Ventricular Septal Defect
In the normal development of the heart, the interventricular foramen closes off to form the membranous part of the interventricular septum. Failure of this structure to close produces a ventricular septal defect that permits shunting of blood from the left to the right ventricle (left-to-right ventricular shunt) during systole. The shunt is left-to-right because left ventricular pressure greatly exceeds right ventricular pressure during systole. For example, right ventricular systolic pressure might be 25 mmHg when left ventricular systolic pressure may be 120 mmHg or higher. This leads to a large pressure gradient across the opening in the septum so that blood flows from the left to right ventricle during systole. The flow of blood across this shunt produces a characteristic holosystolic murmur (i.e., between S1 and S2). Often, the murmur is louder with smaller defects because of increased turbulence.
There can be serious consequences to ventricular septal defects. The shunting of blood increases right ventricular volume and its output by the Frank-Starling mechanism. This increased output can lead to pulmonary hypertension. Furthermore, the increased pulmonary flow leads to left atrial enlargement and increased left ventricular preload and stroke volume by the Frank-Starling mechanism. Over time, these hemodynamic changes can lead to symptoms of congestive heart failure and dyspnea.