ASD ( Atrial Septal Defect)... An Overview

An overview of Atrial septal defect.

1. ASD
(Atrial Septal Defect)

An Overview
By Dr. Amira Aref

2. ASD is a congenital heart
disease due to a spontaneous
malformation of the interatrial
septum.

3. This results in an abnormal
connection between the 2
atria,allowing mixing of
oxygenated and deoxygenated
blood.

4. •It represents 6-10% of CHD.
•It is often diagnosed in childhood, but
sometimes it manifests in adulthood.
•Female to male ratio is 2:1.
•Most cases are sporadic, but some are
part of genetic syndromes ( mutation in
chromosome 5, Holt-Oram syndrom).

5. Types of ASD

The three major types of ASD account for 10%
of all CHD and 25-30% of CHD presenting in
adulthood.
The three main types are:
● Ostium secundum.
● Ostium primum.
● Sinus venosus.

6. Ostium
secundum

•The most common type( 80%).
•Represents 30-40% of CHD in
patients > 40 years.
•Occurs due to a defect in fossa
ovalis ( the middle part of the
septum).

7. Ostium
primum

•The second most common type
(15-20%).
•It is a defect in the
anteroinferior aspect of the
septum ( a form of atrioventricular
septal defect).
•Commonly associated with mitral
valve anomaly.
•Most common type in Down
syndrome.

8. Sinus venosus


•The least common type (5%).
•It is a defect in the superior
aspect of the atrial septum.

9. Pathophysiology

10. •Initially, shunting is from left to right.
•Moderate to large ASD cause RV and RA volume
overload, leading to pulmonary hypertension ,RVH
by the age of 30-40 years if left unreported.
•Atrial arrhythmia, SVT,AF, and flutter can occur.
•Even with left to right shunt, paradoxical embolus
can occur due to transient right to left shunting.

11. Lately, the increased pulmonary artery pressure
and vascular resistance causes bidirectional atrial
shunting and cyanosis ( Eisenmenger’s Syndrome).

12. TIPS:

The clinical deterioration in adults occurs due to:
●Age related decreased in LV compliances and
increase int left to right shunt.
●Atrial arrhythmia.
●Most symptomatic adults >40 years have
pulmonary HTN.
●In premium ASD, symptoms are related to MR.

13. Clinical
picture


Most small to moderate ASD are
asymptomatic.
Large ASD may cause no symptoms in
children.
Common symptoms in children are easy
fatigue, recurrent chest infections,
slow weight gain.

In adults, symptoms may include
exertional dyspnea, palpitations,
stroke, syncope, heart failure.

14. On
examination









●Midsystolic ejection murmur, best
heard on left sternal border.
●Widely fixed split S2.
●Parasternal heave.
●Mid diastolic rumbling murmur on
tricuspid area due to increased flow
across the tricuspide valve in large
left to right shunt.
●In ostium primum, systolic murmur
of MR may be present.

15. Explanation of wide fixed splitting of S2 in ASD:

Normally, during inspiration,S2 is split because
A2 closes before P2. This is caused by the
increased blood return to the RV, causing longer
ejection time , therefore delayed PV closure.
Also, PA tolerate more volume of blood before
the pressure above the valve increases,due to its
lower vascular resistance, so causing delayed PV
closure.

16. In ASD,

S2 Splitting is wide and fixed, due to the
continous blood flow from left to
right,lengthening the cardiac cycle on
right side during inspiration and
expiration.

Reference: Stanford medicine 25.

17. Examination cont.,
In the presence of pulmonary HTN, and RVH,
the findings will be:
•S4.
•The midsystolic pulmonary murmur is softer and
shorter.
• TR flow murmur is absent.
•Splitting of S2 is narrowed.
•Murmur of PR is apparent.

18. Cont.,

In cases of Severe pulmonary HTN, reversal of
the shunt may occur, leading to cyanosis and
clubbing (Eisenmenger’s Syndrome).

19. Investigations
Chest X ray will show
cardiomegaly, prominent
pulmonary artery, and
increased pulmonary vascular
markings.
Echo is diagnostic.
ECG… (next slide).

20. :

Ostium secundum:
●RAD.
●rSR in V1.
●incomplete RBBB.
●Notching of R wave in inferior leads (Crochetage sign).
Ostium Primum:
● LAD.
●rSR in V1.
●RBBB.
Sinus venosus:
●LAD.
●-ve P wave in lead III.

21. Source: Life in the Fast Lane ECG Library.

22. The previous ECG shows:
●RAD.
●Incomplete RBBB.
●Crochetage sign in II, III, avf.
( Ostium Secundum ASD).

23. Treatment of
ASD


●Observation.
●Surgical repair or
transcatheter closure.
●Specific pharmacological
treatments (such as
antiarrhythmics or
diuretics).

24. Small, central ASD < 3 mm closes
spontaneously.

Those between 3-8 mm may close
spontaneously by the age of 3 years.

In asymptomatic child with small shunt,
observe and order echo every 3-5 years.

25. In adults, spontaneous closure is unlikely.
Ostium Primum and Sinus Venosus don't close
spontaneously.
Moderate to large defects with evidence of RV
volume overload in echo should be closed by
2-6years.
Earlier repair should be considered if the child
has chronic lung disease.

26. Cont.,


Transcatheter closure is possible in 80-90% of
defects.
Sinus Venosus and Ostium Primum types are not
amenable to device closure.

27. 2018 AHA/ACC guidelines for adult congenital heart
diseases.
Recommendations of Secundum ASD closure in adults:

●Impaired exertional or functional capacity.
●RA and or RV enlargement.
●Qp:Qs ratio >1.5.
Provided that there is □ no cyanosis, systolic PAP<50%
of systemic systolic pressure, pulmonary vascular
resistance <third of systemic vascular resistance

28. Contraindications
of closure
●Severe pulmonary HTN.
●Eisenmenger’s Syndrome.
●Irrversible pulmonary
vascular disease or
occlussive disease.
●Asymptomatic patient with
Qp:Qs < 1.5

29. Endocarditis
prophylaxis
●Not needed
preoperative.
●Required only for the
first 6 months after
repair, or if there is
a residual defect
adjacent to the
surgical patch.

30. Refrences:
MSD manual.
Medscape.

31. Thank You.