Patent Ductus Arteriosus (PDA) – Hemodynamics

Preoperative Hemodynamics

The patent ductus arteriosus (PDA) is a persistent fetal connection between the descending aorta and the pulmonary artery.

In the postnatal period, systemic pressure exceeds pulmonary arterial pressure, producing a left-to-right shunt (aorta → pulmonary artery).
This shunt causes increased pulmonary blood flow, which can lead to pulmonary overcirculation and pulmonary hypertension, particularly when the ductus is large.
The excess flow returns to the left atrium and left ventricle, producing chronic volume overload and chamber enlargement.
In severe cases, longstanding pulmonary overcirculation increases pulmonary artery pressures, imposing a pressure load on the right ventricle as well.

Following ligation or device closure of the PDA:

Pulmonary overcirculation is eliminated, reducing the volume load on the left atrium and ventricle.
Gradual regression of chamber dilation occurs, and left heart size and function often normalize over time.
Pulmonary hypertension may improve if closure is performed before irreversible vascular remodeling has occurred.

Before closure: PDA physiology is characterized by a continuous left-to-right shunt leading to left heart volume overload, pulmonary overcirculation, and in severe cases, right heart pressure loading.
After closure: Hemodynamics improve with relief of volume overload and potential reversal of pulmonary hypertension if intervention is timely.

The clinical presentation depends on ductal size: small PDAs may be asymptomatic, while large PDAs produce heart failure, failure to thrive, or recurrent respiratory infections.
Eisenmenger physiology can develop if closure is delayed until pulmonary vascular disease becomes fixed, resulting in right-to-left shunting and cyanosis.
In premature infants, PDA is common due to immaturity of ductal smooth muscle, and management may include medical therapy (indomethacin, ibuprofen) before considering surgical or catheter-based closure.