Pulmonary heart. Symptoms and treatment of chronic pulmonary heart disease Features of the clinical picture

The development of cor pulmonale is necessarily preceded by pulmonary hypertension. Although high cardiac output, tachycardia, and increased blood volume may contribute to the development of pulmonary hypertension, right ventricular overload due to increased resistance to pulmonary blood flow at the level of small muscular arteries and arterioles plays a major role in the pathogenesis of the latter. An increase in vascular resistance may be due to anatomical causes or vasomotor disorders; most often there is a combination of these factors (Table 191-2). In contrast to the situation observed with left ventricular failure, with pulmonary hypertension, cardiac output is usually within normal limits and increased, the peripheral pulse is tense, the extremities are warm; all this takes place against the background of clear signs of systemic venous stagnation. Peripheral edema complicating cor pulmonale is usually considered a consequence of heart failure, but this explanation cannot be considered satisfactory, since the pressure in the pulmonary trunk rarely exceeds 65-80 kPa, except in cases where there is a sharp deterioration in the condition with severe hypoxia and acidosis.

It was noted above that an increase in the work of the right ventricle caused by pulmonary hypertension can lead to the development of its failure. However, even in patients with reduced right ventricular stroke volume as a result of pulmonary hypertension, its myocardium is able to function normally when the overload is eliminated.

Anatomical increase in pulmonary vascular resistance. Normally, at rest, the pulmonary circulation is able to maintain approximately the same level of blood flow as in the systemic circulation, while the pressure in it is about 1/5 of the average blood pressure. During moderate physical activity, a 3-fold increase in total blood flow causes only a slight increase in pressure in the pulmonary trunk. Even after pneumonectomy, the remaining vasculature tolerates a sufficient increase in pulmonary blood flow, responding with only a small increase in pulmonary pressure as long as the lungs are free of fibrosis, emphysema, or vascular changes. Likewise, amputation of most of the pulmonary capillary bed in emphysema does not usually cause pulmonary hypertension.

However, when pulmonary vascular reserve is depleted due to progressive reduction in the area and distensibility of the pulmonary vasculature, even small increases in pulmonary blood flow associated with daily life activities can lead to the onset of significant pulmonary hypertension. A necessary condition This is a significant reduction in the cross-sectional area of ​​the pulmonary resistive vessels. A decrease in the area of ​​the pulmonary vascular bed is a consequence of extensive narrowing and obstruction of small pulmonary arteries and arterioles and the accompanying decrease in the distensibility of not only the vessels themselves, but also the surrounding vascular tissue.

Table 191-2. Pathogenetic mechanisms in chronic pulmonary hypertension and cor pulmonale

Pathogenetic mechanism

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Pulmonary heart: etiology, pathogenesis, classification.

HEART PULMONARY - pathological condition, characterized by hypertrophy and dilatation (and then failure) of the right ventricle of the heart due to arterial pulmonary hypertension with lesions of the respiratory system.

Etiology. There are:

1) vascular form of cor pulmonale - with pulmonary vasculitis, primary pulmonary hypertension, mountain sickness, pulmonary embolism;

2) bronchopulmonary form, observed with diffuse damage to the bronchi and pulmonary parenchyma - with bronchial asthma, bronchiolitis, chronic obstructive bronchitis, pulmonary emphysema, diffuse pneumosclerosis and pulmonary fibrosis as a result of nonspecific pneumonia, tuberculosis, pneumoconiosis, sarcoidosis, Hamman-Rich syndrome, etc.;

3) thoradiaphragmatic form of cor pulmonale, which develops with significant disturbances in ventilation and blood flow in the lungs due to deformation chest(kyphoscoliosis, etc.), pathologies of the pleura, diaphragm (with thoracoplasty, massive fibrothorax, Pickwickian syndrome, etc.).

Pathogenesis. Pulmonary arterial hypertension is of leading importance, caused by a pathological increase in resistance to blood flow during hypertension of the pulmonary arterioles - primary (with primary pulmonary hypertension) or in response to alveolar hypoxia (with mountain sickness, impaired alveolar ventilation in patients with bronchial obstruction, kyphoscoliosis, etc.) or due to anatomical reduction in the lumen of the arterial pulmonary bed due to sclerosis, obliteration (in areas of pneumosclerosis, pulmonary fibrosis, vasculitis), thrombosis or thromboembolism, after surgical excision (during pneumonectomy). In case of respiratory failure in patients with extensive damage to the lung parenchyma, the load on the heart is also of pathogenetic importance due to a compensatory increase in blood circulation due to increased venous return of blood to the heart.

Classification. According to the characteristics of development, acute cor pulmonale is distinguished, developing over several hours or days (for example, with massive thromboembolism of the pulmonary arteries, valvular pneumothorax), subacute (developing over weeks, months with repeated thromboembolism of the pulmonary arteries, primary pulmonary hypertension, lymphogenic carcinomatosis of the lungs, severe bronchial asthma, bronchiolitis) and chronic, developing against the background of long-term respiratory failure.

There are three stages in the development of chronic pulmonary heart disease: stage 1 (preclinical) is characterized by transient pulmonary hypertension with signs of intense activity of the right ventricle, which are detected only during instrumental examination; Stage II is determined by the presence of signs of right ventricular hypertrophy and stable pulmonary hypertension in the absence of circulatory failure; Stage III, or the stage of decompensated cor pulmonale (synonym: pulmonary heart failure), occurs from the time the first symptoms of right ventricular failure appear.

Clinical manifestations. Acute cor pulmonale is manifested by pain behind the sternum, sharply rapid breathing, a drop in blood pressure, up to the development of collapse, ash-gray diffuse cyanosis, expansion of the border of the heart to the right, and sometimes the appearance of epigastric pulsation; increasing tachycardia, strengthening and accentuation of the second heart sound over the pulmonary trunk; deviation of the electrical axis of the heart to the right and electrocardiographic signs of overload of the right atrium; increased venous pressure, swelling of the neck veins, enlarged liver, often accompanied by pain in the right hypochondrium.

Chronic pulmonary heart disease to the stage of decompensation is recognized by symptoms of hyperfunction, then hypertrophy of the right ventricle against the background arterial hypertension, detected initially using ECG, chest x-ray and other instrumental methods, and subsequently according to clinical signs: the appearance of a pronounced cardiac impulse (shaking of the anterior chest wall during heart contractions), pulsation of the right ventricle, determined by palpation behind the xiphoid process, strengthening and constant emphasis of the second heart sound over the trunk pulmonary artery with frequent intensification of the first tone over the lower part of the sternum. In the stage of decompensation, right ventricular failure appears: tachycardia;

acrocyanosis; swelling of the neck veins that persists during inspiration (their swelling only during exhalation may be due to bronchial obstruction) nocturia; liver enlargement, peripheral edema (see Heart failure).

Treatment. The underlying disease is treated (elimination of pneumothorax, thrombolytic therapy or surgical intervention for thromboembolism of the pulmonary arteries, therapy for bronchial asthma, etc.), as well as measures aimed at eliminating respiratory failure. According to indications, bronchodilators, expectorants, respiratory analeptics, and oxygen therapy are used. Decompensation of chronic pulmonary heart disease in patients with bronchial obstruction is an indication for continuous therapy with glucocorticoids (prednisolone, etc.), if they are effective. In order to reduce arterial pulmonary hypertension in chronic cor pulmonale, aminophylline (iv, in suppositories) can be used; V early stages-nifedipine (adalat, corinfar); in the stage of circulatory decompensation - nitrates (nitroglycerin, nitrosorbide) under the control of oxygen content in the blood (possible increased hypoxemia). With the development of heart failure, treatment with cardiac glycosides and diuretics is indicated, which is carried out with great caution due to the high sensitivity of the myocardium to toxic effect glycosides against the background of hypoxia and hypocaligistia caused by respiratory failure. For hypocapemia, panangin and potassium chloride are used.

If diuretics are used frequently, potassium-sparing drugs (triampur, aldactone, etc.) have advantages.

To avoid the development of ventricular fibrillation intravenous administration cardiac glycosides cannot be combined with the simultaneous administration of aminophylline, calcium preparations (antagonists in their effect on the heterotopic automatism of the myocardium). If necessary, corglicon is administered intravenously no earlier than 30 minutes after the end of the administration of zufillin. For the same reason, cardiac glycosides should not be administered intravenously against the background of adrenergic agonist intoxication in patients with bronchial obstruction (status asthmaticus, etc.). Maintenance therapy with digoxin or isolanide in patients with decompensated chronic cor pulmonale is selected taking into account the decrease in tolerance to the toxic effects of drugs in the event of increasing respiratory failure.

Prevention consists of prevention, as well as timely and effective treatment diseases complicated by the development of cor pulmonale. Patients with chronic bronchopulmonary diseases are subject to clinical observation in order to prevent exacerbation and conduct rational treatment of respiratory failure. Great importance has proper employment of patients with limited physical activity, which contributes to an increase in pulmonary hypertension.

Coarctation of the aorta: clinical picture, diagnosis, treatment.

Oarctation of the aorta (CA) is a congenital narrowing of the aorta, the degree of which can reach a complete break.

In isolated form, the defect is rare (in 18% of cases). It is usually combined with other anomalies (bicuspid aortic valve, patent ductus arteriosus, ventricular septal defect, etc.).

Typical sites of aortic narrowing are just above and below the origin of the patent ductus arteriosus (infantile and adult types of CA, respectively). The coronary artery can also have an atypical location, even at the level of the abdominal aorta, but this is extremely rare. Narrowing in the area of ​​coarctation can range from moderate (more than 5 mm) to severe (less than 5 mm). Sometimes there is a pinhole no more than 1 mm. The length of the narrowing area also varies and can be either very small (1 mm) or extended (2 cm or more).

There are four types of aortic coarctation:

isolated narrowing of the aorta

narrowing of the aorta in combination with a patent ductus arteriosus

narrowing of the aorta in combination with a ventricular septal defect

narrowing of the aorta in combination with other heart defects.

There are five periods in the natural course of aortic coarctation.

I period critical, age up to 1 year, symptoms of circulatory failure (usually in the pulmonary circulation), also depending on concomitant anomalies; high mortality rate.

II period adaptations, age 15 years, reduction of symptoms of circulatory failure, which by the end of the period are usually represented only by shortness of breath and increased fatigue.

III period compensation, age 515 years, various variants of the course, often asymptomatic.

IV period relative decompensation, age of puberty, increasing symptoms of circulatory failure.

V period of decompensation, age 20-40 years, symptoms of arterial hypertension and its complications, severe circulatory failure in both circles.

Complaints in children early age the symptoms of circulatory failure in the pulmonary circulation predominate (shortness of breath, orthopnea, cardiac asthma, pulmonary edema) In the postductal variant, coronary artery disease can manifest as cardiogenic shock when the PDA closes. In older children, the symptoms of arterial hypertension predominate (cerebral blood supply disorders, headaches, nosebleeds) and, much less frequently, decreased blood flow distal to the aortic narrowing (intermittent claudication, abdominal pain associated with intestinal ischemia) Symptoms of associated abnormalities

The predominance of physical development of the shoulder girdle with thin legs(athletic build) in children of the older age group Pulsation of the intercostal arteries Cyanosis in combination of coronary artery disease with congenital heart disease, accompanied by discharge of blood from right to left Weakening of pulsation in the arteries of the lower extremities Difference in blood pressure in the upper and upper extremities lower limbs more than 20 mm Hg Delay of the pulse wave in the lower extremities compared to the upper extremities Increased apical impulse Increased pulsation of the carotid arteries Systolic murmur over the base of the heart, carried along the left edge of the sternum, in the interscapular region and on carotid arteries Systolic ejection click at the apex and base of the heart Auscultatory symptoms may be completely absent Symptoms of associated anomalies

ECG Signs of hypertrophy and overload of the right (60% of infants), left (20% of infants) or right and left (5% of infants) sections Ischemic changes in the final part of the ventricular complex (50% of infants without fibroelastosis and 100% of children with fibroelastosis myocardium), in 15% of cases there are no signs of myocardial hypertrophy. See also Patent ductus arteriosus, Aortic valve stenosis, Ventricular septal defect.

X-ray of the chest organs Bulging of the arch of the pulmonary artery Cardiomegaly In older children, the shadow formed by the aortic arch and its dilated descending part can take the form of the number 3. The same changes give the esophagus filled with barium the appearance of the letter E. Usuration of the ribs caused by the pressure of the dilated intercostal and internal mammary vessels, found in patients over 5 years of age

EchoCG Myocardial hypertrophy and dilatation of the cavities of the heart depend on the degree of narrowing of the aorta and associated anomalies. In a third of cases, the aortic valve is bicuspid. Visualization of stenosis, determination of its degree. anatomical variant (local, diffuse, tandem) and relation to PDA Measurement of transstenotic pressure gradient Children of older age groups and adults undergo transesophageal echocardiography.

Drug therapy. Conservative treatment of postoperative patients involves correction of systolic hypertension, heart failure, and prevention of aortic thrombosis. In the future, when managing such patients, the issue of prescribing anti-atherosclerotic therapy to prevent possible recoarctation should be decided. Prevention of infective endocarditis. When treating cardiogenic shock, standard regimens are used. In case of postductal or unclear variant of CA, even with a closed PDA, an infusion of PgE1 (alprostadil) 0.05-0.1 mg/kg/min is performed. After hemodynamic stabilization, emergency surgical correction is performed. In the treatment of arterial hypertension in adults, preference is given to ACE inhibitors and calcium antagonists. In the postoperative period, a temporary worsening of hypertension may develop, for which beta-blockers and nitroprusside are prescribed.

Surgical treatment Indications Surgical treatment All patients with coronary artery disease under the age of 1 year are eligible

Complications of myocardial infarction. Cardiogenic shock.

Three groups of MI complications:

Rhythm and conduction disturbances.

Violation of the pumping function of the heart (acute left- and right-ventricular failure, aneurysm, expansion of the infarction zone).

Other complications: epistenocardial pericarditis, thromboembolism, early post-infarction angina, Dresler syndrome.

true cardiogenic shock (with damage to more than 40% of the myocardium) - blood pressure less than 80 mm Hg. Art.

Cardiogenic shock extreme degree of left ventricular failure, characterized by sharp decline contractility of the myocardium (decrease in stroke and cardiac output), which is not compensated by an increase in vascular resistance and leads to inadequate blood supply to all organs and tissues, especially vital important organs. Most often it develops as a complication of myocardial infarction, less often myocarditis or poisoning with cardiotoxic substances. In this case, there are four possible various mechanisms causing shock:

Disorder of the pumping function of the heart muscle;

Severe heart rhythm disturbances;

Ventricular tamponade with effusion or bleeding into the heart sac;

Shock due to massive pulmonary embolism, as a special form of CABG

Pathogenesis

Severe impairment of myocardial contractile function with the additional addition of factors that aggravate myocardial ischemia.

Sympathetic activation nervous system due to a drop in cardiac output and a decrease in blood pressure, it leads to an increase in heart rate and increased myocardial contractility, which increases the heart’s need for oxygen.

Fluid retention due to decreased renal blood flow and an increase in blood volume, which increases preload on the heart, contributes to pulmonary edema and hypoxemia.

Increased peripheral vascular resistance due to vasoconstriction, leading to increased afterload on the heart and increased myocardial oxygen demand.

Violation of diastolic relaxation of the left ventricle of the myocardium due to impaired filling and decreased compliance, which causes an increase in pressure in the left atrium and contributes to increased blood stagnation in the lungs.

Metabolic acidosis due to prolonged hypoperfusion of organs and tissues.

Clinical manifestations

Arterial hypotension systolic blood pressure less than 90 mm Hg. or by 30 mm Hg. below normal levels for 30 minutes or more. Cardiac index is less than 1.8-2 l/min/m2.

Impaired peripheral perfusion of the kidneys oliguria, skin pallor, increased humidity

CNS workload, stupor.

Pulmonary edema as a manifestation of left ventricular failure.

When examining the patient, cold extremities, impaired consciousness, arterial hypotension (average blood pressure below 50-60 mm Hg), tachycardia, muffled heart sounds, oliguria (less than 20 ml/min) are detected. Auscultation of the lungs may reveal moist rales.

Differential diagnosis

Other causes must be excluded arterial hypotension: hypovolemia, vasovagal reactions, electrolyte disturbances (eg, hyponatremia), side effects medications, arrhythmias (for example, paroxysmal supraventricular and ventricular tachycardias).

The main goal of therapy is to increase blood pressure.

Drug therapy

Blood pressure should be increased to 90 mm Hg. and higher. Use the following medicines, which are preferably administered through dispensers:

Dobutamine (selective b 1-adrenergic agonist with positive inotropic effect and minimal positive chronotropic effect, that is, the effect of increasing heart rate is slightly expressed) at a dose of 2.5-10 mcg/kg/min

Dopamine (has a more pronounced positive chronotropic effect, that is, it can increase heart rate and, accordingly, myocardial oxygen demand, thereby somewhat aggravating myocardial ischemia) at a dose of 2-10 mcg/kg/min with a gradual increase in dose every 2-5 minutes to 20- 50 mcg/kg/min

Norepinephrine at a dose of 2-4 mcg/min (up to 15 mcg/min), although it, along with increased myocardial contractility, significantly increases peripheral vascular resistance, which can also aggravate myocardial ischemia.

Cor pulmonale is a condition that develops as a result of pathological processes, occurring in the blood vessels of the lungs and bronchopulmonary system of humans. At the same time, an enlargement () of the right parts of the heart develops.

Pathogenesis

As a result of the study of pathogenesis, a conclusion was made about the significance in the development of the disease. Cor pulmonale develops by two mechanisms:

• Anatomical;
• Functional.

This division is important for prognosis: functional mechanisms can be adjusted.

Anatomical mechanism

This mechanism involves reduction (decrease) of the vascular network of the pulmonary artery. This phenomenon occurs as a result of damage to the walls of the alveoli until they completely die, obliteration and thrombosis of small vessels. The first symptoms begin to appear if about 5% of the small vessels of the lungs fall out of the blood circulation. An enlargement of the right ventricle occurs starting from a 15% reduction, and when the vascular bed is reduced by a third, decompensation of the cor pulmonale occurs.

All of these factors lead to a pathological increase in the size of the right ventricle. As a result, circulatory failure develops. The contractile function of the right ventricle is inhibited already at the earliest stages of development, and the amount of ejected blood decreases accordingly. And after the formation of hypertension, a pathological condition of the ventricle develops.

Functional mechanisms

1. There is an increase in minute blood volume. The more blood passes through the narrowed arterioles of the lungs, the higher the pressure observed in them. However, at the beginning of the development of the disease, the body launches this mechanism to compensate for the existing one (lack of oxygen in the blood).
2. The Euler-Lillestrand reflex develops. This is a mechanism for regulating blood flow. The walls of the small vessels of the lungs react to the lack of oxygen in the blood and narrow. When a normal amount of oxygen enters, the reverse process occurs: blood flow in the capillaries is restored.
3. Vasodilating (vasodilating) factors are insufficiently active. These include prostacyclin and nitric oxide. In addition to vasodilating properties, they have the ability to reduce thrombus formation in blood vessels. If these substances are not enough, then antagonists - vasoconstrictor factors - become more active.
4. Increase in intrathoracic pressure. This leads to a pressing effect on the capillaries, causing pressure to increase in the pulmonary artery. Coughing, which is present in COPD (chronic obstructive pulmonary disease), also contributes to an increase in intrathoracic pressure.
5. The action of vasoconstrictors. If there is an insufficient amount of oxygen in the tissues (hypoxia), the body switches to increased synthesis of substances that cause vasospasm. These substances include histamine, serotonin, and lactic acid. Also, the endothelium of the pulmonary vessels produces endothelin, and platelets produce thromboxane. Under the influence of these substances, vasoconstriction occurs and, as a result, pulmonary hypertension.
6. Increased blood viscosity. helps to increase pressure in the pulmonary vessels. The cause of this phenomenon is the same hypoxia. Microaggregates appear in the blood, which lead to a slowdown in blood flow. This is also facilitated by an increase in thromboxane synthesis.
7. Exacerbation of bronchopulmonary infections. The impact of this factor is two-way: firstly, during infections, ventilation of the lungs worsens, consequently, hypoxia develops and then pulmonary hypertension. Secondly, infections themselves have a depressing effect on the heart muscle, leading to.

Classification

Several classification options for cor pulmonale are generally accepted.

Depending on the speed of symptoms, cor pulmonale is:

• Spicy. The disease develops instantly, literally in minutes.
• Subacute. The development of pathology lasts from several days to several weeks.
• Chronic. A person has been sick for years.

An acute form of pathology can be provoked, which, in turn, is caused by vascular diseases, disorders in the coagulation system, and other pathologies of cardio-vascular system. Recently, the incidence of this particular type of disease has been increasing.

Chronic pathology can develop over several years. Initially, the patient develops insufficiency, which is compensated by hypertrophy, and then, over time, decompensation occurs, characterized by dilatation (expansion) of the right heart and secondary circulatory disorders in the organs. Development chronic illness contribute to frequent bronchitis and pneumonia.

Depending on the etiology there are the following types diseases:

1. Vascular. This type of pulmonary heart occurs as a result of disorders in the blood vessels of the lungs. This is observed with thrombosis, pulmonary hypertension and other vascular pathologies.
2. Bronchopulmonary. Appears in patients suffering from diseases of the bronchopulmonary system. This type of cor pulmonale occurs in tuberculosis, chronic bronchitis, bronchial asthma.
3. Thoradiaphragmatic. The appearance of this type of pathology is facilitated by diseases that affect ventilation of the lungs: pleural fibrosis, kyphoscoliosis, ankylosing spondylitis, Pickwick's syndrome and others. As a result of these ailments, the mobility of the chest is impaired.

Depending on the compensation, the disease is:

• Compensated;
• Decompensated.

Symptoms

Acute pathology manifests itself:

1. Sharp pain in the chest.
2. Severe shortness of breath.
3. Significant reduction in blood pressure.
4. Liver pain, vomiting or nausea.
5. Increased heart rate (about one hundred beats per minute).
6. Swollen neck veins.
7. Common.

Subacute cor pulmonale has the same symptoms as acute cor pulmonale. However, they do not appear as suddenly as in the first case.

With chronic pulmonary heart disease the following are noted:

• Cardiopalmus.
• Increasing shortness of breath. It is initially noticed with increasing load, and then at rest.
• Increased fatigue.
• Possible significant heart pain that does not go away after taking nitroglycerin. This distinguishes cor pulmonale from.
• Widespread cyanosis. It is complemented by blue discoloration of the nasolabial triangle, ears and lips.
• The legs may also swell, the veins of the neck may swell, and fluid may accumulate in the peritoneum (this condition is called ascites).

Diagnostics

Treatment

Different types of diseases require their own specific treatment methods. Cor pulmonale, which develops at lightning speed, is a consequence of massive PE, in which more than half of the vascular bed of the lungs is affected, or submassive, when the lesion covers 25-50% of it. This condition can become a significant threat to human life, so urgent resuscitation is carried out.

Important! should be carried out no later than 6 hours from the onset of the attack. Later measures may not be effective.

Contraindications for thrombolytic therapy should be taken into account: recent, wound, gastric ulcer in the acute stage, etc.

Treating cor pulmonale, despite all scientific advances, is quite difficult. The main goal of medicine so far is to reduce the rate of disease development and improve the quality of life. Since cor pulmonale is, in fact, a complication of the most various diseases, then the main therapeutic methods aimed at their cure. If the cause of the pathology is inflammatory bronchopulmonary diseases, then antibiotics are prescribed. For narrowing of the bronchi, bronchodilators are recommended, and for thromboembolism, anticoagulants. To reduce the edema syndrome caused by, diuretics are prescribed.

Since cor pulmonale is a consequence of various lung diseases, the underlying disease must also be treated.

To reduce oxygen deficiency, oxygen inhalations are performed. Breast massage is prescribed and breathing exercises.

There is evidence of the use of transplantation in the treatment of decompensated cor pulmonale. Both lung and complex lung-heart transplants are performed. It is noted that after such an operation, 60% of people return to normal life.

Important! Treatment methods may be completely useless if the nicotine-dependent patient continues to smoke. It is also necessary to identify possible allergens and prevent their entry into the body.

Cor pulmonale cannot be treated on its own. Self-medication does not produce tangible results and wastes time. The prognosis for the success of therapeutic actions depends on at what stage of the disease they began.

Forecast

Already at the beginning of the development of the disease, the patient’s ability to work suffers, and over time, in the end, the disease turns the person into a disabled person. In this state, there is no way to talk about a normal quality of life. Life expectancy for patients with advanced disease is short.

Prevention

In order to never hear such a diagnosis as “pulmonary heart”, it is necessary to observe all your life simple rules prevention:

• Rejection of bad habits.
• Timely treatment of bronchopulmonary diseases.
• Moderate physical activity.

By following these tips, you can prevent diseases not only of the lungs and heart, but also of the entire body.

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 failure of the left heart, for example, acquired or congenital heart defects.

Hypertrophy of the right ventricle with subsequent depletion of its energy capabilities is mainly caused by pulmonary hypertension (LG) and the associated increase in vascular resistance.

Without pulmonary hypertension there is no chronic pulmonary heart disease (HLS).

In this regard, the European Society for Clinical Respiratory Physiology included the presence of PH in the very definition of CHL.

In addition, in chronic pulmonary heart disease, the left ventricle is involved in the process quite early with the development of its dysfunction. This is due to hypoxemia, infectious-toxic influences and mechanical factors (compression of the left ventricle by the dilated right ventricle, paradoxical movement of the interventricular septum and its protrusion into the cavity of the left ventricle, which complicates its filling). Therefore, there is a tendency to include dysfunction of both ventricles in the definition of CHL.

In our country, the classification of cor pulmonale, proposed back in 1964 by the famous therapist and clinical pharmacologist Academician B.E., is widely used. Votchalom (table).

In a doctor's practice, chronic cor pulmonale is the most common condition. The causes of CHL 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 cor pulmonale are lesions of the thoracodiaphragmatic apparatus: chest deformities (kyphosis, scoliosis), obesity (Pickwick syndrome), extensive pleural cords, myasthenia gravis.

Diseases with primary damage to the pulmonary vessels are somewhat less important: primary pulmonary hypertension (Aerz disease), polyarteritis nodosa and other systemic vasculitis, repeated thromboembolism in small branches of the pulmonary artery.

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

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

Etiology of cor pulmonale:

A) acute(develops in a matter of minutes, hours or days): massive pulmonary embolism, valvular pneumothorax, severe asthma attack, widespread pneumonia

B) subacute(develops over weeks, months): repeated small pulmonary embolism, periarteritis nodosa, pulmonary 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, emphysema, bronchial asthma, pneumoconiosis, bronchiectasis, polycystic pulmonary 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, Pickwickian syndrome in obesity, etc.

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

Pathogenesis of chronic pulmonary heart disease (CPC).

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

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

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

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

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

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

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

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

Classification of cor pulmonale (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 CLS.

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

2. Complex of symptoms caused by respiratory failure and significantly aggravated during the formation of chronic pulmonary heart disease:

– shortness of breath: increases with physical activity, 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 heart area (due to hypoxia and reflex narrowing coronary arteries– pulmonary coronary reflex), decreasing after oxygen inhalation

3. Clinical signs of right ventricular hypertrophy:

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

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

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

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

– systolic murmur in the area of ​​the xiphoid process, increasing with inspiration (Rivero-Corvallo symptom) – a sign of relative tricuspid valve insufficiency, developing with enlargement of the right ventricle

4. Clinical signs of pulmonary hypertension:

– increase in the area of ​​vascular dullness in the 2nd intercostal space due to expansion of the pulmonary artery

– accent of the 2nd tone and its splitting in the 2nd intercostal space on the left

– appearance of a venous network in the sternum area

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

5. Clinical signs of decompensated cor pulmonale:

– orthopnea

– cold acrocyanosis

– swelling of the neck veins that does not decrease with inspiration

– enlarged liver

– Plesch’s symptom (pressure on an enlarged, painful liver causes swelling of the neck veins);

– in severe heart failure, edema, ascites, and hydrothorax may develop.

Diagnosis of CHL.

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

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

3. X-ray of the chest organs - enlargement of the right ventricle and atrium; bulging of the conus and trunk of the pulmonary artery; significant expansion of the hilar vessels with a depleted peripheral vascular pattern; “chopped off” roots of the lungs, etc.

4. Study of the function of external respiration (to identify disorders of the restrictive or obstructive type).

5. Laboratory data: the CBC is characterized by erythrocytosis, high hemoglobin content, slow ESR, and a tendency to hypercoagulation.

Principles of treatment of CHL.

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

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

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

B) improvement bronchial obstruction– xanthines: aminophylline (2.4% solution 5-10 ml IV 2-3 times a day), theophylline (0.3 g tablet 2 times a day) in repeated courses for 7-10 days, b2 – adrenergic agonists: salbutamol (in tablets 8 mg 2 times a day)

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

D) improvement of microcirculation - courses of heparin 5000 units 2-3 times a day subcutaneously until the APTT increases by 1.5-1.7 times compared to the control, low molecular weight heparins(fraxiparine), with severe erythrocytosis - bloodletting followed by infusion of solutions with low viscosity (rheopolyglucin).

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

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

5. If ineffective conservative treatment Lung or lung-heart complex transplantation is indicated.

ITU: the approximate duration of VN for decompensation of the pulmonary heart is 30-60 days.

Causes of cor pulmonale

Acute cor pulmonale develops in a matter of minutes, hours or days as a result of massive pulmonary embolism, valvular pneumothorax, severe attack of bronchial asthma, widespread pneumonia.

Subacute cor pulmonale occurs over weeks, months and is observed with repeated minor pulmonary embolisms, periarteritis nodosa, pulmonary carcinomatosis, repeated attacks of severe bronchial asthma, botulism, myasthenia gravis, and poliomyelitis.

Chronic cor pulmonale develops over several years. There are three groups of diseases that cause chronic cor pulmonale.

1. Diseases affecting the airways and alveoli: chronic obstructive bronchitis, emphysema, bronchial asthma, pneumoconiosis, bronchiectasis, polycystic pulmonary 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, Pickwickian syndrome in obesity, etc.
3. Diseases affecting the pulmonary vessels: primary pulmonary hypertension, repeated thromboembolism in the pulmonary artery system, vasculitis (allergic, obliterating, nodular, lupus, etc.), atherosclerosis of the pulmonary artery, compression of the pulmonary artery trunk and pulmonary veins by mediastinal tumors, aortic aneurysm, etc.

There are compensated and decompensated subacute and chronic pulmonary heart disease.

There are also bronchopulmonary (70-80% of cases), vascular and thoradiaphragmatic forms of cor pulmonale.

The bronchopulmonary form develops with chronic obstructive bronchitis, accompanied by the development of pulmonary emphysema and pneumosclerosis, with bronchial asthma, pulmonary tuberculosis and other lung diseases, both congenital and acquired.

The vascular form occurs with lesions of the vessels of the pulmonary circulation, vasculitis, and pulmonary embolism.

The thoracodiaphragmatic form develops with initial lesions of the spine and chest with its deformation, as well as with Pickwick's syndrome.

Pathogenesis of cor pulmonale

Pathogenetic mechanisms are divided into functional and anatomical. This division is important because functional mechanisms can be corrected.

Functional mechanisms

Development of the Savitsky-Euler-Lillestrand reflex

In patients with COPD, bronchial obstruction syndrome leads to vasoconstriction of small branches of the pulmonary artery, precapillaries (Savitsky-Euler-Lilleslrand reflex). This reflex develops in response to alveolar hypoxia during hypoventilation of central, bronchopulmonary or thoracodiaphragmatic origin. The importance of bronchial obstruction is especially great.

Normally healthy people no more than 1 alveoli are ventilated, the rest are in a state of physiological atelectasis, which is accompanied by a reflex contraction of arterioles and cessation of blood perfusion in these zones, as a result of which the penetration of oxygen-unsaturated blood into the big circle blood circulation In the presence of chronic bronchial obstruction, alveolar hypoventilation, the reflex becomes pathological, spasm of most arterioles and precapillaries leads to increased resistance to blood movement in the pulmonary circulation and increased pressure in the pulmonary artery.

Increase in minute blood volume

A decrease in oxygen tension in the blood causes irritation of the chemoreceptors of the aortic-carotid zone, resulting in an increase in minute blood volume. The passage of increased blood volume through the narrowed pulmonary arterioles leads to a further increase in pulmonary hypertension. However, at the initial stage of the formation of the pulmonary heart, the increase in IOC is compensatory in nature, as it helps to reduce hypoxemia.

The influence of biologically active vasoconstrictors

During hypoxia in tissues, including the lung, a number of biologically active substances (histamine, serotonin, lactic acid, etc.) are released, which cause spasm of the pulmonary arterioles and contribute to an increase in pressure in the pulmonary artery. Metabolic acidosis also contributes to vascular spasm. It is also expected that the endothelium of the pulmonary vessels will increase the production of endothelin, which has a sharp vasoconstrictor effect, as well as thromboxane (produced by platelets, increases platelet aggregation and has a strong vasoconstrictor effect). It is also possible to increase the activity of angiotensin-converting enzyme in the endothelium of the pulmonary vessels, resulting in increased formation of angiotensin II, which leads to spasm of the branches of the pulmonary artery and pulmonary hypertension.

Insufficient activity of vasodilating factors

Insufficient levels of endothelial relaxing factor (nitrogen oxide) and prostacyclin are assumed. Both of these factors are produced by the endothelium, dilate blood vessels and reduce platelet aggregation. With a deficiency of these factors, the activity of vasoconstrictor substances increases.

Increased intrathoracic pressure, bronchial pressure

With obstructive pulmonary diseases, intrathoracic pressure increases significantly, which leads to compression of the capillaries of the alveoli and contributes to an increase in pressure in the pulmonary artery. Intense cough, so characteristic of chronic obstructive pulmonary diseases, also contributes to increased intrathoracic pressure and pulmonary hypertension.

Development of bronchial-pulmonary anastomoses and dilation of bronchial vessels

With pulmonary hypertension, dilation of bronchial vessels and the development of bronchial-pulmonary anastomoses, opening of arteriovenous shunts are observed, which leads to a further increase in pressure in the pulmonary artery system.

Increased blood viscosity

In the development of pulmonary hypertension, an increase in platelet aggregation and the formation of microaggregates in the microcirculation system are important, which contributes to an increase in pressure in the small branches of a.pulmonalis. An increase in blood viscosity and a tendency to hypercoagulation are caused by erythrocytosis (due to hypoxia) and increased production of thromboxane by platelets.

Frequent exacerbations of bronchopulmonary infections

These exacerbations cause, on the one hand, a deterioration in pulmonary ventilation and worsening hypoxemia, and, consequently, a further increase in pulmonary hypertension, on the other hand, intoxication, which has an adverse effect on the condition of the myocardium and contributes to the development of myocardial dystrophy.

Anatomical mechanism of development of pulmonary hypertension

The anatomical mechanism for the development of pulmonary hypertension is a reduction of the vascular bed of the pulmonary artery.

Anatomical reduction of the vascular bed of the pulmonary artery occurs as a result of atrophy of the alveolar walls, their rupture with thrombosis and obliteration of part of the arterioles and capillaries. Reduction of the vascular bed contributes to pulmonary hypertension. Appearance clinical signs chronic pulmonary heart disease occurs when the total area of ​​the pulmonary capillaries is reduced by 5-10%; its reduction by 15-20% leads to pronounced hypertrophy of the right ventricle; a decrease in the surface of the pulmonary capillaries, as well as the alveoli, by more than 30% leads to decompensation of the pulmonary heart.

Under the influence of the above pathogenetic factors, hypertrophy and dilatation of the right parts of the heart occur with the development of progressive circulatory failure. It has been established that a decrease in the contractile function of the right ventricular myocardium occurs in obstructive forms of COPD already at the early, transient stage of pulmonary hypertension and is manifested by a decrease in the ejection fraction of the right ventricle. Subsequently, as pulmonary hypertension stabilizes, the right ventricle hypertrophies and dilates.

Pathomorphology of the pulmonary heart

The main pathomorphological signs of chronic pulmonary heart disease are:

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