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Pulmonary heart

Pulmonary heart (cor pulmonale; synonym: emphysematous heart, kyphoscoliotic heart) is a dilation, or hypertrophy, of the right heart as a result of hypertension of the pulmonary circulation, developed due to lung disease, chest deformities or pulmonary vascular disease and not dependent on congenital malformation or disease hearts. The diagnosis of pulmonary heart is made only after the diagnosis of the underlying disease that caused the hypertension of the pulmonary circulation.

According to the classification of the pulmonary heart adopted in the USSR in 1964 (proposed by B. E. Votchalom), the following are distinguished: acute pulmonary heart (development is calculated in hours or days), subacute pulmonary heart (development over weeks and months) and chronic pulmonary heart (development continues over the years).

Acute pulmonary heart is always decompensated and corresponds to acute pulmonary heart disease. It occurs in connection with vascular or bronchopulmonary disorders. The first are thromboembolism (thrombus, embolism - fat, gas, tumor) of the pulmonary artery and narrowing of its bed (valve pneumothorax, pneumomediastinum); to the second, common pneumonia, which occurs with significant cyanosis, and a severe attack of bronchial asthma (Scheme 1).

In the development of subacute and chronic pulmonary heart, two stages, or forms, are distinguished: compensated, when there is only right ventricular hypertrophy without symptoms of circulatory failure, and decompensated, when right-ventricular type circulatory failure is added (see Pulmonary heart failure).

Subacute and chronic pulmonary heart disease can occur due to vascular, bronchopulmonary and thoraco-diaphragmatic disorders.


In subacute pulmonary heart, vascular causes include repeated thromboembolism (blood clots, parasite eggs, erythrocyte fragments in sickle cell anemia), bronchopulmonary - repeated severe attacks of bronchial asthma and cancerous lymphangitis of the lungs; polio, myasthenia gravis; scheme 2).

In chronic pulmonary heart disease, primary pulmonary hypertension, arteritis, recurrent emboli and vasoconstriction during pulmonary resection are referred to as vascular pathology; to bronchopulmonary - obstructive processes in the bronchi (bronchial asthma, chronic bronchitis, diffuse pneumosclerosis with pulmonary emphysema of various etiologies), restrictive processes in the lung parenchyma (fibrosis and pulmonary granulomatosis) and lung polycystic disease; to thoraco-diaphragmatic - damage to the spine and chest with its deformation, pleural moorings and obesity (Picquick syndrome; scheme 3).

Pathogenesis and pathological anatomy . The main cause of hypertension in the small circle of blood circulation, contributing to the development of pulmonary heart, is an increase in the peripheral resistance of the vascular bed (hypertension appears when it is narrowed by two thirds). An increase in the minute and stroke volume of blood plays a minor role in increasing the pressure in the pulmonary artery, since the resistance in the small circle is 1/16 of the resistance in the large circle, and the pulmonary vessels have a large extensibility. With a simultaneous increase in the minute volume of blood, the degree of narrowing of the vascular bed may be less than two thirds. In addition to the anatomical (closing part of the arteries and capillaries), the functional factor also plays a significant role in the narrowing of the vascular bed: generalized spasm of the arteries and veins of the small circle (pulmo-pulmonary reflex) and reduction of the elongation of the vessel walls due to damage to their walls, as well as from extravascular causes (fibrosis). In addition, arterial hypoxemia and hypercapnia play a large role in increasing pressure in the pulmonary circulation due to reflex-induced spasm of pulmonary arterioles, a compensatory increase in minute blood volume and an increase in deposited blood in the lungs. The cause of arterial hypoxemia and hypercapnia is the so-called alveolar-capillary block, i.e. a violation of diffusion, a change in the relationship between alveolar ventilation and capillary blood flow, and uneven ventilation.


The development of small circle hypertension leads only to that arterial hypoxemia, which is a consequence of a decrease in oxygen tension in the alveolar air during hypoventilation or a decrease in the number of lung capillaries. There is no direct relationship between the degree of arterial hypoxemia and the level of hypertension in the small circle. A known role in increasing the pressure in the pulmonary circulation belongs to the resulting compensatory polycythemia, which increases blood viscosity.

Arising from chronic pulmonary diseases, pulmonary insufficiency is first compensated by the respiratory system, then by the circulatory system. Appears hypertrophy, resp. hyperfunction, “sufficient heart”, compensating for pulmonary insufficiency.

The duration of the stage of compensated pulmonary heart depends on the lifestyle, mainly on the degree of physical activity of the patient, since an increase in blood pressure in a small circle with small degrees of narrowing of the vascular bed appears first only during exercise due to an increase in minute volume of blood. With its equal increase, the work of the right ventricle proceeds in worse conditions compared to the left, since in the small circle the increase in resistance is greater and the supply of the right ventricle with blood is hampered by the deterioration of the possibility of emptying the small veins of the heart (tebesian veins) flowing into the right ventricle.

At the beginning of the development of the pulmonary heart, right ventricular hypertrophy begins with a profound reorganization of the architectonics of the muscular system and hypertrophy of the trabecular muscles and only after that - the outflow pathways. Usually, the left ventricle changes simultaneously. This stage of the pulmonary heart can last for decades.

In the second stage of pulmonary heart development, dystrophic changes occur in the hypertrophied muscle of the right ventricle and circulatory insufficiency appears against the background of existing pulmonary insufficiency.

Clinical picture - see. Pulmonary heart disease.

The diagnosis . The early phases of cardiac changes are not detected by physical methods, but in most cases can be diagnosed radiographically, as well as by electro- and vectorcardiography. At radiological research note protrusion of a pulmonary cone and a pulmonary artery; low standing of the diaphragm and wide lung fields, giving the impression of normal and even reduced heart size; increased pulmonary roots, but, unlike stagnant, they are not blurred and they clearly distinguish the branching of the pulmonary artery. X-ray diagnostics of right ventricular hypertrophy uses X-ray and electromyography and angiocardiography.

Electrocardiographic changes are due to hypertrophy and dilatation of the right ventricle and atrium, a change in the position of the heart (vertical, the tip is deflected posteriorly, the heart is rotated around the longitudinal pox clockwise) and a change in electrical conductivity due to increased air filling in the lungs. In standard leads, deep teeth 5 and low voltage of the QRS complex are defined, in 80% - blockade of the right bundle of His (type Wilson), often combinations S 1 - Q 3 , negative T 2 and T 3 , reduction of the S segment - T in III lead , in V 1 , and V 2 - high P; in the extreme right leads, QRS has the form qR, R, Rs, or qRs; in aVL reduced or negative P, QrS and positive G; in aVF, positive and pointed P, high R and negative T; in aVR - the same, for P - negative. Differential diagnosis of pulmonary heart with a front-partition infarction is aided by the absence of dynamics typical of infarction. The early diagnosis of right ventricular hypertrophy is helped by vectorcardiography (see), because on the vectorcardiogram there are signs of right ventricular hypertrophy (an increase in the end part of the QRS loop in leads BA1,2, I) in many cases appear earlier than on an ECG.

Treatment of compensated pulmonary heart is reduced to the fight against the underlying pulmonary disease in order to prevent the development of hypertension in the pulmonary circulation and the transition to a decompensated pulmonary heart. It is important to limit physical activity, since in the pulmonary heart, physical effort dramatically increases the load on the right heart. Such patients usually spare themselves [effort-saving syndrome (V.L. Ennis)], and the physician should encourage it.