Concept:
Ventricular septal defect (VSD) is the most common congenital heart malformation, characterized by an abnormal communication between the left and right ventricles.
The hemodynamic consequences of a VSD depend directly on the anatomical size of the defect and the ratio of pulmonary to systemic vascular resistance ($Q_p/Q_s$).
Explanation:
• Small (restrictive) VSDs: High resistance to flow generates a large left-to-right pressure gradient, producing a loud, harsh, pansystolic murmur (maladie de Roger) with a systolic thrill, without chamber dilation or left ventricular hypertrophy (LVH). Most small defects close spontaneously ($>75\%$) and do not require surgery.
• Large (non-restrictive) VSDs: Equalize left and right ventricular pressures, resulting in massive left-to-right shunting and pulmonary overcirculation.
• The increased pulmonary venous return overloads the left atrium and left ventricle, leading to left ventricular volume overload, LVH (and biventricular hypertrophy), and congestive heart failure within the first $2$--$8$ weeks of life as pulmonary vascular resistance drops.
• Because there is minimal pressure gradient across a large non-restrictive VSD, its murmur is softer and less harsh than that of a small restrictive defect.
Final Answer:
Large ventricular septal defects cause significant left-to-right shunting, leading to left ventricular volume overload, LVH, and congestive heart failure.