Perimembranous Research Paper

Perimembranous Ventricular Defect A defect in the ventricular septum, the wall dividing the left and right ventricles of the heart. The extent of the opening may vary from pin size to complete absence of the ventricular septum creating one common ventricle. Perimembranous VSDs are located in the left ventricle outflow tract beneath the aortic valve. They are the most common VSD subtype in the United States, occurring 75-80% of cases. Defects may extent into adjacent portions of the ventricular septum. When tissues forms on the right ventricular septal surface (often thought to be tricuspid valvular in origin), it is termed an aneurysm of the membranous septum. Such tissue serves as a mechanism of restriction or spontaneous closure. The defect
It usually manifests a few weeks after birth. VSD is an acyanotic congenital heart defect, a.k.a left-to-right shunt, so there are no signs of cyanosis in the early age. However, uncorrected VSD can increase pulmonary resistance leading to the reversal of the shunt and corresponding cyanosis.
 Pansystolic (Holosystolic) murmur along lower left sternal border (depending upon he size of the defect) +/- palpable thrill (palpable turbulence of blood flow). Heart sounds are normal. Larger VSDs may cause parasternal heave, a displaced apex beat (the palpable heartbeat moves laterally overtime, as the heart enlarges). An infant with a large VSD will fail to thrive and become sweaty and tachypnoeic (breath faster) with feeds.
 The restriction VSDs (smaller defects) are associated with a louder murmur and more palpable thrill (grade IV murmur). Larger defects may eventually be associated with pulmonary hypertension due to the increased blood flow. Over time this may lead to an Eisenmenger’s Syndrome the original VSD operating with a left-to-right shunt, now become right-to-left shunt because of the increased pressures in the pulmonary vascular bed.