5. Types
• Primum – affects the lower part of the
septum
• Secundum – common, affects the upper
part of the septum
• Sinus venosus – affects the upper part
and may be associated with abnormalities
of superior vena cava
7. Incidence
• Sex - female : male = 3:1
• 1/1500 live births
• Ostium secundum counts for 7% of CHD’s
• 100% ASD’s ≤3mm in diameter
• Most of the secundum are associated with Holt-
Oram’s syndrome.
• Holt–Oram syndrome is a disorder that
affects bones in the arms and hands (the
upper limbs) and may also cause heart
problems
8.
9. Pathophysiology
Increased left atrial pressure(02
nated
blood)
↓
Left to right shunt ( no cyanosis)
↓
Burden on right side of the heart
↓
Increased pulmonary blood flow
↓
Pulmonary stenosis / pulmonary HTN
↓
Right ventricular hypertrophy
↓
↑Right atrial pressure
↓
Right to left shunt
↓
cyanosis
10. Clinical Features
In majority remains asymptomatic
Systolic murmer best heard over 2nd
& 3rd
ICS
Dysrrythmias
Increased fatigability
In older children recurrent chest infection,
breathlessness, & bulging of the chest due
to enlargement of right ventricle
Growth failure in some children
11.
12. A hyperdynamic impulse of the right
ventricle may be palpated at the lower left
sternal border
Split S2
Cyanosis in later stages
Cardiomegaly
Pulmonary vascular emboli
Echo shows right ventricular volume
overload
Cardiac catheterization shows increased
02 content in blood
13. Diagnostic measures
• Chest X-Ray
• ECG
• MRI heart
• Cardiac catheterization
• Intracardiac imaging: with special catheters that
are typically placed in the venous system and
advanced to the level of the heart. Involves only
mild sedation.
19. Prognosis
• With a small to moderate atrial septal
defect, a person may live a normal life
span without symptoms.
• Larger defects may cause disability by
middle age because of increased blood
flow and shunting of blood back into the
pulmonary circulation.
20. Ventricular Septal defect
• Abnormal opening between the ventricles
• It can be single pin hole opening to absence of
membrane
• Results in left to right shunt, ultimately right to
left shunt.
21. Types
• Membranous
• Muscular- swiss cheese
• (Perimembranous- lie in the LV outflow
tract just below the aortic valve.
• Infundibular- These defects lie beneath
the pulmonic valve )
23. Pathophysiology
Blood from left ventricle→ right ventricle→ pulmonary artery
↓
Increased pulmonary resistance
↓
Increased pressure in right ventricle
↓
Right ventricular hypertrophy
↓
Enlargement of right ventricle
↓
Enlargement of right atrium
↓
Eisenmengers syndrome
↓
Cyanosis
25. Clinical features
• Pan systolic Murmur
• In large VSD’s
Dyspnoea
Tachypnea
Feeding difficulties
Poor growth
Profuse perspiration
Recurrent pulmonary infections
26. Cardiac failure and its symptoms
Cyanosis seen on exertion specially
while crying
Prominence of left precordium
Digital clubbing
Poor exercise tolerance
S2 is split
29. Management
• Small defects no surgical correction but to
prevent bacterial endocarditis precautions
to be taken
• Moderate to large defects surgical closure
is needed
< 6 months: high risk for surgery usually
open heart surgery is done
30. • 6 to 24 months: in case of pulmonary
hypertension surgery is indicated to
prevent development of hypertensive
vascular disease
• >24 months: depends on pulmonary
vascular resistance
• Surgical interventions done for small
defects are Purse String closure n for
large defects Knitted Dacron patch
• Clamshell type catheter occlusion devices
are tested For closing of apical VSD
33. Prognosis
• Risk depends on
Location of defect
Number of defects
Other associated cardiac defects
Single membrane defect have low
mortality <5%
Multiple defects have a risk of >20%