Atrial Septal Defect (ASD) – Hemodynamics

Preoperative Hemodynamics

An atrial septal defect (ASD) permits communication between the left and right atria.

Because left atrial pressure (LAP) exceeds right atrial pressure (RAP), blood is shunted left-to-right across the defect.
This results in increased pulmonary blood flow; however, pulmonary hypertension is uncommon in isolated ASD because the pressure gradient is relatively small.
The primary consequence is volume overload of the right atrium (RA), right ventricle (RV), and pulmonary arteries (PA).
Chronic shunting leads to dilation of the RA and RV, as well as enlargement of the pulmonary vasculature.
Left ventricular filling may be impaired due to ventricular interdependence and septal shift, producing subtle diastolic dysfunction.

Closure of the defect, whether surgical or transcatheter, normalizes atrial pressures and abolishes the shunt.

Right-sided volume overload is relieved, with gradual remodeling of the RA and RV.
Potential postoperative issues include:

Arrhythmias (PVCs, atrial tachycardia, atrial fibrillation), particularly in adults with longstanding RA/RV dilation.
LV dysfunction or overload, especially in older patients with unrecognized diastolic impairment, since LV preload suddenly increases after shunt closure. Careful perioperative fluid management is therefore critical.

Before closure: ASD physiology is dominated by a left-to-right atrial shunt, causing right heart and pulmonary artery volume overload, with relatively preserved pressures.
After closure: Hemodynamics normalize with relief of right heart dilation, but vigilance is required for arrhythmia management and for left heart adaptation to increased preload.