Ventricular septal defect pathophysiology: Difference between revisions
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==[[Ventricular septal defect image 2-subvalvular ventricular septal defect|Image 2-subvalvular ventricular septal defect]]== | ==[[Ventricular septal defect image 2-subvalvular ventricular septal defect|Image 2-subvalvular ventricular septal defect]]== | ||
==[[Ventricular septal defect image 3- gross, infant heart, pulmonary outlet, muscular septal defect | image 3- gross, infant heart, pulmonary outlet, muscular septal defect]]== | ==[[Ventricular septal defect image 3- gross, infant heart, pulmonary outlet, muscular septal defect | image 3- gross, infant heart, pulmonary outlet, muscular septal defect]]== | ||
==[[Ventricular septal defect image 4-atrioventricular canal: gross, right ventricular view of canal defect | image 4-atrioventricular canal: gross, right ventricular view of canal defect]]== | |||
==[[Ventricular septal defect image 5-gross, left ventricle view of canal defect (very good example) | image 5-gross, left ventricle view of canal defect (very good example)]]== | |||
==[[Ventricular septal defect image 6-perimembranous ventricular septal defect: gross, an excellent example | image 6-perimembranous ventricular septal defect: gross, an excellent example]]== | |||
==[[Ventricular septal defect image 7-gross, subvalvular defect, left ventricle view of tetralogy of Fallot (very good example)| image 7-gross, subvalvular defect, left ventricle view of tetralogy of Fallot (very good example)]]== | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 15:51, 29 June 2011
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] and Leida Perez, M.D.
Associate Editor-in-Chief: Keri Shafer, M.D. [2]
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Pathophysiology
In this lesion, a persistent opening in the upper interventricular septum resulting from failure of fusion with the aortic septum allows blood to flow from the high pressure left ventricle into the low pressure chamber or right ventricle. The subsequent natural history and pathophysiology depend on the size of the defect and the magnitude of left-to-right shunting. Small defects (QP/QS less than 1.5) maybe asymptomatic, but with the high risk for bacterial endocarditis. Large defects are associated with left ventricular failure. Chronic but more moderate left-to-right shunts may lead to pulmonary vascular disease and right sided failure.
The primary variable is the size of the defect. As a child grows, the relative size of the defect may decrease and the defect may even close spontaneously in early childhood.
During the first few months of life the PVR decreases, and the magnitude of left-to-right shunt increases. After the first few months the degree of shunting is dependent on the size of the defect.
Presentations in the adult or adolescent:
a) small defect without significant left-to-right shunting
b) a large defect with severe pulmonary hypertension and cyanosis due to right-to-left shunt.
c) a 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.
Rarely spontaneously close, 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.