Pulmonary heart

Pulmonary heart (cor pulmonale; synonym: emphysematous heart, gipokaliemicski heart) - dilation, or hypertrophy of the right heart in the hypertension in the pulmonary circulation caused by diseases of the lungs, chest deformations or destruction of pulmonary vessels and not dependent on birth defect or disease of the heart. Diagnosis of pulmonary heart is put only after diagnosis of the main disease-causing hypertension in the pulmonary circulation.
According to the adopted in the USSR in 1964 classification pulmonary heart (B. proposed that Votchal) are: acute pulmonary heart (the development is estimated hours or days), subacute HP (development in the weeks and months) and chronic HP (development lasts for years).
Acute HP always decompensirovanna and complies with acute pulmonary-cardiac insufficiency. It arises from vascular or bronchopulmonary disorders. The former include embolism (a blood clot, embolism fat, gas, tumor) of the pulmonary artery and the narrowing of its bed (valve pneumothorax, pneumomediastinum); the second common pneumonia, occurring with significant cyanosis, severe bronchial asthma (scheme 1).
In the development of subacute and chronic pulmonary heart distinguish two stages, or form,is offset when there is only right ventricular hypertrophy and without symptoms of circulatory failure, decompensated, when attached circulatory failure on right ventricular type (see Pulmonary heart disease).
Subacute and chronic HP may arise due to vascular, pulmonary, thoraco-diaphragmatic disorders.
In subacute pulmonary heart to vascular reasons include re thromboembolism (blood clots, eggs of parasites, fragments of erythrocytes in sickle cell anemia), bronchopulmonary - re severe attacks of asthma and cancer lymphangitis the lungs, to the thoraco-diaphragmatic - chronic holding of the Central or peripheral origin (botulism, polio, male; figure 2).
When chronic pulmonary heart to vascular pathology include primary pulmonary hypertension, arteritis, re embolism and narrowing of the vascular bed with lung resection; to broncho - obstructive processes bronchitis (bronchial asthma, chronic bronchitis, diffuse pneumosclerosis with emphysema different etiology), restrictive processes in the lung parenchyma (fibrosis and granulematosny lungs) and polycystic light; to the thoraco-diaphragmatic - defeat of the spine and chest with its deformation, pleural swarthy and obesity (Pickwickian syndrome; figure 3).
Pathogenesis and pathological anatomy. The main cause of hypertension in the pulmonary circulation, contributing to the development of lung heart, is the increase in peripheral resistance of the vascular bed (hypertension appears when narrowing it to two-thirds). The increase in minutes and stroke volume plays a secondary role in increasing the pressure in the pulmonary artery, as the resistance in a small circle is 1/16 resistance in a big circle, and the vessels of the lungs have a great stretch. While increasing cardiac output is the degree of narrowing of the vascular bed can be less than two-thirds. A significant role in reducing vascular bed, in addition to the anatomical (closing part of the arteries and capillaries), plays and functional factor: generalized spasm of the arteries and veins of the small circle (pulmo-pulmonary reflex) and decrease the elasticity of the walls of vessels due to destruction of their walls, and also from extravascular reasons (fibrosis). In addition, a great role in the increase of pressure in the pulmonary circulation play arterial hypoxemia and hypercapnia due to the called reflex spasm of arterioles of the lungs, a compensatory increase in cardiac output and increase the deposited blood in the lungs. The reason of occurrence arterial hypoxemia and hypercapnia is the so-called alveolar-capillary unit, i.e. violation of diffusion, changing relations between the alveolar ventilation and capillary blood flow and irregularity ventilation.
To the development of hypertension small circle leads only the arterial hypoxemia, which is the result of low oxygen tension in the alveolar air with hypoventilation or decrease in the number of capillaries in the lungs. Direct dependence between the degree of arterial hypoxemia and the level of hypertension pulmonary not. Known role in increasing the pressure in the pulmonary circulation belongs arising compensatory polycythemia, increasing blood viscosity.
Resulting in chronic lung diseases, pulmonary insufficiency first offset by the respiratory system, then the circulatory system. Appears hypertrophy, resp. hyperfunction, "enough of the heart", compensating pulmonary insufficiency.
Duration of the stage compensated HP depends on lifestyle, largely on the degree of physical activity of the patient, as increased blood pressure in a small circle with a small degree of narrowing of the vascular channel appears at first only during physical activity due to the increase in cardiac output. When it is equal to the increase in work right ventricle flows in worse conditions than the left, because in a small circle increase resistance more and provision of the right ventricle, blood is difficult due to the worsening of the possibility of emptying the small veins of the heart (tebesjuak veins flowing into the right ventricle.
At the beginning of the development of pulmonary cardiac hypertrophy of the right ventricle begins with a deep restructuring of the architectonics muscular apparatus and hypertrophy of trabecular muscles and only after that - ways outflow. Usually time changes and the left ventricle. This stage HP can last for decades.
In the second stage of development of pulmonary heart happen dystrophic changes hypertrophied muscles of the right ventricle and appears circulatory insufficiency on the background of the existing respiratory failure.
The clinical picture - see Pulmonary heart disease.
The diagnosis. The early phase changes hearts physical methods cannot be detected, but in most cases can be diagnosed radiographically, as well as by the method of electro - vectorcardiography. The radiological examination mark bulging pulmonary cone and pulmonary artery; low position of diaphragm and a wide lung fields, giving the impression of normal and even reduced the size of heart; increased pulmonary roots, but, unlike stagnant, they are not blurred and they clearly distinguish the ramifications of the pulmonary artery. In x-rays hypertrophy of the right ventricle use x - ray and electrotomography and angiocardiography.
Electrocardiographic changes caused by hypertrophy and dilation of the right ventricle and auricle, you change the position of the heart (vertical, upper rejected backwards, heart turned around longitudinal GSP clockwise) and electric conductivity due to the increase in vozduhonosnye lungs. In standard leads determined deep teeth 5 and low voltage of QRS complex, 80% - block of right bundle branch (type Wilson), often combining S1 - Q3, negative T2 and T3, the decrease in segment S - T III lead, V1and V2- high P; in extreme right-lead 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 Tons; in aVR - same, according to R - negative. Differential diagnosis of pulmonary heart with peredneperegorodorn heart helps the absence of typical heart attack dynamics. Early diagnosis of hypertrophy of the right ventricle helps vectorcardiography (see), as vectorcardiographic signs of hypertrophy of the right ventricle (increase of the final part of the loop QRS in leads BA1,2,I) in many cases appear earlier than on the ECG.
Treatment compensated HP is reduced to the struggle with the main pulmonary disease, to prevent the development of hypertension in the pulmonary circulation and the transition to decompensated HP is Important limitation of physical activity, as pulmonary heart physical effort dramatically increases the load on the right heart. Such patients usually themselves cheat [syndrome saving efforts (C. L. Ennis)], and the doctor must be encouraged.