ATRIAL SEPTAL DEFECT (ASD)
DEFINITION
- An atrial septal defect is an abnormal
communication between atria. This is considered to be an acyanotic congenital
heart disease.
- The lesion involves left to right shunting at
the atrial level.
- This defect can occur in any portion of the
atrial septum and are classified into three types:
o
Secundum septum (50%-70%) most common,
involving the focca ovalis - but is a true deficiency of the septum ( i.e., not
a patent foramen ovale)
o
Primum septum (15%) usually associated
with cleft mitral valve. Because of the embryological derivation of the ostium
primum ASD, they may be considered a form of AV (atrioventricular) septal
defect
o
Sinus venosus associated with abnormal
venous return of blood form the left atrium
EPIDEMIOLOGY
- Atrial septal defect is one of the most commonly recognized
forms of congenital heart disease (CHD) in adults.
- This is the second most common congenital heart defect in
children.
- There is a female predominance (Male: Female ratio 1:2)
PATHOPHYSIOLOGY
- Atrial septal defect result from defective development of the
septum secundum or from defective development of the septum primum. After birth,
fusion of the two septa is completed in the region of the foramen ovale. However,
in approximately 25 to 30% of normal adult hearts, the flap of the septum
primum does not completely fuse with the septum secundum permitting shuntiong
across the atrial septum ( i.e an ASD).
CLINICAL
SIGNS AND SYMPTOMS
- Patient are typically asymptomatic early in
life.
- Children may complain of fatigue, have low
weight percentiles and have greater susceptibility to respiratory infections.
- In adults, complication include: atrial arrhythmias,
pulmonary artery hypertension, development of pulmonary vascular obstruction
and congestive heart failure.
- On physical examination the following may be
present:
o
Prominent right ventricle (RV) impulse
o
Palpable pulmonary artery (PA) pulsation
- Auscultatory findings ( may be absent in
infants):
o
S1 may normal or split, with accentuation of T1 (closure
of tricuspid valve), flow across the pulmonic valve may generate a midsystolic
pulmonary ejection murmur
- After the normal postnatal decrease in PVR
(pulmonary vascular resistance), S2 is widely split and fixed in relation to
respiration (with normal Pulmonary artery pressures and low PVR) because of
delay in pulmonic valve closure. With large shunting, flow across the tricuspid
valve may pulmonary cause a mid- diastolic rumbling murmur at the LLSB (left
lower sternal border)
- Apical holosystolic or late systolic murmur
radiation to the axilla may be heard due to associated mitral valve prolapse in
20 – 30% of ASD
- With teenage pts, increase in PVR may diminish
the degree of shunting. Physical findings after that may reflect reflect the following:
o
Pulmonary and tricuspid murmurs may decrease in
intensity
o
P2 is accentuated and the A2 and P2 may fuse
o
Diastolic murmur of PR appears
o
Cyanosis and clubbing accompany development of
right to left shunt
- Pulmonic SEM (systolic ejection murmur), fixed
and widely split s2, and occasional diastolic rumble
- EKG findings:
o
EKG findings includes right axis deciation (+90
to +180), mild right ventricular hypertrophy (RVH), delay in RV activation may
be manifestation of RV overload or true conduction delay in right bundle branch
and peripheral Purkinge system. Left – axis deviation of the P wave (i.e., negative
P in lead 111) suggests presence of a sinus venosus defect. Prolongation of the
PR interval may be seen with all types of ASDs
o
CXR may show cardiomegaly with enlargement of
the right atrium and right ventricle, dilatation of the pulmonary arteries and
its branches, increase pulmonary vascular markings, dilatation of the proximal
superior vena cava may be noted in patients with sunus venosus defect. Left atrial
enlargement is rare but may occur with significant mitral regurgitation.
o
Two dimensional echocardiogram is the diagnostic
tool of choice used to determine size and location of the defect and presence
or absence of pulmonary hypertension.
o
Sinus venosus defect shows a defect in posterior
superior suptum (A below)
o
Secundum type shows dropout in mid- atrial
septum (B)
o
Primum type shows defect in lower atrial septum
(C)
(A)
(B)
(C)
MEDICAL
MANAGEMENT
- Medical management is the first treatment of
choice since these lesions have a high probability of spontaneous closure.
o
In these types of patient, exercise restriction
is unnecessary.
- Subacute bacterial endocarditis (SBE)
prophylaxis is not indicated in absence of mitral valve prolapse.
- For infants in heart failure (unusual), treatment
with anti- heart failure medications:
o
Such as furosemide and Digoxin are usually
prescribed.
SURGICAL
MANAGEMENT
- This is true open heart surgery and requires the
use of cardiopulmonary bypass (CPB). It is the simplest of open heart
procedures that we do. After the establishment of CPB, the right atrium is
opened and the defect is closed by primary stitches or with a pericardial
patch.
- Other options: transcatheter occlusive devices
o
Device closure may be possible in secundum type defects,
provided there is an adequate septa rim.
o
Advantages of nonsurgical closure include short hospital
stay, rapid recovery, and no residual thoracotomy scar.
ASD surgical
closure
ASD Device closure
