The tricuspid valve insufficiency

  • Pathologic anatomy
  • The pathogenesis of disorders of blood circulation
  • The clinical picture
  • Electrocardiographic study
  • Phonocardiographic data
  • Differential diagnosis
  • The tricuspid valve insufficiency - insufficientia valvulae tricuspidalis - develops, as a rule, when a severe, often continuously-recurrent course of rheumatism. Such patients tricuspid insufficiency or tricuspid stenosis joins already against the background formed mitral and aortic vices, which causes certain difficulties in the diagnosis of lesions tricuspid valve. So for the life of sick children these vices are often not diagnosed as pathological studies of the corpses of people who died of rheumatic carditis, vices tricuspid valve was observed in 10-30% (M. A. Skvortsov, 1950; B. the Jonash, 1960).
    The defeat of the tricuspid valve is usually caused by recurrent rheumatic heart disease (A. N. Volovik, 1955; 3. I. Edelman, 1962), but a number of patients in an unfavorable course of the first rheumatic fever, it can occur through 6-11 months from its beginning (I.e. Churakova, S. S. Zelenetsky, 1968). The defeat of the tricuspid valve clinically diagnosed, Etc., according to Churakova and S. S. Zelenetskii, in 0.6% of children with primary rheumatic heart disease and 6.9 percent return.
    Tricuspid insufficiency can be relative and organic, and the child is more likely to occur muscle or relative tricuspid insufficiency, associated with the valvular lesions of the left heart, the compensation which is due to the hard work of the right ventricle. Most often this occurs when the mitral insufficiency and mitral stenosis. Such patients during the development of decompensation, there are signs of tricuspid insufficiency, which take place at the improvement of the patient.
    With the progression of heart failure tricuspid insufficiency relative character becomes more pronounced, which is associated with the development of degenerative changes in the myocardium of the right ventricle, which increase the right atrioventricular holes (G. F. lang, 1958).