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Lutembacher's syndrome pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ayokunle Olubaniyi, M.B,B.S

Overview

Overview

Pathophysiology

Pathophysiology

The presence of both ASD and mitral stenosis occuring together, usually modify the clinical and hemodynamic manifestation of each other. The presence of an ASD creates a second exit (left-to-right shunt) for the blood in the left atrium; consequently reducing the hemodynamic effects of a severe mitral stenosis. In the same fashion, the pressure in the left atrium, pulmonary veins and the pulmonary capillaries decrease if the ASD is large. Therefore, the typical presentation of mitral stenosis as a result of increased hydrostatic pressure such as orthopnea, paroxysmal nocturnal dyspnea, hemoptysis and pulmonary edema are attenuated or diminished, and are often substituted by symptoms of low volume output such as weakness and fatigue.[1]

References

References


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