A congenital anomaly of heart described shortly.

1. VENTRICULAR SEPTAL
DEFECTS
DR.YASNA KIBRIA
Resident , MD(Phase A)
Department of Radiology and Imaging
BSMMU

2. INTERVENTRICULAR SEPTUM
STRUCTURE:
• Inter-ventricular septum (or during development septum inferius) is the stout
wall separating the lower chambers (ventricles) of the heart from one another.
• It is directed obliquely backward to the right,and curved with the convexity
towards the right ventricles.

3. • The greater portion of it is thick
and muscular and constitutes the
muscular interventricular
septum.
• it’s postero-superior part,which
seperates the aortic vestibule
from lower part of right atrium
and upper part of right
ventricle,is thin and fibrous and
is termed as membranous
interventricular septum(septum
membranaceum)

5. DEVELOPMENT OF INTERVENTRICULAR SEPTUM
• The muscular part of the interventricular septum derives from bulboventricular
flange , which is developed due to differencial growth of primitive ventricle and
bulbous cordis.
• The membranous part has a neural crest origin which connects the upper free
margin of bulboventricular flange and anterior and posterior endocardial
cushions of the atrio-ventricular canal.
• It also gets attached to lower border of spiral/aortico-pulmonary septum.

7. VENTRICULAR SEPTAL DEFECT
• A VSD is a defect in the ventricular septum , allowing blood to shunt
between the left and right ventricles.
• Defects can occur any part of the complex curved shaped ventricular
septum.
• It is the commonest of all congenital cardiac anomalies.
• Occur as an isolated condition in 12/10,000 births.
• More common in premature infants.
• Incidence is 36.1%

8. HISTORICAL ASPECT
Henry Roger was the fisrt man to describe ventricular
septal defect,in 1879 he wrote-
“A ventricular defect of the heart occurs from which
cyanosis does not ensue in spite of the fact that a
communication exists between the cavities of two
ventricles and in spite of fact that the admixture of
venous blood and arterial blood occurs.This
congenital defect,which is even compatible with long
life,is a simple one.It comprises a defect in the
interventricular septum”

9. HISTORICAL ASPECT Cont….
 1897 – Eisenmenger syndrome– Autopsy finding
 Pathophysiology by Abbott(1936) and Selzer (1949)
1952-Muller and Danman –pulmonary artery band
 1954 –Lillehei and associates – first VSD repair

10. CLASSIFICATION of VSD
 Perimembranous defect:
• This is the commonest type (80%) of VSD,involving the membranous
septum and adjacent muscular tissue below the aortic root and close
to the upper margin of the tricuspid valve annulus.
• Sometimes this can be large and extend around towards the outlet
part of the septum.
• Types: a)anterior membranous VSD
b)posterior membranous VSD
c)supracristal and infracristal VSD
***Bundle of His runs along the posterior edge-may be damaged during
VSD repair.

11.  MUSCULAR /TRABECULAR DEFECTS : these can
be grouped as follows-
a)Inlet or basal muscular defect: lying in the muscular septum between
the mitral and tricuspid valves.
b)Mid-muscular or apical defect: between the main right and left
ventricular chambers.
c)Outlet defect:which involves either the high anterior trabeculated
part of the septum or the band of the muscle immediately below the
pulmonary valve forming the conus of right ventricles.(sometimes
called conal defect).

13. TYPES OF VSD
1. SMALL: <50% the size of aorta or <5mm
2. MODERATE: >50% the size of the aorta or 5-10 mm
3. LARGE: larger than the size of the aorta or >1 cm
THE GERBODE DEFECT
• A communication through the small portion of the basal septum that
separates the left ventricular outflow tract from the right atrium.(The
atrioventricular septum)
• Very rare but must be diagnosed with care,because it can easily be confused
with perimembranous defect and coexistent tricuspid regurgitation.

14. HAEMODYNAMICS

17. CLINICAL PRESENTATION
• SYMPTOMS: The presentation of this condition depends on the overall size of
interventricular communication-
1. SMALL SIZED VSD: asymptomatic usually,but may present at much later in life.
2. LARGE VSD: asymptomatic at birth,may become symptomatic after 2-3 weeks of life
with breathlessness,feeding difficulties,poor growth,palpitation,recurrent chest
infection etc.
• SIGNS:
i. Children with VSD are malnourished and acyanotic.
ii. Cyanosis and clubbing may be present (eisenmenger syndrome)
iii. Tachypnea,chest indrawing,precordial bulge.
iv. On auscultation-a LOUD pansystolic murmur is present at left sternal border.
v. The liver and spleen may be enlarged.

18. ASSOCIATIONS
 Cardiovascular associations
• Tetralogy of fallot (TOF)
• Truncus arteriosus
• Double outlet right ventricle
• Coarctation of aorta
• Tricuspid atresia
• Aortic regurgitation
• Pulmonary stenosis

19. ASSOCIATIONS
 Extra-cardiac associations
• Aneuploidic / chromosomal anomalies
• Trisomy 21
• Trisomy 18
• Trisomy 13
Other syndrome anomalies:
• Holt-oram syndrome (Heart hand syndrome)

20. IMAGING MODALITIES OF VSD
 NON-INVASIVE
• Plain radiograph
• Echocardiography with Doppler study
• Computed tomography (MDCT/CTA)
• Magnetic resonance imaging
 INVASIVE
• Cardiac catheterization and angiography

21. RADIOLOGICAL FINDINGS
• Plain radiograph:
Chest radiograph can be normal with a small VSD.
Larger VSD may show cardiomegaly (the right and left ventricle are
enlarged , left atrium can also be enlarged).
A large VSD may also show features of pulmonary arterial hypertension,
prominent pulmonary bay, pulmonary oedema , pleural effusion and
increased pulmonary vascular markings.

23. • Two-dimensional echocardiography
oThe diagnosis of VSD is usually confirmed by 2-D echocardiography.
oAllows direct visualization of septal defects.
oFull extent of the interventricular septum should be examined in
suspected VSD.
oThe examination will include,as an absolute minimum ,
the parasternal long and short axis views and
the apical four –chamber view.

26.  Doppler flow assessment:
oMay be needed to detect the presence of of small defects,using the
turbulent jet passing through the defect as a marker.
oMild tricuspid regurgitation is frequently associated with peri-
membranous VSDs.
 Colour flow mapping:
oVery valuable in speeding and simplifying the detection of small or
multiple VSDs , particularly small restless child.
oAn important non invasive method for deducing the right ventricular
pressure. (degree of intracardiac shunting)

28. • COMPUTED TOMOGRAPHY
CT angiogram with ECG-gating allows direct visualization of the defect.
Large VSD may be seen on non-gated studies.
• MAGNETIC RESONANCE IMAGING
May also show added functional information (e.g. quantification/shunt
severity) in addition to anatomy.
Some muscular defect can give rise a “swiss cheese”appearance.
 Black blood imaging at end of diastole
 Bright blood gradient echo dynamic images

30. • Cardiac catheterization and angiography
Is still frequently undertaken if any doubt about intracardiac anatomy
or nature of pulmonary vascular resistance.
If biplane cine angiocardiography if available,the best two views for
initial examination of septum:
I. 65 degree LAO with a 20-25 degree cranial tilt
II. 30 degree RAO
These two views will demonstrate majority of perimembranous,inlet
and mid-muscular septum (LAO) and high anterior and conal
septum(RAO).

31. CONT…
If VSD is large or multiple defects or obscured by additional defects
are shown,at least one additional view may be necessary-
I. 55 degree LAO with a 10-15 degree caudal tilt
II. 40 degree RAO with a 15 degree caudal tilt
*LAO view will distinguish high from low defects,whereas the previous
cranial tilt will distinguish basal from apical defects.
*RAO view will profile the portion of the septum between the inflow
and outflow portions.

34. COMPLICATIONS OF VSDs
• Eisenmenger phenomenon
• Congestive heart failure
• Secondary aortic insufficiency
• Aortic regurgitation
• Infective endocarditis
• Recurrent respiratory tract infections

35. TREATMENT
• Small defects may be left for some years(as long as no significant
pulmonary hypertension) to see if spontaneous closure occurs.
• Larger defects :
medical treatment
surgical treatment
• Primary closure of very large VSD is performed under age of 1 year in many
cases and in some cases in first few weeks of life.
• Closure of VSD is usually performed by prosthetic patch ,sometimes by
direct sutures. (via the right atrium and tricuspid valve)

36. POST OPERATIVE FOLLOW-UP
• In early post operative period, colour flow Doppler may show there is
leakage through the patch.the patch itself is easy to see in two
dimensional imaging as it is highly echogenic.
• Follow up should be done every 1 to 2 years.if no residul shunt is not
present ,SBE prophylaxis should be discontinued after 6 months.
• Activity should not be restricted without post operative
complications.