Atrial septal defect (ASD) is a congenital heart defect caused by an opening in the septum that divides the right and left atria. Because of the pressure gradients, blood typically shunts across the interatrial septum from left to right.
Small defects are often asymptomatic and may go undiagnosed for years.
There is a wide and fixed split S2 due increased blood in the right heart, which delays closure of the pulmonic valve. There may also be a systolic ejection murmur at the upper left sternal border due to increased blood flow through the pulmonic valve.
Large defects often present with easy fatigability, frequent respiratory infections and failure to thrive (FTT). Increased blood flow through the pulmonary vessels may result in pulmonary hypertension. The increased pulmonary resistance leads shunt reversal (Eisenmenger syndrome), causing cyanosis and dyspnea.
Some patients may experience symptoms such as easy fatigability, recurrent respiratory infections, FTT and exertional dyspnea.
Chest radiograph findings include cardiac enlargement secondary to dilation of the right atrium and right ventricle along with increased pulmonary vascular markings.
Using an ultrasound, sound waves are used to visualize the structures of the heart. The transthoracic approach usually confirms the diagnosis of ASD, but the transesophageal approach is often necessary for more precise measurements. The electrocardiogram (ECG) often shows normal sinus rhythm, a right axis deviation and incomplete right bundle branch block.
Surgery or percutaneous transcatheter approach are used in closure of an ASD in patients with symptoms or CHF.
Patients with a repaired ASD requiring prosthetic material or device and patients with repaired ASD with a residual defect must receive prophylactic antibiotics for dental procedures or surgery.
Spontaneous closure is most common in young patients who have small defects. There is no surgery indicated in asymptomatic children without significant left to right shunting.
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