ATRIAL SEPTAL DEFECT (ASD)

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

• Chest x-ray findings:

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.

  

• Echocardiography

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