Ventricular Septal Defect

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Home :: Diseases :: Ventricular Septal Defect
 

Ventricular Septal Defect - defect picture septal ventricular

What is Ventricular Septal Defect

In this lesion, a persistent opening in the upper interventricular septum resulting from failure of fusion with the aortic septum permits blood to pass from the high-pressure left ventricle into the low-pressure right ventricle. The subsequent natural history and pathophysiology depend on the size of the defect and the magnitude of left-to-right shunting. Large defects are associated with early left ventricular failure. Chronic but more moderate left-to-right shunts may lead to pulmonary vascular disease and right-sided failure. Many ventricular defects close spontaneously in early childhood

Clinical Findings of Ventricular Septal Defect

Symptoms and Signs of Ventricular Septal Defect

The clinical features are dependent upon the size of the defect and the presence or absence of a raised pulmonary vascular resistance. Large shunts are associated with loud, harsh holosystolic murmurs in the left third and fourth interspaces along the sternum and, in some cases, middiastolic flow murmurs and an S3 at the apex. Smaller shunts may produce only an early systolic murmur or a diamond-shaped murmur. A systolic thrill is common. Clinical evidence of pulmonary hypertension is often more informative than the murmur itself. High defects may be associated with aortic regurgitation owing to prolapse of a valve leaflet.

Prognosis & Treatment of Ventricular Septal Defect

Patients with the typical murmur as the only abnormality have a normal life expectancy except for the threat of infective endocarditis. Endocarditis is more typical of smaller shunts. Antibiotic prophylaxis is mandatory. With large shunts, congestive heart failure may develop early in life, and survival beyond age 40 years is unusual. Shunt reversal occurs in an estimated 25% of patients, producing Eisenmenger's syndrome.

Small shunts (pulmonary-to-systemic flow ratio < 1.5) in asymptomatic patients do not require surgery. Defects causing large shunts should be repaired to prevent pulmonary hypertension or late heart failure. Once pulmonary hypertension is present (systolic pulmonary arterial pressures > 85 mm Hg), the surgical mortality risk is at least 50%. If right-to-left shunting is present (Eisenmenger's syndrome), surgery is contraindicated. Many defects (up to 40%) close spontaneously. Therefore, surgery should be deferred until late childhood unless there are signs of heart failure or pulmonary hypertension. Surgical mortality rates are low (2–3%). Some defects can be closed percutaneously.





 

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