VSD

• Communication
b/t two ventricles
VSD

• May occur alone or

with other
abnormalities
• About one-third of
small VSDs close
spontaneously
 Ventricular Septal Defect
• Commonest acyanotic CHD (~25%)

• Associated with-Down Syndrome

Fetal hydantoin syndrome
Fetal alcohol syndrome
Trisomy 13, 18
Apert syndrome
 Anatomy
• Compartments of ventricular septum:
- Membranous septum
- Inlet septum
- Trabecular septum
- Outlet or infundibular septum
• Defects result from a deficiency of growth
or failure of alignment or fusion of
component parts
 Classification-pathology
1.Membranous VSD- (perimembranous,
paramembranous , conoventricular, infracristal,
subaortic) – Most common (90%)
2.Muscular VSD- (Swiss cheese ,inlet,
trabecular, central, apical, marginal ,or outlet
types)
3. Supracristal VSD- (subpulmonary, outlet,
infundibular, or conoseptal. subarterial defect)
Least common
Classification-pathology
 Hemodynamics:
• L→R shunt in ventricles occur with high
pressure gradient throughout systole –
pansystolic murmur
• Blood to normal pulmonary valve –
ejection systolic murmur
• Large vol of blood to lungs – pul plethora
• Blood to left atrium – Lt. atrial enlrgement
• Blood to normal mitral valve – delayed
diastolic murmur at apex
 Hemodynamics
• Lt ventricles to outlets – empties relatively
early – early A2
• Rt ventricle & pul artery – increased
ejection time – delayed P2-S2 widely split
&variable
Hemodynamics
 Hemodynamics
• Depends on: a) size of the shunt
b) PVR

• Based on size of VSD:

- Restrictive VSD(<0.5 cm2 )
- Moderately restrictive VSD
- Non-restrictive (>1 cm2 )
 Restrictive VSD
• Small, hemodynamically insignificant
• Size <0.5 cm2
• Between 80% and 85% of all VSDs
• All close spontanously
50% by 2 years
90% by 6 years
10% during school years
• Muscular close sooner than membranous
 A moderately restrictive VSD
• Size -> 0.5 cm2 (>5mm) in diameter

• Moderate shunt (Qp:Qs = 1.5-2.5:1.0)

• May lead to left atrial and LV dilation and

dysfunction, as well as a variable increase in
pulmonary vascular resistance
 Large nonrestrictive VSDs

• Large VSDs with normal PVR

• Usually >1.0 (>10 mm) in diameter

• Usually requires surgery

• Will develop CHF and FTT by age 3-6

months
 Clinical Manifestations:
1. Small VSD: asymptomatic, normal growth

2. Moderate to large: repeated chest

infections, Effort intolerance ,fatigue ,
failure to thrive, pulmonary HTN

3. If unoperated: Pulmonary HTN, cyanosis

and decreased level of activity
 Physical examination
1. Small VSD: well developed, acyanotic

2. Moderate VSD: forceful LV impulse ,

prominent systolic thrill along the lower
left sternal border
 Physical examination
Large VSD: tachypneic, repeated chest infections,
poor weight gain, CHF dyspnea, feeding
difficulties, poor growth, profuse perspiration,
recurrent pulmonary infections, and cardiac failure
in early infancy.

Reversal of shunt: cyanosis, clubbing, respiratory

distress.
 Auscultation
• Heart sounds
• S1 : masked by pansystolic murmur
• S2: masked but can be heard at 2nd lt ICS
– widely split and variable, with
accentuated P2 - single and loud (PAH)
• S3: maybe audible at the apex
 Murmurs
• Shunt - loud, harsh, or blowing pansystolic
murmur grade 3-5/6 best heard at left 3rd & 4th
interspaces is widely transmitted over the
precordium at lower LSB
• Flow –
• Pulmonary : ejection murmur (drowned)
• Mitral : rumbling delayed diastolic murmur at
the cardiac apex, indicates a Qp:Qs of 2:1 or
greater
Fairly large perimembranous
VSD in
 Chest radiography
• Small VSDs -N
• Medium- VSDs -minimal cardiomegaly
and a borderline increase in pulmonary
vasculature
• Large VSDs – gross cardiomegaly . The
pulmonary vascular markings are
increased and frank pulmonary edema
(Plethoric) if pul arterial HTN
• Oligemic lung fields in reversal of shunt,
pul stenosis
 Electrocardiography
• Depends on shunt size & degree of
pulmonary hypertension
• Small VSDs - N tracing
• Medium VSDs – broad, notched P wave
( left atrial overload), LVH
• Large VSDs – RVH with right-axis deviation.
With further progression - biventricular
hypertrophy; P waves may be notched or
peaked
• RVH in Eisenmenger’s complex
 Echocardiography

• Echo - Number, position & size of defect,

chamber size
• Two-dimensional echo – site, size of
defect ,pul. stenosis or pul HTN
 Management:
• Large VSDs Medical:
Treatment of chest infection
Control of heart failure
Infective endocarditis prophylaxis
Dental hygiene
Frequent feeding of high calorie formula, correction of anemia
Non-surgical closure with umbrella device
 Surgical
• Repair of defect under open heart surgery
• Clamshell-type catheter occlusion -closing
apical muscular VSDs.
• Transcatheter device closure - trabecular
(muscular) and perimembranous VSDs
 Indications of surgery:
• Large defects- if CHF not responding to
medical management (within first 6
months of life)

• After 1 year of age, significant LR

shunt, Qp: Qs ratio at least 2:1 without pul
HTN

• Supracristal VSD of any size because of

the high risk of aortic valve regurgitation
 Contraindication of surgery
1. Severe pulmonary vascular disease
2.Muscular septum VSDs , particularly
apical defects and multiple (Swiss
cheese–type)
 Natural history
• Small VSD – Spontaneous closure( 30-50%) during
1st yr of life (membranous & muscular defects)
• Small muscular VSDs are more likely to close 80%
than membranous VSDs 35%
• The vast majority 45% close by age 4 years
• Spontaneous closure has been reported in adults
 Mod to Large VSDs
• Less commonly close spontaneously
• CHF develops in large VSDs after 8 weeks of age

• Repeated chest infection ,FTT

• IE –independent of VSD size – rare in < 2yrs .risk is 2% above

2 yrs
 Natural History:

• Pulmonary hypertension →pulmonary

vascular disease (Eisenmenger syndrome

• Aortic valve regurgitation - the greatest

risk supracristal VSD