Ventricular Septal Defect (VSD) – Hemodynamics

Preoperative Hemodynamics

A ventricular septal defect (VSD) permits direct communication between the left and right ventricles.

Because left ventricular pressure exceeds right ventricular pressure, blood flows left-to-right across the defect, resulting in volume overload of the pulmonary circulation.
The consequence is increased pulmonary blood flow, leading to pulmonary artery dilation and progressive left atrial and left ventricular volume overload.
Over time, persistent high pulmonary flow and pressure may induce pulmonary vascular remodeling and an increase in pulmonary vascular resistance (PVR).
Progressive pulmonary hypertension (PH) increases right ventricular afterload, leading to RV hypertrophy. In severe cases, reversal of shunt direction can occur (Eisenmenger physiology).

Surgical closure of the VSD abolishes the shunt and re-establishes normal ventricular physiology.

Pulmonary blood flow is reduced, unloading the left atrium and left ventricle.
Pulmonary hypertension often improves after closure, depending on the chronicity and severity of preoperative pulmonary vascular disease.
Potential complications include:

Tricuspid regurgitation (TR) if the tricuspid valve is disturbed during patch placement.
Conduction abnormalities, particularly right bundle branch block or complete heart block, due to the proximity of the conduction system to perimembranous defects.

Additionally, closure increases LV afterload, as the low-resistance shunt pathway is eliminated. This may transiently stress the LV, particularly in patients with borderline function.

Before repair: VSD physiology is characterized by left-to-right shunting, pulmonary overcirculation, left heart volume overload, and risk of pulmonary hypertension with secondary RV hypertrophy.
After repair: Hemodynamics normalize with relief of pulmonary overcirculation, but vigilance is required for conduction disturbances, tricuspid valve dysfunction, and the increase in LV afterload.