Ventricular septal defect classification

Template:Ventral septal defect Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Classification

Presentations in the adult or adolescent:

a) small defect without significant left-to-right shunting

b) large defect with severe pulmonary hypertension and cyanosis due to right-to-left shunt.

c) large defect with a large left-to-right shunt that has induced secondary infundibular stenosis (tough to differentiate from tetralogy of Fallot).

Small VSDs

A high resistance to flow across the VSD due to the large pressure difference between the two ventricles. There is a small left-to-right shunt (Qp/Qs < 1.5) and a normal ratio of PA to systemic pressures.

There is little or no increase in the pulmonary vascular resistance. A holosystolic murmur is present due to the pressure gradient across the defect. The majority of these defects close during the first three years of life.

Medium-Sized VSDs

There is a moderate shunt left-to-right present(Qp/Qs = 1.5-2.0) that still has some resistance to flow across the defect. There is also volume overload of the LA and the LV and LVH. There may therefore be a middiastolic mitral murmur and a third heart sound (S3). The ratio of the PA systolic pressure to the systemic pressure is <.5.

The area of the defect is usually less than 1 cm2/m2 of body surface area and is unusual for this group to have a marked increase in PVR. In some cases and depending on the type of VSD, as the child becomes older, the relative size of the defect will decrease.

Large VSDs

There is a large defect on the ventricular septum, > 1 cm2/m2 of BSA, with a large shunt left-to-right (Qp/Qs is > 2), causing volume overload of the LV, which may result in its failure. The defect may approximate the size of the aortic orifice.

The ratio of the PA pressure to the systemic pressure is >.5. Produce the same clinical findings as moderate sized VSD but also pulmonary hypertension.

There is rarely spontaneously closure of the defect, and these patients either die, or progress to adolescence or adulthood with severe pulmonary hypertension or with secondary protective infundibular pulmonary stenosis.

In the group with severe pulmonary hypertension, the left-to-right shunt decreases and the degree of right-to-left shunting increases with accompanying cyanosis (i.e. they develop Eisenmenger's syndrome).

Protective infundibular stenosis may also result in reversal of the shunt, and may be indistinguishable clinically from tetralogy of Fallot.