Ventricular Septal Defect (VSD) CLINICAL FEATURES General examination with Treatment

• There is a shunt from LV to RV due to a defect in the interventricular septum.
• VSD also occurs in combination with other congenital heart defects, as in an atrioventricular canal (AVC),transposition of the great arteries (D-TGA),tetralogy of Fallot (TOF) and occasionally,

CLINICAL FEATURES

• Presentation — Most infants with VSD present in the neonatal period.
• typical presentation of a small VSD in a neonate involves the detection of a cardiac murmur at four to ten days of life

Ventricular Septal Defect (VSD) CLINICAL FEATURES and examination Investigations with Treatment

General examination —

• Infants with small, restrictive VSDs usually remain asymptomatic.
• These include Tachypnea (from increased pulmonary blood flow) Poor feeding (appears hungry but tires easily;
• In contrast, infants with moderate to large VSDs usually manifest signs of heart failure by three to four weeks of age ,
• Tachycardia Hepatomegaly Pulmonary rales, grunting, and retractions (if heart failure is marked) Pallor (from peripheral vasoconstriction)
• sweats with feeds) Poor weight gain (prolonged and severe failure may also affect linear growth and head circumference)

Mild / Small VSD :

• Very small peri membranous and muscular ventricular septal defects may be undetec­ted. There may be normal pulmonary arterial pres­sure.
• There is a prominent left parasternal holosystolic murmur. The murmur may disappear as the defect may spontaneously close.

Moderate VSD :

• There may be congestive heart fail­ure with holosystolic murmurs in the infant.

Large VSD :

• There is failure to thrive, retarded growth and development, hyperdynamic left ventricular im­pulse, left parasternal heave and thrill, harsh holosystolic murmur and apical mid diastolic murmur across the mitral valve.
• Peri membranous or small VSD closes spontaneously. With moderate and large VSD pulmonary vascular resistance increases, there may be congestive heart failure but always there is marked progressive pul­monary vascular disease.
• There is prominent left ventricular impulse due to volume overload and parasternal heave due to di­lated right ventricule due to increased pulmonary vascular resistance.
• VSDs lie just beneath the aortic valve and behind the septal leaflet of the tricuspid valve
• There is systolic thrill and holosystolic murmur, loud P2 and apical mid-diastolic murmur.

ECG

• Shows left atrial ‘P’ wave and tall T waves, or biatrial P waves and biventricular hypertrophy.

X-rays

• Shows increased pulmonary vascularity and pulmo­nary venous congestion. There is cardiomegaly with dilatation of all chambers.
• In moderate to large defects with increased left-to-right shunts, the pulmonary vascular markings are increased, and the left atrium, LV, and PA may be enlarged.
• Later on there is decreased pulmonary blood flow, reversal of shunt (right to left) – Eisenmenger physi­ology.
• In small defects, the radiograph is usually normal.
• All four chambers as well as the pulmonary trunk are dilated but aortic root is small.

2D echocardiography

• Shows the ventricular septal defect.
• Two-dimensional and Doppler echocardiography are useful in identifying the location of the defect and estimating the size of the shunt

Treatment of VSD

• Surgical or non-surgical closure of the defect at ap­propriate age before pulmonary hypertension devel­ops and reversal of shunt (right to left) occurs.