The document discusses atrial septal defect (ASD), a common acyanotic congenital heart defect characterized by a communication between the atria due to septal tissue deficiency. It covers its definition, embryology, surgical anatomy, classification, clinical manifestations, investigative methods, and management strategies, including medical, interventional, and surgical therapies. The detailed classification includes types such as secundum, primum, and sinus venosus ASDs, highlighting their pathophysiological implications and treatment protocols.

1. 10 – Atrial septal defect
Dr. Zeeshan Abdul Nasir
PGY3
Cardiac surgery
MTI - PIC

2. • Definition
• Embryology
• Surgical anatomy of Right Atrium
• Classification
• Pathophysiology
• Clinical manifestation
• Physical examination
• Investigations
• Management

3. Definition
• Communication between the atria resulting from a deficiency of
tissue in the septum causing a left to right flow.
• Acyanotic congenital heart disease.
• Severity depends on:
• Size of defect
• Size of shunt
• Resulting from asymptomatic to right sided overload, PAH.

4. Embryology
• Primitive atrium – partitioned into
right and left atria by growth of the
Septum primum – Thin crescent
shaped membrane that grows from
the roof of the primitive atrium toward
the endocardial cushion.
• Foramen primum – composed of the
free edge of the septum primum and
the endocardial cushions

5. • Fenestrations develop in the
septum primum – coalesce to
form the Ostium secundum.
• Septum primum fuses with the
endocardial cushions.
• Failure of this fusion  Primum
ASD
• Ostium secundum maintains a
right-to-left atrial flow – fetal
circulation.

6. • Septum secundum – forms to
the right of the septum
primum, growing toward the
endocardial cushions and
usually closing the Ostium
secundum.
• Failure to close  Secundum
ASD

7. Surgical anatomy of
the Right atrium
a. Crista terminalis
b. Fossa ovalis
c. Coronary sinus
d. Thebesian valve (Coronary sinus)
e. Eustachian valve (IVC)
f. Tendon of Todaro
g. AV node
h. Bundle of his
• SA node

11. Classification
• According to location
• Secundum ASD
• Primum ASD
• Sinus venosus ASD
• SVC type
• IVC type
• Coronary sinus ASD

12. • According to size
• In younger children:
• Small defect < 3 mm
• Mod defect 3 – 8 mm
• Large defect > 8 mm
• In older children:
• Small < 6 mm
• Mod 6 – 12 mm
• Large > 12 mm

13. Secundum ASDs
• MC type – 70 to 75 % of ASDs
• Location – Midportion of the
atrial septum, within or including
the fossa ovalis
• Single or multiple

14. Primum ASDs
• 15 – 20 %
• Part of the spectrum of Atrioventricular
septal defects (AV Canal defects or
endocardial cushion defects).
• Occur in the inferior – anterior portion
of the atrial septum.
• Cleft in the anterior leaflet of the mitral
valve (mitral valve cleft) – MR
• Mostly associated with Down’s
syndrome.

15. Sinus venosus ASD
• 5 – 10 %
• Involves the portion of the atrial wall derived from the sinus venosus
– no direct communication between the right and left atria
• Typically at the orifice of SVC at the junction of the RA
• Less frequently in the region of the IVC
• Associated with partial anomalous pulmonary venous drainage
(PAPVD) – pulmonary drainage to RA instead of LA.

16. Coronary sinus ASD
• Defect in the roof of the
coronary sinus  direct
communication with the LA.
• Rare
• Usually associated with
complex CHDs.
• Divided into
• CSASD with LSVC
• CSASD without LSVC

17. Pathophysiology
• Moderate – to – large defects – Shunt of oxygenated blood flows from
L  R atrium
• Volume overload and dilation of the RA and RV
• Tricuspid and pulmonary annulus may dilate and become
incompetent
• Inc flow into the lungs  Irreversible pulmonary vascular injury
(Endothelial dysfunction and vascular remodelling) – Inc in PVR 
inverted shunt: R  L
• Eisenmenger syndrome (Cyanosis)

18. Clinical manifestation
• Asymptomatic
• Infants
• Recurrent chest infections
• FTT
• Older children
• Mild fatigue
• Dyspnea that may worsen with age
• Cyanosis

19. Physical examination
• Precordium
• Inspection
• Precordial bulge
• Palpation
• Prominent right ventricular heave felt along the lower left sternal border and
the subcostal area
• Auscultation
• Wide, fixed splitting of the S2
• ESM – Left 2nd
& 3rd
sternal border

20. Investigations
• Non – invasive
• Chest X-Ray
• ECG
• Echocardiography
• Invasive
• Cardiac catheterization

21. Chest X-ray
• Small shunt across the ASD – Normal CXR
• Large shunt –
• Cardiomegaly (RA and RV enlargement)
• Increased pulmonary vascular markings extending to the periphery

23. ECG
• Prolonged PR interval – due to enlargement of RA – 1st
degree heart
block
• Crochetage sign – notched R waves in inferior leads

24. Echo
• Diagnostic

25. Cardiac catheterization
• In whom pulmonary vascular resistance may be a concern.
• Diagnosing associated lesions i.e.
• PAPVD
• MS
• Direct measurement of intracardiac and pulmonary artery pressure
• PVR can be calculated

26. Management
• Medical therapy
• Interventional therapy
• Surgical therapy

27. Spontaneous closure
• In patients with an ASD < 3 mm in size diagnosed before 3 months of
age – 100% of patients at 1 ½ year of age.
• 80% in b/w 3 – 8 mm.
• Spontaneous closure uncommon after 1st
year.

28. Medical management
• Aim to reduce volume overload and to strengthen functions of heart
muscles.
• Symptomatic children:
• Diuretics – relieve ventricular overload, peripheral and pulmonary congestion
• Rate control and anticoagulation – Afib
• Anti hypertensives i.e. Captopril, to reduce afterload

29. Interventional therapy
• Trans-catheter device closure of ASD
• Indicated in:
• Secundum ASD with Qp:Qs ≥ 1.5:1
• 5 mm or more but less than 32 mm
• A significant L  R shunt with clinical evidence of RV volume overload
• There must be enough rim (~4 mm) of septal tissue around the defect for
appropriate placement of the device

30. • Contra-indication:
• Resting pulmonary HTN
• Failed attempted device closure
• No sufficient rim to engage the device
• Sinus venosus defect – device closure would threaten obstruction of
pulmonary veins, IVC and SVC
• Recent infection or sepsis/Bleeding disorders
• Pregnancy
• Intracardiac thrombi

31. • Devices available are:
• Amplatzer septal occlude
• Rashkind ASD occlude
• Cardioseal device
• HELEX
• PFOStar

33. Post device closure follow up
• Aspirin 5 mg/kg/day for 6 months
• F/U echo for:
• Device position
• Residual shunting
• Complications
• F/U echo at
• 24 hours
• 1 month
• 6 months
• 1 year

34. Complications of device closure
• Device misalignment/embolization
• Device erosion of atrial wall or aorta
• Device impingement on adjacent structures i.e. AV valve, Coronary
sinus, SVC
• Infection including endocarditis
• Thromboembolic complications
• Valvular regurgitation
• Residual shunt

35. Surgical closure
• Indications:
• When device closure is not considered appropriate
• CCF in infancy not responding to medical therapy
• Sinus venosus defect
• Secundum ASD + unfavorable anatomy not amenable to p/c closure;
• ASD Diameter > 35 mm
• Inadequate septal rims to permit device deployment
• Close proximity to AV valve, coronary sinus, or venae cavae
• Timing – Usually delayed until the patient is 2 – 4 years old (spont
closure !)

36. Set up
• Standard invasive monitoring and general anesthesia.
• Median sternotomy, heparinization at 300U/kg.
• Standard aorto-bicaval venous cannulation, and patient cooled to 30–
32oC. Antegrade cardioplegia.

37. Secundum ASD
• Primary closure
• Because of the oval shape of most
secundum defects, 80 per cent
can be closed by the primary
suture technique. A double layer
of polypropylene is begun at the
inferior limit of the defect, as this
margin is typically most difficult to
define. Before complete closure of
the defect, entrapped air should
be evacuated from the left atrium.

38. • Patch closure
• If the defect is large or rounder in shape, patch closure should be performed to avoid closure
under tension and distortion of atrial anatomy. A patch of autologous pericardium that is slightly
smaller than the relaxed size of the defect can be used, again beginning the suture line inferiorly.
Polytetrafluoroethylene, Dacron, and bovine pericardium are also suitable patch materials.

39. Sinus venosus defect
• The ASD is generally more superior and posterior than the typical
secundum ASD. The right upper pulmonary veins typically drain into
the junction of the SVC and right atrium.
• Occasionally, multiple veins drain the right upper lobe and may enter
the SVC some distance from its atrial junction.
• Careful circumferential dissection of the SVC allows identification of
these anomalous venous connections for cannulation site selection
and planning of the repair.
• Injury to the right phrenic nerve must be avoided during dissection of
the lateral aspect of the SVC.

40. Baffle repair
• If the pulmonary veins drain to the cavoatrial junction area, baffle repair of the defect using a
pericardial patch is performed.

41. • Patch is sutured from the lower edge of the septal
defect, transitioning up and around the superior edge
of the highest pulmonary vein to direct the flow of
pulmonary venous blood through the septal defect to
the left atrium.
• The patch should be slightly redundant to avoid
obstructing this pathway, especially when it is
extended up the vena cava for more than a few
millimeters

42. Warden repair
• If pulmonary veins enter some
distance up the SVC
• or if the right SVC is unusually small as
seen in the presence of a persistent
left SVC, the so-called Warden repair is
performed,
• directing the lower SVC flow through
the septal defect, with translocation of
the upper SVC to the right atrial
appendage.

43. Thank you