is a defect in the ventricular septum, the wall dividing the left and right ventricles of the heart.
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.
Diagnosis
A VSD can be detected by cardiac auscultation. Classically, a VSD causes a pathognomonic holo- or pansystolic murmur. Auscultation is generally considered sufficient for detecting a significant VSD. The murmur depends on the abnormal flow of blood from the left ventricle, through the VSD, to the right ventricle. If there is not much difference in pressure between the left and right ventricles, then the flow of blood through the VSD will not be very great and the VSD may be silent. This situation occurs a) in the fetus (when the right and left ventricular pressures are essentially equal), b) for a short time after birth (before the right ventricular pressure has decreased), and c) as a late complication of unrepaired VSD. Confirmation of cardiac auscultation can be obtained by non-invasive echocardiography. To more accurately measure ventricular pressures, cardiac catheterization, can be performed.
Signs and symptoms
Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth.
Symptoms
VSD is an acyanotic congenital heart defect, aka a Left-to-right shunt, so there are no signs of cyanosis.
Signs
Pansystolic (Holosystolic) murmur (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.
CAUSES: The cause of VSD ( ventricular septal defect) includes the incomplete looping of the heart during days 24-28 of development. Faults with NKX2.5 gene can cause this.
Complications
- Aortic insufficiency (leaking of the valve that separates the left ventricle from the aorta)
- Damage to the electrical conduction system of the heart during surgery (causing an irregular heart rhythm)
- (failure to thrive in infancy)
- Heart failure
- Infective endocarditis
- Pulmonary hypertension
Treatment
Most cases do not need treatment and heal at the first years of life. Treatment is either conservative or surgical. Smaller 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, i.e. with the following indications:
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 the surgical procedure, 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 (e.g., digoxin 10-20mcg/kg per day), loop diuretics (e.g., furosemide 1–3 mg/kg per day) and ACE inhibitors (e.g., captopril 0.5–2 mg/kg per day).
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