Paediatric VSD is very common. Basic knowledge is must.

1. VENTRICULAR SEPTAL
DEFECT
VSD
VSD – natural history (Nov ’07)
Clinical manifestations and management (Nov ’14)
Hemodynamics of VSD with PAH & treatment. (Apr ’13)

2. • VSD is a congenital defects in the inter- ventricular septum that allow shunting of blood between
the left to Rt ventricle
• most common congenital heart defects in infants and children
• VSD is seen in up to 3.5 infants per 1000 live births
• Most of these close spontaneously in childhood.
• VSD may also accompany other congenital defects.

3. CLASSIFICATION
BASED ON SIZE OF THE DEFECT
LARGE (NONRESTRICTIVE):
Diameter of the defect is approximately equal to diameter of the aortic orifice,
right ventricular systolic pressure is systemic, and
degree of left to right shunt depends on pulmonary vascular resistance.
MODERATE (RESTRICTIVE):
Diameter of the defect is less than that of the aortic orifice.
Right ventricular pressure is 1/2-- 2/3 of systemic and
left to right shunt is >2:1.
SMALL (RESTRICTIVE):
Diameter of the defect is less than one third the size of the aortic orifice.
Right ventricular pressure is normal and the
left to right shunt is <2:1.

4. CLASSIFICATION
• Small VSD : (less than 5 mm) close spontaneously .
• Large VSD : (usually greater than 10 mm) 90% require surgical Intervention

5. • Based on Location of the defect:
• Type I: Subarterial (outlet, subpulmonic,
supracristal or infundibular),
• Type II: Perimembranous (subaortic),
• Type III: Inlet,
• Type IV: Muscular. (commonest)
CLASSIFICATION -VSD

6. CLASSIFICATION -VSD
Four basic types of VSD:
PERIMEMBRANOUS VSD.
• located near the valves.
• one that is most commonly treated by surgery because most do not close on their own.
ATRIOVENTRICULAR CANAL TYPE (INLENT) VSD. This VSD is
• associated with atrioventricular canal defect.
• located underneath the tricuspid and mitral valves.
CONAL SEPTAL VSD.
• The rarest of VSDs
• it occurs in the ventricular septum just below the pulmonary valve.
MUSCULAR VSD.
• The most common type of VSD
• opening in the muscular portion of the lower section of the ventricular septum.
• A large number of these close spontaneously and do not require surgery

8. HEMODYNAMICS -VSD
• VSD results in shunting of oxygenated blood from the left to the right ventricle.
• The left ventricle starts contracting before the right ventricle.
• The flow of blood from the left ventricle to the right ventricle starts early in systole.
• When the defect is restrictive, a high pressure gradient is maintained between the two
ventricles throughout the systole. The murmur, starts early, masking the first sound and
continues throughout the systole with almost the same intensity appearing as a pansystolic
murmur on auscultation and palpable as a thrill.
• Toward the end of systole, the declining left ventricular pressure becomes lower than the aortic
pressure. This results in closure of the aortic valve and occurrence of A2. At this time, however,
the left ventricular pressure is still higher than the right ventricular pressure and the left to right
shunt continues. The pansystolic murmurr, therefore, ends beyond A2 completely masking it

10. HEMODYNAMICS -VSD
• The left to right ventricular shunt occurs during systole at a time when the right ventricle is also
contracting and its volume is decreasing.
• The left to right shunt, therefore, streams to the pulmonary artery more or less directly.
• This flow of blood across the normal pulmonary valve results in an ejection systolic murmur at
the pulmonary valve.
• On the bedside, however, the ejection systolic murmur cannot be separated from the pansystolic
murmur. The effect of the ejection systolic murmur is a selective transmission of the pansystolic
murmur to the upper left sternal border, where its ejection character can be recognized since it
does not mask the aortic component of the second sound.
• The large volume of blood passing through the lungs is recognized in the chest X-ray as pulmonary
plethora. The increased volume of blood finally reaches the left atrium and may result in left
atrial enlargement.

11. HEMODYNAMICS -VSD
• Passing through a normal mitral valve the large volume of blood results in a delayed diastolic
murmur at the apex. The intensity and duration of the delayed diastolic murmur at the apex is
directly related to the size of the shunt. The large flow across the normal mitral valve also results
in accentuated first sound, not appreciable on the bedside as it is drowned by the pansystolic
murmur.
• Since the left ventricle has two outlets, the aortic valve allowing forward flow and the VSD
resulting in a backward leak, it empties relatively early. This results in an early A2. Since the
ejection into the right ventricle and pulmonary artery is increased because of the left to right shunt
the P2 is delayed. Therefore, the second sound is widely split but varies with respiration in
patients with VSD and a large left to right shunt. There is also an increase in the intensity of the
P2.

13. CLINICAL MANIFESTATION
•Fatigue
•Sweating
•Rapid breathing
•Congested breathing
•Anorexia
•Poor weight gain
•Cyanosis
•Murmur sound during auscultation

14. CLINICAL MANIFESTATION
• Patients with VSD can become symptomatic around 6 to 10 weeks of age with congestive cardiac
failure.
• Palpitation, dyspnea on exertion and frequent chest infection are the main symptoms in older
children. The
• precordium is hyperkinetic with a systolic thrill at the left sternal border.
• The heart size is moderately enlarged with a left ventricular type of apex.
• The first and the second sounds are masked by a pansystolic murmur at the left sternal border.

15. CLINICAL MANIFESTATION
• The second sound can, however, be made out at the second left interspace or higher.
• It is widely split and variable with accentuated P2.
• A third sound may be audible at the apex.
• A loud pansystolic murmur is present at the left sternal border.
• The maximum intensity of the murmur may be in the third, fourth or the fifth left interspace.
• It is well heard at the second left interspace but not conducted beyond the apex.
• A delayed diastolic murmur, starting with the third sound is audible at the apex

16. CLINICAL MANIFESTATION
• The electrocardiogram in VSD is variable.
• Initially all patients with VSD have right ventricular hypertrophy. Because of the delay in the fall
of pulmonary vascular resistance due to the presence of VSD, the regression of pulmonary
arterial hypertension is delayed and right ventricular hypertrophy regresses more slowly.
• In small or medium sized VSD, the electrocardiogram becomes normal.
• In patients with VSD and a large left to right shunt, without pulmonary arterial hypertension,
the electrocardiogram shows left ventricular hypertrophy by the time they are six months to a
year old. There are, however, no ST and T changes suggestive of left ventricular strain pattern.
• Patients of VSD who have either pulmonic stenosis or pulmonary arterial hypertension may
show right as well as left ventricular hypertrophy or pure right ventricular hypertrophy.

17. CLINICAL MANIFESTATION
• The cardiac silhouette on chest X-ray is left ventricular type with the heart size determined by
the size of the left to right shunt
• The pulmonary vasculature is increased;
• aorta appears normal or smaller than normal in size.
• There may be left atrial enlargement in patients with large left to right shunts.
• Patients of VSD with a small shunt either because the ventricular defect is small or because of
the associated pulmonic stenosis or pulmonary arterial hypertension have a normal sized heart.

18. Chest x-ray demonstrates prominent pulmonary vasculature
(active congestion) without pleural effusions or convincing
consolidation. The heart is prominent.
cardiac silhouette is enlarged with congestion of the
pulmonary vasculature.

19. CLINICAL MANIFESTATION
• Echocardiogram shows increased left atrial and ventricular size as well as exaggerated mitral
valve motion.
• 2D echo can identify the
• site and size of defect almost all cases ,
• presence or absence of pulmonic stenosis or pulmonary hypertension and
• associated defects.

20. single image from an echocardiogram through the two
ventricles Demonstrate a jet of flow through the
septum consistent with a ventricular septal defect

21. SEVERITY ASSESSMENT
• Thus on the basis of the assessment of physical findings it is possible to separate very small,
small, medium sized and large VSD.
• It is also possible to decide whether there is associated pulmonic stenosis or pulmonary arterial
hypertension of the hyperkinetic or obstructive variety.
• Doppler echo estimates the gradient between the left and right ventricles, thus helping in the
assessment of right ventricular and pulmonary artery pressure.
• If the VSD is small, the left to right shunt murmur continues to be pansystolic but since the shunt
is small, the second sound is normally split and the intensity of P2 is normal.
• There is also absence of the delayed diastolic mitral murmur.
• If the VSD is very small it acts as a stenotic area resulting in an ejection systolic murmur. This is a
relatively common cause of systolic murmurs in young infants that disappear because of the
spontaneous closure.

22. SEVERITY ASSESSMENT
• If the VSD is large it results in transmission of left ventricular systolic pressure to the right
ventricle.
• The right ventricular pressure increases and the difference in the systolic pressure between the
two ventricles decreases.
• The left to right shunt murmur becomes shorter and softer and on the bedside appears as an
ejection systolic murmur
• Patients of VSD may have either hyperkinetic or obstructive pulmonary arterial hypertension.
The P2 is accentuated in both.
• In the former, there is large left to right shunt whereas the latter is associated with a small left to
right shunt.
• In hyperkinetic pulmonary arterial hypertension the cardiac impulse is hyperkinetic with a
pansystolic murmur and thrill, widely split and variable S2 with accentuated P2 and a mitral
delayed diastolic murmur.
• Obstructive pulmonary arterial hypertension is associated with a forcible parasternal impulse, the
thrill is absent or faint, the systolic murmur is ejection type, the S2 is spilt in inspiration (closely
split) with accentuated P2 and there is no mitral murmur.

23. NATURAL HISTORY/COURSE and COMPLICATIONS
• About 10% of large nonrestrictive VSDs die in first year, primarily due to congestive heart failure
• Spontaneous closure is uncommon in large VSDs.
• 30%-40% of moderate or small defects (restrictive) close spontaneously, majority by 3-5 years of
age.
• Decrease in size of VSD is seen in 25%.

24. NATURAL HISTORY/COURSE and COMPLICATIONS
• Patients with VSD have a very variable course.
• They may develop congestive cardiac failure in infancy which is potentially life threatening.
• almost 70% of all ventricular defects become smaller in size.
• A smaller proportion will disappear entirely.
• 90% of patients who have spontaneous closure of the defect, it occurs by the age of 3 years,
though it may occur as late as 25 yr or more.
• Muscular VSD have the highest likelihood of spontaneous closure.
• Perimembranous VSD close with the help of the septal leaflet of the tricuspid valve and
• sub-pulmonic VSDs often become smaller as the aortic valve prolapses through it. However, this
is not a desirable consequence and is often and indication for surgical closure
• Patients born with an uncomplicated VSD may develop pulmonic stenosis due to hypertrophy of
the right ventricular infundibulum, develop pulmonary arterial hypertension or rarely develop
aortic regurgitation due to prolapse of the right coronary or the non-coronary cusp of the aortic
valve.
• Development of pulmonary arterial hypertension is a dreaded complication since if it is of the
obstructive type the patient becomes inoperable.

25. NATURAL HISTORY/COURSE and COMPLICATIONS
• patient with a relatively small VSD often lives a lifetime without any symptoms or difficulty.
• Lastly, the VSD is the commonest congenital lesion complicated by infective endocarditis.
• The incidence of infective endocarditis has been estimated as 2/ 100 patients in a followup of ten
years, that is 1 /500 patient years.
• The incidence of infective endocarditis is small enough that it is not an indication for operation in
small defects.
• However, it is important to emphasize good oral-dental hygiene in all patients with VSD.

26. TREATMENT -VSD
• MEDICAL MANAGEMENT
• consists in control of congestive cardiac failure,
• treatment of repeated chest infections and
• prevention and treatment of anemia and infective endocarditis.
• The patients should be followed carefully to assess the development of pulmonic stenosis,
pulmonary arterial hypertension or aortic regurgitation.
• SURGICAL TREATMENT
• is indicated if:
• (i) congestive cardiac failure occurs in infancy;
• (ii) the left to right shunt is large (pulmonary flow more than twice the systemic flow); and
• (iii) if there is associated pulmonic stenosis, pulmonary arterial hypertension or aortic
regurgitation.
• Surgical treatment is not indicated in patients with a small VSD and in those patients who have
developed severe pulmonary arterial hypertension and significant right to left shunt.

27. TREATMENT -VSD
MODE OF CLOSURE
• SURGICAL CLOSURE.
• DEVICE CLOSURE
✔ muscular VSD in those weighing >15 Kg. (Class IIa).
✔ peri-membranous VSD (Class IIb).
• PULMONARY ARTERY BANDING
is indicated for
✔ multiple (Swiss cheese) (Class I),
✔ Very large VSD, almost single ventricle (Class IIa),
✔ infants with low weight (<2 Kg) (Class IIa), and
✔ associated co-morbidity like chest infection (Class IIb).

28. TREATMENT -VSD
TIMING OF CLOSURE:
• Large VSD with uncontrolled congestive heart failure: As soon as possible.
• Large VSD with severe pulmonary artery hypertension: 3-6 months.
• Moderate VSD with pulmonary artery systolic pressure 50%-66% of systemic pressure: Between 1-2
years of age, earlier if one episode of life threatening lower respiratory tract infection or failure to thrive.
• Small sized VSD with normal pulmonary artery pressure, left to right shunt >1.5:1: Closure by 2-4 years.

29. TREATMENT -VSD
TIMING OF CLOSURE:
• Small outlet VSD (<3mm) without aortic valve prolapse: 1-2 yearly follow up to look for development of
aortic valve prolapse.
• Small outlet VSD with aortic valve prolapse without aortic regurgitation: Closure by 2-3 years of
age irrespective of the size and magnitude of left to right shunt.
• Small outlet VSD with any degree of aortic regurgitation: Surgery whenever aortic regurgitation is
detected.
• Small perimembranous VSD with aortic valve prolapse with no or mild aortic regurgitation: 1-2 yearly
follow up to look for any increase in aortic regurgitation.
• Small perimembranous VSD with aortic cusp prolapse with more than mild aortic regurgitation: Surgery
whenever aortic regurgitation is detected.
• Small VSD with more than one episode of infective endocarditis: Early VSD closure recommended.
• Small VSD with one previous episode of infective endocarditis: Early VSD closure recommended

30. TREATMENT -VSD
TIMING OF CLOSURE:
• Small outlet VSD (<3mm) without aortic valve prolapse: 1-2 yearly follow up to look for development of
aortic valve prolapse.
• Small outlet VSD with aortic valve prolapse without aortic regurgitation: Closure by 2-3 years of
age irrespective of the size and magnitude of left to right shunt.
• Small outlet VSD with any degree of aortic regurgitation: Surgery whenever aortic regurgitation is
detected.
• Small perimembranous VSD with aortic valve prolapse with no or mild aortic regurgitation: 1-2 yearly
follow up to look for any increase in aortic regurgitation.
• Small perimembranous VSD with aortic cusp prolapse with more than mild aortic regurgitation: Surgery
whenever aortic regurgitation is detected.
• Small VSD with more than one episode of infective endocarditis: Early VSD closure recommended.
• Small VSD with one previous episode of infective endocarditis: Early VSD closure recommended

31. TREATMENT -VSD
• Major complications of surgery are:
(i) complete heart block,
(ii) bifascicular block, and
(iii) residual VSD.
These complications are rare and risk of surgery in uncomplicated defects is less than 1 % in most centers.