3. HISTORY
Galen - foramen ovale and normal postnatal closure
Leonardo Da Vinci- Described ASD in
human autopsy
specimen
4. Murray(1948) - external suturing
Charles Bailey - atrioseptopexy
Tyge sondergard – purse string external
suture
Gross(1950) - atrial – well technique
Lewis and Taufic(1953) -inflow – occlusion
technique with surface cooling and
circulatory arrest
1st successful open heart ASD closure
5. Gibbon(1953) - first time used
CPB to close ASD
Mills and King -Device closure of
(1974) ASD
6. EMBRYOLOGY
Embryologically, the septum primum
separates the two atria first, moving inferiorly
toward the endocardial cushions.
The ventricular septum forms by moving
upward from the ventricles to the endocardial
cushions at the same time.
If the atrial septum does not make it all the
way, the residual defect in the septum
primum (ostium primum) results in the
primum ASD.
7. •If the septum primum makes it all the
way, a hole or holes (fenestrations) form
in the middle of the septum (forming the
ostium secundum).
• A second septum then moves down the
right side of the first and normally covers
the ostium secundum hole.
• If it does not cover the hole, a
secundum ASD is present.
8. The septum secundum normally
completely covers the right side of the atrial
septum except for an ovale hole in it (the
foramen ovale). If the septae do not fuse, a
patent path from the RA to the LA persists
(the patent foramen ovale PFO).
9. The most common form of ASD (80%
of cases) is persistence of the ostium
secundum in the mid septum; less
commonly, the ostium primum (which is
low in the septum) persists
14. OSTIUM SECUNDUM ASD
Results either from shortening of the valve of the
foramem ovale,excessive resorption of the septum
primum or deficient growth of septum secundum
Mc type
50-70% of all ASD
APVC is present in 10% case
Female to male ratio – 2 : 1
15. Located in the region of fossa ovalis bounded by
limbus anteriorly, superiorly, and posteriorly
16. OSTIUM PRIMUM ASD
REPRESENT ABSENCE OF THE
ATRIOVENTRICULAR SEPTUM
30% of all ASD
17. Ostium Primum
Next most common type
Located in the lower portion of
the atrial septum.
Will often have a mitral valve
defect associated with it called a
mitral valve cleft.
A mitral valve cleft is a slit-like or
elongated hole usually involves
the anterior leaflet of the mitral
valve.
18. Sinus Venosus
Least common type of ASD
Located in the upper portion of the
atrial septum.
Association with an abnormal
pulmonary vein connection
Four pulmonary veins, two from the
right lung and two from the left lung,
normally return red blood to the left
atrium.
Usually with a sinus venosus ASD, a
pulmonary vein from the right lung
will be abnormally connected to the
right atrium instead of the left
atrium.
This is called an anomalous
pulmonary vein.
..asd-veno.jpg
20. CORONARY SINUS DEFECT
Part of unroofed coronary sinus syndrome
Uncommon
Opening in the wall of distal end of coronary sinus or
unroofing caused by absence of the partition b/w the
coronary sinus and lt atrium.
Accompanied by a left SVC
21.
22. POSTERIOR DEFECT
POSTERIOR AND INFERIOR PART OF ATRIAL
SEPTUM
WITH ABSENCE ,HYPOPLASIA OR ANT.
DISPLACEMENT OF POS. LIMBUS
23. CONFLUENT DEFECT
A confluence of two defects
Fossa ovalis defect with absence of posterior
limbus
Fossa ovalis and coronary ASD
24. Redundancy of the valve of the
foramen ovale can result in an atrial
septal aneurysm.
Respiratory excursion greater then 10
mm.ASA 2-4 % normal population and
70% of cases are associated with a PFO.
25. Patent foramen ovale
Remnant of fetal circulation
Beneath superior limbus, between it and floor of fossa
ovalis
Behaves like flap valve
26. Failure of septum primum and septum secundum
to fuse
1. valve competent “ probe patent “ PFO
2.valvular incompetence with or without an
aneurysm of septum primum component
Incidence at birth (full – term ) - 60%
Incidence in normal adult heart - 25% - 30%
Paradoxical emboli
27. Partial anomalous pulmonary venous connection exist
when one or more but not all pulmonary vein connect
anomalously to the rt atrium.
Total anomalous pulmonary venous connection
applies when all four pulmonary vein connect
anomalously to the rt atrium either directly or
indirectly.
10-15% OS ASD are associated with partial anomalous
PVC.
28. 80-90% SVC sinus venous defect are associated with
anomalous connection of rt sup pulmonary vein to rt
atrium or SVC.
Approximately 90% of PAPVC join the rt upper and
middle lobe pulmonary vein to the rt atrium and SVC.
Anomalous connection of lt pulmonary vein is far less
prevalent (about 10% ) as anomalous connection of rt
pulmonary vein.
b/l partial anomalous pulmonary venous connection
rare.
29. A. rt pulmonary vein
drain into SVC with
sinus venosus ASD
B . rt inferior pulmonary
vein drain in to IVC
C.lt pulmonary vein
drain into lt innominate
vein
D . Lt pulmonary vein
drain into coronary sinus
30. The scimitar syndrome
Described by Chassinat in 1836
Rare anomaly
Characterized by connection of all of the rt pulmonary
vein to inferior vena cava and usually by hypoplasia of
the ipsilateral lung and pulmonary artery.
X ray shadow that resembles the shape of Turkish
sword .
Rarely involve lt side.
31. Lower portion of rt lung perfused by
systematic artery from abdominal aorta.
Associated anomalies
ASD
aortic coarctation
left sided superior vena cava.
32. A –rt pulmonary vein
converge to form a
vascular trunk that drain
in to inferior vena cava
B – levophase following
injection of contrast
material into pulmonary
trunk shows the
common pulmonary
venous channel
C- Turkish sword
33. ASD: Associated cardiac anomalies
ASD must for survival in TGA, TAPVC, and Tricuspid
atresia
PAPVC
VSD-18%
PDA
PS -31%
AS
MS 29%
COA
35. Cardiac chambers in ASD
RT atrium enlarged and thick walled.
RV diastolic size increased.
Normal RV diastolic dimension are b/w .6 and 1.4 cm/
m2. in pt with atrial level large lt to rt shunts average
2.66cm/m2 ,may be large as 4 cm/m2.
Cardiac apex often formed by the RV.
LV normal or slightly decrease in size .
36. Mitral valve and ASD
Mitral valve abnormalities consist of thickening and
fibrosis of leaflets and chordae tendinae attributed to
traumatic cusp movement resulting from left
ventricular deformity.
Mitral prolapse
- prevalence of prolapse is about 20%. Increasing with
age and magnitude of pulmonary to systematic blood
flow ratio (Qp/Qs)
- Schreiber and colleagues have clarified a previously
confused subject by relating mitral valve prolapse to
abnormalities of LV shape in pt with ASD .
37. Mitral regurgitation
-prevalence of severe mitral regurgitation 2-
10%.
Cleft mitral leaflets
-cleft anterior and posterior leaflets that
cause mitral regurgitation are reported to
occurs occasionally.
38. Lung and pulmonary vasculature
Pulmonary artery dilated which tend to compress the
smaller airway which result retention of secretion and
bronchiolitis.
Hypertensive pulmonary vascular disease develops
infrequently in pt with ASD , usually not until the
third or forth decade of life.
This contrast sharply with VSD ,complete AV septal
defect and PDA in which pulmonary vascular disease
may be present early in life.
39. In ASD ,pulmonary vascular disease is caused mainly
by secondary thrombus in the dilated pulmonary
artery branches , with changes in the intima and
media of vessels usually playing minor role.
ASD with pulmonary HTN are relatively common in
pt born at high altitude.
40. Clinical feature and diagnostic
criteria
The female to male ratio 2:1 in pt with an os secundum
ASD while sinus venosus ASD have sex ratio that are
approximately equal.
OS ASD Some time familial
Holt- Oram syndrome -AD
41. ASD may be go unrecognized for decades b/a
symptoms are mild or absent and physical signs are
subtle.
An important exception is the symptomatic infant
with an OS ASD in whom congestive heart failure may
be followed by spontaneous closure.
ASD occurs as an isolated anomaly in 5-10% of all
congenital heart defect.
42. Dyspnea and fatigue are the earliest symptoms of an
OS ASD.
Orthopnea
Platypnea –orthodeoxia rare syndrome
Recurrent lower respiratory tract infection
Older patient deteriorate chiefly on three counts-
1- A decrease lt ventricular destensibility associated with
aging , IHD , systematic HTN or acquired calcific
aortic stenosis augment the lt to rt shunt
43. 2-Age related increase in prevalence paroxysmal atrial
tachycardia , atrial fibrillation and atrial flutter
precipitate congestive heart failure.
3- Mild to moderate pulmonary HTN in older adult
occurs in the face of a persistent lt to rt shunt
Children with ASD may have a delicate gracile habitus
with wt more affected then height. May have lt
Precordial bulge with Harrison's grooves.
44. Cyanosis also occurs when a large
Eustachian valve selectively channels
inferior vena caval blood into the left atrium
through an OS ASD or through an inferior
vena caval sinus venosus defect.
45. Natural history
survival
0.1% of individuals born with large ASD die in infancy
Few die in 1st or 2nd decade of life
5% - 15% die in 3rd decade of life ( PHT, Eisenmenger’s
syndrome)
Premature late death with CHF occurs in increasing
proportion after 5th decade
Lifetime risk of mortality 25%
46. Natural history
Functional status
Presence and severity of functional limitation increase
with age
1% with large ASD have symptoms during 1st yr of life
Most patients asymptomatic through 1st and 2nd decade
, although many are shorter and thin.
Effort intolerance and easy fatigability develop in 2nd
or 3rd decade.
47. CHF common after 40 yr age
Atrial arrhythmia incidence increase with age -
13% in >40 yr age
52%in 60 yr age
Mitral incompetence - 2.5% to 10%
Tricuspid regurgitation - annular
dilation
Bacterial endocarditis - rare
Paradoxical emboli
48. Natural history
Pulmonary hypertension
Occur in 5% - 10% untreated ASD, predominantly
female
Occur after 20 yr age
Higher incidence at high altitude
Incidence increases with advancing age
49. Clinical features
Most infants - asymptomatic
Older children with moderate LTRS
- asymptomatic
- mild fatigue or
dysponea
Children with large LTRS
- fatigue
- dysponea on exertion
- recurrent RTI
- growth retardation
51. Clinical features
cyanosis
Streaming of desaturated IVC blood across ASD,
caused by persistently enlarged Eustachian valve that
baffles blood flow into LA
Advanced irreversible PHT
53. Clinical sign diagnostic of a large (Qp/Qs greater then
1.8 to 2.0) shunt at atrial level are as follow-
- Overactive left parasternal systolic lift
- Fixed splitting second heart sound through out the
respiratory cycle
- A soft pulmonary mid systolic flow murmur(in second
and third ICS)
- A mid –diastolic tricuspid flow murmur(in fourth and
fifth ICS
55. Auscultation
First heart sound-
- split at lower sternal edge and apex and the tricuspid
component is loud.
Pulmonary systolic murmur –
- begins immediately after first heart sound
56. Wide fixed splitting S2-
-wide splitting-
.prolong RV systole
.prolong hang out interval (decrease impedance)
.delayed electrical activation of RV If associated with RBBB
-Fix splitting –
. The phasic changes in systemic venous return during
respiration are associated with reciprocal changes in the
volume of lt to rt shunt minimizing respiratory variation in
the RV filling ie.
(hangout interval-time interval from the cross over of the
pressure to actual closer)
57. -increase venous return during inspiration is associated
with no lt to rt shunt through interatrial
communication
-decrease venous return during expiration is associated
with lt to rt shunt through interatrial communication
minimizing the respiratory variation in RV filling.
Mid – diastolic murmur at tricuspid area
58. The loud second
component of split first
heart sound(T1) is
tricuspid and maximum
at lower sternal edge
A soft pulmonary
systolic murmur in the
2nd ICS lt side followed
by wide fix splitting to
second heart sound
59. ECG
Sinus node dysfunction and accelerated atrial rhythm
Atrial fibrillation, atrial flutter and supraventricular
tachycardia
PR interval prolonged
The P wave axis with OS ASD is inferior and to the left
with upright P waves in leads II,IIIand Avf. The P wave
axis with superior vena caval sinus venosus ASD is
leftward with inverted P wave in lead II,III,avf and
upright P wave in lead v1.
60. rSr or rsR pattern in right Precordial leads
RVH, RAD .
Incomplete or complete right bundle branch
block is present in nearly all cases of ASD,
and superior axis deviation is noted in the
AV canal defect, where complete heart block
is often seen as well
61. The X ray
Increase pulmonary
vascularity extend
periphery of lung field.
Pulmonary trunk and its
branch dilated
Rt atrial enlargement
characteristic
Enlarged rt ventricle
occupies the apex and
form acute angle with lt
hemi diaphragm.
62. Echocardiogram
M - mode
Enlargement of RA and RV dimensions
Paradoxical ventricular septal motion – parasternal
short – axis view
Mitral valve motion - normal
63. Echocardiogram
2 D echocardiography
Subcostal 4 – chamber
view
Echo – free space in
mid – atrial septum
Echo – free space in
posterosuperior atrial
septum in sinus
venosus ASD
Dilated coronary sinus
and communication at
level of orifice of
coronary sinus with LA
64. 2DECHO- sub costal
transducer position
A ,sinus venosus
defect-defect located
in the posterosuperior
atrial septum,beneath
the orifice of SVC
B . Secundum ASD –
the defect is located in
middle portion of the
atrial septum
C . Primum ASD-the
defect is located in the
antero inferior atrial
septum just over the
inflow portion of each
Atrioventricular valve
65. Echocardiogram
Pulsed Doppler Echocardiography
Shunting typically begins in mid – systole
Velocity and volume of blood progressively decrease
until early diastole
Early in ventricular systole – transient RTLS
Determines
Qp : Qs
RV systolic pressure
Pulmonary artery pressure
67. Real time imaging identified a dilated hyperkinetic rt
ventricle with paradoxical motion of the ventricular
septum and vigorous pulsation of pulmonary trunk
and its branch.
68. Cardiac catheterization
Catheter course- across mid –
septal portion
Oxymetry - increase in oxygen saturation
of 10 % or more from svc to RA in one series of blood
samples or increase of 5% in two series of samples
69. Cardiac catheterization
pressure measurement
Equal mean pressure in RA and LA
a and v waves in RA - same magnitude,
appear as M – shaped
RV systolic pressure slightly increased to 25 to 35 mm
Hg
Pulmonary artery pressure normal to slightly
increased
70. Cardiac catheterization
Angiocardiography
cranially angulated LAO projection - defect in
middle of IAS in secundum ASD,defect at the top in
sinus venosus ASD,defect at bottom in AVSD
For coronary sinus ASD selective injection into LSVC,
pulmonary vein, or LA shows passage of contrast into
LA, inferiorly to coronary sinus, and then into right
atrium (in absence of increased RA pressure)
71. Cardiac catheterization- indication
In infants (b/a possible associated anomalies)
In many adult (for assessing possible pulmonary HTN
and status of mitral valve)
In any pt in whom noninvasive test suggest PAPVC
Pt older then 35-40 years
72. Spontaneous closure
In pt with an ASD less then 3 mm in size diagnosed
before 3 month of age , spontaneous closure occurs in
100% of pt at 1 and1/2 yr of age.
More 80 % in b/w 3 and 8 mm
In greater then 8 mm – rarely closes spontaneously
Spontaneous closure of hemodynamically significant
isolated ASD occasionally occurs in 1st year.
Spontaneous closer uncommon after first year.
73. Indication of operation
Elective closer of ASD is generally recommended when
the Qp:Qs is 1.5:1 or greater.
Ideally performed at the age 2-5 yr.
An echo diagnosis of a significant defect with rt
ventricular volume overload is common and sufficient
indication to close ASD.
74. Contraindication
Irreversible pulmonary HTN
Pulmonary vascular disease of sufficient severity to
raise PVR 8-12 wood/m2 at rest and prevent its
decrease to less then 7 wood/m2 with a pulmonary
vasodilator is contraindication for surgery.
75. Trans – catheter Device closure of
ASD
Indicated in-
Os secundum ASD
5mm or more in diameter (but less then 32 mm)
A significant Lt to Rt shunt with clinical evidence of rt
ventricular overload( i.e. Qp/Qs 1.5:1 or greater or RV
enlargement)
There must be enough rim(4mm) of septal tissue
around the defect for appropriate placement of the
device
76. Defect unsuitable for device closer
Failed attempted device closure
Those without sufficient septal rim to engage the
device
Sinus venosus defect for which device closer would
threaten obstruction of pulmonary veins ,IVC and
SVC.
79. Trans-catheter Approach
Device is advance through an introducer sheath
One- half of the device is deployed on left side of atrial
septum, the second half is deployed on the right side
A “sandwich” is formed over the defect
6-8 weeks, device as a frame work for scar tissue to
form
In children the new tissue formation with continue to
grow
84. Care is exercised to place
suture – non coronary
sinus of aorta
SUPERIORLY
tricuspid or mitral valve
ANTERIORLY
the coronary sinus and AV
node
INFEROANTERIORLY
IVC and rt lower
pulmonary vein orifice
INFERIORLY AND
POSTERIORLY
rt upper pulmonary vein
and SVC
SUPERIOPOSTERIORLY
85. Surgical management of sinus
venosus malformation
When pulmonary vein entrance is near the cavoatrial
junction , a simple patch repair can be performed to
channel the pulmonary vein blood across the ASD into
the lt atrium .
When entrance considerable distance from the
cavoatial junction-double patch technique repair done
86. Lateral atriotomy
extending to SVC
Pericardial patch
encompass the orifice
sinus venosus ASD
The SVC and rt atrial
junction are augment
with a second pericardial
patch
88. WARDEN PROCEDURE
When RUPV enters
SVC too high to baffle
Division and over
sewing of SVC
cephalad to entry of
pulmonary vein
Intra atrial patch
baffling the entire SVC
orifice to LA
Re – implantation of
cephalad SVC to RAA
by direct anastomosis
89. Surgical management of coronary
sinus ASD
These defect can be divided into with and those with
out LSVC
Repair of coronary sinus ASD without an LSVC-roofing
procedure
90. the fossa ovalis incised
to view the left atrium,
the unroof coronary
sinus is shown in its
position medial to four
pulmonary vein.
Pericardial patch is used
to repair
91. Repair of coronary sinus ASD with an LSVC-
- when LSVC is small and particularly when there
bridging vein the simplest option is usually to ligate
the LSVC and perform roofing procedure.
- If the LSVC is large intra-atrial baffle technique done.
92. The baffle direct
pulmonary venous
drainage to mitral valve
while the left SVC and
coronary sinus drain to rt
atrium
93. Repair of Scimitar syndrome
1. Baffling of the rt pulmonary vein flow through the rt
atrium across a secundum ASD to the lt atrium.
2. Reimplantation of the anomalous pulmonary higher
into rt atrium with baffling across the ASD.
3. Reimplantation of anomalous pulmonary vein into
the lt atrium with closer of ASD
94. 4. Incise the wall of the rt atrium and the rt common
pulmonary vein as they travel in parallel and then sew
the edge together in a side to side anastomosis and
baffled into the lt atrium through ASD.
95. Repair in presence of increased
pulmonary vascular resistance
Indicated in high Rpi (greater then 6 u-m2 )
Using flap valve patch
The open rt to lt when rt atrial pressure exceed lt atrial
pressure in severe PHT
Ppa and Rpi decrease late postoperatively the flap
valve will close by cicatrix
97. Results
Early (hospital) mortality
Approached zero percent
Fewer then .5%
Causes of death - 1.
pulmonary vascular disease
2. old age (neurologic failure, ch.
CHF)
3. air embolization
4. severe supraventricular arrhythmia
98. Results
Survival rate
Repair during first few yrs of life - survival that of
matched general population
Repair later in childhood or early adult life -survival
very close to that of matched general population
Repair in older patient - life expectancy improves but
survival is not that of matched general population
99. Results
Functional status
Asymptomatic children - no symptoms
before or after operation
Symptomatic infants - complete
relief of symptoms
Older symptomatic patients - improvement
in symptoms
100. Results
Functional status
Prior to ASD closure, > 60% patients older than 40 yr
NYHA class 3 or 4 After ASD closure, > 80% patients
NYHA class 1 or 2.
Improvement in exercise physiology but less
pronounced with older age at operation
101. Results
Hemodynamic Results
Mean pressure in ascending aorta and mean aortic
flow increase
Immediate reduction in pulmonary blood flow
RA pressure decreases; LA pressure increases
Cardiomegaly on chest x – Ray in asymptomatic
children resolve with in 2 yrs in 65% cases but not
regress to normal size in 27% cases
In older patients PVR drops negligibly late after
operation
102. Results
Ventricular function
Striking decrease in RVEDV
in 64% children with surgery before 10 yrs of age -
RVEDV return to normal
In 21% patients with age >25 yrs - RVEDV return to
normal
In 47% adults with impaired RV function, decreased
RV wall motion and EF - less reduction in RV size and
less improvement in EF
103. Results
Ventricular function
LV EF increases normally with maximal exercise
Preoperative abnormal small LV ED dimensions
increase to normal within 6 months.
104. Result
Arrhythmic events
Closure of ASD in children improve AV conduction,
sinus node function, and decrease AVN refractory
period
Incidence in children - 23%
Adult with preoperative AF - postoperative AF
50% patients with age >40 yrs at surgery develop AF.
