VSD

1. VENTRICULAR SEPTAL DEFECT
PART-I
DR DHANESH KUMAR

2. Ventricular Septal Defect
 Henri Roger was the first man to
describe a ventricular septal defect,
in 1879 he wrote:
“A developmental defect of the heart occurs
from which cyanosis does not ensue in spite
of the fact that a communication exists
between the cavities of the two ventricles
and in spite of the 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”

3. .
INTRODUCTION
 2- per 1000 live birth
 Forms 20 % of all CHD
 50 % when associated with other major defect
 10-15% of large VSD’s close spontaneously
 60% of defects close before age 3,
and 90% before age 8

4. .
 Roger in 1879 - First described
 Eisenmenger – 1897 - Autopsy finding
 Pathophysiology by Abbott (1936) & Selzer (1949)
 1952 – Muller and Danman- Pulmonary artery band
 1954 - Lillehei and associates – FirstVSD repair
 1956 – Dushane –Transventricular / Stirling –Transatrial
 1961 – Kirklin- Repair ofVSD in infants
 1976 - Baratt-Boyes – Deep hypothermia & circulatory arrest
HISTORICAL ASPECT

5. Formation of IV septum
 IV septum grows upwards from
floor of the bulboventricular
cavity,division into R and L .
 IVS meets fusedAV cushions
and partially fuses with them.
 Two ridges R and L arise in
conical upper part of
bulboventricular cavity, fuse
with each other to form bulbar
septum.
 Gap between the two is filled
by proliferation of tissue from
the AV cushions.

6. Membranous IV septum
 Anterior part
separates RV and LV.
 Post. part separates
RA and LV.
 This is because the
IAS and IVS don’t
meet in the midline.

7. Associated Defects
 Left Heart Defects
 Aortic stenosis (2%)
 Coarctation of the aorta (5%)
 Right Heart Defects
 TOF
 DORV
 Truncus Arteriosus
 PDA (6%)
 Single ventricle (e.g.Tricuspid atresia, double inlet
left ventricle)

8. Chromosomal Disorders
associated with VSD
 Trisomy 21
 Trisomy 13, 18
 22q11 deletion: Di George syndrome
 TOF is most common anomaly
 VSD with or without aortic arch anomaly is second most common
 Holt-Oram (Hand-heart syndrome):TBX5 gene found on
Chromosome 12
 Recurrence risk forVSD based on parentalVSD
 Paternal 2%
 Maternal 6-10%

9. Ventricular Septum
 The membranous septum-The septal leaflet of theTV
divides membranous septum into:
 1. pars atrioventricularis
 2) pars interventricularis.
 The muscular septum is a nonplanar structure that can
be divided into:
 1) inlet
 2.) trabecular
 3.) infundibular components.

10.  An inletVSD has no muscular
rim between defect and AV
valve annulus.
 The trabecular septum is largest
part of IVS. Defects in the
trabecular septum can be
classified as anterior,
midmuscular, apical, and
posterior.
 The infundibular septum
separates RV and LV outflow
tracts. On the right , it is
bordered by a line from the
membranous septum to the
papillary muscle of the conus
inferiorly and the semilunar
valves superiorly.

11. The Ventricular Septum

12. CLASSIFICATION
ROBERT ANDERSON
 Perimembranous
 Muscular
 Doubly committed Juxta
arterial defects
VAN PRAGH
 AV canal type
 MuscularVSDs
 Conoventricular
 Conal

13. The Ventricular Septum
1. Membranous
2. Outflow
3. Trabecular septum
4. Inflow
5. Subarterial /
Supracristal

14. VSD Size(based on shunt)
Restrictive VSD(Small to Moderate shunt)
– < 0.5 cm2 (Smaller than AVA)
– Small shunt
– Normal RV output
– 75% spontaneously close < 2yrs
– Qp/Qs=1.4-2.2
– Psp/Asp<0.66
Non-restrictiveVSD(Large shunt)
– > 1.0 cm2 (Equal to or greater than to AVA)
– Equal RV and LV pressures
– Large hemodynamically significant shunt
– Rarely close spontaneously
– Qp/Qs >2.2
– Psp/Asp>o.66

15. Based on size(Anatomic)
1) Large : 2/3rd of aortic annular dia. or > 15 mm
or > 1cm/sq. m of BSA
Peak RV sys = LV sys pressure
2) Moderate : Half of aortic annular dia. 5 to 15 mm
RV pressure to ½ of LV
Qp/Qs>2.0
3) Small : One third of aortic annular dia.
insufficient size to raise RV pressure &
Qp/Qs < 1.75

16. Expanded Morphological
Classification of VSD
 CLASSIFICATION EXTENSION
 Perimembranous Inlet, Anterior,Outlet
 Muscular Outlet,Trabecular,
Inlet, Anterior,Apical
 Doubly committed subarterial
 Inlet septal Atrioventricular
septal type
 Malalignment Anterior (TOF)
Posterior(Interrupted arch
or Coarctation)
Rotational(Taussig-Bing)

17. Nomenclature / Classification
 TYPE I-
Conal,
Supracristal,
Infundibular,
Subarterial
 TYPE II –
Perimembranous
 TYPE III-
Inlet/ AV canal type
 Type IV –
Muscular

18. TYPE I VSD
 Conal, Supracristal, Infundibular,
Subarterial
 Maldevelopment of bulbotruncal system
 Located within infundibular portion of RVOT
 Superior margin – no muscular tissue
 Inferior margin – defect is muscular
 Can extend upto right or sometimes
NCC of the aortic valve
 Conduction system is not in surgical proximity

19. Doubly committed subarterial VSD

20. TYPE II VSD
 Perimembranous type
 Most common (80%)
 Margins include membranous septum or remnant
 May have extensions into inlet, outlet or trabecular septum
 Postero-inferior margin very close to the antero-septal
commissure of theTV
 Can extend upto non-coronary cusp of aortic valve
 Danger area- inferior and posterior region of defect

21. Membranous VSD

22. TYPE III VSD
 AV Canal type / InletVSDs
 ~5% of allVSDs
 Located posteriorly – subjacent toTV
septal leaflet in inlet portion
 Superior border- may extend to the
annulus of tricuspid valve
 Conduction system at risk – close
proximity to AV node
Guide- apical area of Triangle of Koch
 Common bundle courses around inf.
aspect of defect

23. Endocardial Cushion (Inlet VSD)

24. INLET VSD

25. TYPE IV VSD
 Muscle all around the defect
 May be either anterior, in the inlet
septum, mid-muscular or apical
 Classification according to location is
important because it determines the
approach for surgical closure.
 Inlet and mid-muscular ----- RA
approach
 Anterior ------- Rt.Ventriculotomy
 Apical ------ May require left
ventriculotomy
 May be Single/ multiple
 Swiss Cheese VSD

26. MUSCULAR VSD

27. Pathophysiology
 Two determinants
 Size of defect
 PVR
 These determine
 Pressure gradient acrossVSD
 Shunt volume acrossVSD
 After birth PVR falls ------ Large
flow across shunt if largeVSD
 Causes increased PA pressure
(initially flow related), increased
PV return, hence LA enlargement
and LV overload
 PAH initially flow related and
reversible

28. Pathophysiology
 Later ----- Intimal proliferation and medial hypertrophy
leads to fixed irreversible PAH
 Flow through the lungs decreases as PVR increases, hence
shunt volume decreases
 Eventually PVR > SVR, hence R  L shunt acrossVSD
Cyanosis  EisenmengerisedVSD

29.  Shunt calculated by Fick’s principle Qp/Qs
Aortic O2 % sat - CentralVenous O2 % sat
Pulm.Vein O2 % sat – Pulm. Art O2 % sat
 SmallVSDs - resistance to flow across theVSD hence
Qp/Qs is rarely > 1.5
 ModerateVSDs - Qp/Qs 1.5 - 2.5, is less likely to cause
pulmonary vascular disease

31. HEATH- EDWARD CLASSIFICATION
 Grade I - hypertrophy of the media of small muscular arteries and arterioles.
 Grade II - intimal cellular proliferation in addition to medial hypertrophy.
 Grade III - progressive intimal proliferation and concentric fibrosis.
 Grade IV - "plexiform lesions"
 GradeV - angiomatous and cavernous lesions and hyalinization of intimal
fibrosis.
 GradeVI - necrotizing arteritis.

32. Natural History
 Spontaneous closure is known,
primarily with perimembranous
and muscularVSDs.
 Subarterial and inletVSDs
rarely close
 Chances differ with age at
detection
 At 1 month = 80% of largeVSDs
close
 At 3 month=60%
 At 6 months =50%
 At 12 months = 25%

34. Natural History
 Patients with largeVSD- symptom develop soon after
birth.
 CHF manifested by- dyspnea on feeding/ rec. pulmonary
infection /hepatomegaly/sweating/failure to thrive.
 Irreversible pulmonary vascular disease after 1-2 yrs of
age.
 Some children with isolatedVSD develop Subpulmonic
stenosis- pt. not at risk of pulmonary vascular disease

35. CLINICAL FEATURES
 Grade I
Small VSD (less than 1.5 cm) Patient is asymptomatic. Murmur can be present since a few days after
birth.
 Grade II
Frequent respiratory tract infections. CHF (rare). Cyanosis is absent even during exercise. Functional
aerobic capacity is usually moderately reduced with early fatigability but unusual CHF.
 Grade III
More frequent respiratory tract infections. Defective growth. Moderate cyanosis at times with exertion
Congestive heart failure frequent in the first years of life (one of the most frequent causes of CHF
during the first year of life). Functional capacity markedly reduced.
 Grade IV or Eisenmenger Complex

36. EISENMENGER COMPLEX
• Infants with Eisenmenger may become easily fatigued,Cyanosed
especially during crying spells and at feeding time
 • Low tolerance for extra exertion
 • Shortness of Breath (dyspnea) and/or rapid breathing
 • Fainting (syncope)
 • Difficulty eating, breathing or sucking
 • Poor weight gain
 • Slow growth or other physical retardation

38. CLINICAL FINDINGS
• Pulse pressure is relatively wide
• Precordium is hyperkinetic with a systolic thrill at LSB
• S1&S2 are masked by a PSM at LSB ,max. intensity of the murmur is best
heard at 3rd,4th&5th Lt ICS .Also well heard at the 2nd space but not conducted
beyond apex
• Lt. 2nd space –widely split &variable accentuated P2
• Delayed diastolic murmur at the apex &S3
• Presence of mid-diastolic ,low pitched rumble at the apex is caused by
increased flow across the mitral valve &indicates Qp:Qs=2:1/greater
• Maladie de Roger –smallVSD presenting in older children as a loud PSM w/o
other significant hemodynamic changes

39. ECG CHEST X-RAY
 May show right/left or combined
ventricular hypertrophy
 Presence of RAD represents
elevated RVP and PAP
 Cardiomegaly : proportional
to the volume overload.
 Mainly LV, LA and RV
enlargement.
 Increased pulmonary blood
flow, PAH.
 Unless LA is significantly
enlarged its difficult to
differentiate from ASD.
 RV may not be as enlarged
as anticipated as it receives
the shunt into its outflow
tract.

40. Ventricular septal defect in a 7-month-old.
Frontal(A)and lateral (B) views of the chest show moderate cardiac enlargement including right
atrial, right ventricular, and left atrial enlargement with posterior displacement of the left main
stem bronchus (arrow in B) and increased pulmonary vascularity

42. VSD IN ADULT
 PSVT & AF prevalent with increasing age.
 VSD+ AR – High risk of bacterial endocarditis
 Right sided failure- due to pulmonary stenosis
 Left sided failure- with assoc. aortic valve prolapse.
 Eisenmenger complex- 2nd & 3rd decade of life
 Pregnancy- spontaneous abortion/small-for-date babies
 Mortality- 27% by 20 years & 69% by 60 years.

43. THANKYOU