Chronic cor pulmonale faculty therapy. Chronic cor pulmonale: causes, symptoms and treatment

PULMONARY HEART. ETIOLOGY, PATHOGENESIS OF ACUTE AND SUB-ACUTE, CHRONIC PULMONARY HEART, CLINIC, DIAGNOSTICS, PRINCIPLES OF TREATMENT.

Pulmonary heart- a pathological condition, characterized by right ventricular hypertrophy caused by hypertension of the pulmonary circulation, which develops when the bronchopulmonary apparatus, pulmonary vessels, chest deformation or other diseases that impair lung function are affected.

Acute heart disease is a wedge symptom complex arising as a result of pulmonary embolism, and with diseases of the cardiovascular and respiratory systems. Etiology: ( sharp lay down my heart with severe course)

1.Massive thromboembolism of the pulmonary artery 2.embolism gas, fatty, tumor 3.thrombosis of the pulmonary artery, pulmonary veins 4.pneumothorax. Clinic: Acute development within a few minutes, hours, against the background of complete well-being, with frequent lethal outcome. It is accompanied by the phenomena of cardiac decompensation. There is a sharp shortness of breath, cyanosis, chest pain, agitation. Pulmonary thromboembolism quickly, within a few minutes to half an hour, leads to the development of shock and death. (Acute cor pulmonale with subacute course):1) embolism of the branches of the pulmonary artery 2) thrombosis of the branches of the pulmonary artery with a recurrent course 3) pulmonary infarction 4) valve pneumotrax 5) widespread acute pneumonia 6) severe course of bronchial asthma 7) arteritis of the pulmonary artery system Clinical picture: Develops within a few hours to several days and is accompanied by increasing shortness of breath, cyanosis and the subsequent development of shock, pulmonary edema. On auscultation, a large number of moist and scattered dry rales are heard, pulsation in 2-3 intercostal space on the left can be detected, an accent of the II tone over the pulmonary artery. The nature of the swelling of the cervical veins, progressive enlargement of the liver, tenderness on palpation. Acute coronary insufficiency often occurs, accompanied by pain, rhythm disturbances, and ECG signs of myocardial ischemia. The development of this syndrome is associated with the occurrence of shock, compression of the venous veins by the dilated right ventricle, irritation of the pulmonary artery receptors. Further, the clinic of a pulmonary infarction is characterized by the renewal or strengthening of the byuols in the chest associated with breathing, shortness of breath, cyanosis, but less compared to the acute phase of the disease. Dry cough, or with scanty sputum, hemoptysis. Fever, tachycardia.

X-ray: unilateral increase in the shadow of the lung root, increased transparency of the lung. High standing of the dome of the diaphragm, dilatation of venous vessels, enlargement of the right heart. Lung infarction - darkening of a triangular shape, fluid in the pleural cavity. ECG: (1-5 days acute) deep S waves in 1 and aVL and Q in 3, V1-V2 negative T, atrial fibrillation. In the subacute phase (1-3 weeks): negative T in 3, aVF, V1-2 leads. Diagnosis: clinical picture, ECG, X-ray, a history of thrombophlebitis of the lower extremities. Pulmonary angiography. Treatment: with the development of a shock state - resuscitation measures (intubation, heart massage, IVL). If resuscitation is successful, an urgent operation is indicated to remove a thrombus from the pulmonary artery trunk and inject thrombolytic drugs into the pulmonary artery through a tube. Therapeutic relief of pain syndrome (analgesics, narcotic drugs, neuroleptanalgesia), lowering pressure in the pulmonary artery (euphyllin, in the absence of hypotension - ganglion blockers), treatment of heart failure. Early anticoagulant therapy - heparin intravenously with a transition to intramuscular and subcutaneous administration under the control of blood clotting. ? -10 days, then indirect anticoagulants. (fibrolysin, streptokinase) Chronic pulmonary heart - develops over a number of years and proceeds at the beginning without heart failure, and then with decompensation according to the right ventricular type. Etiology: 1) lesions in which the ventilation and respiratory function of the lungs is primarily affected (infectious inflammatory diseases of the bronchopulmonary apparatus - chronic bronchitis, chronic pneumonia, bronchiectasis, tuberculosis with the development of emphysema. Bronchial asthma, tumor processes, cystic degeneration of the lungs, collagenosis, silicosis, etc. ) 2) diseases primarily affecting the vessels of the lungs. (Pulmonary arteritis, primary pulmonary hypertension and thromboembolic processes in the system of the small circle) Pathogenesis: hypertension of the small circle as a result of obstructive and restrictive processes. Obstructive processes - violation of bronchial patency, uneven alveolar ventilation, gas diffusion is disturbed and Po2 in the alveolar air decreases - arterial hypoxia. As a result of increased breathing resistance, the intrathoracic pressure increased, which contributes to hypoventilation. Restrictive processes are a decrease in the elasticity and resistance of the lungs, a decrease in the respiratory surface and vascularity of the small circle. Increased blood flow through the pulmonary shunts, resulting in alveolar hypoxia. Alveolar hypoxia leads to increased tone and pressure in the small circle and the development of right ventricular hypertrophy. Hypoxia causes an increase in the number of red blood cells, an increase in viscosity, a slowdown in blood flow and an increase in the BCC. Clinic: severe shortness of breath during physical exertion, increased fatigue, tendency to tachycardia. Sometimes pressing chest pain associated with dilatation of the pulmonary artery, dizziness, short-term episodes of loss of consciousness. The course of the disease is wave-like. With an exacerbation of chronic infections of the respiratory system due to an increase in pressure in the pulmonary artery, there is an increase in the signs of heart failure with blood congestion in a large circle (right ventricular failure) - peripheral edema, enlargement of the liver, etc. II above the pulmonary artery. When the lungs are dilated, the arteries listen to a diastolic murmur (refers to the insufficiency of the valve of the trunk leg) in the 2nd intercostal space. Acrocyanosis, enlargement of the jugular veins, and the appearance of signs of stagnation in a large circle are noted. Diagnostics: ECG: signs of hypertrophy and overload of the right chambers, displacement of the Elos to the right, in lead V1-2, the R wave is increased, S has a small amplitude, T is negative. High P in II and III leads. X-ray: hypertrophy and dilatation of the right ventricle, signs of pulmonary hypertension. EchoCG. Treatment: edema - diuretics. Long-term continuous oxygen therapy with oxygen balloons.

1. RELEVANCE OF THE TOPIC

Chronic cor pulmonale(HLS) is a clinical and functional symptom complex that develops against the background of various bronchopulmonary diseases, ultimately leading to the development of pulmonary hypertension.

In fact, the development of CLS marks a "change in the status of a pulmonary patient to a cardiac" and requires a corresponding shift in emphasis in the management of the patient.

The effectiveness of HLS treatment largely depends on the timely diagnosis. However, the diagnosis of cor pulmonale in the early stages, when this condition remains potentially reversible, is a very difficult problem. At the same time, the treatment of patients with chronic decompensated cor pulmonale is a difficult, sometimes unpromising task. In this regard, the ability to timely suspect and diagnose CLS, taking into account its main etiological factors, acquires great practical importance.

2. PURPOSE OF THE LESSON

To be able to diagnose CLS and draw up a program for managing patients with CLS based on knowledge of the main links of pathogenesis, clinical manifestations, laboratory and instrumental signs, the most informative diagnostic methods, principles of treatment of patients with CLS.

3. QUESTIONS FOR PREPARING FOR THE LESSON

1. The concept of "chronic cor pulmonale", definition.

2. Pathogenesis of CLS.

3. CLS classification.

4. Clinical symptoms of CLS.

5. Diagnostic criteria for CLS.

6. Principles of treatment of patients with chronic pulmonary disease.

7. Forecast.

4. BASE LEVEL TESTS

1. What are the main mechanisms of development of pulmonary hypertension?

with COPD:

A. Alveolar hypoxia.

B. Alveolar hypercapnia.

B. Reduction of the capillary bed due to the destruction of the alveoli. D. Presence of arterio-venous anastomoses in the lungs.

D. Slowing down of blood flow in the pulmonary circulation.

2. What clinical signs may indicate the development of chronic pulmonary disease in a patient with COPD?

A. Cyanosis.

B. Shortness of breath, aggravated by exertion.

B. Bronchial obstruction. D. Epigastric pulsation. D. Sleepiness.

3. Name the symptoms of right ventricular failure:

A. Tachycardia during exercise, persisting for more than 10 minutes after cessation of exercise.

B. Hepatojugular reflux (Plesha symptom). B. Ascites.

D. Enlargement of the spleen. D. Enlargement of the liver.

4. In the analysis of blood in patients with chronic pulmonary disease, they find:

A. Increase in acute phase inflammatory markers. B. Decreased ESR.

B. Erythrocytosis.

D. Hypoproteinemia.

D. Hypercholesterolemia.

5. Auscultatory picture of CLS includes:

A. Systolic murmur over the xiphoid process. B. Accent II tone over the pulmonary artery.

B. Systolic murmur at the apex.

D. Strengthening the I tone in the projection of the tricuspid valve. D. All of the above auscultatory signs.

6. ECG signs of right ventricular hypertrophy:

A. The appearance of a high pointed wave Ρ

B. High Prong Rin V1, V2; deep prong Sin the left chest leads.

B. Complete or incomplete right bundle branch block. D. Deviation of the electrical axis of the heart to the right.

7. Right ventricular hypertrophy develops in the following diseases:

A. Stenosis of the left atrioventricular foramen. B. Stenosis of the pulmonary artery valves.

B. Insufficiency of the aortic valves. D. Subaortic stenosis.

D. Atrial septal defect.

8. With the development of right ventricular failure in patients with chronic cor pulmonale, the appointment is pathogenetically justified:

A. Nitrates.

B. High doses of calcium antagonists.

B. ACE inhibitors.

D. Aldosterone antagonists. D. Cardiac glycosides.

9. Objective clinical signs of right ventricular hypertrophy:

A. Spilled cardiac impulse.

B. Systolic precordial and epigastric pulsation.

B. Expansion of the borders of the heart to the right. D. The appearance of a pathological III tone. D. Swelling of the region of the heart.

10. Choose the correct statements about HLS:

A. Chronic lung diseases cause the development of chronic pulmonary disease in 80-90% of patients.

B. Patients with chronic pulmonary disease are characterized by shortness of breath, aggravated by physical exertion.

B. Erythrocytosis in patients with HLS does not require correction.

D. A sharp drug-induced decrease in pulmonary hypertension can lead to a deterioration in the gas exchange function of the lungs. E. All of the above statements are correct.

11. Criteria for the diagnosis of decompensated chronic cor pulmonale include all of the following, except:

A. Clinical signs of right ventricular failure. B. Stagnation in the pulmonary circulation.

B. Identification of pulmonary hypertension.

D. Presence of tricuspid regurgitation of II-III degree. D. Presence of chronic pulmonary disease.

5. KEY TOPIC ISSUES

5.1. Definition

Chronic cor pulmonale (CLS) - hypertrophy and / or dilation of the right ventricle in combination with pulmonary hypertension, occurring against the background of various diseases that disrupt the structure and / or function of the lungs, except for cases when changes in the lungs are themselves the result of primary damage to the left heart or congenital heart defects and large blood vessels.

5.2. Etiology

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

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

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

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

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

5.3. Classification of chronic pulmonary heart disease (Votchal B.E., 1964)

By the degree of compensation:

Compensated;

Decompensated. By origin:

Vascular genesis;

Bronchopulmonary genesis;

Thoracodiaphragmatic genesis.

5.4. Pathogenesis of chronic cor pulmonale

There are 3 stages in the development of CLS:

Precapillary hypertension in the pulmonary circulation;

Right ventricular hypertrophy;

Right ventricular heart failure.

The development of pulmonary hypertension lies at the heart of the pathogenesis of CLS. Main pathogenetic mechanisms:

Diseases of the lungs, damage to the chest, spine, diaphragm. Violation of ventilation and breathing mechanics. Violation of bronchial patency (obstruction). Decreased respiratory surface (restriction).

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

Hypertensive influence of humoral factors (leukotrienes, PGF 2 a, thromboxane, serotonin, lactic acid).

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

An increase in the minute volume of blood circulation due to hypercatecholaminemia caused by hypoxemia.

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

Development of bronchopulmonary anostomoses.

Increased intra-alveolar pressure in obstructive bronchitis.

In the early stages of CLS formation, compensatory-adaptive reactions predominate, however, a prolonged increase

Figure: 7.1.The main pathogenetic mechanisms of the development of chronic pulmonary heart disease in patients with chronic obstructive pulmonary disease

an increase in pressure in the pulmonary artery leads to hypertrophy, and over time, with repeated exacerbations of bronchopulmonary infection, an increase in obstruction - to dilatation and failure of the right ventricle.

5.5. Clinical picture

Clinical manifestations of HPS include symptoms:

The main disease that led to the development of HLS;

Respiratory failure;

Heart (right ventricular) failure.

5.5.1. Complaints

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

Persistent tachycardia.

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

Arrhythmias are more common with exacerbation of COPD, in the presence of pulmonary decompensation and in patients with concomitant ischemic heart disease, arterial hypertension, obesity.

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

5.5.2. Objective signs

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

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

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

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

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

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

Percussion is determined by the expansion of the absolute and relative cardiac dullness of the right border of the heart; percussion sound above the handle of the sternum - with a tympanic shade, and above the xiphoid process becomes dull-tympanic or completely deaf.

Deafness of heart sounds.

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

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

5.5.3. Laboratory data

In the clinical analysis of blood in patients with HLS, erythrocytosis, high hematocrit, and ESR slowdown are determined.

In a biochemical blood test, with the development of decompensation in the right ventricular type, an increase in residual nitrogen, bilirubin, hypoalbuminemia, hyperglobulinemia are possible.

5.5.4. X-ray signs

Normal or enlarged shadow of the heart in the lateral projection.

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

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

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

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

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

5.5.5. Electrocardiographic signs

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

Direct signs of hypertrophy:

Barb Rin Vi more than 7 mm;

Attitude R / Sin V more than 1;

Inherent deviation in V - 0.03-0.05 s;

The form qRin Vi;

Incomplete right bundle branch block, if Rmore than 10 mm;

Complete block of the right bundle branch block, if Rmore than 15 mm;

The picture of overload of the right ventricle in V1-V2. Indirect signs of hypertrophy:

Chest leads:

Barb Rin V5 less than 5 mm;

Barb Sin V5 more than 7 mm;

Attitude R / Sin V5 less than 1;

Barb Sin V 1 less than 2 mm;

Complete block of the right bundle branch block, if Rless than 15 mm;

Incomplete right bundle branch block, if Rless than 10 mm;

Standard leads:

- P-pulmonalein II and III standard ECG leads;

EOS deviation to the right;

S1S2S3 type.

5.5.6. Echocardiogarphic signs

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

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

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

"D" -shaped shape of the right ventricle.

Tricuspid regurgitation.

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

I - 31-50 mm Hg;

II - 51-75 mm Hg;

III - 75 mm Hg and higher.

5.5.7. Morphological signs

Increase in the wall thickness of the right ventricle (more than 5 mm).

An increase in the mass of the right ventricle: more than 70 g in men, more than 60 g in women.

The ventricular index is more than 0.6 (normal weight of the right ventricle / weight of the left ventricle is 0.4-0.6).

Hypertrophy of the papillary muscles of the right ventricle, which causes the syndrome of relative tricuspid valve insufficiency.

5.6. Treatment

The basic principles of treatment of patients with HLS:

Prevention and treatment of underlying lung diseases.

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

Treatment of right ventricular failure.

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

Treatment and preventionthe underlying disease, for example COPD: bronchodilators - anticholinergic drugs (atrovent *, bero-

dual *), selective P2-agonists (berotek *, salbutamol), methylxanthines, mucolytics. With an exacerbation of the process - antibacterial drugs, if necessary - corticosteroids.

At all stages of the CLS flow pathogenetic treatmentlong-term oxygen therapy is used - inhalation of oxygen-enriched air (30-40% oxygen) through a nasal catheter. The oxygen flow rate is 2-3 liters per minute at rest and 5 liters per minute under load. Criteria for the appointment of long-term oxygen therapy: PaO2 less than 55 mm Hg. and oxygen saturation (saturation of the erythrocyte with oxygen, S A O 2) less than 90%. Long-term oxygen therapy should be prescribed as early as possible in order to correct abnormalities in the blood gas composition, reduce arterial hypoxemia and prevent hemodynamic disorders in the pulmonary circulation, which allows to stop the progression of pulmonary hypertension and remodeling of pulmonary vessels, increases survival and improves the quality of life of patients.

Calcium antagonistscause dilatation of the vessels of the pulmonary and systemic circulation, and therefore refer to direct pulmonary vasodilators. Tactics of prescribing calcium antagonists: treatment begins with small doses of the drug, gradually increasing the daily dose, bringing it to the maximum tolerable; nifedipine is prescribed - 20-40 mg / day, adalat * - 30 mg / day, diltiazem - from 30-60 mg / day to 120-180 mg / day, isradine ^ - 2.5-5.0 mg / day, verapamil - from 80 to 120-240 mg / day, etc. The course of therapy is from 3-4 weeks to 3-12 months. The dose of the drug is selected taking into account the level of pressure in the pulmonary artery and a differentiated approach to the side effects that occur when prescribing calcium antagonists. An immediate effect should not be expected with calcium antagonists.

Nitratescause dilatation of the arteries of the small circle of blood circulation; reduce the afterload on the right ventricle due to venulodilatation, reduce the afterload on the pancreas due to a decrease in the hypoxic vasoconstriction of the PA; reduce pressure in the LA and reduce postcapillary pulmonary hypertension due to a decrease in CDP in the LV. Average therapeutic dose: nitrosorbide - 20 mg 4 times a day.

ACE inhibitorssignificantly improve the survival and prognosis of life in patients with congestive heart failure, including patients with chronic pulmonary disease, since the result of using

ACE inhibitors - decrease in arteriolar and venous tone, decrease in venous return of blood to the heart, decrease in diastolic pressure in the pulmonary artery and right atrium, increase in cardiac output. Prescribe captopril (kapoten *) in a daily dose of 75-100 mg, ramipril - 2.5-5 mg / day, etc., the dose depends on the initial level of blood pressure. With the development of side effects or intolerance to ACE inhibitors, antagonists of AT II receptors (losartan, valsartan, etc.) can be prescribed.

Prostaglandins- a group of drugs that can successfully reduce the pressure in the pulmonary artery with a minimum effect on the systemic blood flow. Their use is limited by the need for long-term intravenous administration, since prostaglandin E1 has a short half-life. For long-term infusion, a special portable pump is used, connected to a Hickman catheter, which is installed in the jugular or subclavian vein. Doses of the drug vary from 5 ng / kg per minute to 100 ng / kg per minute.

Nitric oxideacts similarly to endothelium relaxant factor. During the course of inhalation use of NO in patients with chronic pulmonary disease, a decrease in pressure in the pulmonary artery, an increase in the partial pressure of oxygen in the blood, and a decrease in pulmonary vascular resistance are observed. However, we must not forget about the toxic effect of NO on the human body, which requires a clear dosage regimen.

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

Diureticsprescribed when edema appears, combining them with limiting the intake of fluid and salt (furosemide, lasix *, potassium-sparing diuretics - triamterene, combined drugs). It should be borne in mind that diuretics can cause dryness of the bronchial mucosa, reduce the mucosal index of the lungs and worsen the rheological properties of blood. At the initial stages of CLS development with fluid retention in the body due to hyperaldosteronism, caused by the stimulating effect of hypercapnia on the glomerular zone of the adrenal cortex, it is advisable to prescribe aldosterone antagonists in isolation (veroshpiron * - 50-100 mg daily in the morning or every other day).

The question of the appropriateness of the application cardiac glycosidesin the treatment of patients with chronic pulmonary disease remains controversial. It is believed that the heart

glycosides, possessing a positive inotropic effect, lead to more complete emptying of the ventricles, increase cardiac output. However, in this category of patients without concomitant cardiac pathology, cardiac glycosides do not significantly improve hemodynamic parameters. Against the background of taking cardiac glycosides, symptoms of digitalis intoxication are more often observed in patients with CLS.

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

Use anticoagulantsfor the treatment and prevention of thrombosis, thromboembolic complications. In a hospital, heparin is mainly used in a daily dose of 5,000-20,000 U subcutaneously under the control of laboratory parameters (blood clotting time, activated partial thromboplastin time). Of the oral anticoagulants, preference is given to warfarin, which is prescribed in an individually selected dose under INR control.

Also used antiplatelet agents (acetylsalicylic acid, curantil *), hirudotherapy.

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

5.7. Forecast

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

6. SUPERVISION OF PATIENTS

Supervision tasks:

Formation of skills of interrogation and examination of patients with chronic cor pulmonale;

Formation of skills for making a preliminary diagnosis of CLS based on survey data and patient examination;

Formation of skills in drawing up a plan for the examination and treatment of a patient with HLS.

Patient supervision is an independent work of students. Students personally or in a group of 2-3 people conduct a survey, examination, discussion of the patient's condition, form a preliminary and clinical diagnosis, draw up a plan of examination, treatment, and determine the prognosis of the disease.

The students report the results of the work to the whole group, collectively discuss them.

7. CLINICAL ANALYSIS OF THE PATIENT

Clinical review tasks:

Demonstration of methods of examination and questioning of patients with HLS;

Control of students' skills in examining and interviewing patients with chronic pulmonary disease;

Demonstration of the methodology for making the diagnosis of chronic pulmonary disease based on survey data and examination of patients;

Demonstration of the methodology for drawing up a survey plan;

Demonstration of drawing up a treatment plan.

Clinical analysis is carried out by the teacher or students under the direct supervision of the teacher. During the lesson, the most typical and / or complex clinical examples from a diagnostic and / or therapeutic point of view are analyzed. At the end of the analysis, a structured preliminary or final diagnosis is formulated, and a plan for the examination and treatment of the patient is drawn up.

8. SITUATION TASKS

Clinical challenge? 1

Patient D., 54 years old, was admitted to the therapeutic department with complaints of dyspnea at rest, aggravated by insignificant physical exertion, cough with scanty purulent sputum, general weakness.

Of anamnesisthe disease is known: he considers himself ill for 1.5 months, when, against the background of acute respiratory viral infections, the patient's cough intensified with secretion of purulent sputum, “wheezing” breathing appeared, subfebrile condition persisted, which the patient regarded as an exacerbation of chronic bronchitis of a smoker. As a result of the antibiotic therapy, the temperature returned to normal, but continued

disturb the cough. The patient noted a decrease in exercise tolerance (shortness of breath appeared), as well as an increase in edema of the lower extremities.

Physical examination data.With auscultation of the heart, a systolic murmur is heard along the left edge of the sternum and an accent of the II tone above the pulmonary trunk. Heart rate - 102 per minute, blood pressure - 140/80 mm Hg. The lower edge of the liver protrudes 4 cm from under the costal arch. Dense swelling of the feet and legs.

Clinical blood test:erythrocytes - 6.0x10 11 / l, Hb - 170 g / l, leukocytes - 12.2x10 9 / l, stab leukocytes - 10%, ESR - 7 mm / h.

Electrocardiography:sinus tachycardia, S-type ECG, high pointed Pin II, III, avF leads, predominant Rin V1, V2, deep Sin the left chest leads.

Echocardiographic data:the aorta in the ascending section is 35 mm in diameter. The left heart is not dilated. The left atrium is 36 mm in diameter, the left ventricle is 45 mm in diameter. The thickness of the interventricular septum is 9 mm, the thickness of the posterior wall of the left ventricle is 9 mm. Left ventricular ejection fraction - 62%. The leaflets of the aortic, mitral and pulmonary valves are not changed, the mobility of the leaflets is not limited. The pulmonary artery trunk is dilated. The right parts of the heart are enlarged. The right ventricle is 52 mm in diameter, the right atrium: horizontally - 51 mm in diameter, vertically - 55 mm in diameter. The wall thickness of the right ventricle is 12 mm.

Doppler ultrasonography detects grade II mitral and pulmonary regurgitation, grade II tricuspid regurgitation and pulmonary hypertension (pulmonary artery systolic pressure 38.5 mm Hg).

2. Give an assessment to the results of an objective examination of the patient.

Clinical challenge? 2

Patient L., 37 years old, was admitted to the therapeutic department with complaints of severe weight gain for 7 years, fatigue, severe drowsiness, episodes of sudden falling asleep, snoring during

sleep, dyspnea at rest of a mixed nature, aggravated by physical exertion.

Objective examination.Height - 173 cm.Weight - 110 kg. Kyphosis of the thoracic region. Swelling of the feet, legs. Warm diffuse cyanosis. Vesicular breathing over the lungs, no wheezing. BH - 19 per minute. Heart sounds are rhythmic, muffled, heart rate - 96 per minute. BP - 140/88 mm Hg

General blood analysis:Hb - 174 g / l, leukocytes - 5.5 x 10 9 / l, erythrocytes - 6.7 x 10 11 / l, platelets - 350 000. ESR - 4 mm / h. Increased prothrombin activity of plasma, decreased fibrinolytic activity of plasma, increased platelet adhesion.

Blood gas research:PO2 - 92 mm Hg, PCO2 - 46 mm Hg.

Chest X-ray:high standing of the diaphragm, depletion of the vascular pattern. Relative increase in the RV arch in the left oblique position. Dilation of the common aircraft trunk in the right oblique position. In the lateral projection, an enhanced kyphosis of the thoracic spine is determined.

The study of the function of external respiration: VC is reduced, FVC1 is reduced, the Typhno index is above 70%.

On the electrocardiogram:sinus tachycardia, EOS deviation sharply to the right, blockade of the left posterior branch of the His bundle, blockade of the right bundle of His bundle. Amplitudes RV1 + SV5 - more than 10.5. Weakly negative teeth Tin V1-V2.

EchoCG.The left heart is not dilated. The left atrium is 36 mm in diameter, the left ventricle is 45 mm in diameter. The thickness of the interventricular septum is 12 mm, the thickness of the posterior wall of the left ventricle is 13 mm. Left ventricular ejection fraction - 60%. The leaflets of the aortic, mitral and pulmonary valves are not changed, the mobility of the leaflets is not limited. The right parts of the heart are enlarged. The right ventricle is 54 mm in diameter, the right atrium: horizontally - 49 mm in diameter, vertically - 53 mm in diameter. The wall thickness of the right ventricle is 10 mm.

When dopplerographydetermined pulmonary regurgitation of II degree, tricuspid regurgitation of II degree and pulmonary hypertension (systolic pressure in the pulmonary artery - 42.8 mm Hg).

1. Formulate a preliminary diagnosis.

2. Explain the pathogenesis of obesity breathing disorders.

4. Make a treatment plan for this patient.

9. FINAL TEST PROBLEMS

Choose one or more correct answers.

1. What are the clinical signs of decompensated HPS:

A. Diffuse cyanosis.

B. Peripheral edema.

B. Positive venous pulse. D. Decrease in venous pressure.

D. Systolic murmur at the apex of the heart.

2. Choose the correct statements about pulmonary hypertension:

A. Often develops in patients with COPD.

B. The most informative diagnostic method is a chest x-ray.

B. The main pathogenetic mechanism is alveolar hypoxia. The main clinical sign is swelling of the neck veins during inspiration.

D. All of the above statements are correct.

3. X-ray examination of the chest organs in patients with chronic heart disease reveals:

A. Increase in the cone of the pulmonary artery. B. Aortic configuration of the heart.

B. Mitral configuration of the heart. G. Curly Lines.

D. All of the above.

4. The following are involved in the formation of pulmonary hypertension in patients with COPD:

A. Spasm of pulmonary arterioles. B. Polycythemia.

B. Decompensation of the right ventricle.

D. Vasoactive substances that block the synthesis of nitric oxide. D. Treatment with inhaled corticosteroids.

5. Name the clinical signs of right ventricular hypertrophy:

A. Expansion of the borders of the heart to the right. B. Acrocyanosis.

B. Epigastric pulsation. D. Liver pulsation.

D. Systolic murmur at the xiphoid process.

6. For the diagnosis of chronic cor pulmonale, it is necessary to have all of the following, except:

A. The presence of a patient with chronic pulmonary disease. B. Identification of pulmonary hypertension with echocardiography.

B. Defect of IVS.

D. ECG signs of right ventricular hypertrophy. E. The presence of high pointed teeth Rin II and III standard leads.

7. In the progression of pulmonary hypertension in patients with COPD is important:

A. Treatment with inhaled corticosteroids in combination with long-acting ®2-blockers.

B. Repeated exacerbations of bronchopulmonary infection.

B. Thrombosis of small branches of the pulmonary artery. D. Increased intrathoracic pressure.

D. Secondary erythrocytosis.

8. Treatment of a patient with chronic decompensated cor pulmonale includes:

A. Diuretics.

B. ACE inhibitors.

B. Cardiac glycosides.

D. Aldosterone antagonists. D. Calcium antagonists.

9. In the clinical analysis of blood in patients with HLS, the following are found:

A. Thrombocytosis. B. Erythrocytosis

B. Leukocytosis.

D. Increased ESR.

D. Increase in hemoglobin content.

10. Select the wrong statements:

A. Right ventricular hypertrophy results in increased pulmonary artery pressure.

B. A decrease in the content of carbon dioxide in the alveolar air leads to an increase in the tone of small arteries and arterioles of the lungs.

B. ChPS never develops in restrictive lung diseases.

D. A frequent complication of CLS is atrial fibrillation.

E. All statements are wrong.

11. What medications lower the pressure in the pulmonary artery?

A. Nitroglycerin. B. Theophylline.

B. Digoxin. G. Verapamil.

D. Ipratropium bromide.

12. The reasons for the decompensation of HPS in patients with COPD can be all of the following, except:

A. Infectious exacerbations of COPD. B. Non-infectious exacerbations of COPD.

B. Thromboembolism of the branches of the pulmonary artery. D. Prescription of theophylline preparations.

D. Paroxysms of atrial fibrillation.

13. The reason for the development of HLS can be:

A. Valve pneumothorax. B. Obesity.

B. Recurrent thromboembolism of small branches of the pulmonary artery.

D. Bronchial asthma treated with inhaled corticosteroids.

D. Kyphoscoliosis.

14. EchoCG signs of CLS are all of the following, except:

A. The thickness of the anterior wall of the right ventricle exceeds

B. The end diastolic dimension of the right ventricle is more than 2.5 cm.

B. Mitral regurgitation.

D. Tricuspid regurgitation. D. Dilation of the right atrium.

15. What are the characteristic electrocardiographic signs

A. Amplitudes SV 1 + RV 5 over 38 mm. B. Deviation of EOS to the right.

B. Complete or incomplete right bundle branch block. D. High Prong Rin II and III standard leads.

E. Wide prong Rin I and II standard leads.

16. Auscultatory picture of CLS includes:

A. Mild systolic murmur at the apex.

B. Systolic murmur over the xiphoid process.

B. Weakening of the I tone in the projection of the tricuspid valve. D. Accent II tone over the pulmonary artery.

E. Extra tone at the top.

17. A 62-year-old patient suffering from COPD, chronic respiratory failure, secondary erythrocytosis, decompensated cor pulmonale developed a severe attack of chest pain. Objectively: severe acrocyanosis, number of breaths - 18 per minute, heart rate - 100 per minute, blood pressure - 120/80 mm Hg. Before taking an ECG, it is necessary to stop the pain attack. Which drug should be considered erroneous?

A. Nitroglycerin under the tongue. B. Subcutaneous morphine.

B. Analgin * intravenously. G. Novocaine intravenously. D. Heparin intravenously.

18. Patients with chronic decompensated cor pulmonale are characterized by:

A. Increase in systemic blood pressure.

B. Increased central venous pressure.

B. Tachycardia. D. Bradycardia.

D. Decrease in pulse pressure.

19. Signs of pulmonary hypertension in a patient with COPD are the following ECG signs (Fig. 7.2):

A. Deviation of the electrical axis of the heart.

B. Character of the tooth Rin the II standard lead.

B. Teeth ratio Rand Sin lead V 5. D. Presence of a tooth Rin lead V 1.

D. All of the above signs.

20. The tactics of treating a patient with HPS without signs of right ventricular failure includes:

A. Mandatory appointment of ACE inhibitors. B. Restriction of physical activity.

B. Prescribing osmotic diuretics.

D. Prevention and treatment of chronic lung diseases. D. Prescribing calcium antagonists.

Fig. 7.2.(to question 19).

21. Treatment of chronic pulmonary syndrome in the early stages with isolated hypertension of the pulmonary circulation includes the appointment:

A. Selective ®-blockers. B. Osmotic diuretics.

B. Prolonged nitrates. D. Calcium antagonists.

D. Antiplatelet agents.

10. STANDARDS OF ANSWERS

10.1. Baseline Test Answers

10.2. Answers to situational tasks

Clinical challenge? 1

1. Chronic obstructive bronchitis, in the stage of subsiding exacerbation. HLS, stage of decompensation. Chronic heart failure, III functional class (NYHA classification).

2. A systolic murmur along the left edge of the sternum is heard in the event of tricuspid valve insufficiency. In this case, there is relative failure due to dilatation of the right chambers of the heart. The accent of the II tone over the pulmonary trunk is characteristic of pulmonary hypertension.

3. The electrocardiogram reveals signs of load on the right atrium, right ventricular hypertrophy. During echocardiographic examination, attention is drawn to the intact state of the left heart with hypertrophy in combination with dilatation of mainly the right chambers of the heart, the presence of pulmonary hypertension.

4. Oxygen therapy, bronchodilators (anticholinergic drugs - berodual *, atrovent *), low doses of ACE inhibitors or antagonists of AT II receptors under the control of blood pressure, osmotic diuretics (furosemide - 20-80 mg under diuresis control), aldosterone antagonists (spironolactone - 25-50 mg per day), calcium antagonists, blood pressure and heart rate control.

Clinical challenge? 2

1. Pickwick's syndrome. Obesity III degree. Respiratory failure III degree. HLS, stage of decompensation. Chronic heart failure III functional class (NYHA classification).

2. With excessive obesity, the following respiratory dysfunctions occur:

The mobility of the chest is limited;

The kyphosis of the thoracic spine increases, which causes an almost horizontal position of the ribs and, in connection with this, a barrel-shaped chest;

The mobility of the diaphragm decreases.

All of the above factors fix the chest in an inspiratory position (as in emphysema), as a result of which

the passive act of exhalation is limited, and the tidal volume (DO) and the inspiratory reserve volume (ROVd) decrease. As a result, "shallow" breathing develops, which leads to a deterioration in air flow to the pulmonary alveoli. Increased respiratory movement is a transient compensatory response. With a decrease in DO by 40% (250 ml), even an increase in respiratory movements up to 40 per minute cannot maintain a normal level of ventilation of the pulmonary alveoli, which leads to more or less stable alveolar hypoventilation.

3. Analysis of the gas composition of the blood indicates the presence of the syndrome of alveolar hypoventilation. In the clinical analysis of blood, secondary absolute erythrocytosis is observed. The electrocardiogram shows signs of pulmonary hypertension, right ventricular hypertrophy. Echocardiographic examination revealed hypertrophy in combination with dilatation of the right chambers of the heart, the presence of pulmonary hypertension. The spirogram corresponds to the restrictive type of respiratory failure.

4. Recommended low-calorie diet, restriction of animal fats, consumption of 1 g of protein per 1 kg of proper body weight, sufficient amount of carbohydrates to prevent ketosis, enrichment with vitamins and minerals, reduce consumption of table salt. Shown are anorexigenic agents (Dietrin®, Isolipan®, Minifage®, Fepranon *, Teronac®), lipolysis stimulants (Dietplast®). Consultations of various specialists (endocrinologist, neurologist, geneticist, etc.) are required to establish the possible cause of obesity. Oxygen therapy, antiplatelet agents (acetysalicylic acid - 75-125 mg / day), osmotic diuretics (furosemide under the control of daily diuresis), ACE inhibitors or AT II receptor antagonists, calcium antagonists under control should be prescribed

10.3. Answers to final test items

3.A, D. 4.A, B, D.

20.A, B, D, D.

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PULMONARY HEART (PS) is a clinical syndrome caused by hypertrophy and / or dilatation of the right ventricle resulting from hypertension in the pulmonary circulation, which in turn develops as a result of diseases of the bronchi and lungs, chest deformities or damage to the pulmonary vessels.

Classification

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B.E. Votchal (1964) proposes to classify cor pulmonale according to 4 main characteristics:

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

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

Table 7. Classification of cor pulmonale

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

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

Chronic drugs in 80% of cases, it occurs with damage to the bronchopulmonary apparatus (and in 90% of patients in connection with chronic nonspecific lung diseases); vascular and thoracodiaphragmatic forms of drugs develop in 20% of cases.

Etiology

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

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

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

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

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

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

Pathogenesis

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

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

Scheme 7. Pathogenesis of Chronic Pulmonary Heart

TO anatomical mechanismsinclude:

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

TO functional mechanismsinclude:

• constriction of pulmonary arterioles at low values \u200b\u200bof PaO 2 (alveolar hypoxia) and high values \u200b\u200bof PaCO 2 in the alveolar air;
• increased pressure in the bronchioles and alveoli;
• increased blood levels of substances and metabolites of pressor action;
• an increase in the minute volume of the heart;
• increased blood viscosity.

Functional mechanisms play a decisive role in the formation of pulmonary hypertension. The narrowing of the pulmonary vessels (arterioles) is of primary importance.

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

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

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

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

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

The pressure in the pulmonary artery rises when the capillaries are compressed due to:

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

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

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

Clinical picture (Symptoms)

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Chronic drug manifestations consist of symptoms:

• the underlying disease leading to the development of chronic Drugs;
• respiratory (pulmonary) failure;
• heart (right ventricular) failure.

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

There are three degrees of respiratory failure.

With respiratory failure of the 1st degree shortness of breath and tachycardia occur only with increased physical activity; no cyanosis. The indicators of the function of external respiration (MOD, VC) at rest correspond to the proper values, but change when the load is performed; MVLdecreases. The gas composition of the blood is not changed (there is no lack of oxygen in the body), the function of blood circulation and CBS are normal.

With respiratory failure II degree shortness of breath and tachycardia with slight physical exertion. Indicators MOF, VC are abnormal, MVL is significantly reduced. Cyanosis is expressed. In the alveolar air, the voltage indicators of PaO 2 decrease and PaCO2 increases.

With respiratory failure III degree dyspnea and tachycardia at rest; cyanosis is pronounced. VC indices are significantly reduced, and MVL is impracticable. Lack of oxygen in the body (hypoxemia) and excess carbon dioxide (hypercapnia) are required; the study of CBS reveals respiratory acidosis. The manifestations of heart failure are expressed.

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

The drug develops against the background of respiratory failure IIand, more often, IIIdegree. The symptoms of respiratory failure are similar to those in heart failure, therefore, the doctor faces the difficult task of differentiating them and determining the transition of compensated drugs to decompensated ones.

Diagnosis of pulmonary heart

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

The formulation of a detailed clinical diagnosis takes into account:

1. the underlying disease that led to the formation of drugs;
2. respiratory failure (severity);
3. cor pulmonale (stage):
   • compensated;
   • decompensated (the degree of severity of right ventricular failure is indicated, i.e. its stage).

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

Pulmonary heart disease treatment

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The complex of therapeutic measures includes the impact:

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

Improvement of bronchial patency is facilitated by a decrease in inflammation and edema of the bronchial mucosa (antibiotics, GCS administered intratracheally) and elimination of bronchospasm (sympathomimetic agents; aminophylline, especially its prolonged-acting drugs; anticholinergic agents and calcium channel blockers).

Bronchial drainage is facilitated by means of thinning phlegm, expectorants, as well as postural drainage and a special complex of physiotherapy exercises.

Restoration of bronchial ventilation and improvement of bronchial patency lead to improved alveolar ventilation and normalization of the oxygen transport system of the blood.

Gas therapy plays a major role in improving ventilation, including:

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

According to the indications, the patient carries out breathing with positive pressure at the end of expiration (auxiliary mechanical ventilation or artificial respiration regulator - Lyukevich's nebulator). A special complex of breathing exercises is used to improve pulmonary ventilation.

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

Normalization of the blood oxygen transport system is achieved:

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

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

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

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

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

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

• diuretics,
• aldosterone antagonists,
• peripheral vasodilators (prolonged nitrates are effective).
• The question of the use of cardiac glycosides is decided individually.

Pulmonary heart - clinical syndrome of damage to the right ventricle of the heart, arising from hypertension in the pulmonary circulation.

Etiology, pathogenesis

The cause of hypertension in the pulmonary circulation can be: 1) chronic and specific diseases of the bronchi and lungs; 2) damage to the pulmonary vessels, inflammation or pulmonary embolism; 3) deformation of the chest or spine, causing a violation of the respiratory mechanism.
The pathogenesis of pulmonary heart disease is complex and depends on the etiological factor leading to the development of this disease. At the heart of the pathogenesis is hypertension in the pulmonary circulation (pulmonary hypertension). The reasons for the increase in pressure in the pulmonary artery system can be either organ
natural lesions in the system of small vessels of the lungs, or functional mechanisms. Organic lesions of the pulmonary vessels during obturation of capillaries and precapillaries arise in connection with:
a) obliteration or embolism of the vessels of the lungs;
b) mechanical compression of the pulmonary artery from the outside;
c) pulmonectomy, when there is a significant decrease in the vascular bed.
Functional mechanisms include:
a) alveolar hypoxia, a decrease in oxygen concentration and an increase in the concentration of carbon dioxide in the alveolar air, which leads to a narrowing of the arteries of the lungs;
b) an increase in the concentration in the blood of metabolites that have a pressor effect on the vessels of the lungs;
c) increased air pressure in the bronchioles and alveoli;
d) increased blood viscosity;
e) an increase in the minute volume of the heart.
Alveolar hypoxia develops in all chronic nonspecific lung diseases and is one of the main reasons for the narrowing of the pulmonary vessels and a decrease in blood oxygen saturation. With this pathology, there is an increase in the formation of biologically active substances in the vessels of the lungs (lactic acid, histamine, serotonin, leukotrienes, thromboxin), which increase the tone of the lung vessels. This is the so-called Euler-Liljestrand reflex - a spasm of the arterioles of the lungs with a decrease in the concentration of oxygen in the alveolar air.
In turn, pulmonary vasospasm leads to the development of persistent pulmonary hypertension and ultimately to the formation of hypertrophy of the right heart, first the right ventricle, then the right atrium. Over time, the existing arterial hypoxemia leads to necrobiotic and dystrophic changes in the heart muscle of the hypertrophied right sections, which contributes to the rapid progression of heart failure.

Clinical picture

The clinical picture of cor pulmonale is represented by symptoms of the underlying disease that caused its occurrence, as well as the severity of pulmonary and cardiac (right ventricular) failure. WHO identifies three main groups of diseases leading to the development of cor pulmonale:
1. Diseases that primarily affect the passage of air in the lungs and alveoli:
a) chronic bronchitis;
b) bronchial asthma;
c) bronchiectasis, diffuse interstitial pulmonary sclerosis with or without emphysema (tuberculosis, sarcoidosis, pneumoconiosis, cystic fibrosis, Hammen Rich syndrome, diffuse reticular pneumosclerosis).
2. Diseases primarily affecting the pulmonary vessels:
a) primary pulmonary hypertension;
b) thrombosis and embolism of the pulmonary vessels;
c) compression of the trunk of the pulmonary artery and pulmonary veins by mediastinal tumors and aneurysms;
d) periarteritis nodosa and other arteritis.
3. Diseases primarily affecting the chest:
a) kyphoscoliosis;
b) torocoplasty;
c) pleural fibrosis;
d) chronic pulmonary-muscle diseases (in particular, poliomyelitis);
e) idiopathic alveolar hypoventilation.
With thromboembolism of the trunk, large and small branches of the pulmonary artery, with valvular pneumothorax, repeated, severe attacks of bronchial asthma, a picture of acute and subacute pulmonary heart develops, which is characterized by an acute onset, severe shortness of breath, gray skin color, acrocyanosis, chest pain, often intense, cough, tachycardia, lowering blood pressure, up to collapse, in 20-30% of patients hemoptysis.
At the initial stages of chronic cor pulmonale, only signs of right ventricular hypertrophy can be diagnosed, subsequently a picture of pulmonary heart failure develops. The main symptom of pulmonary and heart failure is shortness of breath, which can be very variable. An increase in shortness of breath is usually observed with an exacerbation of chronic bronchopulmonary disease. Often patients with chronic lung diseases notice increased dyspnea in a horizontal position, when vagal influence and bronchial spasm increase.
With decompensated cor pulmonale, shortness of breath becomes constant. It increases in a horizontal position and decreases in a semi-sitting position. However, shortness of breath cannot serve as the only symptom in making this diagnosis, since it is a sign of respiratory failure in patients with COPD long before the development of circulatory failure in patients with cor pulmonale. Some patients are worried about pain in the region of the heart of an indefinite nature, it is localized to the left of the sternum, is very long and does not stop after taking validol and nitroglycerin. The cause of pain is arterial hypoxemia, which has an infectious-toxic effect on the heart muscle and leads to disruption of metabolic processes in the myocardium. Pain syndrome can also be associated with spasm of the coronary arteries due to coronary pulmonary reflexes and the development of pulmonary hypertension, leading to the expansion of the trunk and large branches of the pulmonary artery.
When examining the patient, attention is drawn to cyanosis of the skin, which is usually diffuse, increases on the tips of the fingers, nose and earlobes. Cyanosis is "warm" as opposed to "cold" in primary heart disease. In patients with chronic cor pulmonale, there is usually no direct correlation between the degree of dyspnea and cyanosis. Cyanosis appears with a decrease in blood saturation to 85-90%, as hypoxemia increases, its degree increases. One of the main symptoms of decompensated right ventricular failure is neck vein swelling. This symptom is observed in about 20% of patients, is associated with an increase in intrathoracic pressure and is combined with an increase in the liver and the appearance of edema of the lower extremities. With pulmonary insufficiency, the swelling of the cervical veins occurs only during inhalation, and with a combination of pulmonary and heart failure, both during inhalation and exhalation. In some patients, there is an increase in pulsation in the epigastric region, due to hypertrophy and overload of the right heart. With dilatation of the right ventricle, relative insufficiency of the atrioventricular valve may develop, which leads to the appearance of a systolic murmur at the xiphoid process of the sternum.
As heart failure develops, heart sounds become muffled, persistent tachycardia appears, hypoxia can lead to increased blood pressure. With decompensation of the disease, patients develop peripheral edema, enlargement of the liver, and the main signs of circulatory failure. As a rule, pastiness and edema of the lower extremities are noted during the period of exacerbation of the bronchopulmonary process, which makes it possible to diagnose circulatory failure in the early stages of its onset. When pulmonary heart disease is combined with atherosclerotic cardiosclerosis or hypertension, ascites and hydrothorax often appear.

Diagnostics

Based on clinical data, as well as methods and X-ray examination. In this phase, there are signs of pulmonary insufficiency and hypertrophy of the right heart. With decompensation, symptoms of circulatory failure join, mainly in the right ventricular type. Percussion in patients with chronic cor pulmonale over the entire surface of the lungs is determined by the box sound due to emphysema. It also determines a decrease in the border of relative cardiac dullness, even with pronounced signs of hypertrophy of the right heart.
Auscultatory picture in the lungs depends on the severity of emphysema, pneumosclerosis and the phase of the process. The most important symptom of heart damage is the deafness of the heart sounds, which occurs due to an increase in the airiness of the lungs and a violation of myocardial contractility. In patients with decompensated cor pulmonale, an increase in the II tone over the pulmonary artery and systolic murmur over the apex of the heart or in the region of the xiphoid process are often heard. An increase in the II tone is associated with an increase in pressure in the pulmonary artery system, and systolic murmur is due to dysfunction of the heart muscle and relative insufficiency of the tricuspid valve. With severe decompensation, a Graham-Still systolic murmur can be heard in the second intercostal space on the left. With the addition of coronary atherosclerosis or cardiosclerosis, cardiac arrhythmias may be observed in patients.
In the CBC in such patients, erythrocytosis can be determined as a reaction to hypoxia, an increase in hematocrit, an increase in blood viscosity, while ESR can remain normal even with an active inflammatory process. In OAM (- hematuria, proteinuria, cylindruria, which helps to confirm circulatory failure. X-ray examination confirms an increase in the right heart, expansion of the trunk and large branches of the pulmonary artery of the heart with depletion of the peripheral vascular pattern, increased pulsation in the center of the lungs and its weakening in the peripheral regions.
In practical medicine, electrocardiography is of great importance in the diagnosis of chronic cor pulmonale. The ECG shows signs of hypertrophy or overload of the right heart. The electrical axis is vertical, the atrial axis is tilted to the right. Its displacement to the right by more than 60 degrees leads to the appearance of a negative P wave in lead aVL, with approximately the same frequency P-pulmonale occurs (high and pointed P wave more than 2-2.5 mm in II, III, aVF leads with normal or its slightly increased width).
One of the popular non-invasive research methods is rheography - the determination of fluctuations in the blood filling of the vessels of the investigated part of the body, associated in time with the cardiac cycle. Rheological signs of cor pulmonale are: a decrease in the angle of inclination of the systolic wave, almost complete absence of diastolic and dicrotic waves, low rheological curve, lengthening of the period of tension, maximum and slow blood filling.
Incomplete blockade of the right bundle branch block can also be a typical sign. Sometimes it is combined with signs of right ventricular myocardial hypertrophy.
Echocardiographic diagnosis depends on the severity of pulmonary emphysema. Echocardiographic signs of cor pulmonale are a decrease in the amplitude of the "a" wave to 1 mm (corresponds to the systole of the right atrium), flattening of the pulmonary valve leaflets, an increase in the amplitude and speed of opening of the valve leaflets, and the appearance of systolic leaflet covering.
One of the early and informative methods of instrumental diagnosis of cor pulmonale is the determination of the pressure in the pulmonary artery (above 45 mm Hg).
When formulating the diagnosis, indicate the underlying disease that caused the occurrence of cor pulmonale, the severity of pulmonary insufficiency (acute, subacute, chronic) and the stage of cor pulmonale (compensated, decompensated).
Differential diagnosis presents certain difficulties, especially when distinguishing between pulmonary heart and heart failure.
See the table "The main clinical and differential diagnostic signs of pulmonary heart and heart failure" (Mukharlyamov NM, 1982).

The main clinical and differential diagnostic signs

pulmonary and heart failure

Symptoms	Pulmonary heart failure	Heart failure
Dyspnea	More often lengthening of exhalation, especially with physical activity	Inhalation is usually not lengthened
Cyanosis	Pronounced and widespread, limbs warm	Predominantly peripheral (phalanges, nose), cold limbs
Patient position	Often horizontal	Semi-seated
Distended neck veins	Increased on exhalation	Expressed equally when exhaling and inhaling
Atrial fibrillation	Seldom	Often
Onset of the disease	Cough, history of colds	History of heart disease; shortness of breath, coughing occurs later, associated with congestion in the lungs
Heart tones	Deaf. Accent 2 tone over the pulmonary artery
Pulsation in the epigastric region	Usually	Seldom
The nature of the defeat	More often obstructive, less often obstructive-restrictive	Usually restrictive
Percussion and auscultation data	Box sound, scattered across all fields, dry, whistling against the background of an elongated exhalation	Moist wheezing in the lower sections, exhalation can be lengthened, box sound is rare
ECG	Signs of right ventricular hypertrophy (pravogram, pulmonary P wave). Right bundle branch block	Depends on heart disease. Absence of pulmonary P wave except for late stages of mitral stenosis
X-ray signs	Enlargement of the right heart, expansion of the trunk and large branches of the pulmonary artery, small branches are narrowed	With severe heart failure, a diffuse increase in all parts of the heart

Treatment

It depends on the course of the process and the underlying disease leading to this complication. So, with pulmonary embolism, emergency thrombolytic therapy is performed under the control of blood clotting. Before emergency hospitalization, the patient is injected with narcotic analgesics, intravenous drip of heparin (20,000-30,000 U), fibrinolysin (40,000-60,000 U) in combination with antihistamines, cardiac glycosides, euphyllin, potassium chloride, glucocorticoids or adrenergic drugs , vitamin B6. If pneumothorax occurs, urgent measures are required. To reduce pain and possible pleuropulmonary shock, narcotic analgesics are administered (1% morphine solution 1-2 ml subcutaneously), puncture of the pleural cavity with air aspiration is performed. Carry out emergency hospitalization in a surgical hospital.
Timely and individually selected complex therapy allows to preserve the ability of patients to work. The traditional treatment regimen for patients with chronic cor pulmonale includes:
1. Treatment of the underlying disease, that is, the elimination of an active inflammatory process in the lung tissue by prescribing antibacterial drugs of the group of penicillins, macrolides, aminoglycosides, cephalosporins, etc. If necessary, antiviral drugs are prescribed rimantadine, acyclovir.
2. Restoration of bronchial conductivity, which is achieved with the help of adrenergic agents (alupent, astmopent, salbutamol, berotek, bricanil, ipradol, fenothyrol, etc.). For this purpose, methylxanthines (aminophylline, theophylline, theoder, theotard, theolong) and anticholinergics (berodual, eudur, etc.) can be prescribed. To reduce the edema of the bronchial mucosa, glucocorticoids (prednisolone, triamcinolone) are prescribed, preference is given to the use of glucocorticoids in the form of aerosols (becotide, beclamethasone).
Proteolytic enzymes (trypsin, chymotrypsin, profesim) are prescribed to dilute bronchial secretions. In order to rehydrate the secretion, mineral salts, essential oils are prescribed. Suppress persistent unproductive cough with bromhexine, syrup and sinecode tablets, inhalation of lidocaine.
3. Correction of impaired immunity, which is achieved through the appointment of thymosin, zixorin, amiksin, immunal, etc.
4. Improvement of hemodynamics, treatment of circulatory failure and pulmonary hypertension. For this purpose, four groups of drugs are prescribed:
a) cardiac glycosides (digoxin, strophanthin, korglikon, convallatoxin, etc.);
b) peripheral vasodilators (nitroglycerin, sodium nitroprusside, Molsidomin, hydralazine, etc.). In order to reduce the pressure in the pulmonary artery, calcium ion antagonists (nifedipine, verapamil), angiotensin-converting enzyme inhibitors (Enalapril, kapoten, etc.) and vasodilators are prescribed;
c) diuretics (furasemide, hypothiazide, lasix, aldactone, etc.);
d) glucocorticoids, progesterone to influence the main links of the pathogenesis of pulmonary heart failure, and also carry out gravitational blood surgery (hemosorption, erythrocytopoiesis) and cardiopulmonary transplantation.
5. Decrease in intravascular fibrin formation and thrombin formation, which is achieved by the appointment of aspirin, heparin, fibrinolysin, thrombokinase, trental, curantil.
6. Fight against hypoxemia and hypercapnia, which is carried out with the help of oxygen therapy - the most effective method of treating chronic cor pulmonale (inhalation of a 40-60% mixture through a nasal catheter at a rate of 6-9 liters per minute), hyperbolic oxygenation, assisted ventilation lungs. In the recovery period, chest massage and physiotherapy exercises are widely prescribed to restore the normal type of breathing. Indications for spa treatment in chronic pulmonary heart disease are determined by the underlying disease. The prognosis depends on the underlying disease, the nature of the pulmonary process.

Clinical examination

In order to prevent the development of cor pulmonale, it is necessary to carry out regular medical examinations, as well as timely and adequate therapy for diseases leading to this complication. Patients are subject to dispensary observation at least 1 time per month, courses of supportive and anti-relapse treatment are conducted for them on an outpatient basis and in a hospital. Indications for hospitalization are acute and subacute cor pulmonale, chronic cor pulmonale with an increase in symptoms of respiratory and right ventricular failure, heart rhythm disturbances, life-threatening.

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, Beck's sarcoidosis (Boeck), fibrosing alveolitis (endo- and exogenous);
• - dr.

Diseases primarily affecting the chest, diaphragm with limited mobility:

• - kyphoscoliosis;
• - multiple injuries to the ribs;
• - Pickwick's syndrome in obesity;
• - ankylosing spondylitis;
• - pleural suppuration after suffering pleurisy.

Diseases primarily affecting the pulmonary vessels:

• - primary arterial hypertension (Ayerza's disease);
• - recurrent pulmonary embolism (PE);
• - compression of the pulmonary artery from the veins (aneurysm, tumor, etc.).

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

• - bronchopulmonary;
• - thoracodiaphragmatic;
• - vascular.

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

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

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

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

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

There are 3 stages of pulmonary failure.

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

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

The second stage of pathogenesis: arterial hypoxemia will lead to a restructuring of the central hemodynamics - in particular, an increase in the amount of circulating blood, polycythemia, polyglobulia, an increase in blood viscosity. Alveolar hypoxia will lead to hypoxemic vasoconstriction by a reflex pathway called the Euler-Liestrand reflex. Alveolar hypoxia led to hypoxemic vasoconstriction, an increase in intra-arterial pressure, which leads to an increase in hydrostatic pressure in the capillaries. Violation of the non-respiratory function of the lungs leads to the release of serotonin, histamine, prostaglandins, catecholamines, but most importantly, in conditions of tissue and alveolar hypoxia, the interstitium begins to produce a greater amount of angiotensin-converting enzyme. The lungs are the main organ where this enzyme is produced. It converts angiotensin 1 into angiotensin 2. Hypoxemic vasoconstriction, release of biologically active substances under conditions of restructuring of central hemodynamics will lead not only to an increase in pressure in the pulmonary artery, but to a persistent increase in it (above 30 mm Hg), that is, to the development of pulmonary hypertension.

If the processes continue further, if the underlying disease is not treated, then naturally some of the vessels in the pulmonary artery system die due to pneumosclerosis, and the pressure steadily increases in the pulmonary artery. At the same time, persistent secondary pulmonary hypertension will lead to the opening of shunts between the pulmonary artery and bronchial arteries and unoxygenated blood enters the systemic circulation through the bronchial veins and also contributes to an increase in the work of the right ventricle.

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

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

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

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

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

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