VSD is the most common cardiac malformation and accounts for 25% of congenital heart disease. Defects may occur in any portion of the ventricular septum, but most are of the membranous type.
The clinical findings of patients with a VSD vary according to the size of the defect and pulmonary blood flow and pressure.
Small VSDs with trivial left-to-right shunts and normal pulmonary arterial pressure are the most common. These patients are asymptomatic, and the cardiac lesion is usually found during routine physical examination. Characteristically, a loud, harsh, or blowing holosystolic murmur is present and heard best over the lower left sternal border, and it is frequently accompanied by a thrill.
Large VSDs with excessive pulmonary blood flow and pulmonary hypertension are responsible for dyspnea, feeding difficulties, poor growth, profuse perspiration, recurrent pulmonary infections, and cardiac failure in early infancy. Cyanosis is usually absent, but duskiness is sometimes noted during infections or crying. Prominence of the left precordium is common, as are a palpable parasternal lift, a laterally displaced apical impulse and apical thrust, and a systolic thrill. The holosystolic murmur of a large VSD is generally less harsh than that of a small VSD and more blowing in nature because of the absence of a significant pressure gradient across the defect. It is even less likely to be audible in the newborn period.
In patients with small VSDs, the chest radiograph is usually normal, although minimal cardiomegaly and a borderline increase in pulmonary vasculature may be observed. The electrocardiogram is generally normal.
In large VSDs, the chest radiograph shows gross cardiomegaly with prominence of both ventricles, the left atrium, and the pulmonary artery. Pulmonary vascular markings are increased, and frank pulmonary edema, including pleural effusions, may be present. The electrocardiogram that you can check my blog shows biventricular hypertrophy; P waves may be notched or peaked.
The two-dimensional echocardiogram shows the position and size of the VSD.
The natural course of a VSD depends to a large degree on the size of the defect. A significant number (30–50%) of small defects close spontaneously, most frequently during the 1st 2 yr of life. Small muscular VSDs are more likely to close (up to 80%) than membranous VSDs are (up to 35%).
In patients with small VSDs, parents should be reassured of the relatively benign nature of the lesion, and the child should be encouraged to live a normal life, with no restrictions on physical activity. Surgical repair is currently not recommended.
Indications for surgical closure of a VSD include
patients at any age with large defects in whom clinical symptoms and failure to thrive cannot be controlled medically;
infants between 6 and 12 mo of age with large defects associated with pulmonary hypertension,even if the symptoms are controlled by medication;
and patients older than 24 mo with a Qp : Qs ratio greater than 2 : 1.
Patients with supracristal VSD of any size are usually referred for surgery because of the high risk for aortic valve regurgitation