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 mmHg) than the right ventricle (~20 mmHg), 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<unk> s, who may present with breathlessness, poor feeding and failure to thrive in infancy. Patients with smaller<unk> s may be asymptomatic. Four different septal<unk> s exist, with perimembranous most common, outlet, atrioventricular, and muscular less commonly.
Ventricular septal defect
Heart septal defect
Atrioventricular septal defect
Atrial septal defect
Aortopulmonary septal defect
Tricuspid atresia
Double aortic arch
Double inlet left ventricle