Ventricular Septal Defects

Background/Epidemiology

  • Most common congenital heart defect; ~2/1000 live births, usually in conjunction with other heart defects but not uncommon to be isolated
  • Not uncommonly associated with genetic abnormalities e.g. Down’s syndrome; Edward’s syndrome; Patau’s syndrome

Pathophysiology

  • The size of the VSD, the pressures in the right and left ventricles and pulmonary resistance will determine the physiological effect of a VSD
  • At birth, the pressure difference between the left and right side of the heart are almost equal and so the effect is minimal.  With time, the pressure gradient increases and symptoms manifest.
    • If there is persistent high pulmonary resistance e.g. in Down’s syndrome, this can further halt the effect of a VSD (therefore patients with Down’s are always screened for heart defects shortly after birth)
  • Without increased pulmonary resistance/obstruction, the shunt is left to right.
    • This rarely has a significant effect on the right heart (as might be expected); but instead, the increased pre-load returning to the left side of the heart causes symptoms of heart failure
  • Only in severe disease, can subsequent pulmonary hypertension cause a right-left shunt

Presentation

  • Small lesions may cause few or no symptoms
    • Only sign may be a harsh pansystolic murmur (often loudest in small lesions- may have a palpable thrill)
  • Moderate defects may present with increased respiration rate and effort and fatigue, particularly after feeding (exertion for a baby)
    • Poor weight gain/failure to thrive (normal length but low weight)

Investigations

  • Echocardiography is the main investigation
  • CXR/ECG may also be useful to monitor any heart failure

Management

  • Small VSDs may resolve themselves
  • Larger defects will require surgery to close them
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