Acute pulmonary vasodilatory properties of amlodipine in humans with pulmonary hypertension. Heart. 1996; 75(2):171–173.

This file is taken from the Medinfo collection

http://www.doktor.ru/medinfo

http://medinfo.home.ml.org

Email: [email protected]

or [email protected]

or [email protected]

FidoNet 2:5030/434 Andrey Novicov

We write essays to order - e-mail: [email protected]

Medinfo has the largest Russian collection of medical

abstracts, case histories, literature, training programs, tests.

Visit http://www.doktor.ru - Russian medical server for everyone!

LECTURE ON INTERNAL DISEASES.

TOPIC: HEART PULMONARY.

Relevance of the topic: Diseases of the bronchopulmonary system and chest are of great importance in affecting the heart. Damage to the cardiovascular system in diseases of the bronchopulmonary apparatus is referred to by most authors as cor pulmonale.

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

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

Hypertrophy of the right ventricle and its dilatation due to 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 dilatation 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:

“Pulmonary heart is a complex of hemodynamic disorders in the pulmonary circulation, developing as a result of diseases of the bronchopulmonary apparatus, deformations of the chest, and primary damage to the pulmonary arteries, which at the final stage manifests itself as right ventricular hypertrophy and progressive circulatory failure.”

ETIOLOGY OF HEART PULMONARY.

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, as post-tuberculosis outcomes

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

Diseases that primarily affect chest, a diaphragm with limited mobility:

kyphoscoliosis

multiple rib injuries

Pickwickian syndrome in obesity

ankylosing spondylitis

pleural suppuration after 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 cause the development of cor pulmonale in 20% of cases. That's why they say that depending on etiological factor There are three forms of cor pulmonale:

bronchopulmonary

thoradiaphragmatic

vascular

Standards for values ​​characterizing the hemodynamics of the pulmonary circulation.

Systolic pressure in the pulmonary artery is approximately five times less than 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 mmHg, the diastolic pressure is more than 15, and the mean pressure is more than 22 mmHg.

PATHOGENESIS.

The pathogenesis of cor pulmonale is based on pulmonary hypertension. Since cor pulmonale most often develops in bronchopulmonary diseases, we’ll start with that. 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 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 of chronic heart diseases, especially chronic obstructive bronchitis.

All 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 intra-alveolar pressure increases. Under conditions of arterial hypoxemia, the non-respiratory function of the lungs is disrupted - biological active substances begin to be produced, which have not only a bronchospastic, but also a vasospastic effect. At the same time, a violation of the vascular architecture 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, and increased blood viscosity. Alveolar hypoxia will lead to hypoxemic vasoconstriction through a reflex called the Euler-Liestrand reflex. Alveolar hypoxia led to hypoxemic vasoconstriction, increased intra-arterial pressure, which leads to increased 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 under conditions of tissue and alveolar hypoxia, the interstitium begins to produce angiotensin converting enzyme in greater quantities. The lungs are the main organ where this enzyme is formed. It converts angiotensin 1 into angiotensin 2. Hypoxemic vasoconstriction, the release of biologically active substances in conditions of restructuring of central hemodynamics will lead not just to an increase in pressure in the pulmonary artery, but to a persistent increase in it (above 30 mmHg), 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 persistently increases in the pulmonary artery. At the same time, persistent secondary pulmonary hypertension will lead to the fact that shunts open between the pulmonary artery and the bronchial arteries and unoxygenated blood enters the big circle blood circulation through the bronchial veins and also helps to increase 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 in itself, and hypertrophy with elements of dilatation quickly develops in it.

The fourth stage is hypertrophy or dilatation 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 dilatation and the development of predominantly right ventricular circulatory failure.

Pathogenesis of the development of cor pulmonale in the thoradiaphragmatic form: in this form, the leading one 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, in contrast to the obstructive type that is caused by chronic pulmonary heart disease. 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 cor pulmonale in the vascular form is that with thrombosis of the main branches of the pulmonary arteries, the blood supply to the pulmonary tissue sharply decreases, since along with thrombosis of the main branches, there is a concomitant reflex narrowing of the 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, angiotensin-converting enzyme.

The pathogenesis of cor pulmonale is multistage, multistage, and in some cases not entirely clear.

CLASSIFICATION OF HEART PULMONARY.

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

bronchopulmonary heart

thoradiaphragmatic

vascular

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

• subacute

  chronic

Acute cor pulmonale develops over a period of hours, minutes, or 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, it requires immediate assistance. Subacute can be compensated and decompensated mainly according to the right ventricular type. Chronic cor pulmonale can be compensated, subcompensated, or decompensated.

According to its genesis, acute cor pulmonale develops in vascular and bronchopulmonary forms. Subacute and chronic cor pulmonale can be vascular, bronchopulmonary, or thoradiaphragmatic.

Acute cor pulmonale develops primarily:

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

with pneumothorax (especially valvular),

during an attack of bronchial asthma (especially with status asthmaticus - a qualitatively new condition of patients with bronchial asthma, with complete blockade of beta2-adrenergic receptors, and with acute cor pulmonale);

for acute confluent pneumonia

right-sided total pleurisy

A practical example of subacute cor pulmonale is recurrent thromboembolism of small branches of the pulmonary arteries during an attack of bronchial asthma. A classic example is cancerous lymphangitis, especially with chorionepitheliomas and peripheral lung cancer. The thoracodiaphragmatic form develops with hypoventilation of central or peripheral origin - myasthenia gravis, botulism, poliomyelitis, etc.

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

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

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

stage of pulmonary heart failure of varying degrees (swelling in the extremities, enlarged abdomen, etc.).

Chronic cor pulmonale is divided into 4 stages according to the level of pulmonary insufficiency, arterial blood oxygen saturation, right ventricular hypertrophy and circulatory failure:

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

pulmonary failure 2 - VC/BVC 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.

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

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

CLINIC OF ACUTE PULMONARY HEART.

The most common cause of development is pulmonary embolism, 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 severe shortness of breath turning into inspiratory suffocation, rapidly increasing cyanosis, chest pain of various types, shock or collapse, rapidly increasing liver size, swelling in the legs, ascites, epigastric pulsation, tachycardia (120-140), harsh breathing , in some places weakened vesicular; Moist, varied rales are heard, especially in the lower parts of the lungs. Additional research methods, especially ECG, are of great importance in the development of acute pulmonary heart disease: a sharp deviation of the electrical axis to the right (R 3 >R 2 >R 1, S 1 >S 2 >S 3), P-pulmonale appears - a pointed P wave, in the second , third standard leads. Right bundle branch block is complete or incomplete, ST inversion (usually elevation), 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 signs may also occur in acute myocardial infarction of the posterior wall.

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

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

For valvular pneumothorax - surgical treatment. In case of confluent pneumonia, along with antibiotic treatment, diuretics and cardiac glycosides are necessarily prescribed.

CLINIC OF CHRONIC PULMONARY HEART.

Patients are concerned 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, shortness of breath of an expiratory nature with an unchanged respiratory rate, with restrictive processes, the duration of exhalation decreases and the respiratory rate increases. Upon objective examination, 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, edema of the lower extremities, ascites. The pulse is increased, the boundaries of the heart expand to the right, and then to the left, the tones are dull due to emphysema, the accent of the second tone is over the pulmonary artery. Systolic murmur at the xiphoid process due to dilatation 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 - a Graham-Still murmur, which is associated with relative insufficiency of the pulmonary valve. Above the lungs percussion there is a box sound, breathing is vesicular and harsh. In the lower parts of the lungs there are congestive, silent moist rales. On palpation of the abdomen - enlarged liver (one of the reliable, but not early signs pulmonary heart, since the liver can be displaced due to emphysema). The severity of symptoms depends on the stage.

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

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

The third stage - signs of right ventricular failure are added - an increase in the right border of cardiac dullness, an increase in the size of the liver. Constant swelling in the lower extremities.

The fourth stage is shortness of breath at rest, forced position, often accompanied by respiratory rhythm disorders such as Cheyne-Stokes and Biot. The swelling is constant, cannot be treated, the pulse is weak and frequent, the heart is bullish, the sounds are muffled, the systolic murmur at the xiphoid process. There is a lot of moist rales in the lungs. The liver is of considerable size and does not contract under the influence of glycosides and diuretics as fibrosis develops. Patients are constantly dozing.

Diagnosis of thoradiaphragmatic heart is often difficult; one must always remember about the possibility of its development in kyphoscoliosis, ankylosing spondylitis, etc. The most important sign is the early appearance of cyanosis, and a noticeable increase in shortness of breath without attacks of suffocation. 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. Associated with traumatic brain injury, obesity is accompanied by thirst, bulimia, and arterial hypertension. Diabetes mellitus often develops.

Chronic cor pulmonale in primary pulmonary hypertension is called Aerz's disease (described in 1901). A polyetiological disease of unknown origin, it mainly affects women from 20 to 40 years old. Pathomorphological studies have established that with primary pulmonary hypertension, thickening of the intima of the precapillary arteries occurs, that is, in the arteries muscular type thickening of the media is noted, 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 joints; 1/3 of patients may experience fainting, dizziness, and Raynaud's syndrome. And then shortness of breath increases, which is a sign that indicates that primary pulmonary hypertension is entering a stable final stage. Cyanosis quickly increases, which is expressed to the degree of a cast-iron tint, becomes permanent, and swelling quickly increases. The diagnosis of primary pulmonary hypertension is established by exclusion. Most often this diagnosis is pathological. In these patients, the entire clinical picture 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 cor pulmonale: for 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 findings: appear very late. One of the early symptoms is bulging of the pulmonary artery trunk on x-ray. The pulmonary artery bulges, often flattening the waist of the heart, and this heart is mistaken by many doctors for the mitral configuration of the heart.

ECG: indirect and direct signs of right ventricular hypertrophy appear:

deviation of the electrical axis of the heart to the right - R 3 >R 2 >R 1, S 1 >S 2 >S 3, angle greater than 120 degrees. The most basic indirect sign is an increase in the interval of the R wave in V1 by more than 7 mm.

direct signs are blockade of the right bundle branch, the amplitude of the R wave in V 1 is more than 10 mm with complete blockade of the right bundle branch. 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 the 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 are Doppler cardiography, echocardiography - enlargement of the right side of the heart, increased pressure in the pulmonary artery.

PRINCIPLES OF TREATMENT OF HEART PULMONARY.

Treatment of cor pulmonale involves treating the underlying disease. In case of exacerbation of obstructive diseases, bronchodilators and expectorants are prescribed. For Pickwick's syndrome - treatment of obesity, etc.

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

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

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

PREVENTION.

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

Increased pressure in the pulmonary capillary system (pulmonary hypertension, hypertension) is most often a secondary disease not directly related to vascular damage. The primary conditions have not been sufficiently studied, but the role of the vasoconstrictor mechanism, thickening of the arterial wall, and 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 symptoms are added as complications to the underlying chronic disease.

Some features of the blood supply to the lungs

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

The pulmonary artery is divided into 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 narrowing, resistance to blood flow increases and internal pressure in the vessels increases; expansion reduces pressure and reduces the force of resistance. The occurrence of pulmonary hypertension depends on this mechanism. The total network of pulmonary capillaries covers an area of ​​140 m2.

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

How is pressure in the pulmonary vessels regulated?

The amount of blood pressure in the pulmonary vessels is regulated by:

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

Extensive receptor zones are located in large and medium-sized arteries, at branching points, and in veins. Arterial spasm leads to impaired oxygen saturation of the blood. And tissue hypoxia promotes the release of substances into the blood 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 contrary, causes a vasoconstrictor effect. Under normal conditions, their interaction is balanced.

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

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

Pulmonary arterial hypertension, according to international experts, begins at the upper level – 30 mmHg. Art.

Factors causing hypertension in the pulmonary circulation

The main factors of pathology, according to V. Parin’s classification, are divided into 2 subtypes. Functional factors include:

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

Anatomical factors include:

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

What causes secondary pulmonary hypertension?

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

• chronic inflammatory diseases bronchi and lung tissue (pneumosclerosis, emphysema, tuberculosis, sarcoidosis);
• thoracogenic pathology in violation of the structure of the chest and spine (Bechterew's disease, consequences of thoracoplasty, kyphoscoliosis, Pickwick's syndrome in obese people);
• mitral stenosis;
• congenital heart defects (for example, patent ductus arteriosus, “windows” in the interatrial and interventricular septum);
• tumors of the heart and lungs;
• diseases accompanied by thromboembolism;
• vasculitis in the area of ​​the pulmonary arteries.

What causes primary hypertension?

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

It has been established that women make up 60% of patients. Pathology is detected both in childhood and in old age, but average age identified patients - 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 bone protein gene, angioproteins, their influence on the synthesis of serotonin, and increased blood clotting due to the blocking of anticoagulant factors has been established.

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

The result is hypertrophy, then expansion of the cavity, loss of right ventricular tone 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 lobes of the lung tissue, causing a lack of surfactant substance on its surface);
• severe diffuse inflammation (pneumonitis) associated with the development of massive allergic reaction on inhaled odors of paint, perfume, flowers.

However, pulmonary hypertension can be caused by food, drugs and folk remedies therapy.

Pulmonary hypertension in newborns can be caused by:

• continued fetal circulation;
• meconium aspiration;
• diaphragmatic hernia;
• general hypoxia.

In children, hypertension is promoted by enlarged tonsils.

Classification according to the nature of the flow

It is convenient for clinicians to divide hypertension in the pulmonary vessels according to the timing of development into acute and chronic form. Such a classification helps to “combine” the most common causes and clinical course.

Acute hypertension occurs due to:

• pulmonary embolism;
• severe status asthmaticus;
• 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;
• increase in 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;
• proliferation of myxoma or thrombus in the left atrium;
• gradual decompensation of chronic left ventricular failure, for example, with coronary disease or cardiomyopathies.

The following 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 injuries, mechanical breathing;
• mechanical (obstructive) origin, associated with narrowing of the arteries - 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, which worsens with physical activity (can develop in paroxysms);
• general weakness;
• rarely loss of consciousness (as opposed to neurological causes without convulsions and involuntary urination);
• paroxysmal chest pains, similar to angina pectoris, but accompanied by an increase in shortness of breath (scientists explain them by a reflex connection between the pulmonary and coronary vessels);
• the admixture of blood in the sputum when coughing is characteristic of significantly increased pressure (associated with the release of red blood cells into the interstitial space);
• hoarseness is detected in 8% of patients (caused by mechanical compression of the recurrent nerve on the left by the dilated pulmonary artery).

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

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

• a blue tint to the lips, fingers, ears, which intensifies as shortness of breath becomes more severe;
• the symptom of “drum” fingers is detected only with prolonged inflammatory diseases, vices;
• the pulse is weak, arrhythmias are rare;
• blood pressure is normal, with a tendency to decrease;
• palpation in the epigastric zone makes it possible to determine increased impulses of the hypertrophied right ventricle;
• On auscultation, an accentuating second sound on the pulmonary artery is heard, and a diastolic murmur is possible.

Association of pulmonary hypertension with permanent reasons and certain diseases allows us to identify variants in the clinical course.

Portopulmonary hypertension

Pulmonary hypertension leads to a simultaneous increase in portal vein pressure. In this case, the patient may or may not have cirrhosis of the liver. It accompanies chronic liver diseases in 3–12% of cases. The symptoms are no different from those listed. Swelling and heaviness in the hypochondrium on the right are more pronounced.

Pulmonary hypertension with mitral stenosis and atherosclerosis

The disease varies in severity. 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. Functional and organic mechanisms of hypertension are combined.

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

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

Vascular changes progress and become irreversible. Atherosclerotic plaques do not grow to large sizes, but they are sufficient to narrow 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 artery embolization;
2. subacute - develops with bronchial asthma, lung carcinomatosis;
3. chronic - caused by emphysema, a functional spasm of the arteries, turning into an organic narrowing of the artery, characteristic of chronic bronchitis, pulmonary tuberculosis, bronchiectasis, frequent pneumonia.

An increase in resistance in the vessels puts 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). Clinical signs of pulmonary hypertension gradually increase.

Hypertensive crises in the vessels of the “small circle”

A 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;
• feeling of external compression of the chest;
• severe cough, sometimes with hemoptysis;
• pain in the interscapular region radiating to the anterior sections and sternum;
• cardiopalmus.

Upon examination, the following is revealed:

• patient's agitated state;
• inability to lie in bed due to shortness of breath;
• pronounced cyanosis;
• weak rapid pulse;
• visible pulsation in the area of ​​the pulmonary artery;
• swollen and pulsating neck veins;
• excretion of copious amounts of light-colored urine;
• involuntary defecation is possible.

Diagnostics

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

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

Russian scientists F. Uglov and A. Popov proposed to distinguish between 4 elevated levels 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 hypertrophy of the right chambers of the heart:

1. X-ray - indicates an expansion of the right borders of the cardiac shadow, an increase in the arch of the pulmonary artery, and reveals its aneurysm.
2. Ultrasound methods (ultrasound) - allow you to accurately determine the size of the heart chambers and the thickness of the walls. A type of ultrasound - Dopplerography - shows disturbances in blood flow, flow speed, and the presence of obstacles.
3. Electrocardiography - reveals early signs of hypertrophy of the right ventricle and atrium by a characteristic deviation to the right of the electrical axis, an enlarged atrial “P” wave.
4. Spirography is a method of studying the possibility of breathing; it determines 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 more in a modern way- computed tomography.

More complex methods (radionuclide scintigraphy, angiopulmonography). A biopsy to study the condition of 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 oxygen saturation of the blood is measured. This helps in identifying the causes of secondary hypertension. During the procedure, vasodilators are administered and the reaction of the arteries is checked, 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-asthmatic drugs and vasodilators provide assistance. Folk remedies can further enhance the allergic mood of the body.

If a patient has chronic embolization, the only remedy is surgical removal of the thrombus (embolectomy) by excision from the pulmonary trunk. The operation is carried out in specialized centers; a transition to artificial blood circulation is necessary. Mortality 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 good review seriously ill patients. This is considered a favorable sign.

An analogue of Prostacyclin, Epoprostenol, is administered intravenously through a subclavian catheter. Apply inhalation forms medications (Iloprost), Beraprost tablets orally. 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, and anticoagulants.

The use of solutions of Eufillin and No-shpa has a temporary effect.

Are there any folk remedies?

It is impossible to cure pulmonary hypertension with folk remedies. Recommendations on the use of diuretics and cough suppressants are used very carefully.

You should not get carried away with healing for this pathology. Lost time in diagnosis and initiation of therapy may be lost forever.

Forecast

Without treatment, the average survival time for patients is 2.5 years. Treatment with Epoprostenol increases the lifespan to five years in 54% of patients. The prognosis of pulmonary hypertension is unfavorable. Patients die from increasing right ventricular failure or thromboembolism.

Patients with pulmonary hypertension due to heart disease and arterial sclerosis live up to 32–35 years of age. The crisis course aggravates the patient’s condition and is regarded as an unfavorable prognosis.

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

Clinic, 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 heart tissue, causing defects. At the same time, joints and nerve fibers in the body are affected.

The inflammatory response is triggered predominantly hemolytic streptococcus group A, which causes diseases of the upper respiratory tract(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 onset of the disease. It has been established that every fourth patient with rheumatic heart disease has isolated mitral valve stenosis. In 40% of cases, combined valve damage develops. According to statistics, mitral stenosis is more common in women.

Inflammation leads to damage to the edge of the valve leaflets. After the acute period, thickening and fibrosis of the edges of the valves occurs. When tendon cords and muscles are involved in the inflammatory process, they shorten and scar. 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 reduction in the valve opening by half. Now, higher pressure is needed to push blood through the narrow opening from the left atrium into the left ventricle. Increased pressure in the left atrium leads to “jamming” in the pulmonary capillaries. Clinically, this process manifests itself as dyspnea on exertion.

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

Clinical features

Rheumatic heart disease with damage to the mitral valve 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 loads pathological processes are getting worse. As the disease progresses, the patient is unable to breathe normally when lying down (orthopnea). Only when taking a forced sitting position does the patient breathe. In some cases, severe shortness of breath occurs at night with attacks of suffocation, which forces the patient to sit.

Patients can withstand moderate stress. However, they are at risk of developing pulmonary edema, which can be caused by:

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

During a coughing attack, hemoptysis may occur. The causes of the complication are associated with rupture of the bronchial veins. Such profuse bleeding is rarely life-threatening. During choking, blood-stained sputum may appear. With a long course of the disease, against the background of heart failure, pulmonary infarction may occur.

Thromboembolism poses a threat to life. During atrial fibrillation, a detached blood clot can travel through the bloodstream to the kidneys, arteries of the heart, the area of ​​the aortic bifurcation, or the brain.

Symptoms include:

• chest pain;
• hoarseness (due to compression of the laryngeal nerve);
• ascites;
• liver enlargement;
• swelling.

Diagnostics

In order to make a diagnosis, a series of examinations are carried out. The doctor examines the pulse, blood pressure, and interviews the patient. In cases where pulmonary hypertension has not yet developed, pulse and blood pressure are normal. In severe pulmonary hypertension, a change in heart rhythm occurs. During auscultation, changes in heart sounds are detected and the severity of stenosis is assessed.

Instrumental examination methods include:

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

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

Doppler ultrasound reveals the severity of the stenosis and the speed of blood flow. If the patient is planning to undergo valve replacement surgery, cardiac catheterization is included in the examination.

Treatment

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

• Lifestyle changes.
• Prevention of relapses of rheumatic fever.
• Antibiotic therapy for endocarditis (if any).
• Prescription of anticoagulants (Warfarin).
• Diuretics (Furosemide, Lasix, etc.).
• Nitrates (when present) chronic failure valve).
• 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 valve leaflets, cleaning them from calcifications and blood clots during surgery);
• mitral valve replacement;
• percutaneous balloon valvuloplasty.

Balloon plasty is performed on patients whose valve leaflets are sufficiently flexible and movable. The catheter is inserted through femoral vein into the interatrial septum. A balloon is placed at the site of stenosis of the hole and inflated. 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 the operation to be performed on women who are expecting a child.

If the patient has a severe degree of calcification, pronounced changes in the valve, 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, treatment with anticoagulants (Warfarin) under the control of blood clotting is important. With inadequate therapy after prosthetics, there is a possible risk of thromboembolism.

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

Rheumatic disease of the aortic valve

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

During attacks of rheumatism, valvulitis (inflammation of the valves) develops. This leads to gluing 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.

Due to chronic processes, patients adapt to pathological changes. Myocardial hypertrophy maintains cardiac output for a long time without symptoms or valve dilatation. The disease is characterized by a long asymptomatic period. The patient may complain of angina attacks after exercise.

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

The development of pathology leads to shortness of breath, dizziness, suffocation in a lying position (orthopnea). During the examination, the doctor detects a low-fill pulse, a disturbance in heart sounds, and a rough systolic murmur of ejection into the aorta. Additionally, the doctor prescribes an echocardiogram.

Treatment includes:

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

To relieve attacks of angina, patients are prescribed long-acting nitrates. Treatment includes the administration of cardiac glycosides and diuretics. The progression of the disease worsens the prognosis, so patients at a late stage of valvular stenosis are indicated for valve replacement, since drug treatment does not provide improvement in the condition.

Prevention

Chronic rheumatic pathology is prevented timely treatment laryngitis, pharyngitis caused by hemolytic streptococcus A. Diseases are treated with antibiotics penicillin series or erythromycin for allergies to penicillins.

Secondary prevention consists of preventing rheumatic attacks and fever. Patients are prescribed antibiotics on an individual basis. If there are signs of carditis, patients continue to receive a course of antibiotic treatment for ten years after a rheumatic attack. It is worth noting that neglect of primary prevention leads to the risk of developing defects after rheumatism. Conservative treatment of defects helps slow the progression of pathology and increases patient survival.

Signs, degrees and treatment of pulmonary hypertension

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

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

This disease sometimes occurs in children. With pulmonary hypertension in newborns, the pulmonary circulation is unable to maintain or reduce the already reduced vascular resistance of the lungs at birth. This condition is usually observed in post-term or premature babies.

Causes

There are many causes 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 disrupted 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 close.
• Fibrosis of lung tissue. This condition is characterized by changes in lung tissue when connective tissue replaces normal cells.

Normal lung and with bronchiectasis

The causes of pulmonary hypertension may also lie in heart disease. Among them, importance is attached to congenital defects, such as patent ductus ductus, septal defects and patent foramen ovale. The prerequisite may be diseases in which the functionality of the heart muscle is impaired, contributing to blood stagnation in the pulmonary circulation. Such ailments include cardiomyopathy, ischemic heart 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. When it occurs, the alveoli do not receive enough oxygen. This is observed with uneven pulmonary ventilation, which gradually increases. If a reduced amount of oxygen enters the lung tissue, the blood vessels of the pulmonary system narrow.
2. Changes in the structure of lung tissue when connective tissue grows.
3. Increased red blood cell count. This condition is caused by constant hypoxia and tachycardia. Microthrombi appear as a result of vascular spasm and increased adhesion of blood cells. They clog 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 damage to the vessels of the pulmonary circulation of an autoimmune nature.

Several other factors may contribute to the development of pulmonary hypertension. It may be taking some medicines that affect 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 hypertension. These include pregnancy, female gender, hypertension. Liver cirrhosis, HIV infection, blood diseases, hyperthyroidism, hereditary diseases, portal hypertension and other rare diseases can help develop pulmonary hypertension. Compression of the pulmonary vessels by a tumor, the effects of obesity and a deformed chest, as well as elevation at high altitudes can have an effect.

Classification

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

Primary pulmonary hypertension

With this form, there is a persistent increase in pressure in the artery, however, not against the background of cardiovascular diseases 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 according to a dominant type.

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

Primary hypertension can develop against the background of concentric fibrosis of the pulmonary artery. This leads to a narrowing of its lumen and an increase in blood flow pressure. As a result of this, and also due to the inability of healthy pulmonary vessels to support the movement of blood with high pressure or the inability of altered vessels to support the movement of blood with normal pressure, a compensatory mechanism develops. It is based on the emergence of bypass pathways, which are open arteriovenous shunts. The body is trying to lower the level high pressure due to the transfer of blood through them. However, the muscle wall of the arterioles is weak, so the shunts quickly fail. This creates areas that also increase the pressure value. Shunts disrupt proper blood flow, which leads to disruption of blood oxygenation and oxygen supply to tissues. Despite 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, which contribute to the development of the secondary form:

• Diseases that cause LV dysfunction. The diseases that are the root cause of hypertension and accompany diseases of this group include: ischemic myocardial damage, aortic valve defects, myocardial and cardiomyopathic damage to the LV.
• Diseases leading to increased pressure in the left atrium chamber: developmental anomalies, tumor lesions of the atrium and mitral stenosis.

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

• Functional mechanisms. Their development is due to the disruption of normal and or the formation of new functional pathological features. Drug therapy is aimed specifically at their correction and elimination. Functional links include an increase in blood volume per minute, an increase in blood viscosity, the pathological Savitsky reflex, the influence of frequent bronchopulmonary infections and the effect of biologically active elements on the artery.
• Anatomical mechanisms. Their occurrence is preceded by certain anatomical defects in the pulmonary artery or pulmonary circulatory system. Drug therapy in this case brings virtually no benefit. Some defects can be corrected with surgery.

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

1. Pulmonary hypertension stage 1. This form occurs without disrupting the activity of the physical plane. Normal exercise does not lead to shortness of breath, dizziness, weakness or chest pain.
2. 2 degree. The disease causes minor impairment of activity. 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. Minor physical activity causes shortness of breath and the other symptoms listed above.
4. Grade 4 is accompanied by the mentioned symptoms at the slightest load and at rest.

There are two more forms of the disease:

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

Depending on the pressure, three more types of 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 pressure greater than 45 mm Hg.

Symptoms

The disease can occur without symptoms in the compensation stage. Because of this, it is most often discovered when a severe form has begun to develop. Initial manifestations are observed when the pressure in the pulmonary artery system is increased two or more times compared to normal. As the disease progresses, symptoms such as weight loss, shortness of breath, fatigue, hoarseness, cough and palpitations appear. A person cannot explain them. At an early stage of the disease, fainting may occur 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 that somehow indicate 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 secondary disease is a complication of other diseases, during diagnosis it is important to identify the underlying disease. This is possible thanks to the following measures:

• Study of the medical history. This includes collecting information about when shortness of breath, chest pain and other symptoms began, what the patient associates with 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, enlarged liver, swelling lower limbs, pulsation of neck veins. Listening to the lungs and heart with a phonendoscope is also performed.
• ECG. Allows you to see signs of enlargement of the right heart.
• A chest x-ray can help identify an enlarged heart.
• Ultrasound of the heart. Helps estimate the size of the heart and indirectly determine the pressure in the arteries of the lungs.
• Arterial catheterization. Using this method, you can determine the pressure in it.

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

Treatment

Treatment of pulmonary hypertension is based on several methods.

1. Non-drug treatment. It includes drinking liquid in an amount of no more than 1.5 liters per day, as well as reducing the amount of table salt consumed. Oxygen therapy is effective, as it helps eliminate acidosis and restore nervous function. central system. It is important for patients to avoid situations that cause shortness of breath and other symptoms, so avoiding physical activity 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: thromboendarectomy, atrial septostomy.
4. Traditional methods. Traditional treatment can only be used on the recommendation of a doctor.

Consequences

A common complication of the disease is RV heart failure. It is accompanied by cardiac arrhythmia, which manifests itself as atrial fibrillation. Severe stages of hypertension are characterized by the development of thrombosis of pulmonary arterioles. In addition, in the blood vessels can develop hypertensive crises 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 severe stages of the disease, thrombosis of pulmonary arterioles is possible

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

Prevention

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

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

By leaving a comment, you accept the User Agreement

• Arrhythmia
• Atherosclerosis
• Varicose veins
• Varicocele
• Haemorrhoids
• Hypertension
• Hypotension
• Diagnostics
• Dystonia
• Stroke
• heart attack
• Ischemia
• Blood
• Operations
• Heart
• Vessels
• Angina pectoris
• Tachycardia
• Thrombosis and thrombophlebitis

• Heart tea
• Hypertension
• Pressure bracelet
• Normalife
• Allapinin
• Asparkam
• Detralex

Cor pulmonale (CP) is hypertrophy and/or dilatation of the right ventricle (RV) resulting from pulmonary arterial hypertension caused by diseases affecting the function and/or structure of the lungs, and not associated with primary pathology of the left heart or congenital heart defects. LS is formed as a result of diseases of the bronchi and lungs, thoracodiaphragmatic lesions or pathology of the pulmonary vessels. The development of chronic pulmonary heart disease (CPP) is most often caused by chronic pulmonary failure (CPF), and the main reason for the formation of CPP is alveolar hypoxia, causing spasm of the pulmonary arterioles.

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

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

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

DEFINITION

Pulmonary heart- is hypertrophy and/or dilatation of the right ventricle resulting from pulmonary arterial hypertension caused by diseases affecting the function and/or structure of the lungs and not associated with primary pathology of the left heart or birth defects hearts.

The pulmonary heart (CP) is formed on the basis pathological changes the lung itself, violations of extrapulmonary respiratory mechanisms that provide ventilation of the lung (damage to the respiratory muscles, disturbance of the central regulation of breathing, elasticity of the osteochondral formations of the chest or conduction nerve impulse By n. diaphragmicus, obesity), as well as pulmonary vascular damage.

CLASSIFICATION

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

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

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

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

The development of CHL is directly related to chronic pulmonary failure (CPF). In clinical practice, a classification of CLN is used based on the presence of shortness of breath. There are 3 degrees of CLN: the appearance of shortness of breath with previously available efforts - I degree, shortness of breath with normal exertion - II degree, shortness of breath at rest - III degree. It is sometimes appropriate to supplement the above classification with data on the gas composition of the blood and the pathophysiological mechanisms of the development of pulmonary failure (Table 7.2), which allows the selection of pathogenetically based therapeutic measures.

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

Table 7.1.

End of table. 7.1.

Note. The diagnosis of cor pulmonale is made after the diagnosis of the underlying disease: when formulating the diagnosis, only the first two columns of the classification are used. Columns 3 and 4 contribute to an in-depth understanding of the essence of the process and the choice of therapeutic tactics

Table 7.2.

Clinical and pathophysiological classification of chronic pulmonary failure

(Alexandrov O.V., 1986)

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

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

The main cause of the development of chronic pulmonary heart disease is chronic obstructive pulmonary disease.

PATHOGENESIS

The development of chronic drugs is based on the gradual formation of pulmonary arterial hypertension, caused by several pathogenetic mechanisms. The main cause of PH in patients with bronchopulmonary and thoracodiaphragmatic forms of CHL is alveolar hypoxia, the role of which in the development of pulmonary vasoconstriction was first shown in 1946 by U. Von Euler and G. Lijestrand. The development of the Euler-Lillestrand reflex is explained by several mechanisms: the effect of hypoxia is associated with the development of depolarization of vascular smooth muscle cells and their contraction due to changes in the function of potassium channels of cell membranes;

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

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

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

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

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

Patients with severe obesity develop Pickwick's syndrome (named after the work of Charles Dickens), which is manifested by hypoventilation with hypercapnia, which is associated with a decrease in the sensitivity of the respiratory center to CO 2, as well as impaired ventilation due to mechanical restriction by adipose tissue with dysfunction (fatigue) respiratory muscles.

Increased blood pressure in the pulmonary artery may initially contribute to an increase in the volume of perfusion of the pulmonary capillaries, but over time, hypertrophy of the RV myocardium develops, followed by its contractile failure. Pressure indicators in the pulmonary circulation are presented in table. 7.3.

Table 7.3

Pulmonary hemodynamic parameters

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

CLINIC

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

A characteristic complaint of patients is shortness of breath. First, during physical activity (stage I of CLN), and then at rest (stage III of CLN). It is expiratory or mixed in nature. A long course (years) of COPD dulls the patient’s attention and forces him to consult a doctor when shortness of breath appears during light physical exertion or at rest, that is, already in stage II-III chronic pulmonary disease, when the presence of chronic pulmonary disease is indisputable.

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

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

Tachycardia is a common complaint in patients with CHL and appears even at the stage of development of CHL in response to arterial hypoxemia. Heart rhythm disorder is uncommon. Availability atrial fibrillation, especially in people over 50 years of age, is usually associated with concomitant ischemic heart disease.

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

With decompensation of the cor pulmonale, swelling may appear in the legs, which first appears most often during an exacerbation of bronchopulmonary disease and is first localized in the area of ​​the feet and ankles. As right ventricular failure progresses, edema spreads to the area of ​​the legs and thighs, and rarely, in severe cases of right ventricular failure, an increase in the volume of the abdomen due to the formation of ascites is noted.

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

In patients with CLN and CLS, encephalopathy may develop due to chronic hypercapnia and cerebral hypoxia, as well as impaired vascular permeability. With severe encephalopathy, some patients experience increased excitability, aggressiveness, euphoria and even psychosis, while other patients experience lethargy, depression, drowsiness during the day and insomnia at night, and headaches. Fainting rarely occurs during exercise as a result of severe hypoxia.

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

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

Blood pressure in patients with compensated CHL is often increased, and in decompensated patients it is decreased.

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

The clinical picture of chronic pulmonary heart disease is determined by the severity of pulmonary pathology, as well as pulmonary and right ventricular heart failure.

INSTRUMENTAL DIAGNOSTICS

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

Electrocardiographic diagnosis of CHL comes down to identifying RV hypertrophy. The main (“direct”) ECG criteria for pancreatic hypertrophy include: 1) R in V1>7mm; 2) S in V5-6 > 7 mm; 3) RV1 + SV5 or RV1 + SV6 > 10.5 mm; 4) RaVR > 4 mm; 5) SV1,V2 =s2 mm; 6) RV5,V6<5 мм; 7) отношение R/SV1 >1; 8) complete blockade of the right bundle branch with RV1>15 mm; 9) incomplete blockade of the right bundle branch with RV1>10 mm; 10) negative TVl and decreased STVl,V2 with RVl>5 mm and the absence of coronary insufficiency. If there are 2 or more “direct” ECG signs, the diagnosis of pancreatic hypertrophy is considered reliable.

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

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

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

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

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

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

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

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

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

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

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

4. RV diastolic function is assessed using transtricuspid diastolic flow in pulse-mode

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

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

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

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

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

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

1. In PH, the pattern of movement of the posterior leaflet of the pulmonary artery valve changes, which is determined in M-mode: a characteristic indicator of PH is the presence of a mid-systolic wave due to partial closure of the valve, which forms a W-shaped movement of the valve in systole.

2. In patients with pulmonary hypertension, due to increased pressure in the right ventricle, the interventricular septum (IVS) is flattened, and the left ventricle resembles the letter D along its short axis (D-shaped left ventricle). With a high degree of PH, the IVS becomes like a wall of the RV and moves paradoxically in diastole towards the left ventricle. When the pressure in the pulmonary artery and right ventricle becomes more than 80 mmHg, the left ventricle decreases in volume, is compressed by the dilated right ventricle and takes on a crescent shape.

3. Possible regurgitation on the pulmonary valve (normally, first-degree regurgitation is possible in young people). With a continuous wave Doppler study, it is possible to measure the velocity of pulmonary regurgitation with further calculation of the value of the end-diastolic pressure gradient of the PA-RV.

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

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

Catheterization of the right heart and pulmonary artery

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

Radionuclide ventriculography (RVG)

RVG measures right ventricular ejection fraction (RVEF). RVEF is considered abnormal if it is below 40-45%, but RVEF itself is not a good indicator of right ventricular function. It allows you to evaluate systolic function right ventricle, which strongly depends on afterload, decreasing when the latter increases. Therefore, a decrease in RVF is recorded in many patients with COPD, not being an indicator of true right ventricular dysfunction.

Magnetic resonance imaging (MRI)

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

The presence of chronic pulmonary disease (as the cause of chronic pulmonary disease) requires a special study of the function of external respiration. The doctor is tasked with clarifying the type of ventilation failure: obstructive (impaired passage of air through the bronchi) or restrictive (reduced gas exchange area). In the first case, examples include chronic obstructive bronchitis, bronchial asthma, and in the second case, pneumosclerosis, lung resection, etc.

TREATMENT

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

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

2) treatment of chronic pulmonary hypertension and pulmonary hypertension;

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

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

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

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

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

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

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

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

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

In patients with hypoventilation associated with reduced activity of the respiratory center, medications that increase central inspiratory activity - respiratory stimulants - can be used as auxiliary methods of therapy. They should be used in cases of moderate respiratory depression that do not require the use of O2 or mechanical ventilation (sleep apnea syndrome, obesity-hypoventilation syndrome), or when oxygen therapy is not possible. A few drugs that increase arterial oxygenation include nicetamide, acetozalamide, doxapram and medroxyprogesterone, but all of these drugs have a large number of side effects when used over a long period of time and therefore can only be used for a short time, for example during an exacerbation of the disease.

Currently, almitrina bismesylate is one of the drugs that can correct hypoxemia for a long time in patients with COPD. Almitrin is a specific ago-

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

Vasodilators

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

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

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

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

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

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

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

In Russia, from the group of prostanoids for the treatment of patients with drugs, only prostaglandin E 1 (vasaprostan) is currently available, which is prescribed intravenously by drip at a rapid rate.

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

Endothelin receptor antagonists

Activation of the endothelin system in patients with PH served as a rationale for the use of endothelin receptor antagonists. The effectiveness of two drugs of this class (bosentan and sitaxentan) in the treatment of patients with CHL that developed against the background of primary PH or against the background of systemic connective tissue diseases has been proven.

Phosphodiesterase type 5 inhibitors

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

Long-term oxygen therapy

In patients with bronchopulmonary and thoracodiaphragmatic forms of CHL the main role in the development and progression of the disease belongs to alveolar hypoxia, therefore oxygen therapy is the most pathogenetically substantiated method of treating these patients. The use of oxygen in patients with chronic hypoxemia is critical and must be constant, long-term, and usually carried out at home, which is why this form of therapy is called long-term oxygen therapy (LOT). The goal of DCT is to correct hypoxemia to achieve paO 2 values ​​>60 mm Hg. and Sa0 2 >90%. It is considered optimal to maintain paO 2 within 60-65 mm Hg, and exceeding these values ​​leads to only a slight increase in Sa0 2 and oxygen content in arterial blood, but may be accompanied by CO 2 retention, especially during sleep, which has negative consequences.

effects on the function of the heart, brain and respiratory muscles. Therefore, VCT is not indicated for patients with moderate hypoxemia. Indications for DCT: RaO 2<55 мм рт.ст. или Sa0 2 < 88% в покое, а также раО 2 56-59 мм рт.ст. или Sa0 2 89% при наличии легочного сердца или полицитемии (гематокрит >55%). For most patients with COPD, an O2 flow of 1-2 l/min is sufficient, and in the most severe patients the flow can be increased to 4-5 l/min. The oxygen concentration should be 28-34% vol. It is recommended to conduct VCT at least 15 hours a day (15-19 hours/day). The maximum breaks between oxygen therapy sessions should not exceed 2 hours in a row, because breaks of more than 2-3 hours significantly increase pulmonary hypertension. Oxygen concentrators, liquid oxygen tanks and cylinders with compressed gas. The most commonly used are concentrators (permeators), which release oxygen from the air by removing nitrogen. VCT increases the life expectancy of patients with CLN and CHL by an average of 5 years.

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

Long-term oxygen therapy is the most effective method of treating chronic pulmonary insufficiency and congestive heart disease, increasing the life expectancy of patients by an average of 5 years.

Long-term home ventilation

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

NO inhalation therapy

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

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

CPAP therapy

Continuous positive airway pressure therapy method (continuous positive airway pressure- CPAP) is used as a treatment method for chronic respiratory failure and chronic pulmonary hypertension in patients with obstructive sleep apnea syndrome, preventing the development of airway collapse. The proven effects of CPAP are the prevention and straightening of atelectasis, increasing lung volumes, reducing ventilation-perfusion imbalance, increasing oxygenation, lung compliance, and redistributing fluid in the lung tissue.

cardiac glycosides

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

Diuretics

In the treatment of patients with decompensated CHL with edematous syndrome, therapy with diuretics, including antagonists, is used

aldosterone (aldactone). Diuretics should be prescribed cautiously, with small doses, since with the development of RV failure, cardiac output is more dependent on preload, and, therefore, excessive reduction in intravascular fluid volume can lead to a decrease in RV filling volume and a decrease in cardiac output, as well as an increase in blood viscosity and a sharp decrease in pressure in the pulmonary artery, thereby worsening the diffusion of gases. Other serious side effect diuretic therapy is metabolic alkalosis, which in patients with COPD with respiratory failure can lead to inhibition of the activity of the respiratory center and deterioration of gas exchange rates.

Angiotensin-converting enzyme inhibitors

In the treatment of patients with decompensated cor pulmonale in recent years, angiotensin-converting enzyme inhibitors (ACEIs) have come to the forefront. ACEI therapy in patients with CHL leads to a decrease in pulmonary hypertension and an increase in cardiac output. In order to select effective therapy for CHL in patients with COPD, it is recommended to determine the polymorphism of the ACE gene, because Only patients with ACE II and ID gene subtypes exhibit a pronounced positive hemodynamic effect of ACE inhibitors. It is recommended to use ACE inhibitors in minimal therapeutic doses. In addition to the hemodynamic effect, there is a positive effect of ACE inhibitors on the size of the heart chambers, remodeling processes, exercise tolerance and an increase in life expectancy in patients with heart failure.

Angiotensin II receptor antagonists

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

Atrial septostomy

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

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

Lung or heart-lung transplantation

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

PULMONARY HEART.

Relevance of the topic: Diseases of the bronchopulmonary system and chest are of great importance in affecting the heart. Damage to the cardiovascular system in diseases of the bronchopulmonary apparatus is referred to by most authors as cor pulmonale.

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

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

Hypertrophy of the right ventricle and its dilatation due to 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 dilatation 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:

“Pulmonary heart is a complex of hemodynamic disorders in the pulmonary circulation, developing as a result of diseases of the bronchopulmonary apparatus, deformations of the chest, and primary damage to the pulmonary arteries, which at the final stage manifests itself as right ventricular hypertrophy and progressive circulatory failure.”

ETIOLOGY OF HEART PULMONARY.

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, as post-tuberculosis outcomes

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

Diseases that primarily affect the chest and diaphragm with limitation of their mobility:

kyphoscoliosis

multiple rib injuries

Pickwickian syndrome in obesity

ankylosing spondylitis

pleural suppuration after 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 cause 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

thoradiaphragmatic

vascular

Standards for values ​​characterizing the hemodynamics of the pulmonary circulation.

Systolic pressure in the pulmonary artery is approximately five times less than 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 mmHg, the diastolic pressure is more than 15, and the mean pressure is more than 22 mmHg.

PATHOGENESIS.

The pathogenesis of cor pulmonale is based on pulmonary hypertension. Since cor pulmonale most often develops in bronchopulmonary diseases, we’ll start with that. 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 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 of chronic heart diseases, especially chronic obstructive bronchitis.

All 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 intra-alveolar pressure increases. Under conditions of arterial hypoxemia, the non-respiratory function of the lungs is disrupted - biological active substances begin to be produced, which have not only a bronchospastic, but also a vasospastic effect. At the same time, a violation of the vascular architecture 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, and increased blood viscosity. Alveolar hypoxia will lead to hypoxemic vasoconstriction through a reflex called the Euler-Liestrand reflex. Alveolar hypoxia led to hypoxemic vasoconstriction, increased intra-arterial pressure, which leads to increased 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 under conditions of tissue and alveolar hypoxia, the interstitium begins to produce angiotensin converting enzyme in greater quantities. The lungs are the main organ where this enzyme is formed. It converts angiotensin 1 into angiotensin 2. Hypoxemic vasoconstriction, the release of biologically active substances in conditions of restructuring of central hemodynamics will lead not just to an increase in pressure in the pulmonary artery, but to a persistent increase in it (above 30 mmHg), 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 persistently increases in the pulmonary artery. At the same time, persistent secondary pulmonary hypertension will lead to the fact that the shunts between the pulmonary artery and the bronchial arteries open 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 in itself, and hypertrophy with elements of dilatation quickly develops in it.

The fourth stage is hypertrophy or dilatation 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 dilatation and the development of predominantly right ventricular circulatory failure.

Pathogenesis of the development of cor pulmonale in the thoradiaphragmatic form: in this form, the leading one 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, in contrast to the obstructive type that is caused by chronic pulmonary heart disease. 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 cor pulmonale in the vascular form is that with thrombosis of the main branches of the pulmonary arteries, the blood supply to the pulmonary tissue sharply decreases, since along with thrombosis of the main branches, there is a concomitant reflex narrowing of the 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, angiotensin-converting enzyme.

The pathogenesis of cor pulmonale is multistage, multistage, and in some cases not entirely clear.

CLASSIFICATION OF HEART PULMONARY.

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

bronchopulmonary heart

thoradiaphragmatic

vascular

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

• subacute

  chronic

Acute cor pulmonale develops over a period of hours, minutes, or 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, it requires immediate assistance. Subacute can be compensated and decompensated mainly according to the right ventricular type. Chronic cor pulmonale can be compensated, subcompensated, or decompensated.

According to its genesis, acute cor pulmonale develops in vascular and bronchopulmonary forms. Subacute and chronic cor pulmonale can be vascular, bronchopulmonary, or thoradiaphragmatic.

Acute cor pulmonale develops primarily:

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

with pneumothorax (especially valvular),

during an attack of bronchial asthma (especially with status asthmaticus - a qualitatively new condition of patients with bronchial asthma, with complete blockade of beta2-adrenergic receptors, and with acute cor pulmonale);

for acute confluent pneumonia

right-sided total pleurisy

A practical example of subacute cor pulmonale is recurrent thromboembolism of small branches of the pulmonary arteries during an attack of bronchial asthma. A classic example is cancerous lymphangitis, especially with chorionepitheliomas and peripheral lung cancer. The thoracodiaphragmatic form develops with hypoventilation of central or peripheral origin - myasthenia gravis, botulism, poliomyelitis, etc.

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

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

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

stage of pulmonary heart failure of varying degrees (swelling in the extremities, enlarged abdomen, etc.).

Chronic cor pulmonale is divided into 4 stages according to the level of pulmonary insufficiency, arterial blood oxygen saturation, right ventricular hypertrophy and circulatory failure:

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

pulmonary failure 2 - VC/BVC 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.

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

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

CLINIC OF ACUTE PULMONARY HEART.

The most common cause of development is pulmonary embolism, 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 severe shortness of breath turning into inspiratory suffocation, rapidly increasing cyanosis, chest pain of various types, shock or collapse, rapidly increasing liver size, swelling in the legs, ascites, epigastric pulsation, tachycardia (120-140), harsh breathing , in some places weakened vesicular; Moist, varied rales are heard, especially in the lower parts of the lungs. Additional research methods, especially ECG, are of great importance in the development of acute pulmonary heart disease: a sharp deviation of the electrical axis to the right (R 3 >R 2 >R 1, S 1 >S 2 >S 3), P-pulmonale appears - a pointed P wave, in the second , third standard leads. Right bundle branch block is complete or incomplete, ST inversion (usually elevation), 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 signs may also occur in acute myocardial infarction of the posterior wall.

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

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

For valvular pneumothorax - surgical treatment. In case of confluent pneumonia, along with antibiotic treatment, diuretics and cardiac glycosides are necessarily prescribed.

CLINIC OF CHRONIC PULMONARY HEART.

Patients are concerned 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, shortness of breath of an expiratory nature with an unchanged respiratory rate, with restrictive processes, the duration of exhalation decreases and the respiratory rate increases. Upon objective examination, 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, edema of the lower extremities, ascites. The pulse is increased, the boundaries of the heart expand to the right, and then to the left, the tones are dull due to emphysema, the accent of the second tone is over the pulmonary artery. Systolic murmur at the xiphoid process due to dilatation 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 - a Graham-Still murmur, which is associated with relative insufficiency of the pulmonary valve. Above the lungs percussion there is a box sound, breathing is vesicular and harsh. In the lower parts of the lungs there are congestive, silent moist rales. When palpating the abdomen, there is 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.

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

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

The third stage - signs of right ventricular failure are added - an increase in the right border of cardiac dullness, an increase in the size of the liver. Constant swelling in the lower extremities.

The fourth stage is shortness of breath at rest, forced position, often accompanied by respiratory rhythm disorders such as Cheyne-Stokes and Biot. The swelling is constant, cannot be treated, the pulse is weak and frequent, the heart is bullish, the sounds are muffled, the systolic murmur at the xiphoid process. There is a lot of moist rales in the lungs. The liver is of considerable size and does not contract under the influence of glycosides and diuretics as fibrosis develops. Patients are constantly dozing.

Diagnosis of thoradiaphragmatic heart is often difficult; one must always remember about the possibility of its development in kyphoscoliosis, ankylosing spondylitis, etc. The most important sign is the early appearance of cyanosis, and a noticeable increase in shortness of breath without attacks of suffocation. 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. Associated with traumatic brain injury, obesity is accompanied by thirst, bulimia, and arterial hypertension. Diabetes mellitus often develops.

Chronic cor pulmonale in primary pulmonary hypertension is called Aerz's disease (described in 1901). A polyetiological disease of unknown origin, it mainly affects women from 20 to 40 years old. Pathomorphological studies have established that with primary pulmonary hypertension, thickening of the intima of the precapillary arteries occurs, that is, in muscular-type arteries, thickening of the media is noted, 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 joints; 1/3 of patients may experience fainting, dizziness, and Raynaud's syndrome. And then shortness of breath increases, which is a sign that indicates that primary pulmonary hypertension is entering a stable final stage. Cyanosis quickly increases, which is expressed to the degree of a cast-iron tint, becomes permanent, and swelling quickly increases. The diagnosis of primary pulmonary hypertension is established by exclusion. Most often this diagnosis is pathological. In these patients, the entire clinical picture 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 cor pulmonale: for 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 findings: appear very late. One of the early symptoms is bulging of the pulmonary artery trunk on x-ray. The pulmonary artery bulges, often flattening the waist of the heart, and this heart is mistaken by many doctors for the mitral configuration of the heart.

ECG: indirect and direct signs of right ventricular hypertrophy appear:

deviation of the electrical axis of the heart to the right - R 3 >R 2 >R 1, S 1 >S 2 >S 3, angle greater than 120 degrees. The most basic indirect sign is an increase in the interval of the R wave in V1 by more than 7 mm.

direct signs are blockade of the right bundle branch, the amplitude of the R wave in V 1 is more than 10 mm with complete blockade of the right bundle branch. 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 the 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 are Doppler cardiography, echocardiography - enlargement of the right side of the heart, increased pressure in the pulmonary artery.

PRINCIPLES OF TREATMENT OF HEART PULMONARY.

Treatment of cor pulmonale involves treating the underlying disease. In case of exacerbation of obstructive diseases, bronchodilators and expectorants are prescribed. For Pickwick's syndrome - treatment of obesity, etc.

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

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

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

PREVENTION.

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