A ventricular septal defect (VSD) 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.
VSD is the most common congenital cardiac defect, occurring once in 500 live births. It may occur as an isolated abnormality or part of complex congenital heart disease.
Symptoms: Usually no symptoms but symptoms develop when Eisenmenger’s syndrome develops. Symptoms are: dyspnoea, fatigue, heart failure.
- Small VSD: Presents with a loud systolic murmur over left lower sterna edge. In asymptomatic patient such VSD usually closed spontaneously.
- Moderate VSD:
- Systolic thrill over left sterna edge.
- A loud pansystolic murmur.
- Cardiac enlargement.
- Large VSD:
- Increasing pulmonary hypertension.
- Right ventricular parasternal heave.
- Loud pulmonary component of 2nd heart sound.
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 cardiac ultrasound (echocardiography). To more accurately measure ventricular pressures, cardiac catherization, can be performed.
- Small VSD : No findings.
- Moderate to large VSD:
- X-ray: cardiomegaly, enlargement of pulmonary arteries.
- ECG: Features of LVH and RVH.
- Echo: Demonstrate the defect, biventricular enlargement, pulmonary artery enlargement.
- Small VSD: Usually closed spontaneously.
- Moderate to large VSD: Surgical repaired before development of severe pulmonary hypertension. Prophylaxis for infective endocarditis should be advice.
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:
- Failure of congestive cardiac failure to respond to medications
- VSD with pulmonic stenosis.
- Large VSD with pulmonary hypertension.
- 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 10-20 µg/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).
- Davidson’s Principles and Practice of Medicine, 21st
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