A ventricular septal defect (VSD) is a defect in the ventricular septum, the wall dividing the left and right ventricles of the heart.
The extent of the opening may vary from pin size to complete absence of the ventricular septum, creating one common ventricle.
The ventricular septum consists of an inferior muscular and superior membranous portion and is extensively innervated with conducting cardiomyocytes.
The membranous portion, which is close to the atrioventricular node, is most commonly affected in adults and older children in the United States.
It is also the type that will most commonly require surgical intervention, comprising over 80% of cases.
Membranous ventricular septal defects are more common than muscular ventricular septal defects, and are the most common congenital cardiac anomaly.
Signs and symptoms
Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth.
VSD is an acyanotic congenital heart defect, aka a left-to-right shunt, so there are no signs of cyanosis in the early stage.
However, uncorrected VSD can increase pulmonary resistance leading to the reversal of the shunt and corresponding cyanosis.
Pansystolic (Holosystolic) murmur along lower left sternal border (depending upon the size of the defect) +/- palpable thrill (palpable turbulence of blood flow). Heart sounds are normal.
Larger VSDs may cause a parasternal heave, a displaced apex beat (the palpable heartbeat moves laterally over time, as the heart enlarges).
An infant with a large VSD will fail to thrive and become sweaty and tachypnoeic (breathe faster) with feeds.
The restrictive ventricular septal defects (smaller defects) are associated with a louder murmur and more palpable thrill (grade IV murmur).
Larger defects may eventually be associated with pulmonary hypertension due to the increased blood flow.
Over time this may lead to an Eisenmenger’s syndrome the original VSD operating with a left-to-right shunt, now becomes a right-to-left shunt because of the increased pressures in the pulmonary vascular bed.
Congenital VSDs are frequently associated with other congenital conditions, such as Down syndrome.
A VSD can also form a few days after a myocardial infarction (heart attack) due to mechanical tearing of the septal wall, before scar tissue forms, when macrophages start remodeling the dead heart tissue.
The causes of congenital VSD (ventricular septal defect) include the incomplete looping of the heart during days 24-28 of development.
Faults with gene are usually associated with isolated (non syndromic) ASD in humans when one copy is missing.
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 than the right ventricle , 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.