Ventricular Septal Defect - Pathophysiology

Pathophysiology

During ventricular contraction, or systole, some of the blood from the left ventricle leaks into the right ventricle, passes through the lungs and reenters the left ventricle via the pulmonary veins and left atrium. This has two net effects. First, the circuitous refluxing of blood causes volume overload on the left ventricle. Second, because the left ventricle normally has a much higher systolic pressure (~120 mm Hg) than the right ventricle (~20 mm Hg), the leakage of blood into the right ventricle therefore elevates right ventricular pressure and volume, causing pulmonary hypertension with its associated symptoms.

In serious cases, the pulmonary arterial pressure can reach levels that equal the systemic pressure. This reverses the left to right shunt, so that blood then flows from the right ventricle into the left ventricle, resulting in cyanosis, as blood is by-passing the lungs for oxygenation.

This effect is more noticeable in patients with larger defects, who may present with breathlessness, poor feeding and failure to thrive in infancy. Patients with smaller defects may be asymptomatic. Four different septal defects exist, with perimembranous most common, outlet, atrioventricular, and muscular less commonly.