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Ventricular Septal Defects. Tate Gisslen, MD Mentor: Bradley S. Marino, MD, MPP, MSCE May 6, 2011. Anatomy. 4 morphological components of septum Membranous Inlet Outlet/Infundibular Muscular/Trabecular. Anatomy. Membranous-70-80% Small Located at base, between inlet and outlet

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Ventricular Septal Defects

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ventricular septal defects

Ventricular Septal Defects

Tate Gisslen, MD

Mentor: Bradley S. Marino, MD, MPP, MSCE

May 6, 2011

  • 4 morphological components of septum
    • Membranous
    • Inlet
    • Outlet/Infundibular
    • Muscular/Trabecular
  • Membranous-70-80%
    • Small
    • Located at base, between inlet and outlet
    • Perimembranous - Extends to adjacent septum



  • Inlet
    • Inlet 5-8%,
    • AV valve to chordae attachments


  • Outlet/Infundibular
    • 5-7%
    • Separates L and R outflow tracts


  • Muscular/Trabecular (5-20%)
    • Anterior/Marginal (anterior to septal band)
    • Midmuscular/Central (posterior to septal band)
    • Apical (inferior to moderator band)
    • Posterior (beneath septal leaflet)


  • Blood flow (which way and how much) dependent on multiple factors
    • Small and restrictive
      • Lesion size
    • Large and non-restrictive
      • Balance between pulmonary and systemic vascular resistance
lesion size
Lesion Size
  • Restrictive VSD
    • < 0.5 cm2 (Smaller than Ao valve orifice area)
    • Small L to R shunt
    • Normal RV output
    • 75% spontaneously close < 2yrs
  • Non-restrictive VSD
    • > 1.0 cm2 (Equal to or greater than to Ao valve orifice area)
    • Equal RV and LV pressures
    • Large hemodynamically significant L to R shunt
    • Rarely close spontaneously
vascular resistance
Vascular Resistance
  • Pulmonary resistance may remain high longer in infants with large VSD
    • Minimal L to R shunt
  • Decreasing pulmonary resistance leads to significant L to R shunt
    • Clinical symptoms of CHF
  • Persistent L to R shunt leads to hypertrophy of the medial smooth muscle layer of the pulmonary arteries which increases PVR and potential R to L shunting
  • Long-standing L to R shunting that results in chronically increased PVR may lead to persistent R to L shunting described as “Eisenmenger Physiology”
clinical features small lesions
Clinical Features-Small Lesions
  • Murmur
    • 4 to 10 days, early with rapid decrease in PVR
  • Asymptomatic
    • normal feeding, growth and development
  • Restrictive VSD - Holosystolic murmur
    • correlates with continuous pressure gradient
  • Non-restrictive large VSD – no murmur (no turbulence if no gradient)
clinical features large lesions
Clinical Features-Large Lesions
  • Accentuated precordial activity
    • More prominent as LV volume increases
  • Signs/symptoms of CHF
    • Diaphoresis
    • Tachypnea
    • Fatigue with feeding
    • Hepatomegaly
    • Rales
    • Duskiness with crying
  • May develop as early as 2 weeks
  • Severity increases as PVR decreases
  • Chest Radiography
    • Cardiomegaly
    • Increased pulmonary vasculature
    • Pulmonary edema
  • EKG
    • Small: normal or LVH
      • Prominent Q, R, and T waves in II, III, aVF and V6
    • Large: Biventricular hypertrophy
      • RVH- rsR’ in V1, S wave in V6
  • Assess indication in consultation with Cardiology
  • Assess location, size, and multiplicity
  • RV and PA pressure
  • Assess for LA and LV dilation
  • Assess LV function
  • Note relation to great vessels, AV valves
cardiac catheterization
Cardiac Catheterization
  • Able to document
    • Number of defects
    • Presence of associated defects
    • Magnitude of shunt
    • Estimate PVR
  • Not used if information apparent by other means
    • Most information available through Echocardiography
  • Most common congenital heart lesion
  • Occurs in 50% of children with heart lesions
  • 15-20% in isolation
  • 5-50 per 1000 live births
  • 56% female
associated defects
Associated Defects
  • Left Heart Defects
    • Aortic stenosis
    • Coarctation of the aorta
  • Right Heart Defects
    • Tetrology of Fallot
    • Double Outlet Right Ventricle
  • Truncus Arteriosus
  • Some single ventricle (e.g. Tricuspid atresia, double inlet left ventricle)
chromosomal disorders associated with vsd
Chromosomal Disorders associated with VSD
  • Trisomy 21: 40% of T21 will have VSD
  • Trisomy 13, 18: 18% of T13, 31% of T18 will have VSD
  • 22q11 deletion:
    • Tetrology of Fallot is most common anomaly
    • VSD with or without aortic arch anomaly is second most common
  • Holt-Oram (Hand-heart syndrome): TBX5 gene found on Chromosome 12
  • Recurrence risk for VSD based on parental VSD
    • Paternal 2%
    • Maternal 6-10%
treatment for small vsd
Treatment for Small VSD
  • No medication or surgery if asymptomatic
    • 75-80% close by 2 years
  • Observation
  • No antibiotic prophylaxis for procedures
treating a moderate to large vsd
Treating a Moderate to Large VSD
  • Treatment of CHF
  • Determining when to repair
chf treatment
CHF Treatment
  • High-calorie formula
  • Medication
    • Diuretics
      • Furosemide with or without spironolactone
    • Afterload reduction
      • Enalapril or Captopril
    • Digoxin (maybe)
    • Symptoms of CHF improve as L to R shunt decreases
indications for intervention
Indications for Intervention
  • Decompensated CHF
  • Compensated CHF with:
    • Large hemodynamically significant VSD - L to R shunting with Qp/Qs > 2:1, even if asymptomatic, ideally before 1 year
    • Growth failure, unresponsive to medical therapy is an indication for surgery
not indicated
Not Indicated
  • Small VSDs - 6 months without CHF or ↑PVR
  • Small hemodynamically insignificant VSD – L to R shunting with Qp/Qs < 1.5:1
  • Eisenmenger physiology
post intervention
  • Most infants have normal growth and development
  • Early closure (< 1 year) associated with better LV function and regression of hypertrophy
  • Residual VSD is not common
  • RBBB is common following surgery
    • Rare complete heart block
  • Typically dacron patch closure
  • Sometimes primary closure
  • Surgical mortality < 1%
catheter closure
Catheter Closure
  • Location
    • Muscular
    • Perimembranous
  • Complications
    • Heart block
    • Valve insufficiency
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