Ventricular septal defects (VSDs)


Refers to a defect in the ventricular septum, the wall dividing the left and right ventricles of the heart.

The opening varies from pin size to complete absence of the ventricular septum, creating one common ventricle.

The most common of congenital cardiac abnormalities.

VSDs are found in 30-60% of all newborns with a congenital heart defect, or about 2-6 per 1000 births.

Has a prevalence of 2-5 per 100 births of trabecular VSDs that close shortly after birth in 80-90% of the cases.

The ventricular septum consists of an inferior muscular and superior membranous portion.

The ventricular septum is extensively innervated with conducting cardiomyocytes.

There are various forms of ventricular septal defects:

1. Conoventricular, malaligned

2. Perimembranous

3. Inlet

4. Muscular

The membranous portion type, is close to the atrioventricular node.

In the US, the membranous portion is most commonly affected in adults and older children.

The membranous portion type most commonly required surgical intervention, accounting for over 80% of cases.

Membranous ventricular septal defects are the most common congenital cardiac anomaly.

Ventricular septal defect is usually symptomless at birth manifesting a few weeks after birth.

VSD is an acyanotic congenital heart defect.

It is a left-to-right shunt, so there are no signs of cyanosis in the early stage.

Uncorrected VSD can lead to increased pulmonary resistance leading to the reversal of the shunt and cyanosis.

A pansystolic murmur along lower left sternal border, depending upon the size of the defect can be heard on auscultation.

A palpable thrill may be felt along the left sternal border.

Heart sounds are normal.

Larger VSDs may cause a parasternal heave, and a laterally displaced apex beat as the heart enlarges.

An infant with a large VSD is associated with failure to thrive, diaphoresis and tachypnea with feeding.

Smaller VSDs with restrictive disease are associated with a louder murmur and more palpable thrill.

Larger defects may be associated with pulmonary hypertension due to the increased blood flow to the pulmonary artery, leading to an Eisenmenger’s syndrome.

During ventricular contraction, 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 circuitous refluxing of blood causes volume overload on the left ventricle.

The left ventricle normally has a much higher systolic pressure, about 120 mmHg, than the right ventricle, about 20 mmHg), the leakage of blood into the right ventricle therefore elevates right ventricular pressure and volume, causing pulmonary hypertension with its associated symptoms.

The original VSD has with a left-to-right shunt, now becomes a right-to-left shunt because of the increased pressures in the pulmonary vascular bed.

This reversal in the left to right shunt, results in blood flowing from the right ventricle into the left ventricle, resulting in cyanosis, as blood is by-passing the lungs for oxygenation.

In advanced cases, the pulmonary arterial pressure can reach levels that equal the systemic pressure.

Diagnosis can be made by cardiac auscultation.

A VSD causes a pathognomonic holo- or pansystolic murmur.

The murmur is made by the abnormal flow of blood from the left ventricle, through the VSD, to the right ventricle.

The intensity of the murmur varies with the size of the VSD and the status of the pressures of the right and left ventricles, at any point in time.

Confirmation of cardiac auscultation findings can be obtained by non-invasive cardiac echocardiography, cardiac catheterization.

Congenital VSDs are frequent in congenital conditions, such as Down syndrome.

Mechanical tearing of the septal wall with myocardial infarction can form a VSD.


Most cases do not need treatment and heal at the first years of life.

Small congenital VSDs often close on their own, as the heart grows, and in such cases may be treated conservatively.

Some cases may necessitate surgical intervention:

1. Failure of congestive cardiac failure to respond to medications

2. VSD with pulmonic stenosis

3. Large VSD with pulmonary hypertension

4. VSD with aortic regurgitation

For surgical repair, a heart-lung machine is required and a median sternotomy is performed.

Percutaneous endovascular procedures are less invasive and can be done on a beating heart, but are only suitable for certain patients.

Repair of most VSDs is complicated by the fact that the conducting system of the heart is in the immediate vicinity.

Ventricular septum defect in infants is initially treated medically with cardiac glycosides, loop diuretics and ACE inhibitors.

The Amplatzer muscular VSD occluder, may be used to close some VSDs.

The Amplatzer septal occluder has full closure of the ventricular defect within the 24 hours of placement.

Surgical closure of a Perimembranous VSD is performed on cardiopulmonary bypass with ischemic arrest.

Exposure is achieved through the right atrium, as the tricuspid valve septal leaflet is retracted or incised to expose the defect margins.

Percutaneous device closure of these defects is rarely performed because of the reported incidence of both early and late onset complete heart block after device closure, presumably secondary to device trauma to the AV node.

Patch materials are available, including native pericardium, bovine pericardium, Gore-or Dacron.

Suture techniques avoid injury to the conduction system located on the left ventricular side of the interventricular septum near the papillary muscle of the conus, and to avoid injury to the aortic valve with sutures.

Intraoperative transesophageal echocardiography confirms secure closure of the VSD, normal function of the aortic and tricuspid valves, ventricular function, and the elimination of all air from the left side of the heart.

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