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Ventricular Septal Defect (VSD)
In ventricular septal defect there is abnormal communication between right and left ventricle. Anatomically 90 per cent of all VSD are located in the membranous part of the ventricular septum with a variable extension into adjoining muscular part of the ventricular septum. Ventricular septal defect is the most common congenital cardiac lesion.
Pathophysiology and Hemodynamics
In ventricular septal defect there is shunting of oxygenated blood from the left to the right ventricle as the pressure in the left ventricle is higher than in the right ventricle. This results in passage of oxygenated blood in greater amounts from left to the right ventricle, leading to pulmonary hypertension. In extreme cases there may be only one ventricle. The muscles, hypertrophy, because of increased pressure in the right ventricle due to left to right shunt and pulmonary resistance. The muscles of right atrium also enlarge due to increased pressure. If pulmonary vascular resistance increases, the left to right shunt gets reduced, resulting in right to left shunt. Unoxygenated blood then crosses to the left ventricle and enters the systemic circulation. This phenomenon is known as Eisenmenger syndrome, a combination of pulmonary hypertension with reversed shunting.
Isonzerization of glucose-6-phosphate Isonzerization of glucose-6-phosphate : This step is catalyzed by phosphoglucoisomerase to form fructose-6-phosphate.
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