What is Ventricular Septal Defect?
VSDs may be subdivided into membranous and muscular defects. Muscular VSDs 10-20% are described according to their location on the ventricular septum. They have a higher rate of spontaneous closure than membranous VSD. The majority of VSDs, 70-80% are located in the membranous portion of the interventricular septum.
Less common VSD types include outlet VSD 5% located just below the aortic and pulmonary valves. The outlet VSD also known as doubly committed subaortic and subpulmonic or supracristal VSD accounts for 30-35% of VSDs in Asian patients. The atrioventricular septal defects 5% is located near the junction of the mitral and tricuspid valves.
Large VSDs are usually detected in childhood due to a murmur or the presence of congestive heart failure. Without closure, large VSDs cause pulmonary hypertension with irreversible pulmonary vascular disease and eventual reversal of the shunt from right to left Eisenmenger syndrome. Children and adults with isolated small VSDs rarely require closure and follow up suggests a low risk of complications, however endocarditis prophylaxis is recommended.
The management of VSD depends on the size of the defect and the pulmonary vascular resistance. Surgery is recommended for patients with moderate or large VSD if the magnitude of pulmonary vascular obstructive disease is not prohibitive. Once the ratio of pulmonary to systemic vascular resistance exceeds 0.7, the risk associated with surgery is very high.
The small VSD causes a loud systolic murmur, which obliterates the second heart sound. A displaced apical left ventricular impulse and mitral diastolic flow rumble suggests a hemodynamically important VSD, causing volume overload. It is noted that Transthoracic echocardiography demonstrates the size, number, location and hemodynamic impact of the VSD.