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 with damage to the bronchopulmonary apparatus, pulmonary vessels, chest deformation or other diseases that impair lung function.
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 Clinic: 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 wet and scattered dry rales are heard, pulsation in 2-3 intercostal space on the left, an accent of the II tone over the pulmonary artery can be detected. The nature of the swelling of the cervical veins, progressive enlargement of the liver, pain 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 buoles 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 (aminophylline, 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 was increased, which promotes 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. Alveoli 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 erythrocytes, 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 signs of heart failure with blood congestion in a large circle (right ventricular failure) - peripheral edema, enlargement of the liver, etc. During examination, the appearance of a heart beat or pulsation in the epigastric region, accent 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.
Pulmonary heart - a complex of hemodynamic disorders in the pulmonary circulation, which develops as a result of diseases of the bronchopulmonary apparatus, deformation of the chest or primary lesion of the pulmonary arteries, manifested at the final stage by hypertrophy and dilatation of the right ventricle and progressive circulatory failure.
Etiology of cor pulmonale:
A) acute (develops in minutes, hours or days): massive PE, valvular pneumothorax, severe asthma attack, widespread pneumonia
B) subacute (develops over weeks, months): repeated small PE, periarteritis nodosa, lung carcinomatosis, repeated attacks of severe asthma, botulism, myasthenia gravis, poliomyelitis
B) chronic (develops over several years):
1.diseases affecting the airways and alveoli: chronic obstructive bronchitis, pulmonary emphysema, bronchial asthma, pneumoconiosis, bronchiectasis, polycystic lung disease, sarcoidosis, pneumosclerosis, etc.
2.diseases affecting the chest with limited mobility: kyphoscoliosis and other chest deformities, ankylosing spondylitis, condition after thoracoplasty, pleural fibrosis, neuromuscular diseases (poliomyelitis), diaphragm paresis, Pickwick syndrome in obesity, etc.
3.Diseases affecting the pulmonary vessels: primary pulmonary hypertension, repeated thromboembolism in the pulmonary artery system, vasculitis (allergic, obliterating, nodular, lupus, etc.), pulmonary atherosclerosis, compression of the pulmonary artery trunk and pulmonary veins by mediastinal tumors, etc.
Pathogenesis of chronic pulmonary heart (CP).
The main pathogenetic factor in the formation of CLS is pulmonary hypertension, which occurs due to a number of reasons:
1) in diseases with hypoventilation of the pulmonary alveoli in the alveolar air, the partial pressure of oxygen decreases, and the partial pressure of carbon dioxide increases; the onset of alveolar hypoxia causes spasm of the pulmonary arterioles and an increase in pressure in the small circle (alveolar-capillary reflex Euler-Liljestrand)
2) hypoxia causes erythrocytosis with a subsequent increase in blood viscosity; increased blood viscosity contributes to increased platelet aggregation, the formation of microaggregates in the microcirculation system and an increase in pressure in small branches of the pulmonary artery
3) a decrease in the oxygen tension in the blood causes irritation of the chemoreceptors of the aortic carotid zone, as a result, the minute volume of blood increases; its passage through spasmodic pulmonary arterioles leads to a further increase in pulmonary hypertension
4) during hypoxia, a number of biologically active substances (histamine, serotonin, etc.) are released in the tissues, which also contribute to the spasm of the pulmonary arterioles
5) atrophy of the alveolar walls, their rupture with thrombosis and obliteration of a part of arterioles and capillaries due to various diseases of the lungs leads to anatomical reduction of the vascular bed of the pulmonary artery, which also contributes to pulmonary hypertension.
Under the influence of all of the above factors, hypertrophy and dilatation of the right heart with the development of progressive circulatory failure occur.
Pathomorphological signs of CLS: expansion of the diameter of the trunk of the pulmonary artery and its large branches; hypertrophy of the muscle layer of the pulmonary artery wall; hypertrophy and dilatation of the right heart.
Pulmonary heart classification (according to Votchal):
1. Downstream: acute cor pulmonale, subacute cor pulmonale, chronic cor pulmonale
2. Depending on the level of compensation: compensated, decompensated
3. Depending on the genesis: vascular, bronchial, thoracodiaphragmatic
The main clinical manifestations of HLS.
1. Clinical manifestations of chronic obstructive and other lung diseases.
2. A complex of symptoms due to respiratory failure and significantly aggravated by the formation of chronic cor pulmonale:
- shortness of breath: increases with physical exertion, orthopnea is not typical, decreases with the use of bronchodilators and oxygen inhalation
- severe weakness, constant headaches, drowsiness during the day and insomnia at night, sweating, anorexia
- warm diffuse gray cyanosis
- palpitations, constant pain in the region of the heart (due to hypoxia and reflex narrowing of the coronary arteries - pulmocoronary reflex), decreasing after inhalation of oxygen
3. Clinical signs of right ventricular hypertrophy:
- expansion of the right border of the heart (rarely)
- displacement of the left border of the heart outward from the midclavicular line (due to displacement by an enlarged right ventricle)
- the presence of a heart beat (pulsation) along the left border of the heart
- pulsation and better auscultation of heart sounds in the epigastric region
- systolic murmur in the xiphoid process, increasing on inspiration (Rivero-Corvallo symptom) - a sign of relative tricuspid valve insufficiency, which develops with an increase in the right ventricle
4. Clinical signs of pulmonary hypertension:
- an increase in the zone of vascular dullness in the II intercostal space due to the expansion of the pulmonary artery
- accent II tone and splitting it in the II intercostal space on the left
- the appearance of a venous mesh in the sternum
- the appearance of diastolic murmur in the area of \u200b\u200bthe pulmonary artery due to its dilatation (Graham-Still symptom)
5. Clinical signs of decompensated cor pulmonale:
- orthopnea
- cold acrocyanosis
- swelling of the neck veins, not diminishing with inspiration
- enlarged liver
- Plesha symptom (pressure on an enlarged painful liver causes swelling of the neck veins);
- with severe heart failure, the development of edema, ascites, hydrothorax is possible.
ChLS diagnostics.
1. Echocardiography - signs of right ventricular hypertrophy: an increase in the thickness of its wall (normally 2-3 mm), expansion of its cavity (the index of the right ventricle is the size of its cavity in terms of the body surface - normal is 0.9 cm / m2); signs of pulmonary hypertension: an increase in the rate of opening of the pulmonary artery valve, its easy detectability, W-shaped movement of the pulmonary valve semilunar in systole, an increase in the diameter of the right branch of the pulmonary artery by more than 17.9 mm; paradoxical movements of the interventricular septum and mitral valve, etc.
2. Electrocardiography - signs of right ventricular hypertrophy (increase in RIII, aVF, V1, V2; depression of the ST segment and changes in the T wave in leads V1, V2, aVF, III; rightogram; displacement of the transition zone in V4 / V5; complete or incomplete right blockade legs of the bundle of His; an increase in the interval of internal deviation\u003e 0.03 in V1, V2).
3. Chest x-ray - enlargement of the right ventricle and atrium; bulging of the cone and trunk of the pulmonary artery; significant expansion of hilar vessels with a depleted peripheral vascular pattern; “Chopped off” roots of the lungs, etc.
4. Research function external respiration (to identify violations of the restrictive or obstructive type).
5. Laboratory data: erythrocytosis, high hemoglobin content, delayed ESR, and a tendency to hypercoagulability are characteristic of the UAC.
Principles of HPS treatment.
1. Etiological treatment - aimed at treating the underlying disease that led to chronic pulmonary disease (AB in bronchopulmonary infection, bronchodilators in broncho-obstructive processes, thrombolytics and anticoagulants in PE, etc.)
2. Pathogenetic treatment - aimed at reducing the severity of pulmonary hypertension:
A) long-term oxygen therapy - reduces pulmonary hypertension and significantly increases life expectancy
B) improvement of bronchial patency - xanthines: aminophylline (2.4% solution 5-10 ml i.v. 2-3 times / day), theophylline (in a tablet of 0.3 g 2 times / day) by repeated courses of 7-10 days, b2 - adrenergic agonists: salbutamol (in a tablet, 8 mg 2 times / day)
C) decrease in vascular resistance - peripheral vasodilators: prolonged nitrates (sustac 2.6 mg 3 times a day), calcium channel blockers (nifedipine 10-20 mg 3 times / day, amlodipine, isradipine - have an increased affinity for the SMC of the pulmonary vessels ), antagonists of endothelin receptors (bosentan), prostacyclin analogs (iloprost i.v. and inhalation up to 6-12 times / day, beraprost inside 40 mg up to 4 times / day, treprostinil), nitrous oxide and nitrous oxide donors (L- arginine, sodium nitroprusside - have a selective vasodilating effect, reduce the effects of pulmonary hypertension, without affecting systemic blood pressure).
D) improvement of microcirculation - courses of heparin 5000 U 2-3 times / day s / c until APTT increase by 1.5-1.7 times compared to control, low molecular weight heparins (fraxiparin), with severe erythrocytosis - bloodletting followed by infusion solutions with low viscosity (rheopolyglucin).
3. Symptomatic treatment: to reduce the severity of right ventricular failure - loop diuretics: furosemide 20-40 mg / day (be careful, because it can cause hypovolemia, polycythemia and thrombosis), in case of combination of HF with MA - cardiac glycosides, to improve the work of the myocardium - metabolic agents (oral mildronate 0.25 g 2 times / day in combination with potassium orotate or panangin), etc.
4. Physiotherapy (breathing exercises, chest massage, hyperbaric oxygenation, exercise therapy)
5. In case of ineffective conservative treatment, transplantation of the lungs or the "lung-heart" complex is indicated.
ITU: approximate time of VL with decompensation of cor pulmonale is 30-60 days.
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LECTURE ON INTERNAL DISEASES.
TOPIC: PULMONARY HEART.
Relevance of the topic: Diseases of the bronchopulmonary system, chest are of great importance in heart damage. Most authors designate the defeat of the cardiovascular system in diseases of the bronchopulmonary system by the term cor pulmonale.
Chronic cor pulmonale develops in about 3% of patients suffering from chronic lung diseases, and in the general structure of mortality from congestive heart failure, chronic cor pulmonale accounts for 30% of cases.
Cor pulmonale is hypertrophy and dilation or only dilation of the right ventricle resulting from hypertension of the pulmonary circulation, which developed as a result of diseases of the bronchi and lungs, chest deformities, or primary lesions of the pulmonary arteries. (WHO 1961).
Right ventricular hypertrophy and its dilatation with changes as a result of primary heart damage, or congenital malformations do not belong to the concept of cor pulmonale.
Recently, clinicians have noticed that hypertrophy and dilation of the right ventricle are already late manifestations of cor pulmonale, when it is no longer possible to rationally treat such patients, so a new definition of cor pulmonale was proposed:
“Cor pulmonale is a complex of hemodynamic disorders in the pulmonary circulation, which develops as a result of diseases of the bronchopulmonary apparatus, chest deformities, and primary lesions of the pulmonary arteries, which at the final stage manifested by right ventricular hypertrophy and progressive circulatory failure ”.
ETIOLOGY OF THE PULMONARY HEART.
Cor pulmonale is a consequence of diseases of three groups:
Diseases of the bronchi and lungs, primarily affecting the passage of air and alveoli. This group includes approximately 69 diseases. They cause the development of cor pulmonale in 80% of cases.
chronic obstructive bronchitis
pneumosclerosis of any etiology
pneumoconiosis
tuberculosis, not by itself, like post-tuberculosis outcomes
SLE, Boeck's sarcoidosis, fibrosing alveolitis (endo- and exogenous)
Diseases primarily affecting the chest, diaphragm with limited mobility:
kyphoscoliosis
multiple rib injuries
obesity Pickwick syndrome
ankylosing spondylitis
pleural suppuration after suffering pleurisy
Diseases primarily affecting the pulmonary vessels
primary arterial hypertension (Ayerza`s disease)
recurrent pulmonary embolism (PE)
compression of the pulmonary artery from the veins (aneurysm, tumor, etc.).
Diseases of the second and third groups are the cause of the development of cor pulmonale in 20% of cases. That is why they say that, depending on the etiological factor, three forms of cor pulmonale are distinguished:
bronchopulmonary
thoracodiaphragmatic
vascular
Standards for values \u200b\u200bcharacterizing the hemodynamics of the pulmonary circulation.
The systolic pressure in the pulmonary artery is approximately five times less than the systolic pressure in the systemic circulation.
Pulmonary hypertension is said to be if the systolic pressure in the pulmonary artery at rest is more than 30 mm Hg, the diastolic pressure is more than 15, and the mean pressure is more than 22 mm Hg.
PATHOGENESIS.
Pulmonary hypertension is the cornerstone of the pathogenesis of cor pulmonale. Since cor pulmonale develops most often 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 failure is a condition in which the normal blood gas composition 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 pulmonary fibrosis, 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, with this, a violation of the vascular architectonics of the lungs occurs - some of the vessels die, some expand, etc. Arterial hypoxemia leads to tissue hypoxia.
The second stage of pathogenesis: arterial hypoxemia will lead to a restructuring of central hemodynamics - in particular, an increase in the amount of circulating blood, polycythemia, polyglobulia, an increase in blood viscosity. Alveolar hypoxia will lead to hypoxemic vasoconstriction by a reflex pathway called the Euler-Liestrand reflex. Alveolar hypoxia led to hypoxemic vasoconstriction, an increase in intra-arterial pressure, which leads to an increase in hydrostatic pressure in the capillaries. Impaired non-respiratory function of the lungs leads to the release of serotonin, histamine, prostaglandins, catecholamines, but the most important thing is that, under conditions of tissue and alveolar hypoxia, the interstitium begins to produce more angiotensin-converting enzyme. The lungs are the main organ where this enzyme is produced. It converts angiotensin 1 into angiotensin 2. Hypoxemic vasoconstriction, release of biologically active substances under conditions of restructuring of central hemodynamics will lead not only to an increase in pressure in the pulmonary artery, but to a persistent increase in it (above 30 mm Hg), that is, to the development of pulmonary hypertension. If the processes continue further, if the underlying disease is not treated, then naturally some of the vessels in the pulmonary artery system die due to pneumosclerosis, and the pressure steadily increases in the pulmonary artery. At the same time, persistent secondary pulmonary hypertension will lead to the opening of shunts between the pulmonary artery and bronchial arteries and unoxygenated blood enters the systemic circulation through the bronchial veins and also contributes to an increase in the work of the right ventricle.
So, the third stage is persistent pulmonary hypertension, the development of venous shunts, which enhance the work of the right ventricle. The right ventricle is not powerful by itself, and hypertrophy with dilatation elements rapidly develops in it.
The fourth stage is hypertrophy or dilation of the right ventricle. Myocardial dystrophy of the right ventricle 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.
PULMONARY HEART CLASSIFICATION.
There is no single classification of cor pulmonale, but the first international classification is mainly etiological (WHO, 1960):
bronchopulmonary heart
thoracodiaphragmatic
vascular
A domestic classification of cor pulmonale is proposed, which provides for the division of cor pulmonale according to the rate of development:
subacute
chronic
Acute cor pulmonale develops within a few hours, minutes, maximum days. Subacute cor pulmonale develops over several weeks or months. Chronic cor pulmonale develops over several years (5-20 years).
This classification provides for compensation, but acute cor pulmonale is always decompensated, that is, requires immediate assistance. The subacute can be compensated and decompensated mainly by the right ventricular type. Chronic cor pulmonale can be compensated, subcompensated, decompensated.
By genesis, acute cor pulmonale develops in vascular and bronchopulmonary forms. Subacute and chronic cor pulmonale can be vascular, bronchopulmonary, thoracodiaphragmatic.
Acute cor pulmonale develops primarily:
with embolism - not only with thromboembolism, but also with gas, tumor, fat, etc.,
with pneumothorax (especially valve),
with an attack of bronchial asthma (especially with asthmatic status - a qualitatively new state of patients with bronchial asthma, with complete blockade of beta2-adrenergic receptors, and with acute pulmonary heart);
with acute drainage pneumonia
right-sided total pleurisy
A practical example of a subacute pulmonary heart disease is recurrent thrombolism of small branches of the pulmonary arteries, with an attack of bronchial asthma. A classic example is cancerous lymphangitis, especially in chorionepitheliomas, in peripheral lung cancer. The thoracodiphragmatic form develops with hypoventilation of central or peripheral origin - myasthenia gravis, botulism, poliomyelitis, etc.
To distinguish at what stage the cor pulmonale passes from the stage of respiratory failure to the stage of heart failure, another classification was proposed. Cor pulmonale is divided into three stages:
latent latent insufficiency - there is a violation of the function of external respiration - VC / FVC is reduced to 40%, but there are no changes in the gas composition of the blood, that is, this stage characterizes respiratory failure of stage 1-2.
stage of severe pulmonary insufficiency - the development of hypoxemia, hypercapnia, but without signs of heart failure in the periphery. There is dyspnea at rest, which cannot be attributed to heart damage.
stage of pulmonary heart failure of varying degrees (edema in the limbs, an increase in the abdomen, etc.).
Chronic cor pulmonale in terms of pulmonary insufficiency, arterial oxygen saturation, right ventricular hypertrophy and circulatory failure is divided into 4 stages:
the first stage - pulmonary insufficiency of the 1st degree - VC / CVC is reduced to 20%, the gas composition is not disturbed. Right ventricular hypertrophy is absent on the ECG, but there is hypertrophy on the echocardiogram. There is no circulatory insufficiency at this stage.
pulmonary insufficiency 2 - VC / VC up to 40%, oxygen saturation up to 80%, the first indirect signs of right ventricular hypertrophy appear, circulatory failure +/-, that is, only shortness of breath at rest.
the third stage - pulmonary insufficiency 3 - VC / FVC less than 40%, arterial blood saturation up to 50%, signs of right ventricular hypertrophy appear on the ECG in the form of direct signs. Circulatory insufficiency 2A.
fourth stage - pulmonary insufficiency 3. Blood oxygen saturation less than 50%, right ventricular hypertrophy with dilation, circulatory insufficiency 2B (dystrophic, refractory).
CLINIC OF ACUTE PULMONARY HEART.
The most common cause of development is PE, an acute increase in intrathoracic pressure due to an attack of bronchial asthma. Arterial precapillary hypertension in acute cor pulmonale, as in the vascular form of chronic cor pulmonale, is accompanied by an increase in pulmonary resistance. Next comes the rapid development of right ventricular dilatation. Acute right ventricular failure is manifested by pronounced shortness of breath that turns into an inspiratory dyspnea, rapidly growing cyanosis, pain behind the breastbone of a different nature, shock or collapse, rapidly increasing liver size, edema on the legs, ascites, epigastric pulsation, tachycardia (120-140), hard breathing , in some places weakened vesicular; wet, variegated 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\u003e R 2\u003e R 1, S 1\u003e S 2\u003e S 3), P-pulmonale appears - a pointed tooth P, in the second , the third standard leads. The right bundle branch block is complete or incomplete, ST inversion (often ascending), S in the first lead is deep, Q in the third lead is deep. Negative S wave in the second and third leads. The same symptoms can occur in acute myocardial infarction of the posterior wall.
Emergency care depends on the cause of the acute cor pulmonale. If there was PE, then pain relievers, fibrinolytic and anticoagulant drugs (heparin, fibrinolysin), streptodecase, streptokinase) are prescribed, up to surgical treatment.
In case of status asthmaticus - large doses of intravenous glucocorticoids, bronchodilators through a bronchoscope, transfer to mechanical ventilation and bronchial lavage. If this is not done, the patient dies.
With valvular pneumothorax - surgical treatment. With drainage pneumonia, along with antibiotic treatment, diuretics and cardiac glycosides are necessarily prescribed.
CLINIC OF CHRONIC PULMONARY HEART.
Patients are worried about shortness of breath, the nature of which depends on the pathological process in the lungs, the type of respiratory failure (obstructive, restrictive, mixed). With obstructive processes, dyspnea of \u200b\u200ban expiratory nature with an unchanged breathing rate, with restrictive processes, the duration of exhalation decreases, and the respiratory rate increases. In an objective study, along with signs of the underlying disease, cyanosis appears, most often diffuse, warm due to the preservation of peripheral blood flow, in contrast to patients with heart failure. In some patients, cyanosis is so pronounced that the skin acquires a cast-iron color. Swollen neck veins, swelling of the lower extremities, ascites. The pulse is speeded up, the borders of the heart expand to the right, and then to the left, the tones are muffled due to emphysema, the accent of the second tone over the pulmonary artery. Systolic murmur at the xiphoid process due to dilation of the right ventricle and relative insufficiency of the right tricuspid valve. In some cases, with severe heart failure, you can listen to a diastolic murmur on the pulmonary artery - the Graham-Still murmur, which is associated with the relative insufficiency of the pulmonary valve. Above the lungs, percussion sound is boxy, vesicular breathing, hard. In the lower parts of the lungs, stagnant, non-sounding moist rales. On palpation of the abdomen - an enlarged liver (one of the reliable, but not early signs of cor pulmonale, since the liver can be displaced due to emphysema). The severity of symptoms depends on the stage.
The first stage: against the background of the underlying disease, shortness of breath increases, cyanosis appears in the form of acrocyanosis, but the right border of the heart is not enlarged, the liver is not enlarged, physical data in the lungs depend on the underlying disease.
The second stage - shortness of breath turns into attacks of suffocation, with difficulty breathing, cyanosis becomes diffuse, from the data of objective research: pulsation appears in the epigastric region, the tones are muffled, the accent of the second tone over the pulmonary artery is not constant. The liver is not enlarged, it can be omitted.
The third stage - signs of right ventricular failure join - an increase in the right border of cardiac dullness, an increase in the size of the liver. Constant edema in the lower limbs.
The fourth stage - shortness of breath at rest, forced position, often accompanied by respiratory rhythm disorders such as Cheyne-Stokes and Biota. Edema is constant, not amenable to treatment, the pulse is weak, fast, bovine heart, muffled tones, systolic murmur at the xiphoid process. There is a mass of moist wheezing in the lungs. The liver is of considerable size, does not contract under the influence of glycosides and diuretics, as fibrosis develops. Patients are constantly asleep.
Diagnostics of the thoracodiaphragmatic heart is often difficult, one must always remember about the possibility of its development in kyphoscoliosis, ankylosing spondylitis, etc. The most important sign is the early appearance of cyanosis, and a noticeable increase in shortness of breath without asthma attacks. Pickwick's syndrome is characterized by a triad of symptoms - obesity, drowsiness, severe cyanosis. This syndrome was first described by Dickens in the Posthumous Papers of the Pickwick Club. It is associated with traumatic brain injury, obesity is accompanied by thirst, bulimia, arterial hypertension. Diabetes mellitus often develops.
Chronic cor pulmonale in primary pulmonary hypertension is called Aerza's disease (described in 1901). A polyetiological disease, of unknown origin, mainly affects women from 20 to 40 years old. Pathomorphological studies have established that in primary pulmonary hypertension, the intima of the precapillary arteries thickens, that is, thickening of the media is noted in the arteries of the muscle type, and fibrinoid necrosis develops, followed by sclerosis and the rapid development of pulmonary hypertension. Symptoms are varied, usually complaints of weakness, fatigue, pain in the heart or joints, 1/3 of patients may experience fainting, dizziness, Raynaud's syndrome. And in the future, shortness of breath increases, which is the sign that indicates that primary pulmonary hypertension passes into a stable final stage. Cyanosis rapidly grows, which is expressed to the degree of a cast-iron shade, becomes permanent, swelling rapidly increases. The diagnosis of primary pulmonary hypertension is established by exclusion. Most often, this diagnosis is pathological. In these patients, the entire clinic progresses without a background in the form of obstructive or restrictive breathing disorders. With echocardiography, the pressure in the pulmonary artery reaches its maximum values. Treatment is ineffective, death occurs from thromboembolism.
Additional research methods for cor pulmonale: in a chronic process in the lungs - leukocytosis, an increase in the number of red blood cells (polycythemia associated with increased erythropoiesis due to arterial hypoxemia). X-ray data: appear very late. One of the early symptoms is a bulging of the pulmonary artery trunk on radiographs. The pulmonary artery is bulging, often flattening the waist of the heart, and many doctors mistake this heart for the mitral configuration of the heart.
ECG: there are indirect and direct signs of right ventricular hypertrophy:
deviation of the electrical axis of the heart to the right - R 3\u003e R 2\u003e R 1, S 1\u003e S 2\u003e S 3, the angle is more than 120 degrees. The most basic indirect sign is an increase in the interval of the R wave in V 1 by more than 7 mm.
direct signs - blockade of the right bundle of His bundle, the amplitude of the R wave in V 1 is more than 10 mm with complete blockade of the right bundle of His bundle. The appearance of a negative T wave with a displacement of the wave below the isoline in the third, second standard lead, V1-V3.
Of great importance is spirography, which reveals the type and degree of respiratory failure. On ECG, signs of right ventricular hypertrophy appear very late, and if only deviations of the electrical axis to the right appear, then they already speak of pronounced hypertrophy. The most basic diagnostics is Doppler cardiography, echocardiography - an increase in the right heart, increased pressure in the pulmonary artery.
PRINCIPLES OF PULMONARY HEART TREATMENT.
Treatment of cor pulmonale consists in treating the underlying disease. With an exacerbation of obstructive diseases, bronchodilators, expectorants are prescribed. With Pickwick's syndrome - obesity treatment, etc.
Reduce the pressure in the pulmonary artery with calcium antagonists (nifedipine, verapamil), peripheral vasodilators that reduce preload (nitrates, corvaton, sodium nitroprusside). Of greatest importance is sodium nitroprusside in combination with angiotensin-converting enzyme inhibitors. Nitroprusside 50-100 mg intravenously, kapoten 25 mg 2-3 times a day, or enalapril (second generation, 10 mg per day). They also use treatment with prostaglandin E, antiserotonin drugs, etc. But all these drugs are effective only at the very beginning of the disease.
Treatment of heart failure: diuretics, glycosides, oxygen therapy.
Anticoagulant, antiaggregant therapy - heparin, trental, etc. Due to tissue hypoxia, myocardial dystrophy develops rapidly, so cardioprotectors (potassium orotate, panangin, riboxin) are prescribed. Cardiac glycosides are prescribed very carefully.
PREVENTION.
Primary is the prevention of chronic bronchitis. Secondary - treatment of chronic bronchitis.
1960 0
According to the definition of the WHO Expert Committee, cor pulmonale is hypertrophy or a combination of hypertrophy with dilatation of the right ventricle, arising from diseases affecting the structure or function of the lungs or both at the same time and not associated with primary insufficiency of the left heart, for example, with acquired or congenital heart defects.
To hypertrophy of the right ventricle with the subsequent depletion of its energy capabilities leads mainly pulmonary hypertension (LH)and the associated increase in vascular resistance.
No pulmonary hypertension chronic pulmonary heart (HLS).
In this regard, the European Society for the Clinical Physiology of Respiration included the presence of LH in the very definition of HPS.
In addition, in chronic cor pulmonale, the left ventricle is involved in the process quite early with the development of its dysfunction. This is due to hypoxemia, infectious and toxic influences and mechanical factors (compression of the left ventricle by the dilated right, paradoxical movement of the interventricular septum and its protrusion into the cavity of the left ventricle, which makes it difficult to fill it). In this regard, there is a tendency to include dysfunction of both ventricles in the definition of HPS.
In our country, the classification of pulmonary heart is widely used, proposed back in 1964 by a well-known therapist and clinical pharmacologist, academician B.E. Votchalom (table).
In the practice of a doctor, chronic cor pulmonale is most common. The causes of chronic pulmonary disease in 80% are diseases of the bronchopulmonary apparatus: chronic obstructive pulmonary disease (COPD), fibrosing alveolitis, granulomatosis (sarcoidosis, disseminated pulmonary tuberculosis, etc.), systemic scleroderma. In second place as a cause of chronic pulmonary heart disease are lesions of the thoracodiaphragmatic apparatus: chest deformities (kyphosis, scoliosis), obesity (Pickwick syndrome), extensive pleural mooring, myasthenia gravis.
Diseases with primary lesions of the pulmonary vessels are somewhat less important: primary pulmonary hypertension (Aerz's disease), polyarteritis nodosa and other systemic vasculitis, repeated thromboembolism in small branches of the pulmonary artery.
Table. Classification of pulmonary heart (B.E. Votchal, 1964)
| The nature of the flow |
condition compensation |
Predominant pathogenesis |
Features of clinical paintings |
| I. Acute cor pulmonale: development within a few hours, days II. Subacute cor pulmonale: develops over several weeks, months Diagnostics of the compensated chronic pulmonary heartDiagnosis of compensated HPS is the identification of hypertrophy and dilatation of the right ventricle, as well as PH in the diseases listed above.Clinical signs of right ventricular hypertrophy: diffuse cardiac impulse, defined in the area of \u200b\u200babsolute cardiac dullness or in the epigastric region (not to be confused with the transmitting pulsation of the aorta). Epigastric pulsation is a less reliable sign, since it can be observed with pulmonary emphysema and without right ventricular hypertrophy due to the downward displacement of the heart. Clinical and radiological methods to reveal hypertrophy are far from being possible in all cases. This is due to the downward displacement of the heart due to emphysema ("hanging" heart) and clockwise rotation of the heart, as a result of which the right ventricle shifts to the left and can take the place of the left. Therefore, percussion and X-ray enlargement of the heart to the right is not associated with hypertrophy of the right ventricle, but is due to dilatation of the right atrium and already indicates decompensation of HPS. It is sometimes possible to reveal hypertrophy of the right ventricle during X-ray examination in the first oblique and lateral positions in the form of an arcuate protrusion into the anterior mediastinum. Electrocardiographic signs of right ventricular hypertrophy are divided into direct and indirect. Direct signs are conventionally designated as R-type or S-type of right ventricular hypertrophy. The first is manifested by a high R wave in V 1 and V 2, the second by a sharp decrease in the R wave and deep S waves in V 5 and V 6. A combination of both types of symptoms is often observed. Along with this, there is a shift of ST below the isoline in V 1, V 2 and the appearance of a Q wave in these leads, a shift of the transition zone to the left, complete or incomplete blockade of the right bundle branch. Indirect signs include, in particular, an increase in the amplitude of the P wave in leads II, III and aVF (P-pulmonale), which indicates right atrial hypertrophy. It should be noted that the information content is rather low. emission computed tomography (ECG) in chronic cor pulmonale, which is associated with the above-mentioned positional changes in the heart, as well as with the fact that hypertrophy of the right ventricle develops against the background of prolonged hypoxia, as a result of which it cannot reach significant sizes. Even with decompensation of CLS, the frequency of detection of right ventricular hypertrophy by this method does not exceed 50-60%. Even lower is the information content of the X-ray research method. Currently, echocardiography (in M-mode, two-dimensional and Doppler echocardiography in pulsed and continuous wave mode) is of primary importance for detecting pulmonary heart. The most important echocardiographic signs of cor pulmonale are right ventricular hypertrophy (the thickness of its anterior wall exceeds 0.5 cm), dilatation of the right heart, paradoxical movement of the interventricular septum in diastole towards the left ventricle, and an increase in tricuspid regurgitation. The advantage of Doppler echocardiography in CLS is the ability to simultaneously determine the pressure in the pulmonary artery. Pathogenesis of chronic pulmonary heart decompensationIt is believed that progressive dystrophy of the hypertrophied myocardium is of primary importance in the development of decompensation of chronic cor pulmonale. However, in patients with CLS, there is often no correspondence between the degree of PH, on which myocardial hypertrophy and dystrophy mainly depend, and the severity of right ventricular failure. Therefore, in the development and progression of heart failure (HF) in chronic cor pulmonale, importance is attached to other factors.Among them, the main ones are: 1. Previously noted increase in activity renini-angiotensin-aldosterone system (RASC). 2. Hypoxia in combination with inflammatory intoxication. When disseminated lung diseases (DZL) accumulate pro-inflammatory cytokines that have a direct damaging effect on cardiomyocytes. A clear relationship was established between an increase in the level of proinflammatory cytokines (tumor necrosis factor, interleukin-6) and the severity of hypoxia, endogenous intoxication and inflammation activity. 3. In recent years, evidence has appeared that due to the violation of immune mechanisms in patients with DLP, sensitization to the cardiac antigen develops, which leads to autoimmune damage to the myocardium. Diagnostics of the decompensated chronic pulmonary heartTo assess severe heart failure in CHD, the classification can be used circulatory failure (NK)proposed by N.D. Strazhesko and V.Kh. Vasilenko. However, its application in these cases has some peculiarities. As you know, NK stage I according to this classification is characterized mainly by shortness of breath during exercise.In patients with COPD and other PDD, cor pulmonale decompensation develops against the background of severe pulmonary insufficiency, manifested, in particular, by shortness of breath and cyanosis. This does not make it possible, according to clinical data, to establish NK stage I in CLS. The possibility of using phase analysis of the cardiac cycle for this purpose is still subject to further study. The second feature of using the classification of N.D. Strazhesko and V.Kh. Vasilenko is the difficulty (often impossibility) of differentiation in decompensated chronic pulmonary heart disease NK IIA and IIB stages. NK stage II, according to this classification, is characterized by the retention of NK at rest: at stage IIA - in one, at IIB - in both circles of blood circulation. With DLP, decompensation for a long time is manifested only by right ventricular failure, and dyspnea at rest, which in heart disease indicates mainly stagnation in the pulmonary circulation, is primarily associated with pulmonary insufficiency. Thus, with decompensated CLS, it is recommended to isolate only stages II and III. In stage II NK, the following symptoms appear: 1. Constant swelling of the neck veins. This is preceded for a long time by a change in the filling of the cervical veins, depending on the phases of breathing (swelling on exhalation and collapse on inspiration). This "play" of veins is associated with fluctuations in intrathoracic pressure and does not indicate decompensation of the right ventricle. 2. Enlargement of the liver. A slight (1-2 cm) enlargement of the liver may be associated with a downward displacement of the organ due to the low standing of the diaphragm. A convincing sign of decompensation is a more significant increase in the size of the liver, especially the left lobe, the presence of at least slight pain on palpation, and a decrease in the size of the liver after treatment with cardiotonic drugs. 3. Peripheral edema. However, it is necessary to bear in mind the possibility of developing pasty legs, sometimes significant, not due to cardiac decompensation, but in connection with respiratory failure and hypercapnia (apparently due to the effect on the mineralocorticoid function of the adrenal glands). 4. "Cold" cyanosis (cold extremities), which indicates its stagnant origin. In case of pulmonary insufficiency, cyanosis is "warm", which indicates its hypoxemic nature. However, stagnant cyanosis "overlaps" with hypoxemic, and the latter predominates for a long time. Therefore, in many patients with decompensated CLS stage II, cyanosis is still warm. "Cold" cyanosis is more typical for stage III NK. With decompensation of chronic respiratory syndrome, there are some features of the manifestations of shortness of breath. These include the absence or weakness of orthopnea, which, as a rule, is observed only in the presence of ascites. Diagnostics of stage III NK is based on well-known signs (development of congestive cirrhosis of the liver, common and refractory to treatment edema, including cavity, degenerative changes in internal organs, etc.). As already noted, the symptoms of HPS decompensation are superimposed on the manifestation of pulmonary insufficiency that appeared earlier. Therefore, in the complication of the underlying disease, such as COPD, it is necessary to indicate the degree of FN and the stage of heart failure. For example, after the formulation of the underlying disease (COPD), grade III LN, grade III pulmonary hypertension, decompensated chronic pulmonary heart disease, stage II NK are noted as complications. To express functional disorders of the apparatus of external respiration and heart in patients with DLP, you can use the term "Pulmonary heart failure" (PPF) and express it as a fraction: in the numerator - the degree of pulmonary, in the denominator - the degree of heart failure. In this case, the complication is formulated as follows: chronic cor pulmonale, pulmonary heart failure III / II degree. It must be emphasized that the degrees of pulmonary and heart failure usually do not coincide: more often the degree of pulmonary failure is higher than the degree of heart failure. Therefore, it is strictly necessary to separately indicate the degree of pulmonary and heart failure. Saperov V.N., Andreeva I.I., Musalimova G.G. |
The reasons leading to the development of chronic pulmonary heart disease can be divided into several groups.
The first group of reasons unites chronic diseases lungs, proceeding with the development of obstructive syndrome. These are bronchial asthma, chronic obstructive bronchitis, chronic emphysema of the lungs, occupational diseases of the lungs, etc. Chronic cor pulmonale develops in connection with the formation of irreversible obstruction of the bronchi, the development of connective tissue in their walls, thickening of the muscle layer of the bronchial wall, as a result of which air permeability is impaired. bronchi and the triggering mechanism of the pathogenesis of chronic cor pulmonale is turned on - hypertension in the pulmonary circulation.
The second group of reasons that naturally lead to the development of hypertension in the pulmonary circulation are diseases of the skeleton - various deformities of the spine and ribs, leading to a decrease in the volume of the chest and disruption of the mutual arrangement of internal organs (scoliosis, kyphosis and other diseases; obesity, accompanied by a high standing of the diaphragm and constriction of the lungs). All these reasons also contribute to the activation of the mechanism leading to the formation of pulmonary hypertension.
And the last, third, group of causes is diseases of the vessels that feed the lung tissue (atherosclerosis of the pulmonary vessels, etc.). As a rule, for the formation of chronic cor pulmonale, it is necessary that the etiological factor exerts its influence on the patient for a long time, for many years.
Pathogenesis
Etiological factors for various reasons cause disruption of the passage of air into the bronchi and an increase in pressure in the pulmonary vessels.
For the implementation of pulmonary hypertension, the Euler-Liljestrandt reflex is of great importance, which consists in the development of pulmonary vasospasm, which occurs in response to a decrease in the partial pressure of oxygen in the pulmonary vessels.As a result, the right ventricle is forced to perform intensive work to promote blood into the pulmonary vessels. Due to this, compensatory hypertrophy of the walls of the right ventricle occurs, and then its dilatation.
Excessive body weight often leads to a high standing of the diaphragm, resulting in constriction of the lungs, pulmonary hypoxia and hypertension of the pulmonary arterioles. This condition is called Pickwick's syndrome.
On examination, you can identify indirect signs that indicate the presence of chronic inflammatory diseases of the lung tissue - fingers in the form of drumsticks and nails that resemble watch glasses.
Since the development of chronic pulmonary heart disease is preceded by the formation of respiratory failure, the examination can reveal signs that indicate its presence.
Chronic pulmonary failure leads to the development of hypoxia, resulting in a characteristic clinical symptom - shortness of breath.
On examination, an increase in the number of respiratory movements and the involvement of additional respiratory muscles in the act of breathing are determined. Cyanosis may be noted as a manifestation of hypoxemia and hypercapnia. In addition, swelling of the cervical veins is noted in chronic cor pulmonale.
Respiratory failure is classified according to the degree of arterial oxygen saturation and carbon dioxide content.
There are 3 degrees of respiratory failure.
The first degree is the presence of chronic obstructive diseases with a slight decrease in the partial pressure of oxygen in the blood, CBS is not disturbed. With excessive physical exertion, a decrease in the indicators of the function of external respiration is observed. Clinically, respiratory failure of the first degree is manifested by the onset of symptoms only with excessive physical exertion, daily activities are not limited. On examination, cyanosis is not noted.
The second degree corresponds to the partial pressure of oxygen in the blood in the range from 79 to 55 mm Hg. Art., a decrease in the indicators of samples characterizing the function of external respiration, a change in CBS (respiratory alkalosis develops). Clinically characteristic symptoms (shortness of breath) occur during daily physical activity, but are absent at rest. On examination, cyanosis of the tips of the fingers and toes, ears, lips, cyanotic skin areas, cool to the touch, are determined.
The third degree of respiratory failure is accompanied by a decrease in the partial pressure of oxygen below 55 mm Hg. Art., CBS changes (respiratory acidosis). The indicators characterizing the function of external respiration are significantly reduced. The symptoms of respiratory failure appear already at rest and significantly disrupt the social and everyday activity of patients. On examination, diffuse cyanosis of the skin is noted, the skin is cold to the touch.
Interviewing a patient reveals a variety of complaints indicating both a disease of the bronchopulmonary system and the presence of complications - chronic respiratory failure, chronic pulmonary heart disease.
On palpation of the patient's pulse, an increase in pulse is noted, with physical exertion, the pulse becomes even more frequent. On palpation, the presence of a heart beat is noted. The heart beat is formed by the right ventricle and is determined by hypertrophy of the latter. A heart beat is detected in the epigastric region, if it is present, its characteristics are determined - diffuse, uplifting. Palpation allows you to determine the presence of edema in the lower extremities, indicating heart failure.
With percussion, an increase in the boundaries of relative cardiac dullness to the right is determined, due to hypertrophy of the right heart. In a number of cases, signs of pulmonary emphysema are noted - the presence of a box sound with comparative lung percussion, displacement of the boundaries of the lower edge of the lung downward and a decrease in the mobility of the lower pulmonary edge.
Auscultatory data, in addition to signs of diseases of the bronchopulmonary system, can reveal changes in heart sounds. So, the main sign of hypertension in the pulmonary circulation is the appearance of an accent of the II tone over the pulmonary artery. In some cases, an auscultatory phenomenon such as Graham Steele's diastolic murmur is determined.
It should be noted that with decompensation of chronic pulmonary heart disease, the formation of chronic heart failure is noted, the main signs of which are determined during a general clinical study, which should not be forgotten during an objective examination of the patient.
Diagnostics
X-ray examination is one of the simple and informative research methods. It allows you to identify hypertrophy of the right heart - the contour of the heart increases to the right, there is a bulging of the pulmonary artery cone and deviation of the esophagus. In the lungs, there is an increase in the pulmonary pattern.
Electrocardiogram data are of great importance for determining hypertrophy of the right heart. The main signs of chronic cor pulmonale are deviation of the cardiac axis to the right, the presence of a large P wave in leads II and III, in AVF and right chest leads, blockade of the right bundle branch, negative T wave in leads V 1-2.
The phonocardiogram reveals an increase in the amplitude of 1 and I tone over the pulmonary artery.
Treatment
Treatment of chronic pulmonary heart disease is carried out using certain measures. The first group of measures is aimed at treating the underlying disease that caused the development of such a complication, that is, chronic obstructive pulmonary diseases are treated according to general rules. Such patients need to facilitate the passage of air through the bronchial tree, this will help reduce hypertension in the pulmonary vessels. For this purpose, drugs are prescribed that affect the liquefaction of sputum, and drugs that promote its discharge, as well as bronchodilators that eliminate spasm of the muscles of the bronchial tree.
Non-drug measures that improve sputum drainage include massage therapy and breathing exercises.
The use of drugs that reduce pulmonary hypertension is of great importance. These drugs include α-2-blockers, ACE inhibitors, aldosterone blockers. Reducing hypertension in the pulmonary artery system affects the main link in the pathogenesis of chronic pulmonary heart disease.
In the formation of cardiopulmonary insufficiency, treatment is supplemented with a number of components. Therapy for heart failure includes drugs such as diuretics, aldosterone blockers, ACE inhibitors, calcium channel blockers. Therapy for pulmonary insufficiency is aimed at enriching the blood with oxygen. For this, methods of artificial lung ventilation, hyperbaric oxygenation, hemosorption are used.