Ventricular Septal Defect (VSD)

VSD is the most common congenital heart condition. It may occur as an isolated defect, or it may be a component of anomalies such as tetralogy of Fallot, transposition of great arteries, coarctation of aorta etc.




1/500. Commonest congenital heart defect.

Defect may be small or large.
With a small defect, the murmur is rarely present at birth but appears as pulmonary vascular resistance falls and left to right shunt occurs. The key feature is that not enough blood can pass through the hole to overload the right heart – overcirculation is mild and there is no heart failure. The murmur is the most significant feature.
In patients with larger defect and thus larger left-to-right shunt, large amounts of blood cross the defect leading to pulmonary overcirulation and depriving the systemic circulation of cardiac output. This therefore overloads right and left heart. Signs and symptoms are of pulmonary oedema, right heart failure and compensated shock. Failure to thrive become more apparent at around 6-8 weeks.

Children with small VSD are usually asymptomatic and are reviewed at a regular basis. Most do not require active treatment. The defects tend to grow become smaller with time and majority undergo spontaneous closure.

Moderate VSDs require regular reviews, medical therapy with diuretics +/- ACE inhibitors for infants of cardiac failure and optimisation of calorie intake. Patients who respond to medical therapy are followed closely to see whether the defect diminishes in size during the first year of life, or even closes spontaneously.

With large VSDs, the initial treatment is medical therapy with diuretics +/- ACE inhibitors to control congestive cardiac failure and prevent pulmonary vascular disease. Sometimes pulmonary artery banding manages overcirculation and allows the baby to grow before surgery.

Indications of surgical closure of VSD :

1.    Infants <6 months (<3 months for those with trisomy 21) who have uncontrolled heart failure despite maximal medical and dietary interventions or who have pulmonary hypertension.

2.     Children with a persistent significant shunt (Qp:Qs >2:1) with elevated PA pressures

3.    Subpulmonic and membranous defects, with aortic regurgitation should be surgically corrected before the aortic valve is permanently damaged.
Procedures may involve Intracardiac repair ( direct patch closure of the defect under cardiopulmonary bypass and/or deep hypothermia ) or transcatheter closure.

Surgical closure of a VSD is generally contraindicated if PA pressure is suprasystemic or if PVR is greater than >12 mmHg/L/min/m2 as these patients are at high risk for persistent pulmonary hypertension and closure of defects with such elevated PVR may result in low cardiac output and increased peri-operative mortality.

(small defect)
Asymptomatic (80 – 90%)
May have a thrill at left lower sternal edge
Loud pansystolic mumur at lower left sternal edge (the louder the murmur, the smaller the hole within reason)
Quiet P2

(large defect)
Symptomatic with heart failure after age 1 week (tachypnoea, poor feeding)
Right ventricular heave
Soft or no systolic murmur
Apical mid-diastolic heart murmur
Loud P2
Displaced apex beat

ECG – Small defect: normal. Large defect : biventricular hypertrophy by 2 months
CXR – Small defect: normal. Large defect:  increased pulmonary markings; cardiomegaly

Exam vignette
I examined Harry, a 9-year-old boy  who looks well-grown for his age. I would like to plot his height and weight on a growth chart.
He is pink and not in respiratory distress. There are no dysmorphic features or finger clubbing. There are no scars on his chest.
He has a grade 3/6 pansystolic murmur audible all over his praecordium but loudest on his left lower sternal edge.
My differential diagnoses include Ventricular Septal Defect, tricuspid regurgitation or mitral regurgitation.

Filed in Cardiovascular
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