Elaborates the Pathophysiology of ventricular septal defect?

The shunt in the VSD is left to right. The magnitude of the shunt is determined by the size of the VSD and the, level of pulmonary vascular resistance. The lower the PVR, the greater the magnitude of L>R shunt. This type of shunt is called dependent shunt. In VSD the LV starts contracting before RV, and high-pressure gradient is maintained between two ventricles throughout systole. Hence the murmur is pansystolic. Towards the end of the systole, the declining LV pressure becomes lower than the aortic valve with occurrence of A2. However the LVSP > RVSP, and left to right shunt continues.

The pansystolic murmur therefore ends beyond A2 completely masking it. The increased volume of blood finally reaches the LA I LV resulting in volume overload if LA/ LV. Passing through a normal mitral valve, the large volume of blood results in MDM at the apex. This is a very useful clue indicating a large flow and operability of the lesion. Since the left ventricle has two outlets it empties relatively early, this results in early A2.Since ejection into RV and PA is increased, P2 is delayed. Therefore the S2 is widely split but varies with respiration. In a large VSD with increasing PVR, 52 splitting become less and less obvious. It is single once PVR is significantly elevated.