[Differential use of peripheral vasodilators in the treatment of chronic circulatory failure in patients with mitral valve insufficiency].
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Biomedical subjects
Publications and source records attributed to B I Vorob'ev.
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Comparative hemodynamic studies, making use of different techniques, have demonstrated that tetrapolar transthoracic rheoplethysmography is a very accurate instrument of determining effective stroke volume in cases of mitral regurgitation, and that the latter can be detected by echocardiography and rheoplethysmography. Intracardiac hemodynamic disorders can be assessed on the basis of echographic estimates of left-atrial mean dynamic pressure.
A comprehensive clinical sample (375 cases of myocardial infarction, with uncomplicated course in 115, pulmonary edema in 80, cardiac asthma in 37, pulmonary edema combined with cardiogenic shock in 55, and other complications in 88; 89 fatal cases altogether) was used to demonstrate that the shock lung associated with myocardial infarction was rooted in strained operation of various pulmonary functions other than gaseous exchange and inadequate inactivation of vasoactive substances (histamine, serotonin, kinins). The ultrastructural pattern of the shock lung is characterized by damaged aerohematic barrier edema, hypercoagulation, atelectases and the sludging of aggregated erythrocytes. Acute respiratory insufficiency is not always associated with cardiogenic shock and may develop spontaneously in myocardial infarction.
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A total of 347 patients with myocardial infarction were investigated. Of those, 115 had uncomplicated course of the disease, while pulmonary edema developed in 80, cardiac asthma in 37, pulmonary edema and cardiogenic shock in 35, and various other complications in 80; the outcome was lethal in 80 cases. The pathogenetic contribution of increased permeability to the development of myocardial infarction and its complications is demonstrated. Transendothelial pinocytosis is a trigger mechanism of pulmonary edema. Its pathomorphism is achieved in five steps, each corresponding to a certain degree of ultrastructural transformation of endothelial and alveolar cells. Pulmonary surfactant damage adds to the effect of tissue factors of increased aerohematic barrier permeability.
The investigations have shown the pathogenetic role of enhanced capillary permeability on the development of myocardial infarction and its complications. To a definite degree the above disorders are conditioned by the activation of the kallikrein-kinin system. This made us try contrykal with heparin in the comprehensive system of treatment of these patients. A clear-cut clinical and laboratory effect has been obtained which justifies recommending the use of protease inhibitors in complicated myocardial infarction.
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