Atrial
Septal
Defect (ASD)
General: A defect in the atrial septum that allows
shunting
of blood between the atria. The
direction of the shunt depends on the relative pressures between the
two
systems (pulmonic and systemic).
Prevalence: Accounts for 10% of all congenital heart
disease. Occurs in 4/100K of the
general population. The male:
female ratio is 1:2
Embryology: The atrial septum arises from two
components. The
septum primum grows from the upper primitive atrium while the septum
secundum
grows from the posterosuperior portion.
The endocardial tube twists to form the four-chambered heart. The septum secundum covers the inferior
aspect of the septum primum known as the ostium primum. The superior
portion of
the septum primum becomes the foramen ovale.
Location: Four types:
- ostium secundum is most common.
- sinus venosus, located high in the
septum where the vena cava intersects with the right atrium, associated
with anomalous venous return
- ostium primum, located low in the
septum and considered a type of AV septal defect.
- Coronary sinus septal defect
Typical Presenting symptoms-
- Usually small defect is asymptomatic
- May rarely have symptoms of CHF in
infancy and failure to gain weight.
- Larger defects may present in second
decade of life. May begin with exercise
intolerance and shortness of breath
- Larger defects will often develop
atrial arrhythmias
- Some are discovered after neurologic
symptoms secondary to stroke. From cerebral
emboli
Physical findings:
- III/VI systolic ejection LUSB secondary to increased flow across pulmonic
valve. The ASD itself does not cause a
murmur.
- S2 widely
split and fixed (i.e. does not vary with inspiration). If diastolic
murmur heard, implies increased flow across tricuspid and elevated
pulmonary blood flow
- With increased Lto R shunting, may
have ventricular heave
CXR: Enlarged heart and increased pulmonary
vascular
markings with large left to right shunts.
EKG- With
dilated RV
may have right bundle branch block.
May also have atrial arrhythmias like fibrillation and flutter.
Echo: Dilated RV, visualization of defect.
Complications:
- Growth failure,
- Atrial tachyarrhythmia
- Pulmonary hypertension
- Paradoxical emboli to brain and body
Treatment:
- Closure via surgery or
catheterization. Usually done electively by age 3 to avoid RV
dysfunction. If no significant shunt
(<2:1), pt can be monitored periodically for development of
arrhythmia or pulm HTN.
- 20% will
spontaneously close in the first year of life, higher likelihood if
less than 4 mm in diameter. Unlikely to
spontaneously close after age 3.
Treatment prognosis: Complication rate of
surgery <1%. Closure via
catheter appears to have similar success rate. Pts
usually have no restrictions.
Endocarditis prophy: Varies by study and
practitioner.
References
1.
Univeresity of Chicago Cardiolog Page