Ventricular septal defects a brief and easy understanding of embryogenesis, pathophysiology, clinical features, types, diagnosis and management of various types of Ventricular septal defects

1. VENTRICULAR SEPTAL
DEFECTS
Dr. Chintan

2.  Most common congenital malformation of the heart – 25-30%
(Excluding Bicuspid Aortic valve) ( Ref: Nadas pediatric
cardiology)

3. Embryogenesis
At Gestational age 44, Interventricular septum
is closed.

4. Genetics and Associations
 Chromosomal
1. Downs
2. Di-George
3. Turners
 Gene disorders
1. NKX2.5
2. TBX5
3. GATA4
With Paternal VSDs, the recurrence risk in an offspring is 2% and with Maternal
VSDs have a recurrence risk of 6% to 10%*
*Nora JJ, Nora AH. Update on counseling the family with a first-degree relative
with a congenital heart defect. Am J Med Genet. 1988; 29: 137–142.

5. Types
 Based on Location
1. Perimembraneous
2. Muscular
3. Doubly committed
and juxta-arterial

6. Perimembranous

7. Swiss cheese pattern

8. Doubly commited and juxta-arterial

9. Types
 Based on

10. Pathophysiology
The size of the VSD, the pressure in the right and left
ventricular chambers, and pulmonary resistance are
factors that influence the hemodynamic significance of
VSDs
Small VSD  restrictive defects shunting is
hemodynamically insignificant
Large VSD  shunting depends on pulmonary vascular
resistance  excessive shunting leads to increase in
pulmonary blood flow and CHF

12. Pathophysiology
 During Systole  Bypasses the RV cavity LR
shunting  Increase in PBF, LVH, LVEDV
 Adaptive mechanism  increase SV, contractility, HR,
myocardial mass
 Leads to : CHF(2* to volume overload) at 6-10 weeks
recurrent RTI
Pulmonary HTN
Eisenmenger Syndrome

14. Presentation
Small VSD :
 Most often asymptomatic .
 Loud , harsh , blowing , holo systolic murmur
heard best over LLSB frequently accompanied by
thrill .
** more chances of Infective Endocarditis

15. LARGE VSDs
 Dyspnea, feeding difficulties, poor growth, profuse
perspiration, recurrent chest infection & cardiac failure in
early infancy .
 Cyanosis usually absent , duskiness noted during crying or
infection .
 Physical signs :
 Prominent L precordium , palpable parasternal lift .
 Lateral displacement of apex beat , apical thrust .
 Holosystolic murmur ( less harsh , more blowing ).
 Pulmonary component of S2 may be increased 
pulmonary hypertension

16. Patients with
Eisenmenger
syndrome often are
cyanotic with clubbing.
They have a right
ventricular heave on
palpation of the
precordium and a loud
pulmonary component
of the second heart
sound. A VSD murmur
may not be present.

18. 2D ECHOCARDIOGRAPHY is the diagnostic modality of
choice

19. Management
 SMALL VSD
Most will close spontaneously usually within 1st 2 years of
life. Ensure by the disappearance of the murmur, normal
ECG on follow up, normal Echocardiogram.
While the VSD is present, for prevention of bacterial
endocarditis:
Maintain good oral hygiene
Antibiotic prophylaxis before dental extraction or any
operation where there will be bleeding is NO LONGER
RECOMMENDED (Nelson 20th Edition)
Surgical closure may not be required

20. Management
 LARGE VSDs :
AIM : Control Heart Failure( diuretics + digoxin +
afterload reducing agents) and prevent development
of pulmonary vascular disease.
Indications for surgical closure of a VSD :
 patients at any age with large defects in whom clinical
symptoms and failure to thrive cannot be controlled
medically;
 infants between 6 and 12 mo of age with large defects
associated with pulmonary hypertension, even if the
symptoms are controlled by medication;
 patients older than 24 mo with a Qp : Qs ratio greater than 2
: 1.
 Patients with a supracristal VSD of any size are usually

22. Surgical Options