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1. Atrial Septal Defects
By: Dr Richa Malik
Moderator: Dr Ajay Kumar

2. HISTORY
Leonardo da vinci describes the patent foramen ovale. “I have found from a, left auricle, to b
right auricle, like perforating channel from a to b”
1875
Karl Von Rokitansky provided a superb account of the pathological anatomy of atrial septal
defect together with its embryological basis
1921 Assmann described radiological features of ASD
1934
Roesler analysed 62 recorded necropsy cases of ASD in which only one was diagnosed
during life
1941 Bedford et al defined the clinical features of ASD
1955 Hudson described normal and abnormal interatrial septum
1979 Sweeney and Rosenquist – normal and abnormal interatrial septum was redefined

3. Introduction
• An atrial septal defect (ASD) is a hole of variable size in the
atrial septum.
• Atrial septal defect (ASD) is detected in 1 child per 1500
live births, and accounts for 5-10% of congenital heart
defects.
• ASDs make up 30-40% of all congenital heart disease
detected in adults (second only to bicuspid aortic valve).
• ASDs occur in women 2-3 times as often as men.

4. Introduction
• ASDs can occur in different anatomic portions of
the atrial septum.
• ASDs can be isolated or occur with other
congenital cardiac anomalies.
• Functional consequences of ASDs are related to
the anatomic location of the defect, its size, and the
presence or absence of other cardiac anomalies.

5. Embryology

7. This sequence of atrial septation given by- Van Meirop.
Septum secundum forms- limbus of fossa ovalis; septum
primum forms- valve and the channel for interatrial blood
flow thr os.sec-k/a-foramen ovale -persists in fetal life.
Functional closure postnatally -LAP>RAP
d/t increase in LAP, valve of fossa ovalis gets pressed
against limbus- competent seal
Ist yr of life- fibrous adhesions between limbus and valve,
permanent anatomical closure

8. Classification
• Primum ASD
• Secundum ASD
• Sinus venosus defects
• Coronary sinus defects
• Patent foramen ovale
• Common Atrium

9. Primum ASD
• Make up ~15% of all ASDs.
• Occur if the septum primum does not fuse with the endocardial cushions,
leaving a defect at the base of the interatrial septum that is usually large.
• Usually not isolated – primum ASDs are typically associated with
anomalies of the AV valves (such as cleft mitral valve) and defects of the
ventricular septum (VSDs) or a common AV canal.

10. Secundum ASD
• Make up ~70% of all ASDs.
• Occur twice as often in females.
• Typically located within the area bordered by the limbus of
the fossa ovalis. • Defects vary in size, from <3 mm to >20
mm.

11. Secundum ASD
• May be associated with other ASDs.
• Multiple defects can be seen if the floor of the fossa ovalis (AKA valve of the
foramen ovale) is fenestrated.
• Ten to twenty percent have a functional mitral valve prolapse -
May be related to changing LV geometry associated with RV volume overload

12. Sinus venosus ASD
• Make up ~10% of ASDs, posterior and superior to fossa ovals
• Characterized by malposition of the insertion of the SVC or
IVC straddling the atrial septum.
• Often associated with anomalous pulmonary venous return –
the RUL/RML pulmonary veins may connect with the junction of
the SVC and RA in the setting of a superior sinus venosus
ASD.

13. Coronary Sinus Septal Defects
• Less than 1% of ASDs, inferior and anterior to fossa ovals
• Defects in the inferior/anterior atrial septum region that includes the
coronary sinus orifice.
• Defect of at least a portion of the common wall separating the
coronary sinus and the left atrium – AKA “unroofed coronary sinus”
• Can be associated with a persistent left SVC draining into the
coronary sinus.
• Can be associated with Complete atrioventricular septal defect with
asplenia syndrome

14. Patent Foramen Ovale
•Not truly an “ASD” because no septal
tissue is missing.
•Oxygenated blood from the IVC crosses
the foramen ovale in utero.
•At birth, the flap normally closes due to •
Reduced right heart pressure and PVR
• Elevated LA pressure.
•Flap fusion is complete by age two in
70-75% of children; the remainder have
a PFO.

15. Scimitar syndrome
• rare anomaly characterized by connection of all of
the right pulmonary veins into the inferior vena cava.
• The ipsilateral lung and pulmonary artery are usually
hypoplastic.
• The syndrome rarely involves the left lung.
• The term scimitar refers to a radiologic shadow that
resembles the shape of a Turkish sword.

16. Pathophysiology of ASD
• in utero interatrial flow is normally from right to left through a patent
foramen ovale
• At birth, there is little or no shunt in either direction across an atrial
septal defect because the compliance of the right and left ventricles is
virtually identical.
• When the defect is restrictive, size per se determines the magnitude of
the shunt
• When the defect is nonrestrictive, there is no pressure difference
between the right and left atrium, so shunt volume is determined by the
relative compliance of the two ventricles.

17. • Factors for L R shunt : R chamber compliance
1. RA COMPLIANT
2. TV - larger
3. RV –compliant, thin walled as muscle growth is less rapid than LV
4. PVR RV stroke volume.
RV tolerates extra vol load quite well as it handle large vol at low ejection pressures
5. Qp / Qs > 3:1 --> case of PDA, AS, CoA, VSD (L A enlargement - Foraman ovale
is stretched and incompetent)
RV tolerates VOLUME OVERLOAD, while LV tolerates PRESSURE OVERLOAD

18. Changes due to left to right shunt
Hypertensive proximal pulmonary arteries dilate aneurysmally and contain mural
calcification and intraluminal thrombi that can be massive and occlusive. Fibrosis of
PA lead to high PAH
•the right ventricle is volume overloaded and the left ventricle is volume
underloaded which displaces the ventricular septum into the left ventricular cavity,
reducing its size and changing its shape from ovoid to crescentic.
•volume overload of the right atrium provokes atrial fibrillation and atrial flutter,
which further increase the left-to-right shunt and result in heart failure
•Superior systolic displacement of the mitral leaflets (mitral valve prolapse) occurs
because leaflets with normal area and chordal length are housed in a left
ventricular cavity that is reduced in size and abnormal in shape
•coronary reserve is compromised in the volume-overloaded right ventricle if the left
main coronary artery is compressed by a dilated pulmonary trunk

19. Patterns of shunting
1. Effect of respiration
- Inspiration : Intrathoracic negative pressure, Increases venous return to RA and decrease
return to LA
In valsalva maneuvre - decrease venous return and increase peripheral pooling
2. Effect of cardiac cycle
• The shunt reaches its peak in late systole and early diastole;
• it diminishes throughout diastole
• In late diastole, it is supplemented by atrial contraction
3. Pattern of blood flow
Pulmonary blood flow that is received by the right pulmonary veins is channelled into the right
atrium because of proximity of the right pulmonary veins to the rim of the atrial septal defect.

20. 4. Effect of posture
- Erect - venous pooling --> decrease IVC return
- Recumbent —> increase IVC flow --> R-L
shunt
5. ASD patients have good exercise tolerance

21. NATURAL HISTORY
< 1 Year
Spontaneous closure
Death uncommon < 0.1%
10 - 20
Years
Usually asymptomatic
- 13% have Pulmonary Hypertension
- - 9% have Eisenmengers
30 Years
80 - 86 % asymptomatic
4% may have Rheumatic disease of Mitral valve
> 40
Years
Pulmonary Hypertension 6 – 14%
Arrhythmias
Eisenmengers
CCF

22. Natural History of ASDs
• Most ASDs <8mm close spontaneously in infants.
• Spontaneous closure is unusual in children and adults; defects often
become progressively larger.
• Most patients with a significant shunt flow ratio (Qp:Qs > 2:1) will be
symptomatic and require closure by age 40.
• Increasing size of the ASD may preclude percutaneous closure.
• Weight is more affected then height
• Association
A. • Holt oram syndrom
B. • Patau’s syndrome , Edward’s syndrome

23. Natural History of ASDs
• Life expectancy is not normal, though many patients live to
advanced age.
• Natural survival beyond age 40-50 is <50%.
• The attrition rate after age 40 is ~6% per year.
• Advanced pulmonary hypertension seldom occurs before the
third decade.
• Atrial fibrillation is a late complication; stroke is a potential
complication of ASD (ongoing investigation into this issue).

24. Clinical Manifestations
•Children may be asymptomatic; may have easy
fatigability, exertional dyspnea. Underdeveloped, more
prone to respiratory infections.
•Most patients with shunt flow ≥ 2:1 will be symptomatic
and require correction by age 40.
•large left-to-right shunt is responsible for a decrease in
pulmonary compliance and an increase in the work of
breathing

25. Clinical Manifestations
Risk of atrial arrhythmias increases with age
and PA pressure.

26. Physical Exam Findings
•Prominent Jugular venous pulse
•Wide, fixed splitting of S2 (delayed closure of pulmonic valve with
reduced respiratory variation)
•Midsystolic pulmonary flow or ejection murmur
Usually over 2nd intercostal space
Peaks in early-to-mid systole, ends before S2
•Palpable RV heave
•Mid-diastolic murmurs are the result of augmented tricuspid flow.

27. Pregnancy and ASD
• Despite the gestational increase in cardiac output and stroke volume,
young gravida with an atrial septal defect generally endure pregnancy,
even multiple pregnancies, without tangible ill effects.
• However, brisk hemorrhage during delivery provokes a rise in
systemic vascular resistance and a fall in systemic venous return, a
combination that augments the left-to-right shunt, sometimes
appreciably.
• There is also a peripartum risk of paradoxical embolization from leg
veins or pelvic veins because emboli carried by the inferior vena cava
traverse the atrial septal defect and enter the systemic circulation.

28. ECG Findings
• Right atrial enlargement d/t vol overload (tall P wave)
• The P wave axis with an ostium secundum atrial septal defect is inferior and to the left with upright P
waves in leads 2, 3, and aVF
• RVH – RAD, rSR’ in V1, R>S in V1.
• Atrial tachyarrhythmias – a.fib, atrial flutter
• AV delay – often with primum ASD in association with LAFB and RBBB (the rim of an ostium primum
defect is near the His bundle).
• A notch near the apex of the R waves in inferior leads 2,3 and aVF of ostium secundum and sinus
venosus atrial septal defects has been called crochetage.

29. Chest X-Ray Findings
• Dilation of RA and RV
• Enlarged main pulmonary
arteries and pulmonary vessels,
without redistribution to apical
vessels.
• Left atrial enlargement if
associated mitral regurgitation.
• enlarged main pulmonary
artery with oligemic lung fields in
c/o PAH

30. Echocardiography and ASDs
• Some clues to the presence of ASD:
Abrupt discontinuity of the septum, and slight thickening at its termination
RA enlargement, RV enlargement/dilation
Dilated pulmonary arteries
Increased flow velocity in the PA and across TV
Paradoxical motion and diastolic flattening of the ventricular septum
• TTE is usually definitive in secundum ASDs.
• TEE will help with sizing defects, and identifying sinus venosus defects.

31. Two-Dimensional TTE
Apical four-chamber view
Can often see ostium primum ASD in this view.
Shadowing and echo dropout (especially in the
area of the fossa ovalis) may lead to false
positives.
Subcostal view
• Often more reliable - can visualize entire atrial
septum.
• Sensitivity for ASD detection:
1. Primum ASD: 100%
2. • Secundum ASD: 89%
3. Sinus venosus ASD: 44%

38. Color Doppler TTE
• Can confirm the presence of the
ASD, estimate the defect size,
and evaluate the efficacy of
surgery.
• Flow extends from mid-systole
to mid-diastole; second phase of
flow coincident with atrial systole.
• May have brief R-L shunting. •
Usually not a high velocity jet.

39. Contrast Echo
•Administer agitated saline contrast through IV- into central or arm vein
•Apical four-chamber view is usually optimal.
•Bubbles in the LA suggests right-to-left shunting -POSITIVE STUDY
at the atrial level if 3 bubbles within 3 cardiac cycles following complete
opacification of the RA. Delayed bubbles may be due to pulmonary AVMs – may
be less phasic in appearance ( FALSE POSITIVE).
•Large ASDs may have nearly continuous shunting, but smaller ASDs may be
more phasic with respiration.
•May see “negative contrast effect” if mainly left-to right shunt- non-contrast
blood appears in the contrast filled RA( NEGATIVE STUDY).

40. Transesophageal Echo
•TEE is superior to TTE in visualizing the interatrial septum and
identifying all types of ASDs.
•With contrast or Doppler, TEE can detect any brief right-to-left
shunting that may occur with transient increases in right-sided
pressure.
•TEE is much more sensitive than TTE for detection of left-to-right
shunt as negative right atrial contrast (93% vs. 58% in one study).
•TEE can detect flow through multiple ASDs.

41. Transesophageal Echo
•Estimation of defect size using the diameter of the Doppler color flow jet correlates
with surgical findings.
•Since ASDs are not necessarily round, TEE helps with determining both their size
and shape. This is especially important when percutaneous closure is being
contemplated.
•FOUR Rims of ASD :
•Posterosuperior ( SVC rim): ME bicaval view
•Posterior rim: ME 4 chamber view
•AV Rim ( Anterosuperior rim) : ME AV SAX view
•Anteroinferior rim : ME 4 chamber view

42. Transesophageal Echo

43. Estimation of Shunt Flow Ratio
•Operative closure of an ASD traditionally recommended
when the ratio of pulmonary blood flow to systemic blood
flow (Qp/Qs) is greater than 1.5:1 or 2:1.
•Can estimate Qp/Qs from TTE measurements using
Pulsed Doppler echocardiography. Cardiac MR is also
useful for further assessment of Qp/Qs ratio.
•Correlation between Doppler imaging and cardiac
catheterization techniques for this measurement is good.

44. Estimation of Shunt Flow Ratio
•First measure stroke volume through each valve:
Stroke Volume (Q) = CSA x VTI
•Left-sided stroke volume is measured from LVOT (diameter measured in
parasternal long axis view).
•Maximum Doppler flow velocity apical to aortic valve (VTILVOT) taken in
apical four-chamber view.
•Right-sided velocity time integral (VTIPA) measured in PA well before
bifurcation.
•PA diameter measured at the same level as VTIPA.

45. Estimation of Shunt Flow Ratio
•Substitution into stroke volume ratio gives:
Qp/Qs = (PAdiam)2 x VTIPA
-------------------------------------
(LVOTdiam)2 x VTILVOT
• Diameters of LVOT and PA are squared – exact measurement of these
values is especially important.
• PA diameter can be difficult to assess in some patients; this is the term
that is most often responsible for inaccurate estimates of the shunt ratio.

46. Estimation of Shunt Flow Ratio By
Cath Data
Qp = O2 consumption
-----------------------------
(PVO2- PAO2) * Hb * 13.6
Qs = O2 consumption
-----------------------------
(SAO2- MVO2) * Hb * 13.6
PVR = PA Pressure – LA
----------------------
Qp
SVR = Systemic Pressure – RA
------------------------------
Qs

47. Indications for Defect Closure
• 1.) Symptoms
• Exercise intolerance, fatigue, dyspnea, heart failure
• Atrial tachyarrhythmias?
Occur in 20% and often the presenting symptom
Not an indication by itself (incidence may not be
reduced after surgery).

48. Indications for Defect Closure
• 2.) Defect Size and Qp/Qs
• Larger ASDs impose a greater hemodynamic burden on the RV.
• In the absence of pulmonary hypertension, Qp/Qs is closely correlated with the
size of the ASD.
• Qp/Qs > 2:1 is a well-established indication, though many authors advocate
1.7:1 or even 1.5:1.
• AHA recommends a threshold Qp/Qs ≥ 1.5:1, but these guidelines exclude
patients > 21 years of age.
• Canadian Cardiac Society recommends Qp/Qs >2:1, or >1.5:1 in the presence
of reversible pulmonary hypertension.

49. Surgical Closure
•Median sternotomy is the traditional approach
•minimally invasive approaches- partial sternotomy, mini-
incision, anterolateral 4th interspace thoracotomy- are
emerging- only cosmetic benifits, no improvement in surgical
morbidity.
•Pericardial or Dacron patches are used.
•Primary closure of the defect is not recommended.
•Can repair other defects at the same time (such as cleft mitral
valve if primum ASD).

50. In sinus veNosus ASD, patch closure+ baffle anomalous
PV to LA
2 PATCH technique- one pericardial patch to baffle PV and
other to augment SVC-RA Jxn to avoid SVC obstruction
WARDEN procedure- when PV drain into high SVC- SVC
divided above PV entry, CARDIAC END containing PV is
baffled close to LA and remaining SVC reattached to RAA

51. In CORONARY SINUS ASD, if no LSVC- patch
closure of CS orifice. CS drains into LA, causing
minimal cyanosis
LSVC +nt -CS covered in LA, and the osmium is
allowed to drain in RA
If bridging vein +nt- LSVC ligation
+ patch closure of CS orifice

52. Right Sided Maze
In patients with preoperative documented
Atrial Flutter
Biatrial maze procedure- arrythmias having
both right and left sided component
Adds very little time to operation

53. Contraindications for Sx
Irreversible pulmonary hypertension
mPAP > 10U/m2, >7U/m2 with vasodilators
PVR > 2/3 rd of SVR
PAP > 2/3 rd of systemic pressures
Qp:Qs < 1.5:1
Lung biopsy with Heath Edwards > II
Biventricular end stage heart failure

54. •ANAESTHETIC MANAGEMENT
• Premedication
• Light premedication is given.
Morphine 0.1-0.2mg/kg , Fentanyl 1-2 ug/kg ,
Benzodiazepenes can be given ( reduce dose of morphine)
Midazolam 0.05-0.1 mg/kg
Avoid dehydration
Avoid 100% O2 - l/t decrease in PVR, increase in left to right shunting
Avoid any Air during IV injection
• Connect iv line with running fluid • Syringe should be up right

55. • Monitoring
• ECG, IBP, Spo2, capnography, temperature
• Invasive monitoring-
-Direct arterial pressure
-CVP- measure loading conditions and means of transfusing
inotropes/vasodilators
- Do Direct LA pressure monitoring whenever there is MR pre and
post surgery.

56. • ANAESTHETIC MANAGEMENT
• Induction
• In left to right shunt inhlation induction will be accelerated.
• So sevoflurane up to 3-5% can be used
• Avoid halothan and isoflurane because of myocardial depressant action
• Or use IV inductin agents like ketamine, propofol, etomidate
• Midazolam, Narcotic( morphine 0.5mg/kg or Fentanyl 5-10 ug/kg)
•Muscle relaxants- Vecuronium + Narcotics-
• Avoid atracurium- histamine release

57. • Maintainence
• A balanced anesthesia that includes low
concentrations of a volatile anesthetic is desirable.
Avoid halothane- arrythmogenic
• Isoflurane(tachy cardia),Sevoflurane(ideal).
• Intraoperative fluid replacement must be done
adequately to maintain hydration.

58. WEANING FROM CPB
Deair of heart should be done properly and if possible under TEE guidance
•Before the last few stitches are pulled up, a clamp or tissue forceps is placed in
the aperture, and the anesthesiologist inflates the lung to expel any air from the
left atrium. The suture line is snugged while lung inflation is maintained, and an
additional bite is taken with the stitch, which is then tied.
•After the right atrium is sucked dry, once again the lungs are inflated to drive
through left atrial blood and thus identify any defects in the suture line.
•left atrial pressure is measured at this time (or estimated by palpation of the
pulmonary artery) and noted to be 5 to 15 mmHg higher than right atrial
pressure. This increase is related to small size and decreased compliance of the
LV compared with that of the RV.

59. Rx of right ventr dysfxn or
pulmonary hypertension
Adequate sedation and paralysis
pH>7.45: hyperventilation for target PCO2 = 25 to 30mm Hg, Bicarbonate
iv
Arterial O2 saturation approx 100%
Adequate RV vol loading with CVP=15 TO 18mmHg
Prevent and treat lung disease/lesions, atelectasis, pneumonia, pulmonary
oedema
Pulmonary vasodilators: SNP, NTG, Milrinone/ Amrinone, PGE1, NO
Inotropic support : Dobutamine, Milrinine/ Amrinone

60. Post operative
management
• left atrial pressure is routinely monitored intraoperatively and for about 24 hours
postoperatively in older patients.
• Occasionally, when mitral regurgitation has been underestimated preoperatively
and there are signs of severe pulmonary venous hypertension postoperatively, an
urgent echocardiographic study may be required.
• With proper use of anesthetic agent, can be extubated in OT or within 4 hrs in
ICU.
• All patients over age 35 years at operation receive sodium warfarin
prophylactically beginning on the evening of the second postoperative day and
continuing for 8 to 12 weeks after repair.
• Endocarditis prophylaxis is used for 6 month a/f Sx

61. Post-operative
Complication
• LV Dysfunction
• Air Embolism
• Pulmonary vascular disease
• Ventricular dysfunction
• Arrhythmic events
• Thromboembolism
• reintrvention
• Postpericardiotomy syndrome and effusions- associated with Ist 6weeks a/f Sx

62. Percutaneous Closure
•An alternative to surgical closure for secundum ASDs ,PFO with appropriate
anatomic characteristics.
1. Defect < 30mm diameter(32MM for Amplatzer septal occluder, 18mm for
HELEX septal occluder).
2. Prefer a rim of tissue at least 4mm around the defect to prevent obstruction
of coronary sinus, R pulmonary veins, vena cavae, or AV valves.
3. Weight > 15kg - for technical reasons
•Approximately half to two-thirds of secundum ASDs in adults meet these
criteria.

63. Amplatzer Occlusion Device
•Introduced in 1996.
•Approved for percutaneous ASD
closure in 2001 by F.D.A.
•Over 90,000 have been
manufactured and delivered to date.
•Consists of two round disks made of
Nitinol (nickel + titanium) wire mesh
linked together by a short connecting
waist.

64. Amplatzer Occlusion Device
Advantages over surgery:
• Can be delivered through smaller catheters
• It is self-centering but can be repositioned
easily
• Has round retention disks that extend
radially beyond the defect, which results in a
much smaller overall size and firmer contact
with the atrial septum
• Shape enhances endothelialization and
reducing the risk of residual shunting

65. Amplatzer – deployment of right
atrial disc

66. Anesthesia for Percutaneous
closure
•Controlled ventilation should be preferred
•Airway anesthesia
•TEE guidance to cardiologist
•LA Pressure measurement
•Avoid any Air during IV injection

67. Percutaneous Closure -
Complications
•Early complications
A. Device embolization or malposition requiring surgery (2.4%)
B. Atrial fibrillation (2.4%)
C. Heart block, effusion, thrombus in LAA (2.2%)
•Thrombus formation (both in LA and RA)
1. Need aspirin and plavix for at least 6 months
•Rare complications: cardiac perforation, sudden death
•Long-term complication: device erosion (0.1% of cases) – risk factors include deficient
aortic rim , deficient superior rim, and oversized device.
• Allergic reaction to NICKEL released from device( peak at 1 month)

68. Cryptogenic Stroke Risk?
• Data are widely conflicting on the relationship between PFO, atrial septal aneurysm,
and/or ASD and recurrent cerebral emboli.
Increased prevalence of PFO and cryptogenic stroke; less clear for ASD.
• The role of defect closure vs. medical therapy for prevention of recurrent stroke is not
well defined.
• Aspirin is often used in setting of PFO or an isolated atrial septal aneurysm, and
especially if PFO + ASA.
Role of coumadin is not as clear – coumadin recommended if patient has a documented
DVT/PE. Less data available for ASDs.
• Surgical excision of an atrial septal aneurysm (without PFO or ASD) may be
considered if aspirin or coumadin fail to prevent a recurrent embolic event.

69. Recommendations for Transcatheter
Device Closure of Secundum ASD

71. THANK YOU FOR YOUR
PATIENCE