Acyanotic congenital heart diseases VSD ASD AVSD PDA

1. Yapa Wijeratne
Acyanotic Congenital Heart Diseases
VSD ASD AVSD PDA
Commonest – 32% all CHD
Occurs alone or in
association with other
defects
Usually small
2 main types
Perimembranous
Muscular
1. Perimembranous
2. Outlet / subarterial
3. Muscular
4. inlet
Classified according to the
position in the septum
Types
1.Ostium secundum
Most common
Situated in the region of
fossa ovalis
Usually single / multiple small
lesions
2. Ostium primum
(partial A-V septal defect)
3. Superior sinus venosus
4. Inferior sinus venosus
5. Coronary sinus
High association with Down
syndrome
All are symptomatic
All require surgery
Types
Normal
Partial AVSD
Complete AVSD
Arterial duct is kept open by
prostaglandins in foetal life
Usually closes in first few
days after birth
Delayed closure seen in
- preterms,
- those born at high
altitudes,
- those with defective
duct wall
Present in congenital rubella
syndrome
Rarely familial
Presentation depends on the size of the
defect and pulmonary artery
pressure
 asymptomatic
 heart failure
 failure to thrive
 recurrent infection
 cyanosis
 endocarditis (rare)
Large VSD
Presents at 2 – 8 weeks of
age
 Symptoms of heart
failure
 Recurrent respiratory
Most present at 1- 5 yrs with
asymptomatic murmur
Rarely it is familial
Few have failure to thrive /
heart failure
Partial AVSD / Ostium
primum defect
Surgery 2 – 5 yrs
30 % mortality
20 year survival 80%
Complete AVSD
Early surgery (3 – 6 mths)
10 % Mortality
10 year survival 83 %
Usually present with
asymptomatic murmur
(Continuous machinery
murmur beneath L. clavicle)
Wide pulse pressure
bounding / collapsing pulse
In more severe disease (large
PDA)
- mdm at apex (flow
murmur)
- evidence of PHT
(loud P2, R.
ventricular
hypertrophy)

2. Yapa Wijeratne
infection
 Tachypnoea /
dyspnoea
 Intercostal /
subcostal recessions
With PHT – symptoms↓
develops cyanosis
(Eisenmenger’s)
- Eisenmenger’s - late
Precordial
findings
psm+
maximum at L.
parasternal region
 mdm at apex (flow
murmur)
gallop rhythm
 Loud P2
Delayed P2 & fixed splitting of
2nd
heart sound
Systolic murmur at
pulmonary area (increased
flow)
DD
1. Venous hum
Varies with posture / head
movement
Best heard on right side
2. AV malformation
Coronary, chest-wall,
pulmonary
3. VSD with aortic
regurgitation
4. Ruptured sinus of Valsalva
aneurysm
ECG biventricular hypertrophy (in
PHT)
Upright “T” wave in V1 in
PHT
incomplete RBBB > 90 %
(10 % normal will also have
RBBB)
R axis deviation
CXR Cardiomegaly
Enlarged pulmonary arteries
Peripheral pruning
Increased hilar vascular
markings
Pulmonary oedema.
Cardiomegaly
Enlarged pulmonary arteries
Pulmonary plethora
Cardiomegaly
Enlarged pulmonary arteries
Peripheral pruning
Pulmonary plethora
Prognosis > 2/3 of muscular defects &
1/3 of perimembranous
defects
- close spontaneously within

3. Yapa Wijeratne
6 yrs.
Management Small VSD with normal pul.
artery pressure
 review regularly
 antibiotic prophylaxis
for SABE
 long term survival is
excellent
Large VSD with symptoms
Treat heart failure
NG feeding + added calories
Surgery
If primary repair not possible
- pulmonary artery banding
Surgery for VSD
Indications for surgery within
first year
1. severe symptoms
with failure to thrive
2. PHT
If pul. Artery pressure > 75%
of systemic pressure surgery
in 2nd year
Large VSD with pulmonary :
systemic flow ratio > 2 : 1
surgery in 4-5 yrs.
Operative mortality < 5 %
long term survival - excellent
Spontaneous closure is
unusual
Defects < 6 mm may close
spontaneously in the
neonatal period
Defects > 8 mm in diameter
unlikely to close
Surgery recommended from
the age of 2 yrs. (usually
before school age)
Bacterial endocarditis very
rare
Transcatheter procedure
It is possible to close central
defects by using varies
devices
Low risk
High closure rates
Surgical closure
Direct suture / patch
< 1 % mortality
10 % post-cardiotomy
syndrome with pericardial
effusion
Survival similar to that of
general population
Fluid restriction / diuretics
Indomethacin – in neonates
Transcatheter closure
Method of choice
Occlusion rate > 98 %
Surgical ligation for large
defects
Mortality < 0.5 %
Outcome is excellent
Risk of recurrent laryngeal
nerve palsy, recanalization,
inadvertent ligation of L.
pulmonary artery