Ventricular septal defect (VSD)


A ventricular septal defect (VSD) occurs when there is direct communication between the left and right ventricles. This can be a congenital anomaly or acquired as a complication of a myocardial infarction.

Ventricular septal defects are classified as membranous, perimembranous, supracristal (infundibular or subpulmonic) or muscular.

vsd_defects_labelled

Membranous VSDs are the most common type and originate inferior to the crista supraventricularis, yet still towards the left ventricular outflow tract.

Perimembranous VSDs are also inferior to the crista supraventricularis, however extend into the muscular septum.

Supracristal VSDs occur just beneath the aortic valve at the left ventricular outflow tract. A Venturi effect can occur from the left to right shunt causing the aortic valve leaflet to prolapse into the VSD resulting in significant aortic valve regurgitation.

Muscular VSDs occur in the mid to apical interventricular septum and do not involve cardiac valves.

A Gerbode defect is technically a type of ventricular septal defect, although this results in a left ventricular to right atrial shunt.

Pathophysiology

Significant left to right shunting can occur resulting in a high left ventricular cardiac output. Forward systemic flow can be reduced if the shunt is large resulting in symptoms of congestive heart failure.

The Qp/Qs ratio can be measured during cardiac catheterization or via echocardiography and helps to determine the size of the cardiac shunt. The Qp (flow through the pulmonary vascular bed) is compared to the Qs (flow through the systemic vascular bed). In a normal individual without a cardiac shunt this ratio should be 1, however the pulmonary flow increases significantly compared to systemic flow when a left to right shunt is present. If the Qp/Qs ratio reaches > 2, then clinical symptoms usually manifest.

Physical Examination

A ventricular septal defect produces a holosystolic murmur. Blood abnormally flows from the LV (high pressure) to the RV (low pressure) creating turbulent blood flow and a holosystolic murmur heard best at "Erb's point". The smaller the ventricular septal defect, the louder the murmur. A very small VSD can cause a palpable thrill (vibration on the chest). A small VSD with a loud murmur is called "Maladie de Roger" after the initial describer.

VSD

Diagnosis

Diagnosis is predominantly made via echocardiography which directly images the shunt and can can measure important hemodynamic parameters such as cardiac chamber sizes, the Qp/Qs ratio and pulmonary pressures.

Left ventriculography can visualized VSDs as well. During right heart catheterization, oxygen saturations are frequently measured from different cardiac chambers in order to identify left to right shunts. If a ventricular septal defect is present, the oxygen saturation will be markedly higher in the right ventricle due to shunting of well oxygenated blood from the left ventricle to the right ventricle. This diagnostic technique can be helpful when a patient presents after an acute myocardial infarction with pulmonary edema and shock to diagnose an acute ventricular septal defect.

Treatment

There is no specific medical therapy that is recommended in the treatment of a ventricular septal defects. Ventricular septal defects can be closed surgically or percutaneously.

The indications to close a ventricular septal defect include:

  1. Qp/Qs is > 1.5 and there is LV systolic or diastolic dysfunction causing clinical heart failure.
  2. Prior endocarditis on the VSD
  3. Qp/Qs is > 1.5 and the pulmonary pressures are no more than two thirds of systemic pressure.
  4. Qp/Qs is > 2 and there is evidence of volume overload of the LV
  5. Acute VSD after myocardial infarction

If Eisenmenger’s syndrome is present, closure of a VSD is NOT recommended and can be fatal. In this situation, the only remedy is heart-lung transplantation.

References:

1. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine

2. Hurst's the Heart, 13th Edition

Image reference: CC Patrcik J Lynch and C. Carl Jaffe, Yale University, 2006.