With birth, the pulmonary circulation increases dramatically as the low resistance placenta is removed, the lungs inflate with air, the pulmonary vascular resistance begins to fall and the organ of oxygenation is transferred from the placenta to the lungs. As the ductus arteriosus closes in the first hours or days of life, there is separation of the pulmonary and systemic circulation allowing for discrepancy between the pulmonary and systemic resistances and the resulting changes and differences in right and left ventricular pressures. The pulmonary vascular resistance continues to fall in neonatal and early infancy as the pulmonary vasculature remodels, intra-acinar arterioles multiply and are arranged in parallel, and the infant develops a normal physiologic anemia. All of these changes lead to a systemic resistance that exceeds the pulmonary resistance, a corresponding decrease in the right ventricular pressure, and a pressure gradient between the left and right ventricle. Progressive shunting across a given ventricular septal defect will ensue as the pressure difference between the ventricles increases with the passage of time. The size of the defects and to some degree its location will determine the clinical manifestations.

With small ventricular septal defects, the pressure gradient is well maintained between the left and right ventricle and with each systole, there shunt of blood from the high pressure ventricle to the lower pressure chamber. While the shunt may be small in the small defect, the high pressure gradient will produce significant turbulence of blood as it moves from left to right. This turbulence will produce the murmur on auscultation, and as a result, a small ventricular septal defect often has a loud, easily audible systolic murmur. This murmur is frequently holosystolic as there is flow throughout systole Ð from the onset of AV valve closure through the closure of the semilunar valves.

With larger ventricular septal defects, the volume of the left to right shunt will increase as the pulmonary vascular resistance falls during infancy. Because the larger size of the defect does not restrict flow, the pulmonary arterial bed is exposed to this high volume of flow and to a higher pressure than would be present in the absence of a ventricular septal defect. In fact, in truly large ventricular septal defects, the pulmonary artery pressure will equal the aortic pressure (if there is no obstruction to either systemic or pulmonary blood flow), as the defect allows for equalization of pressures between the two ventricles. While the flow across the defect may be high in large ventricular septal defects, the turbulence is minimized, as there is no significant pressure gradient between the two ventricles. As a result, the large ventricular septal defect may not produce a significant murmur from its flow. However, one may appreciate turbulence across the pulmonary outlet from the increased volume of blood being ejected into the pulmonary artery. In addition, there may turbulence across the mitral valve during diastole as the volume of blood returning from the lungs is significantly increased.

Ventricular septal defects produce almost all of their shunting during systole when the ventricles are exposed to increasing pressure as the ventricles are depolarized and then exposed their downstream resistances as the semilunar valves open. While the defect obviously exists during diastole, the ventricular pressures are often nearly if not equal so that there is essentially no shunting during this phase of the cardiac cycle. The isovolumic phase of ventricular systole does not truly exist as there is communication between the ventricles and their volumes will change. Shunting continues from this early phase of systole through its completion when the semilunar valves close. While ventricular septal defects do in fact shunt blood from the high pressure left ventricle to the lower pressure right ventricle, it is the pulmonary circuit that experiences the true volume load. Again, during systole, the right ventricle is contracting, ejecting its contents into the pulmonary artery so that it essentially serves as a conduit for the left ventricular blood to enter the pulmonary artery. As a result, the pulmonary artery, the pulmonary capillaries, the pulmonary veins, the left atrium and left ventricle all become volume loaded and dilate in response to a significantly large ventricular septal defect.