Pulmonary Heart - Causes and Pathogenesis

Causes of pulmonary heart disease

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

Subacute pulmonary heart disease occurs over weeks or months and is observed with repeated small pulmonary embolisms, periarteritis nodosa, pulmonary carcinomatosis, repeated attacks of severe bronchial asthma, botulism, myasthenia, and poliomyelitis.

Chronic pulmonary heart disease develops over several years. There are three groups of diseases that cause chronic pulmonary heart disease.

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, Bechterew's disease, condition after thoracoplasty, pleural fibrosis, neuromuscular diseases (poliomyelitis), diaphragmatic 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.

A distinction is made between compensated and decompensated subacute and chronic pulmonary heart disease.

There are also bronchopulmonary (70-80% of cases), vascular and thoracodiaphragmatic forms of pulmonary heart disease.

The bronchopulmonary form develops in chronic obstructive bronchitis, accompanied by the development of pulmonary emphysema and pneumosclerosis, in 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 Pickwickian syndrome.

Chronic bronchopulmonary cor pulmonale is discussed next.

Pathogenesis of pulmonary heart disease

Pathogenetic mechanisms are divided into functional and anatomical. This division is important, since functional mechanisms are subject to correction.

Functional mechanisms

Development of the Savitsky-Euler-Liljestrand reflex

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

Normally, in healthy people, no more than y 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 areas, as a result of which the penetration of oxygen-depleted blood into the systemic circulation is prevented. In the presence of chronic bronchial obstruction, alveolar hypoventilation, the reflex becomes pathological, spasm of most arterioles, precapillaries leads to an increase in resistance to blood flow in the pulmonary circulation, an increase in pressure in the pulmonary artery.

Increase in minute blood volume

A decrease in the oxygen tension in the blood causes irritation of the chemoreceptors of the aortic-carotid zone, resulting in an increase in the minute blood volume. The passage of an increased volume of blood 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 the cardiac output is compensatory in nature, since it helps to reduce hypoxemia.

The influence of biologically active vasoconstrictors

During hypoxia in tissues, including pulmonary tissue, 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 assumed that the endothelium of the lung vessels produces 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 that the activity of angiotensin-converting enzyme in the endothelium of the pulmonary vessels increases, resulting in increased formation of angiotensin II, which leads to spasm of the branches of the pulmonary artery and pulmonary hypertension.

Insufficient activity of vasodilatory factors

It is assumed that there is an insufficient content of endothelial relaxing factor (nitric oxide) and prostacyclin. 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 vasoconstrictors increases.

Increased intrathoracic pressure, pressure in the bronchi

In obstructive pulmonary diseases, intrathoracic pressure increases significantly, which leads to compression of the alveolar capillaries and contributes to an increase in pressure in the pulmonary artery. An increase in intrathoracic pressure and pulmonary hypertension is also facilitated by intense coughing, so characteristic of chronic obstructive pulmonary diseases.

Development of bronchial-pulmonary anastomoses and expansion of bronchial vessels

In pulmonary hypertension, there is expansion of the bronchial vessels and development of bronchial-pulmonary anastomoses, opening of arteriovenous shunts, 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 the a.pulmonalis. An increase in blood viscosity and a tendency to hypercoagulation are caused by erythrocytosis (due to hypoxia), increased production of thromboxane by platelets.

Frequent exacerbations of bronchopulmonary infections

These exacerbations cause, on the one hand, a deterioration in pulmonary ventilation and a worsening of hypoxemia, and, consequently, a further increase in pulmonary hypertension, and 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 pulmonary hypertension development

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

Anatomical reduction of the pulmonary artery vascular bed 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. The appearance of clinical signs of chronic pulmonary heart disease occurs with a reduction in the total area of pulmonary capillaries 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 disease.

Under the influence of the above pathogenetic factors, hypertrophy and dilatation of the right heart chambers 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 dilation of the right chambers of the heart.

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