Atrial septal defects (ASDs) are holes in the atrial septum that allow blood to pass from the left to the right atrium. There are several types of ASDs that can occur in different locations in the septum. Over time, the excess blood flow to the right side of the heart can lead to enlargement of the right atrium and ventricle, pulmonary hypertension, and heart failure if left untreated. Echocardiography is the primary imaging test used to diagnose ASDs and estimate the size of shunting. Small ASDs may close on their own, but larger defects often require closure via catheterization or surgery to prevent long term complications.

1. Atrial Septal Defects
Dr. Harshil Joshi
DM Cardiac Anesthesia Resident
UNMICRC

2. 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”
Sweeney and Rosenquist – normal and abnormal interatrial septum was redefined1979
Hudson described normal and abnormal interatrial septum1955
Bedford et al defined the clinical features of ASD1941
Roesler analysed 62 recorded necropsy cases of ASD in which only one was diagnosed
during life
1934
Assmann described radiological features of ASD1921
Karl Von Rokitansky provided a superb account of the pathological anatomy of atrial
septal defect together with its embryological basis
1875

3. Introduction
• An atrial septal defect (ASD) is a hole of variable size in the
• atrial septumAtrial 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. Classification
• Primum ASD
• Secundum ASD
• Sinus venosus defects
• Coronary sinus defects
• Patent foramen ovale
• Common Atrium

8. 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.

9. 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.

10. 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

11. Sinus venosus ASD
• Make up ~10% of ASDs.
• 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.

12. Coronary Sinus Septal Defects
• Less than 1% of ASDs
• 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.

13. 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.

14. 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.

15. 15
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.

16. • 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)
PATHOPHYSIOLOGY …. Contd ……
RV tolerates VOLUME OVERLOAD, while LV tolerates PRESSURE OVERLOAD

17. 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
•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
•which displaces the ventricular septum into the left ventricular cavity,
reducing its size and changing its shape from ovoid to crescentic.
•thickening and fibrosis of mitral leaflets and chordae tendineae
•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

18. 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.

19. 19
4. Effect of posture
- Erect - venous pooling --> decrease IVC return
- Recumbent --> increase IVC flow --> R-L shunt
5. ASD patients have good exercise tolerance

20. 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

21. 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
• Holt oram syndrome
• Patau’s syndrome
• Edward’s syndrome

22. 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).

23. 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

24. Clinical Manifestations
• Platypnea-orthodeoxia is a rare syndrome characterized by
orthostatic provocation of a right-to-left shunt across an atrial
septal defect or a patent foramen ovale.Platypnea (dyspnea
induced by the upright position and relieved by recumbency)
and orthodeoxia (arterial desaturation in the upright position
with improvement during recumbency) are features of this
rare disorder
• Risk of atrial arrhythmias increases with age and PA
pressure.

25. Physical Exam Findings
•Arterial Pulse
•Jugular venous puls
•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.

26. 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.

27. 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
secundumand sinus venosus atrial septal defects has been called crochetage.

28. 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.
• Ascending aorta is seldom border
forming because the intracardiac
shunt does not traverse the aortic
root

29. 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.

30. 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:
• Primum ASD: 100%
• Secundum ASD: 89%

31. 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.

32. Contrast Echo
•Administer agitated saline contrast through IV.
•Apical four-chamber view is usually optimal.
•Bubbles in the LA suggests right-to-left shunting
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.
•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.

33. 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.

34. 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.
•Five Rim of ASD
•Posterosuperior
•Posterior
•AV Rim
•SVC and IVC Rim

35. TEE

36. 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.

37. 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.

38. 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.

39. 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

40. Indicator Dilution Method
•More Sensitive for smaller shunts
•Cannot localize the level of left to right shunt
•Left to Right : Dye (indocyanine green) is injected
into pulmonary artery and a sample is taken from the
systemic artery
•Right to Left: dye injected just proximal to the
presumed shunt and blood sample is taken from
systemic artery

41. Interpretation of Indicator Dilution
Method

42. 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).

43. 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.

44. Surgical Closure
•Median sternotomy is the
traditional approach
•minimally invasive approaches are emerging.
•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).

45. • ANAESTHETIC MANAGEMENT
• Premedication
• Light premedication is given.
Morphine 0.1-0.2mg/kg
Fentanyle 1-2 ug/kg
Benzodiazepenes can be given ( reduce dose of morphine)
Midazolam 0.05-0.1 mg/kg
Avoid dehydration
Avoid 100% O2
Avoid any Air during IV injection
• Connect iv line with running fluid
• Syringe should be up right

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

47. • 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
• 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
.

48. • 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.

49. 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.

50. 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.
• 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.

51. Post-operative
Complication
• LV Dysfunction
• Air Embolism
• Pulmonary vascular disease
• Ventricular dysfunction
• Arrhythmic events
• Thromboembolism
• reintrvention

52. Percutaneous Closure
•An alternative to surgical closure
for secundum ASDs with
appropriate anatomic
characteristics.
• Defect < 30mm diameter
• Prefer a rim of tissue at least 5mm
around the defect to prevent
obstruction of coronary sinus, R
pulmonary veins, vena cavae, or AV
valves.
•Approximately half to two-thirds
of secundum ASDs in adults
meet these criteria.

53. 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.

54. 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

55. Amplatzer – deployment of right
atrial disc

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

57. Percutaneous Closure - Complications
•Early complications
• Device embolization or malposition requiring surgery (2.4%)
• Atrial fibrillation (2.4%)
• Heart block, effusion, thrombus in LAA (2.2%)
•Thrombus formation (both in LA and RA)
• 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 (25/28
cases), deficient superior rim, and oversized device.

58. 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.

59. ACC/AHA 2008 Guidelines for the
Management of Adults
With Congenital Heart Disease

65. Recommendations for Transcatheter Device
Closure of Secundum ASD

67. Thank You!