Ventricular Septal Defect
(VSD)
Meru Yale
 Most common congenital cardiac malformation
 25% of all CHD
 90% are in the membranous part of septum.
 VSD vary from a few mm in diameter ,to a defect so large –
no interventricular septum( single ventricle)
 Associated with ASD,PDA or PS
Embryology
embryology
Classification
according to number
 Single VSD  Multiple VSD
 (Swiss-cheese type)
According to size
 Small VSD - <0.5 cm2/m2 BSA
 Maladie de Roger- these defects close spontaneously.
 Moderate VSD is 0.5-1 cm2/m2
 Large VSD is >1cm2/m2
According to site
 Supracristal
 Infracristal
membranous muscular
inlet trabecular infundibular
Conditions associated with VSD
Chromosomal Anomalies
 Trisomy 21,18 13
 Cri-du-chat syndrome
Syndromes
 CATCH 22
 VATER
 Holt Oram
 CHARGE
Maternal conditions
• Diabetes
• Phenylketonuria
Teratogenic agents
• Alcohol
• Hydantoin
• Valproate
• Trimethadone
Haemodynamics
 Right ventricle pressure is 1/5th left ventricle pressure- causes pressure
gradient across vsd.
 Magnitude of shunt depends on size of defect and pulmonary
resistance.
 In large vsd rt to lft ventricular pressure is equalized.in these defects
direction is determined by ratio of pulmonary to systemic vascular
resistance.
Natural History
 Spontaneous closure in 40% cases
 25-30% defects may become small enough not to require surgical intervention.
 Majority of defects close by age 2,most close by age 5-7yrs.
 Pulmonary vascular obstructive disease may develop in 10%
 Infundibular stenosis (Gasul’s transformation) may occur in 8%of the defects.
 Aortic insufficiency develops in 5% of patients.
Clinical Features
 It depends on size of VSD
 Small vsd- asymptomatic.
 Moderate to large vsd – symptomatic at 6-10 wks of age.
exercise intolerance
delayed growth
CCF
recurrent respiratory tract infection
cardiomegaly
 Large vsd with pulmonary HTN
cyanosis
clubbing
polycythaemia
General examination
 Pulse
small vsd-normal
moderate vsd-normal
large vsd with CCF- pulsus alternans
 JVP
increased with large vsd with CCF
CVS
 Inspection
small vsd- normal
moderate vsd- moderate parasternal lift
Large vsd- hyperdynamic precordium
 Palpation
small vsd – normal
moderate and large vsd-
• Precordium-prominent(cardiomegaly)
• Parasternal heave (RV hypertrophy)
• P2 palpable (pulmonary HTN)
• Thrill (systolic)- 3rd and 4th ICS
Auscultation
 Small vsd- S2 normal , pansystolic murmur.
 Moderate vsd- S1 loud at apex
S2 widely split
P2 is loud
S3 may be heard over apex
murmur grade 4-6 ,holosystolic at left sternal border
short systolic murmur in 2nd left ICS
middiastolic murmur flow murmur – mitral valve area
 Large VSD-
• S2 loud with loud P2
• PSM with thrill - lower left sternal border
• S3
• Mid-diadtolic rumble in apical area
• Murmur in upper left parasternal area
• Pulmonary ESM preceded by EC
INVESTIGATIONS
 ECG
 Moderate VSD –
 Large VSD-
• Left axis deviation
• Left atrial enlargement- notched p in lead I , aVR and V6
• Left ventricular enlargement – tall R in lead I, II and aVF
• Prominent Q and tall R in V5 and V6
• Right axis deviation
• Biventricular enlargement- tall R in V1, deep Q in V5 and V6
• V3/V4 – equiphasic RS complex
• RBBB may be seen
Tracing from a 3-month-old infant with a large ventricular septal defect, patent ductus arteriosus,
and pulmonary hypertension. The tracing shows
combined ventricular hypertrophy with left dominance. Note that V2 and V4 are in ½
standardization.
X-RAY
 Moderate VSD –
 Large VSD –
• Mild – moderate cardiac enlargement
• Mild prominence of pulmonary artery
• Increase in pulmonary vasculature
• Significant cardiomegaly with left atrial enlargement
• Right atrial enlargement(with CCF)
• Dilated pulmonary artery
• Pulmonary plethora
Posteroanterior and lateral views of chest roentgenograms of a ventricular septal
defect with a large shunt and pulmonary hypertension. The heart size is
moderately increased, with enlargement on both sides. Pulmonary vascular markings
are increased, with a prominent main pulmonary artery segment.
 Eisenmenger’s complex
• Minimal cardiomegaly
• Oligaemic lung fields with central plethora
• Moderately dilated pulmonary trunk
 ECHO – site and size of defect can be visualized.
 Cardiac catheterisation-
 Doppler study detects direction of flow of blood across shunt.
• Visualisation of defect
• Oxygen studies
• Pressure studies
Complications
 CCF
 Pulmonary HTN
 Eisenmenger’s syndrome
 AR
 IE
Treatment
 Small VSD require no treatment – close spontaneously
 Operative correction is indicated in Qp:Qs ratio >1.5:1.0
 Medical
• Control CCF
• Treat repeated chest infections
• Anemia
• IE
 Surgical
• In CCF
• Large L R shunt
• Associated PS, pulmonary HTN, AR
 Closure of VSD with a patch
 Catheter closure of VSD is best for muscular defects
Thank You

Vsd

  • 1.
  • 4.
     Most commoncongenital cardiac malformation  25% of all CHD  90% are in the membranous part of septum.  VSD vary from a few mm in diameter ,to a defect so large – no interventricular septum( single ventricle)  Associated with ASD,PDA or PS
  • 5.
  • 6.
  • 7.
    Classification according to number Single VSD  Multiple VSD  (Swiss-cheese type)
  • 8.
    According to size Small VSD - <0.5 cm2/m2 BSA  Maladie de Roger- these defects close spontaneously.  Moderate VSD is 0.5-1 cm2/m2  Large VSD is >1cm2/m2
  • 9.
    According to site Supracristal  Infracristal membranous muscular inlet trabecular infundibular
  • 10.
    Conditions associated withVSD Chromosomal Anomalies  Trisomy 21,18 13  Cri-du-chat syndrome Syndromes  CATCH 22  VATER  Holt Oram  CHARGE Maternal conditions • Diabetes • Phenylketonuria Teratogenic agents • Alcohol • Hydantoin • Valproate • Trimethadone
  • 11.
  • 13.
     Right ventriclepressure is 1/5th left ventricle pressure- causes pressure gradient across vsd.  Magnitude of shunt depends on size of defect and pulmonary resistance.  In large vsd rt to lft ventricular pressure is equalized.in these defects direction is determined by ratio of pulmonary to systemic vascular resistance.
  • 17.
    Natural History  Spontaneousclosure in 40% cases  25-30% defects may become small enough not to require surgical intervention.  Majority of defects close by age 2,most close by age 5-7yrs.  Pulmonary vascular obstructive disease may develop in 10%  Infundibular stenosis (Gasul’s transformation) may occur in 8%of the defects.  Aortic insufficiency develops in 5% of patients.
  • 18.
    Clinical Features  Itdepends on size of VSD  Small vsd- asymptomatic.  Moderate to large vsd – symptomatic at 6-10 wks of age. exercise intolerance delayed growth CCF recurrent respiratory tract infection cardiomegaly  Large vsd with pulmonary HTN cyanosis clubbing polycythaemia
  • 19.
    General examination  Pulse smallvsd-normal moderate vsd-normal large vsd with CCF- pulsus alternans  JVP increased with large vsd with CCF
  • 20.
    CVS  Inspection small vsd-normal moderate vsd- moderate parasternal lift Large vsd- hyperdynamic precordium  Palpation small vsd – normal moderate and large vsd- • Precordium-prominent(cardiomegaly) • Parasternal heave (RV hypertrophy) • P2 palpable (pulmonary HTN) • Thrill (systolic)- 3rd and 4th ICS
  • 21.
    Auscultation  Small vsd-S2 normal , pansystolic murmur.  Moderate vsd- S1 loud at apex S2 widely split P2 is loud S3 may be heard over apex murmur grade 4-6 ,holosystolic at left sternal border short systolic murmur in 2nd left ICS middiastolic murmur flow murmur – mitral valve area
  • 22.
     Large VSD- •S2 loud with loud P2 • PSM with thrill - lower left sternal border • S3 • Mid-diadtolic rumble in apical area • Murmur in upper left parasternal area • Pulmonary ESM preceded by EC
  • 23.
    INVESTIGATIONS  ECG  ModerateVSD –  Large VSD- • Left axis deviation • Left atrial enlargement- notched p in lead I , aVR and V6 • Left ventricular enlargement – tall R in lead I, II and aVF • Prominent Q and tall R in V5 and V6 • Right axis deviation • Biventricular enlargement- tall R in V1, deep Q in V5 and V6 • V3/V4 – equiphasic RS complex • RBBB may be seen
  • 25.
    Tracing from a3-month-old infant with a large ventricular septal defect, patent ductus arteriosus, and pulmonary hypertension. The tracing shows combined ventricular hypertrophy with left dominance. Note that V2 and V4 are in ½ standardization.
  • 26.
    X-RAY  Moderate VSD–  Large VSD – • Mild – moderate cardiac enlargement • Mild prominence of pulmonary artery • Increase in pulmonary vasculature • Significant cardiomegaly with left atrial enlargement • Right atrial enlargement(with CCF) • Dilated pulmonary artery • Pulmonary plethora
  • 28.
    Posteroanterior and lateralviews of chest roentgenograms of a ventricular septal defect with a large shunt and pulmonary hypertension. The heart size is moderately increased, with enlargement on both sides. Pulmonary vascular markings are increased, with a prominent main pulmonary artery segment.
  • 29.
     Eisenmenger’s complex •Minimal cardiomegaly • Oligaemic lung fields with central plethora • Moderately dilated pulmonary trunk
  • 30.
     ECHO –site and size of defect can be visualized.  Cardiac catheterisation-  Doppler study detects direction of flow of blood across shunt. • Visualisation of defect • Oxygen studies • Pressure studies
  • 31.
    Complications  CCF  PulmonaryHTN  Eisenmenger’s syndrome  AR  IE
  • 32.
    Treatment  Small VSDrequire no treatment – close spontaneously  Operative correction is indicated in Qp:Qs ratio >1.5:1.0  Medical • Control CCF • Treat repeated chest infections • Anemia • IE  Surgical • In CCF • Large L R shunt • Associated PS, pulmonary HTN, AR  Closure of VSD with a patch  Catheter closure of VSD is best for muscular defects
  • 33.