VENTRICULAR SEPTAL DEFECT

VSDVSD
BY DR. VIKAS, DEPTT. OFBY DR. VIKAS, DEPTT. OF
CTVS, PGIMER ,CTVS, PGIMER ,
CHANDIGARHCHANDIGARH

CASE PRESENTATIONCASE PRESENTATION
 Natik 2 year m childNatik 2 year m child
Magholi Chopal shimla .Magholi Chopal shimla .
 History of 1 Recurrent chest infection .History of 1 Recurrent chest infection .
2 Difficulty in breathing .2 Difficulty in breathing .
3 Failure to thrive.3 Failure to thrive.

 h/o fever present.h/o fever present.
 h/o cough present.no h/o hemoptysis.h/o cough present.no h/o hemoptysis.
 h/o dyspnea at rest present . No PNDh/o dyspnea at rest present . No PND
 No h/o wheeze.No h/o wheeze.
 Ho palpitation presentHo palpitation present
 No h/o cynosis.Squatting ,orNo h/o cynosis.Squatting ,or Syncopal attack.Syncopal attack.
 h/o puffiness of face distention of abdomenh/o puffiness of face distention of abdomen
present .present .

 Family history - no h/o D M. HT .TB.Family history - no h/o D M. HT .TB.
 Past history . antinatal normal,Past history . antinatal normal,
 General examination .General examination .
 Height 82 CM Weight . 8 KGHeight 82 CM Weight . 8 KG
66% GRADE 11 PEM`66% GRADE 11 PEM`
RAO’S INDEX .12 N (.15 to .16) SPO2RAO’S INDEX .12 N (.15 to .16) SPO2
 H R 130 / min R-R 34/minH R 130 / min R-R 34/min
 Pallor is presentPallor is present
 No cynosis ,icterus,clubbing ,No cynosis ,icterus,clubbing ,
 JVP ,LAP,Edema.JVP ,LAP,Edema.

 CARDIOVASCULAR EXAMINATION .CARDIOVASCULAR EXAMINATION .
 precordium bulging present.precordium bulging present.
Apex beat 5Apex beat 5thth
ICS -ICS -
Thrill presentThrill present
PSM GRADE .3PSM GRADE .3

InvestigationInvestigation
 .Hb 13.5 g% TLC 4700..Hb 13.5 g% TLC 4700.
 Glucose . 79 mg% .Glucose . 79 mg% .
 Na 138 k 4.5. Cl 31Na 138 k 4.5. Cl 31
 S urea 43 S Creatinine .4S urea 43 S Creatinine .4

 INTRODUCTIONINTRODUCTION
 AA VSDVSD is a defect in the ventricular septumis a defect in the ventricular septum
 The ventricular septum consists of an inferiorThe ventricular septum consists of an inferior
muscular and superior membranous portionmuscular and superior membranous portion
 The membranous portion -most commonlyThe membranous portion -most commonly
affected in adults and older childrenaffected in adults and older children
 most common congenital cardiac anomalies.most common congenital cardiac anomalies.
 3-3.8 per 1000 live births3-3.8 per 1000 live births

Ventricular Septal DefectVentricular Septal Defect
 Most common CHD in children (25%)Most common CHD in children (25%)
 75-80% of small VSD’s close75-80% of small VSD’s close
spontaneously by late childhoodspontaneously by late childhood
 10-15% of large VSD’s close10-15% of large VSD’s close
spontaneouslyspontaneously
 60% of defects close before age 3, and60% of defects close before age 3, and
90% before age 890% before age 8
 Risk factors for decreased survival forRisk factors for decreased survival for
unoperated patients include:unoperated patients include:
 Cardiomegaly on CXR, Elevated PASPCardiomegaly on CXR, Elevated PASP
(>50 mmHg), and CV symptoms.(>50 mmHg), and CV symptoms.

 Henri Roger was the first man toHenri Roger was the first man to
describe a ventricular septal defect,describe a ventricular septal defect,
in 1879 he wrote:in 1879 he wrote:
““A developmental defect of the heart occursA developmental defect of the heart occurs
from which cyanosis does not ensue in spitefrom which cyanosis does not ensue in spite
of the fact that a communication existsof the fact that a communication exists
between the cavities of the two ventriclesbetween the cavities of the two ventricles
and in spite of the fact that the admixture ofand in spite of the fact that the admixture of
venous blood and arterial blood occurs. Thisvenous blood and arterial blood occurs. This
congenital defect, which is even compatiblecongenital defect, which is even compatible
with long life, is a simple one. It comprises awith long life, is a simple one. It comprises a
defect in the interventricular septum”defect in the interventricular septum”

Development of IVSDevelopment of IVS
 Muscular septumMuscular septum ––
primordial IV septumprimordial IV septum
 Closure ofClosure of
interventricularinterventricular
foramen&foramen& membranousmembranous
septumseptum formation-formation-
Rt & Lt bulbar ridgesRt & Lt bulbar ridges
endocardial cushionsendocardial cushions

Morphology – The VentricularMorphology – The Ventricular
SeptumSeptum
1. Membranous
2. Outflow
3. Trabecular
septum
4. Inflow
5. Subarterial /
Supracristal

AnatomyAnatomy
 4 morphological components of septum4 morphological components of septum
 MembranousMembranous
 InletInlet
 Outlet/InfundibularOutlet/Infundibular
 Muscular/TrabecularMuscular/Trabecular

AnatomyAnatomy
 Membranous-70-80%Membranous-70-80%
 SmallSmall
 Located at base, between inlet and outletLocated at base, between inlet and outlet
 Perimembranous - Extends to adjacentPerimembranous - Extends to adjacent
SSEseptumSSEseptumMembranous Membranous

AnatomyAnatomy
 InletInlet
 Inlet 5-8%,Inlet 5-8%,
 AV valve to chordae attachmentsAV valve to chordae attachments
Inlet

AnatomyAnatomy
 Outlet/InfundibularOutlet/Infundibular
 5-7%5-7%
 Separates L and R outflow tractsSeparates L and R outflow tracts
Infundibular

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

Types of VSD (kirklin)Types of VSD (kirklin)
1
23
4

Hemodynamic classificationHemodynamic classification
 RestrictiveRestrictive- resistance that limits the shunt at the site of- resistance that limits the shunt at the site of
vsdvsd
LVSP > RVSPLVSP > RVSP
pulm /aortic systolic pressure ratio < 0.3pulm /aortic systolic pressure ratio < 0.3
Qp / Qs<1.4/1Qp / Qs<1.4/1
 Moderately restrictiveModerately restrictive - RVSP high, but less than LVSP- RVSP high, but less than LVSP
- Qp/Qs 1.4/2.2- Qp/Qs 1.4/2.2
 Non restrictiveNon restrictive -Shunt not limited at the site of defect-Shunt not limited at the site of defect
RVSP , LVSP, PA , Aortic systolicRVSP , LVSP, PA , Aortic systolic
pressurespressures equalequal
Qp/Qs >2.2Qp/Qs >2.2
Flow determined by PVRFlow determined by PVR

Natural historyNatural history
 Spontaneous closure :75-85 % allSpontaneous closure :75-85 % all
VSDs:35% perimemb .VSDs:35% perimemb .
 80% at age 1month . 60% at 380% at age 1month . 60% at 3
month.50%at age 6 month and 25% ofmonth.50%at age 6 month and 25% of
those at age 12 monththose at age 12 month..
 More frequent in small defectsMore frequent in small defects
 Decrease in size with ageDecrease in size with age
 Inlet & outlet defects donot become smaller /close spontInlet & outlet defects donot become smaller /close spont
 Large & nonrestrictive defects : 10- 15%Large & nonrestrictive defects : 10- 15%
 EndocarditisEndocarditis – risk of endocarditis 4-10% for the first 30 years– risk of endocarditis 4-10% for the first 30 years
of lifeof life
 25 yr survival for all pts with a VSD 87%25 yr survival for all pts with a VSD 87%

Mechanisms of closureMechanisms of closure
 Adherence of tricuspid leaflet , or chordal tissue toAdherence of tricuspid leaflet , or chordal tissue to
the edges of VSD.the edges of VSD.
 Growth & hypertrophy of septum around the defectGrowth & hypertrophy of septum around the defect
 By development of subacute bacterial endocarditisBy development of subacute bacterial endocarditis
adherence of STL tissue to the marginsadherence of STL tissue to the margins
 (Negative pressure effect exerted by a high velocity(Negative pressure effect exerted by a high velocity
stream flowing through the defect )stream flowing through the defect )
 Ventricular septal aneurysmVentricular septal aneurysm
 prolapse of aortic cuspprolapse of aortic cusp
 intrusion of a sinus of valsalva aneurysmintrusion of a sinus of valsalva aneurysm

Associated LesionsAssociated Lesions
 PDA --6% 25% infants with heartPDA --6% 25% infants with heart
failure.failure.
 Coarctation of the aorta 5%.Coarctation of the aorta 5%.
 Congenital aortic stenosis 2% .Congenital aortic stenosis 2% .
 Congenital mitral valve disease 2%Congenital mitral valve disease 2%

Special situations IN VSDSpecial situations IN VSD
 VSD WITH PDAVSD WITH PDA
 VSD WITH COARCTARION OFVSD WITH COARCTARION OF
AORTA.AORTA.
 RIGHT ATRIAL VERSUS RIGHTRIGHT ATRIAL VERSUS RIGHT
VENTRICULAR APPROACH.VENTRICULAR APPROACH.
 PERCUTANEOUS CLOSURE OFPERCUTANEOUS CLOSURE OF
VSD.VSD.
 VSD WITH PUL RESISTANCE HIGH .VSD WITH PUL RESISTANCE HIGH .

Timing of surgery in VSDTiming of surgery in VSD
 <3months<3months - if symptomatic- if symptomatic
 3-6 months3-6 months - symptomatic, growth- symptomatic, growth
failure, increasing PAH.failure, increasing PAH.
 >6 months>6 months – primarily based on PAH– primarily based on PAH
 Wait till 1 yr , if no PAHWait till 1 yr , if no PAH

PathophysiologyPathophysiology
 Defect size is often compared to aorticDefect size is often compared to aortic
annulusannulus
 Large: > 75% of annulus size , flow velocity 1mLarge: > 75% of annulus size , flow velocity 1m
ss
 Medium: 33-75% of annulus size flow velocityMedium: 33-75% of annulus size flow velocity
1 to 4 m s1 to 4 m s
 Small: <33% of annulus size flow velocity >4 mSmall: <33% of annulus size flow velocity >4 m
ss

 Restrictive VSD is typically small, such that aRestrictive VSD is typically small, such that a
significant pressure gradient exists between thesignificant pressure gradient exists between the
LV and RV (high velocity), with small shuntLV and RV (high velocity), with small shunt
(Qp/Qs ≤ 1.4 : 1)(Qp/Qs ≤ 1.4 : 1)
 Moderately restrictive VSDModerately restrictive VSD  moderate shuntmoderate shunt
(Qp/Qs 1.4 to 2.2 : 1)(Qp/Qs 1.4 to 2.2 : 1)
 Large / non-restrictive VSDLarge / non-restrictive VSD  large shunt (Qp/Qslarge shunt (Qp/Qs
> 2.2 : 1)> 2.2 : 1)
 Eisenmenger VSDEisenmenger VSD  irreversible pulmonary HTNirreversible pulmonary HTN
and shunt may be zero or reversed (i.e. Rand shunt may be zero or reversed (i.e. RL)L)

 During systole, blood is shunted from LV to RVDuring systole, blood is shunted from LV to RV
 passes through the lungs and re enters the LV via thepasses through the lungs and re enters the LV via the
pulmonary veins and LA causes volume overload onpulmonary veins and LA causes volume overload on
the LV Shunt into the RV elevates RV pressure andthe LV Shunt into the RV elevates RV pressure and
volume, leading to pulmonary hypertension.volume, leading to pulmonary hypertension.
 More noticeable in patients with larger defectsMore noticeable in patients with larger defects
Magnitude of shunt: size, PVRMagnitude of shunt: size, PVR
 Small defect: large resistance occurs at the defectSmall defect: large resistance occurs at the defect
 Larger defect: resistance offered by the defectLarger defect: resistance offered by the defect
minimumminimum

Heath-Edwards ClassificationHeath-Edwards Classification
Grade I: Medial hypertrophy
Grade II: Cellular intimal
proliferation in an
abnormally muscular artery
Grade III: Occlusive changes Grade IV: Dilatation
Grade V: Plexiform lesions
Grade VI: Acute necrotizing
arteritis

 Enlargement of LA,Enlargement of LA,
LV,PALV,PA
 Shunt mainly inShunt mainly in
systole, when thesystole, when the
RV also contractsRV also contracts
 Shunted blood goesShunted blood goes
directly to PAdirectly to PA

ManagementManagement
 Observation & follow upObservation & follow up
Small VSDsSmall VSDs
 Medical managementMedical management
Medium sized vsdMedium sized vsd
CCF- treat with diuretics & digitalis,CCF- treat with diuretics & digitalis,
ACEIACEI
failure ppted by LRTI- Treat bothfailure ppted by LRTI- Treat both
2-3 months follow up2-3 months follow up
RV & PA pressures assessedRV & PA pressures assessed
Failure to thriveFailure to thrive
 SurgicalSurgical
Large vsdLarge vsd

 drugsdrugs
digoxin 10-20mcg/kg per daydigoxin 10-20mcg/kg per day
furosemide 1–3 mg/kg per dayfurosemide 1–3 mg/kg per day
captopril 0.5–2 mg/kg per daycaptopril 0.5–2 mg/kg per day
enalapril 0.1mg/kg per dayenalapril 0.1mg/kg per day

Indications of surgicalIndications of surgical
interventionintervention
 Large VSD with pulmonaryLarge VSD with pulmonary
hypertensionhypertension
 VSD with aortic regurgitationVSD with aortic regurgitation
 VSD with associated defectsVSD with associated defects
 Failure of CCF to respond toFailure of CCF to respond to
medications.medications.

 ACC/AHA guidelines 2008 forACC/AHA guidelines 2008 for
management of adults with CHDmanagement of adults with CHD

Surgical VSD closureSurgical VSD closure
 Closure of vsd indicated when Qp/QsClosure of vsd indicated when Qp/Qs
2 or more & clinical e/o LV volume2 or more & clinical e/o LV volume
overloadoverload
When pt has a history of IEWhen pt has a history of IEIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

Surgical VSD closureSurgical VSD closure
 Closure of vsd is reasonable when LClosure of vsd is reasonable when LR shunt isR shunt is
present at a Qp/Qs >1.5, with a PA pressure <2/3present at a Qp/Qs >1.5, with a PA pressure <2/3rdrd
of systemic pressure & pulse volume recording <of systemic pressure & pulse volume recording <
2/32/3rdrd
of SVRof SVR
 Closure of vsd is reasonable when LClosure of vsd is reasonable when LR shunt isR shunt is
present at a Qp/Qs >1.5, in the presence of LVpresent at a Qp/Qs >1.5, in the presence of LV
systolic or diastolic failuresystolic or diastolic failure
 Vsd closure not recommended in pts with severeVsd closure not recommended in pts with severe
irreversible PAHirreversible PAH
III IIaIIaIIaIIbIIbIIbIIIIIIIIIIII IIaIIaIIaIIbIIbIIbIIIIIIIIIIII IIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII
III IIaIIaIIaIIbIIbIIbIIIIIIIIIIII IIaIIaIIaIIbIIbIIbIIIIIIIIIIII IIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII
III IIaIIaIIa IIbIIbIIbIIIIIIIIIIII IIaIIaIIa IIbIIbIIbIIIIIIIIIIII IIaIIaIIa IIbIIbIIbIIIIIIIII

PA bandingPA banding
 PA banding- palliative procedure , whenPA banding- palliative procedure , when
additional lesions make repair difficult, patientadditional lesions make repair difficult, patient
in severe heart failure.in severe heart failure.
 Done in multiple VSDsDone in multiple VSDs
 30-50% of original diameter is narrowed30-50% of original diameter is narrowed
 Systolic pressure of 25-30 mmHg beyond theSystolic pressure of 25-30 mmHg beyond the
constriction.constriction.

Technique of operation. VSDTechnique of operation. VSD

Transventricular approach for closureTransventricular approach for closure
of conal septal defectof conal septal defect

COMPLICATIONSCOMPLICATIONS
 AV Dissociation . RBBB.AV Dissociation . RBBB.
 Ventricular arrhythmias.Ventricular arrhythmias.
 Heart block.Heart block.
 Poor hemodynamic state.Poor hemodynamic state.
 Residual shunting.2%Residual shunting.2%
 AR/TRAR/TR
 Cardiac dysfunction.Cardiac dysfunction.
 Pulmonary hypertension.Pulmonary hypertension.
 Early hospital death.<1%Early hospital death.<1%

Post op follow upPost op follow up
 Every 1-2 yrsEvery 1-2 yrs
 VSD & mild PAH& repair after 3 yrs ofVSD & mild PAH& repair after 3 yrs of
age-age- watch for progressivewatch for progressive
pulmonary vascular disease.pulmonary vascular disease.
 Surgical cureSurgical cure. (. (surviving the earlysurviving the early
postoperative period and being alivepostoperative period and being alive
late postoperativelylate postoperatively ..

Endocarditis Prophylaxis forEndocarditis Prophylaxis for
VSDVSD
 Uncomplicated VSD – no Abx for dental or otherUncomplicated VSD – no Abx for dental or other
procedures required .procedures required .
 Post repair:Post repair:
 Abx for 6 months following surgical or percutaneousAbx for 6 months following surgical or percutaneous
repairrepair
 Indefinite Abx if there is residual shuntIndefinite Abx if there is residual shunt
 Focus should be on optimal dental hygiene for those withFocus should be on optimal dental hygiene for those with
CHDCHD

Eisenmenger SyndromeEisenmenger Syndrome
 InIn 1897 Victor Eisenmenger published a paper1897 Victor Eisenmenger published a paper
entitled “congenital defects of the ventricular septum”entitled “congenital defects of the ventricular septum”
 In 1958, Paul Wood summarized Eisenmenger’sIn 1958, Paul Wood summarized Eisenmenger’s
accounts:accounts:
““The patient was a powerfully built man of 32 whoThe patient was a powerfully built man of 32 who
gave a history of cyanosis and moderategave a history of cyanosis and moderate
breathlessness since infancy. He managed well untilbreathlessness since infancy. He managed well until
January of 1894 when dyspnea increased andJanuary of 1894 when dyspnea increased and
edema set in. Seven months later he was admitted toedema set in. Seven months later he was admitted to
the hospital in a state of heart failure……Hethe hospital in a state of heart failure……He
improved with rest and digitalis, but collapsed andimproved with rest and digitalis, but collapsed and
died suddenly on November 13 following a largedied suddenly on November 13 following a large
hemoptysishemoptysis

 As disease progresses, more advanced morphologicAs disease progresses, more advanced morphologic
changes (plexiform lesions, necrotizing arteritis)changes (plexiform lesions, necrotizing arteritis)
occur which are irreversibleoccur which are irreversible
 As the increased PVR approaches or exceeds theAs the increased PVR approaches or exceeds the
SVR, the shunt is reversedSVR, the shunt is reversed
 As R to L shunting develops, cyanosis appearsAs R to L shunting develops, cyanosis appears
 Most patients will develop exertional dyspnea andMost patients will develop exertional dyspnea and
impaired exercise toleranceimpaired exercise tolerance

 Palpitations occur in >50% of patients (A. fib/flutter inPalpitations occur in >50% of patients (A. fib/flutter in
40% and VT in 10%)40% and VT in 10%)
 Hemoptysis in ~20%Hemoptysis in ~20%
 PE, angina, syncope, endocarditis ~10%PE, angina, syncope, endocarditis ~10%
 Signs of PHTN (RV heave, palpable PSigns of PHTN (RV heave, palpable P22, and right, and right
sided Ssided S44) are typically present) are typically present
 Pulmonary ejection click and a soft scratchy SEM (dPulmonary ejection click and a soft scratchy SEM (d/t/t
dilated pulmonary trunk)dilated pulmonary trunk)
 High pitched decrescendo diastolic murmur (Graham-High pitched decrescendo diastolic murmur (Graham-
Steele) audible in most patientsSteele) audible in most patients
 Usually no peripheral edema until right heart failureUsually no peripheral edema until right heart failure
ensuesensues

CXR reveals prominent central pulmonary arteries and
decreased vascular markings (pruning) of the peripheral vessels

 Large variation in life expectancy in adults withLarge variation in life expectancy in adults with
Eisenmenger syndromeEisenmenger syndrome
 Rate of survival among patients withRate of survival among patients with
Eisenmenger syndrome isEisenmenger syndrome is
 80% at 10 years, 77% at 15 years, and 42% at 2580% at 10 years, 77% at 15 years, and 42% at 25
yearsyears
 Recent study of 109 adults revealed following asRecent study of 109 adults revealed following as
independent predictors of mortality:independent predictors of mortality:
 Age at presentationAge at presentation
 Supraventricular arrhythmiasSupraventricular arrhythmias
 Poor NYHA functional class (III or IV)Poor NYHA functional class (III or IV)

 Pregnancy is discouraged due to high maternalPregnancy is discouraged due to high maternal
(50%) and fetal (60%) mortality(50%) and fetal (60%) mortality
 CVA may occur secondary to paradoxical emboliCVA may occur secondary to paradoxical emboli
 Also at higher risk for cerebral abscessesAlso at higher risk for cerebral abscesses
 Patients should avoid intravascular volume depletion,Patients should avoid intravascular volume depletion,
heavy exertion, high altitudes, and use ofheavy exertion, high altitudes, and use of
vasodilatorsvasodilators
 IV epoprostenol may be beneficial in decreasing PVRIV epoprostenol may be beneficial in decreasing PVR

 Phlebotomy with isovolumic replacement isPhlebotomy with isovolumic replacement is
recommended for patients with moderate torecommended for patients with moderate to
severe symptoms of hyperviscosity and ansevere symptoms of hyperviscosity and an
elevated hematocrit >65%elevated hematocrit >65%
 Prevention of iron deficiency is importantPrevention of iron deficiency is important
 Supplemental oxygen reduces episodes ofSupplemental oxygen reduces episodes of
dyspnea (?survival benefit)dyspnea (?survival benefit)
 Lung transplantation (with repair of cardiacLung transplantation (with repair of cardiac
defect) or heart/lung transplantation is andefect) or heart/lung transplantation is an
option.option.

 Successful closure is associated with excellentSuccessful closure is associated with excellent
survival if ventricular fx is normal. Elevated PAPsurvival if ventricular fx is normal. Elevated PAP
preop may progress, regress, or remain the samepreop may progress, regress, or remain the same
postoppostop
 A. fib may occur, especially if there has beenA. fib may occur, especially if there has been
longstanding volume overload of the left heart. Latelongstanding volume overload of the left heart. Late
VT and sudden death are potential risks, especially inVT and sudden death are potential risks, especially in
patients repaired late in life. CHB may also occurpatients repaired late in life. CHB may also occur
after surgical repairafter surgical repair
 Pregnancy is well tolerated in women with small orPregnancy is well tolerated in women with small or
moderate VSD and in women with repaired VSDmoderate VSD and in women with repaired VSD
 Pregnancy is contraindicated in women withPregnancy is contraindicated in women with
Eisenmenger syndrome due to both high maternalEisenmenger syndrome due to both high maternal
((>50%) and fetal (~60%) mortality>50%) and fetal (~60%) mortality

 Follow-up:Follow-up:
 Patients with following problems benefit fromPatients with following problems benefit from
periodic evaluation by cardiologistperiodic evaluation by cardiologist
 Patch leaks or residual VSDs (which seldom requirePatch leaks or residual VSDs (which seldom require
reoperation)reoperation)
 Elevated PVR at time of surgeryElevated PVR at time of surgery
 Aortic valve surgeryAortic valve surgery
 Late repair of moderate or large defectsLate repair of moderate or large defects
 Significant atrial or ventricular arrhythmiasSignificant atrial or ventricular arrhythmias
 Associated cardiac lesions (eg RVOTO, AR)Associated cardiac lesions (eg RVOTO, AR)
 Endocarditis prophylaxis is recommended for 6/12Endocarditis prophylaxis is recommended for 6/12
following VSD closure or for life if residual defectfollowing VSD closure or for life if residual defect
persistspersists

VENTRICULARVENTRICULAR
SEPTAL DEFECTSEPTAL DEFECT

Morphology – The VentricularMorphology – The Ventricular
SeptumSeptum

AnatomyAnatomy
 Membranous-70-80%Membranous-70-80%
 SmallSmall
 Located at base, between inlet and outletLocated at base, between inlet and outlet
 Perimembranous - Extends to adjacentPerimembranous - Extends to adjacent
septumseptumMembranous Membranous

 Perimembranous(membranous/Perimembranous(membranous/
 infracristal )-70-80%infracristal )-70-80%
 Muscular- 5-20%Muscular- 5-20%
Central- mid muscularCentral- mid muscular
ApicalApical
Marginal- along RV septal junctionMarginal- along RV septal junction
Swiss cheese septum – multipleSwiss cheese septum – multiple
defectsdefects
 Inlet/ AV canal type-5-8%Inlet/ AV canal type-5-8%
 Supracrital/ subaortic- 5-7%Supracrital/ subaortic- 5-7%

 Defect size is often compared to aorticDefect size is often compared to aortic
annulusannulus
 Large: > 50% of annulus sizeLarge: > 50% of annulus size
 Medium: 25-50% of annulus sizeMedium: 25-50% of annulus size
 Small: <25% of annulus sizeSmall: <25% of annulus size

 Large VSDLarge VSD Size equal to the aorticSize equal to the aortic
rootroot
 Equalization of pressures in RV& LVEqualization of pressures in RV& LV
 Increased LA pressureIncreased LA pressure opening ofopening of
foramen ovalforamen oval

 Medium sized VSDMedium sized VSDVSD size about half – equal toVSD size about half – equal to
the size of the aortic orificethe size of the aortic orifice
 When PA & RVSP are > 50% of systemic arterialWhen PA & RVSP are > 50% of systemic arterial
pressurepressure
 mm od-large Lod-large L R shunt developsR shunt develops
 Small VSD in infancySmall VSD in infancy <1/3<1/3rdrd
size of aortic rootsize of aortic root
 shunt limited by size of the defectshunt limited by size of the defect
 Shunt entirely during ventricular systoleShunt entirely during ventricular systole
 LL R shunt <50% LV outputR shunt <50% LV output
 Pulmonary:systemic flow ratio < 2:1Pulmonary:systemic flow ratio < 2:1

 Restrictive VSD is typically small, such thatRestrictive VSD is typically small, such that
a significant pressure gradient existsa significant pressure gradient exists
between the LV and RV (high velocity), withbetween the LV and RV (high velocity), with
small shunt (Qp/Qs ≤ 1.4 : 1)small shunt (Qp/Qs ≤ 1.4 : 1)
 Moderately restrictive VSDModerately restrictive VSD  moderatemoderate
shunt (Qp/Qs 1.4 to 2.2 : 1)shunt (Qp/Qs 1.4 to 2.2 : 1)
 Large / non-restrictive VSDLarge / non-restrictive VSD  large shuntlarge shunt
(Qp/Qs > 2.2 : 1)(Qp/Qs > 2.2 : 1)
 Eisenmenger VSDEisenmenger VSD  irreversibleirreversible
pulmonary HTN and shunt may be zero orpulmonary HTN and shunt may be zero or

 During systole, blood is shunted from LV to RVDuring systole, blood is shunted from LV to RV
 passes through the lungs and re enters the LV via thepasses through the lungs and re enters the LV via the
pulmonary veins and LApulmonary veins and LA
 causes volume overload on the LVcauses volume overload on the LV
 Shunt into the RV elevates RV pressure andShunt into the RV elevates RV pressure and
volume, leading to pulmonary hypertension.volume, leading to pulmonary hypertension.
 More noticeable in patients with larger defectsMore noticeable in patients with larger defects

pathophysiologypathophysiology
 Magnitude of shunt: size, PVRMagnitude of shunt: size, PVR
 Small defect: large resistance occurs atSmall defect: large resistance occurs at
the defectthe defect
 Larger defect: resistance offered by theLarger defect: resistance offered by the
defect minimumdefect minimum
: Shunt depends largely: Shunt depends largely
on PVRon PVR
 Lower the PVR, greater the LLower the PVR, greater the LRR
ShuntShunt

 Spontaneous closureSpontaneous closure :75-85 % all VSDs:75-85 % all VSDs
 :35% perimemb ( 1:35% perimemb ( 1stst
6/12)6/12)
 More frequent in small defectsMore frequent in small defects
 Decrease in size with ageDecrease in size with age
 Inlet & outlet defects donot become smaller /close spontInlet & outlet defects donot become smaller /close spont
 Large & nonrestrictive defects : 10- 15%Large & nonrestrictive defects : 10- 15%
 endocarditisendocarditis – risk of endocarditis 4-10% for the first 30– risk of endocarditis 4-10% for the first 30
years of lifeyears of life
 High velocity turbulent jet into RVHigh velocity turbulent jet into RV

Mechanisms of closureMechanisms of closure
 Growth & hypertrophy of septum around the defectGrowth & hypertrophy of septum around the defect
 By development of subacute bacterial endocarditisBy development of subacute bacterial endocarditis
 adherence of STL tissue to the marginsadherence of STL tissue to the margins
 (Negative pressure effect exerted by a high velocity(Negative pressure effect exerted by a high velocity
stream flowing through the defect )stream flowing through the defect )
 Ventricular septal aneurysmVentricular septal aneurysm
 prolapse of aortic cuspprolapse of aortic cusp
 intrusion of a sinus of valsalva aneurysmintrusion of a sinus of valsalva aneurysm

 CHFCHF
 Large VSDsLarge VSDs
 Mod sized VSDs survive into adulthoodMod sized VSDs survive into adulthood
 Increased rt sided flowIncreased rt sided flow  pulmonarypulmonary
vascular diseasevascular disease  Eisenmenger’sEisenmenger’s
physiology if left untreatedphysiology if left untreated

 Risk factors for decreased survivalRisk factors for decreased survival
 Shortness of breath, fatigue,Shortness of breath, fatigue,
DOE,progressive ARDOE,progressive AR
 CardiomegalyCardiomegaly
 PASP >60mm Hg/ >1/2 of systemic pressurePASP >60mm Hg/ >1/2 of systemic pressure
 Good prognosticatorsGood prognosticators
Lack of symptomsLack of symptoms
normal LV size & functionnormal LV size & function
small Lsmall LR shuntR shunt
normal pulmonary pressures / resistancenormal pulmonary pressures / resistance
Intact vasodilator response in pulmonaryIntact vasodilator response in pulmonary
vasculaturevasculature

 genetic factorsgenetic factors
 Affected father- 2%Affected father- 2%
 Affected mother – 6%Affected mother – 6%
 25 yr survival for all pts with a VSD 87%25 yr survival for all pts with a VSD 87%
 Mortality increases with the size of VSDMortality increases with the size of VSD

History & clinical featuresHistory & clinical features

HistoryHistory
 Incidence unrelated to maternal age,Incidence unrelated to maternal age,
sex, birth ordersex, birth order
 3.3% 13.3% 1stst
degree relatives of indexdegree relatives of index
patientspatients
 Among 1Among 1stst
degree relatives with CHD,degree relatives with CHD,
1/31/3rdrd
have vsdhave vsd
 30-60% siblings of index patients have30-60% siblings of index patients have
vsdvsd
 Parents with spontaneously closed vsdParents with spontaneously closed vsd

Small VSD - infancySmall VSD - infancy
 Normal wt gain & developmentNormal wt gain & development
 2-8 wks – tachycardia & tachypnea2-8 wks – tachycardia & tachypnea
especially with infectionespecially with infection
 2-4/6 systolic mr, medium frequency2-4/6 systolic mr, medium frequency

Large VSD - infancyLarge VSD - infancy
 Infant well in the immediate postnatal periodInfant well in the immediate postnatal period
 Systolic mr LLSB after 1-7 daysSystolic mr LLSB after 1-7 days
 develop respiratory distress , in 2-8 wksdevelop respiratory distress , in 2-8 wks
 Systolic thrill , along LSBSystolic thrill , along LSB
 S1 normal/ soft: s2loud narrow splitS1 normal/ soft: s2loud narrow split
 Systolic mr , 2-3/6 intensity at birth, louder & harsh asSystolic mr , 2-3/6 intensity at birth, louder & harsh as
shunt increasesshunt increases
 S3 & MDM at apexS3 & MDM at apex
 If the infant survives - subsequent course with persistentIf the infant survives - subsequent course with persistent
dyspnea, sweating, poor feeding, failure to thrive, LRTIdyspnea, sweating, poor feeding, failure to thrive, LRTI

Beyond infancyBeyond infancy
 Arterial pulse- brisk ( vigorous ejection from aArterial pulse- brisk ( vigorous ejection from a
volume overloaded ventricle)volume overloaded ventricle)
 N pulse in eisenmenger’s - systemic strokeN pulse in eisenmenger’s - systemic stroke
volume maintainedvolume maintained
 Cyanosis & clubbing : eisenmenger’sCyanosis & clubbing : eisenmenger’s
 JVP – N in small defectsJVP – N in small defects
elevated - Mod restr & nonrestrictive vsdelevated - Mod restr & nonrestrictive vsd
withwith ccfccf
 Precordial bulge ( large shunt 5-6 months)Precordial bulge ( large shunt 5-6 months)
 Harrison’s sulcusHarrison’s sulcus

 RV heave in pts with RV vol overloadRV heave in pts with RV vol overload
 Features of PAHFeatures of PAH
 Grade 2-5/6 systolic regurgitantGrade 2-5/6 systolic regurgitant
mrLLSBmrLLSB
 MDM preceeded by S3MDM preceeded by S3
 Infundibular vsd: early diastolicInfundibular vsd: early diastolic
decrescendo mr of ARdecrescendo mr of AR

Improvement of symptomsImprovement of symptoms
 Closing defectClosing defect
findings :findings : soft s2soft s2
high frequency & shorter murmurhigh frequency & shorter murmur
 Increasing PVRIncreasing PVR
findings :findings : increased RV pulsationsincreased RV pulsations
s2 loud, narrow splits2 loud, narrow split
 Infundibular hypertrophyInfundibular hypertrophy
decreased Ldecreased LR shunt,R shunt,
findings :findings : s2 decreases in intensity ,s2 decreases in intensity ,
crescendo-decrescendo systolic murmur in thecrescendo-decrescendo systolic murmur in the
ULSB,ULSB,
cyanosis (shunt reversal )cyanosis (shunt reversal )

 Eisenmenger’sEisenmenger’s
 apex by RVapex by RV
 Palpable dilated hypertensive pulmonaryPalpable dilated hypertensive pulmonary
trunktrunk
 Loud pulmonary closure soundLoud pulmonary closure sound
 Very short or no systolic mr of vsdVery short or no systolic mr of vsd
 Short pulmonary ejection mr ULSBShort pulmonary ejection mr ULSB
 EDM of pulmonary regurgitationEDM of pulmonary regurgitation
 Loud harsh s1 coincident holosystolicLoud harsh s1 coincident holosystolic
mr of TRmr of TR

ECGECG
 small defects unremarkablesmall defects unremarkable
 LA enlargementLA enlargement - Mod restrictive, large- Mod restrictive, large
LLR shuntsR shunts
 left axis deviationleft axis deviation
Inlet vsd /AV septal defectInlet vsd /AV septal defect
5% moderately restrictive vsds5% moderately restrictive vsds
Ventricular septal aneurysmsVentricular septal aneurysms
multiple vsdsmultiple vsds

 LV enlargementLV enlargement in larger defectsin larger defects
 RVHRVH - Mild or moderate elevation of RV- Mild or moderate elevation of RV
pressure (rsR’ in V4R or V1)pressure (rsR’ in V4R or V1)
- Large VSD, equal ventricular- Large VSD, equal ventricular
pressures , elevatedpressures , elevated PVRPVR
 RVH , RADRVH , RAD - Eisenmenger’s- Eisenmenger’s
 RBBBRBBB - Surgical repair- Surgical repair

Chest x rayChest x ray Small defects that were mod restrictive at birth –Small defects that were mod restrictive at birth –
increased LV size, dilated pulmonary trunk & itsincreased LV size, dilated pulmonary trunk & its
branchesbranches
 Large shunts – hyperinflated lungs with flat hemiLarge shunts – hyperinflated lungs with flat hemi
diaphragmsdiaphragms
 LA enlargement best appreciated in the lateralLA enlargement best appreciated in the lateral
positionposition
 Increased PVR, decreases LIncreased PVR, decreases LR shunt, decreasesR shunt, decreases
heart size, enlargement of pulmonary trunk& itsheart size, enlargement of pulmonary trunk& its
branches persistsbranches persists

Common locations of vsdCommon locations of vsd -2d-2d
echoecho

EchocardiographyEchocardiography

Echocardiography- dopplerEchocardiography- doppler
 CFM-Direction, timing of flowCFM-Direction, timing of flow
 IVG (mmHg) = 4v²IVG (mmHg) = 4v²
 PG = LVSP - RVSPPG = LVSP - RVSP

Cardiac catheterizationCardiac catheterization
Hemodynamic assessmentsHemodynamic assessments
cardiac index oximetry quantification ofcardiac index oximetry quantification of
shuntshunt
To assess pulmonary vascular resistanceTo assess pulmonary vascular resistance
 Pts with increased PVR, with mod or largePts with increased PVR, with mod or large
LLR shuntR shunt
 If PVR is increased, response to 100%If PVR is increased, response to 100%
oxygen,NO testedoxygen,NO tested

cineangiographycineangiography
 Defect best imaged in LAO(70°)cranialDefect best imaged in LAO(70°)cranial
(25°)(25°)
 Inlet defect - hepatoclavicular viewInlet defect - hepatoclavicular view
( 40°LAO,cranial( 40°LAO,cranial
angulation)angulation)
 Anterior muscular VSD- RAO viewAnterior muscular VSD- RAO view
 Aortography - r/o PDA ,coarctationAortography - r/o PDA ,coarctation

Indications of surgicalIndications of surgical
interventionintervention
 Large VSD with pulmonaryLarge VSD with pulmonary
hypertensionhypertension
 VSD with aortic regurgitationVSD with aortic regurgitation
 VSD with associated defectsVSD with associated defects
 Failure of congestive cardiac failure toFailure of congestive cardiac failure to
respond to medicationsrespond to medications

Timing of surgeryTiming of surgery in VSDin VSD
 <3months<3months - if symptomatic- if symptomatic
 3-6 months3-6 months - symptomatic, growth- symptomatic, growth
failure, increasing PAHfailure, increasing PAH
 >6 months>6 months – primarily based on PAH– primarily based on PAH
 Wait till 1 yr , if no PAHWait till 1 yr , if no PAH

VSD closureVSD closure
 Direct closure of the defectDirect closure of the defect
 Surgical mortality <1%Surgical mortality <1%
 Complications – RBBB- direct injury to rtComplications – RBBB- direct injury to rt
bundle, disruption of purkinje fibersbundle, disruption of purkinje fibers
 Residual shunt (<5% )Residual shunt (<5% )
 Injuries to tricuspid valve & aortic valveInjuries to tricuspid valve & aortic valve

PA bandingPA banding
 PA banding- palliative procedure , whenPA banding- palliative procedure , when
additional lesions make repair difficultadditional lesions make repair difficult
 Done in multiple VSDsDone in multiple VSDs
 30-50% of original diameter is narrowed30-50% of original diameter is narrowed
 Systolic pressure of 25-30 mmHg beyond theSystolic pressure of 25-30 mmHg beyond the
constrictionconstriction
 RV/PA pressure gradient > 45 associatedRV/PA pressure gradient > 45 associated
with hypoxemiawith hypoxemia

Post op follow upPost op follow up
 Every 1-2 yrsEvery 1-2 yrs
 VSD & mild PAH& repair after 3 yrs ofVSD & mild PAH& repair after 3 yrs of
age-age- watch for progressivewatch for progressive
pulmonary vascularpulmonary vascular diseasedisease
 long term follow up neededlong term follow up needed

ATRIAL WAVESATRIAL WAVES
 a= atrial contractiona= atrial contraction
 c= contraction of ventricle and closure of tricuspid valvec= contraction of ventricle and closure of tricuspid valve
 x=x descentx=x descent
 v=venous fillingv=venous filling
 y= y descent due to opening of tricuspid valvey= y descent due to opening of tricuspid valve

RIGHT HEART PRESSURESRIGHT HEART PRESSURES

Haemodynamic ParametersHaemodynamic Parameters

 The following criteria suggest left atrial enlargement/abnormality whenThe following criteria suggest left atrial enlargement/abnormality when
correlated with echocardiographic data:correlated with echocardiographic data:
 Negative phase of P in V1>0.04 sec — sensitivity 83 percent; specificityNegative phase of P in V1>0.04 sec — sensitivity 83 percent; specificity
80 percent80 percent
 Negative phase of P in V1>1 mm — sensitivity 60 percent; specificityNegative phase of P in V1>1 mm — sensitivity 60 percent; specificity
93 percent93 percent
 P-terminal force >0.04 mm/sec — sensitivity 69 percent; specificity 93P-terminal force >0.04 mm/sec — sensitivity 69 percent; specificity 93
percentpercent
 Notched P, interpeak interval >0.04 sec — sensitivity 15 percent;Notched P, interpeak interval >0.04 sec — sensitivity 15 percent;
specificity 100 percentspecificity 100 percent
 P wave duration >0.11 sec — sensitivity 33 percent; specificity 88P wave duration >0.11 sec — sensitivity 33 percent; specificity 88
percentpercent
 P wave/PR duration >1.6 — sensitivity 31 percent; specificity 64P wave/PR duration >1.6 — sensitivity 31 percent; specificity 64
percentpercent

Special situationsSpecial situations

VSD with ARVSD with AR
 Peri membranous VSD with AR - 5-8%Peri membranous VSD with AR - 5-8%
 Subarterial VSDs – 30%Subarterial VSDs – 30%
 Sagging or herniation of RCC or RCC+ NCCSagging or herniation of RCC or RCC+ NCC
 May cause RVOT obstructionMay cause RVOT obstruction
 Due to morphological abnormality of valveDue to morphological abnormality of valve
 LV volume – regurgitant volume & shuntLV volume – regurgitant volume & shunt
volumevolume
 VSD murmur dates from infancyVSD murmur dates from infancy
 AR murmur appears (5-9 yrs)AR murmur appears (5-9 yrs)

OutlineOutline
 Morphology, Types & PathophysiologyMorphology, Types & Pathophysiology
 Natural History and Clinical PresentationNatural History and Clinical Presentation
 Some Echo examplesSome Echo examples
 Clinical Scenarios and RecommendationsClinical Scenarios and Recommendations
 Interventions: Indications, Surgery,Interventions: Indications, Surgery,
PercutaneousPercutaneous
 Pregnancy and Endocarditis ProphylaxisPregnancy and Endocarditis Prophylaxis
 Review QuestionsReview Questions

IntroductionIntroduction
 The most common form of CHD, accountingThe most common form of CHD, accounting
for up to 20-40% of patients diagnosed withfor up to 20-40% of patients diagnosed with
CHDCHD
 Impact may range from asymptomatic toImpact may range from asymptomatic to
pulmonary HTN, LV volume overload andpulmonary HTN, LV volume overload and
RVHRVH
 Morphology: 4 typesMorphology: 4 types
 Membranous – most common type in adultsMembranous – most common type in adults
(80%)(80%)
 Muscular – most common type in youngMuscular – most common type in young

Natural HistoryNatural History
 Restrictive: typically does not haveRestrictive: typically does not have
hemodynamic impact and may closehemodynamic impact and may close
 Location Location Location: Subaortic mayLocation Location Location: Subaortic may
result in progressive AIresult in progressive AI
 Moderately restrictive: does create LVModerately restrictive: does create LV
overload and dysfunction along withoverload and dysfunction along with
variable increase in PVRvariable increase in PVR
 Large / non-restrictive: LV volume overloadLarge / non-restrictive: LV volume overload
earlier in life with progressive pulm HTNearlier in life with progressive pulm HTN

Clinical FeaturesClinical Features
 Peds:Peds:
 MurmurMurmur
 Dyspnea, CHF, Failure to thriveDyspnea, CHF, Failure to thrive
 Adults:Adults:
 Asymptomatic murmur – harsh, pansystolic, leftAsymptomatic murmur – harsh, pansystolic, left
sternal bordersternal border
 Mod restrictive – dyspnea, a.fib, displacedMod restrictive – dyspnea, a.fib, displaced
apex, murmur, S3apex, murmur, S3
 Non-restrictive Eisenmenger VSD – centralNon-restrictive Eisenmenger VSD – central
cyanosis, clubbing, RV heave, loud P2cyanosis, clubbing, RV heave, loud P2

tt
Outlet VSD – Para long axis

Supracristal VSD, with pulm outflow tract obstruction

Echo Example 3Echo Example 3
 Type:Type:
 Size:Size:
Membranous
Restrictive

Echo Example 3Echo Example 3
Type:
Size:
Shunt:
Muscular
Large / Non-restrictive
RL (inc RH
pressures)
RV dilated
Eisenmengers

Clinical Scenarios &Clinical Scenarios &
RecommendationsRecommendations
 Eisenmenger SyndromeEisenmenger Syndrome
 SupportiveSupportive
 Bosentan (Endothelin receptor antagonist) –Bosentan (Endothelin receptor antagonist) –
improves functional capacity, QOLimproves functional capacity, QOL
 SildenafilSildenafil
Penny DJ, Vick GW. Lancet 2011; 377: 1103-12

InterventionsInterventions
 Indications for Surgical Closure in adults:Indications for Surgical Closure in adults:
 Evidence of LV volume overload (Class I ifEvidence of LV volume overload (Class I if
Qp/Qs >2, Class IIa if Qp/Qs > 1.5)Qp/Qs >2, Class IIa if Qp/Qs > 1.5)
 History of bacterial endocarditis (Class I)History of bacterial endocarditis (Class I)
 Significant LSignificant LR shunt with PA pressure < 2/3R shunt with PA pressure < 2/3
systemic and PVR is < 2/3 SVRsystemic and PVR is < 2/3 SVR
 Surgical ClosureSurgical Closure
 Considered the first-line choice of therapy forConsidered the first-line choice of therapy for
those with indicationsthose with indications
 Usually involves direct patch closure w cardio-Usually involves direct patch closure w cardio-

Long Term Surgical OutcomesLong Term Surgical Outcomes
 Retrospective review of 46 pts with surgicalRetrospective review of 46 pts with surgical
VSD repair at Mayo ClinicVSD repair at Mayo Clinic
Mongeon et al. JACC Int 2010; 3: 290-7

Interventional OptionsInterventional Options
 Percutaneous Device ClosurePercutaneous Device Closure
 Muscular VSDs can typically be closedMuscular VSDs can typically be closed
percutaneouslypercutaneously
 Class IIb recommendation in Guidelines (i.e. surgeryClass IIb recommendation in Guidelines (i.e. surgery
still preferred)still preferred)
 No FDA approved devices for perimembranousNo FDA approved devices for perimembranous
VSDs, although there are specific devices forVSDs, although there are specific devices for
this purposethis purpose
 Concern re proximity of defect to AV node and highConcern re proximity of defect to AV node and high
risk of complete AV block requiring pacemakerrisk of complete AV block requiring pacemaker

Pregnancy and VSDsPregnancy and VSDs
 Pregnancy well tolerated in women withPregnancy well tolerated in women with
small to moderate sized VSDs as long assmall to moderate sized VSDs as long as
there is no pulmonary vascular involvementthere is no pulmonary vascular involvement
 Eisenmenger syndrome: PregnancyEisenmenger syndrome: Pregnancy
contraindicated due to exceptionally highcontraindicated due to exceptionally high
risk of maternal and fetal deathrisk of maternal and fetal death

Question 1Question 1
 An isolated VSD will generally causeAn isolated VSD will generally cause
enlargement of which chamber(s):enlargement of which chamber(s):
 A: Left atrium, left ventricleA: Left atrium, left ventricle
 B: Right ventricleB: Right ventricle
 C: Right ventricle, pulmonary arteryC: Right ventricle, pulmonary artery
 D: AortaD: Aorta
 E: Right ventricle, right atriumE: Right ventricle, right atrium

An isolated VSD will generally causeAn isolated VSD will generally cause
enlargement of which chamber(s):enlargement of which chamber(s):
 A: Left atrium, left ventricleA: Left atrium, left ventricle
 B: Right ventricleB: Right ventricle
 C: Right ventricle, pulmonary arteryC: Right ventricle, pulmonary artery
 D: AortaD: Aorta
 E: Right ventricle, right atriumE: Right ventricle, right atrium

 The defect shown on the previous slide is a:The defect shown on the previous slide is a:
 A: Muscular VSDA: Muscular VSD
 B: Sinus venosus VSDB: Sinus venosus VSD
 C: Perimembranous VSDC: Perimembranous VSD
 D: Inlet VSDD: Inlet VSD
 E: Supracristal VSDE: Supracristal VSD

The defect shown on the previous slide is a:The defect shown on the previous slide is a:
 A: Muscular VSDA: Muscular VSD
 B: Sinus venosus VSDB: Sinus venosus VSD
 C: Perimembranous VSDC: Perimembranous VSD
 D: Inlet VSDD: Inlet VSD
 E: Supracristal VSDE: Supracristal VSD

 A common complication of this defect is:A common complication of this defect is:
 A: Pulmonary valve endocarditisA: Pulmonary valve endocarditis
 B: Aortic regurgitationB: Aortic regurgitation
 C: Aortic dissectionC: Aortic dissection
 D: Tricuspid regurgitationD: Tricuspid regurgitation
 E: Right ventricular enlargementE: Right ventricular enlargement

A common complication of this defect is:A common complication of this defect is:
 A: Pulmonary valve endocarditisA: Pulmonary valve endocarditis
 C: Aortic dissectionC: Aortic dissection
 D: Tricuspid regurgitationD: Tricuspid regurgitation
 E: Right ventricular enlargementE: Right ventricular enlargement

 There is no diastolic flow in thisThere is no diastolic flow in this
perimembranous VSDperimembranous VSD
 A: TrueA: True
 B: FalseB: False

There is no diastolic flow in thisThere is no diastolic flow in this
perimembranous VSDperimembranous VSD
 A: TrueA: True
 B: FalseB: False

 A restrictive VSD is a simple lesion with aA restrictive VSD is a simple lesion with a
good long term prognosis. However,good long term prognosis. However,
complications can occur. All of the followingcomplications can occur. All of the following
are possible complications of a VSD except:are possible complications of a VSD except:
 A: EndocarditisA: Endocarditis
 C: Aortic valve prolapseC: Aortic valve prolapse
 D: Eisenmenger SyndromeD: Eisenmenger Syndrome
 E: Right sided volume overloadE: Right sided volume overload

A restrictive VSD is a simple lesion with aA restrictive VSD is a simple lesion with a
good long term prognosis. However,good long term prognosis. However,
complications can occur. All of the followingcomplications can occur. All of the following
are possible complications of a VSD except:are possible complications of a VSD except:
 A: EndocarditisA: Endocarditis
 C: Aortic valve prolapseC: Aortic valve prolapse
 D: Eisenmenger SyndromeD: Eisenmenger Syndrome
 E: Right sided volume overloadE: Right sided volume overload

 The pulmonary artery systolic pressure inThe pulmonary artery systolic pressure in
this patient with a VSD is:this patient with a VSD is:
 A: NormalA: Normal
 B: Moderately elevatedB: Moderately elevated
 C: Systemic / Supra-systemicC: Systemic / Supra-systemic

The pulmonary artery systolic pressure inThe pulmonary artery systolic pressure in
this patient with a VSD is:this patient with a VSD is:
 A: NormalA: Normal
 B: Moderately elevatedB: Moderately elevated
 C:C: Systemic / Supra-systemicSystemic / Supra-systemic

 A patient with a VSD undergoes TTE. BPA patient with a VSD undergoes TTE. BP
measured at the time of the study is 125/75measured at the time of the study is 125/75
(right arm), MAP 92. CW doppler across the(right arm), MAP 92. CW doppler across the
VSD gives a peak velocity of 5 m/s.VSD gives a peak velocity of 5 m/s.
Assuming RA pressure of 5, what is theAssuming RA pressure of 5, what is the
estimated PASP?estimated PASP?
 A: 20mmHgA: 20mmHg
 B: 25 mmHgB: 25 mmHg
 C: 30 mmHgC: 30 mmHg
 D: 72 mmHgD: 72 mmHg

VSD HemodynamicsVSD Hemodynamics
 Peak gradient = 4 x vPeak gradient = 4 x v22
(Simplied Bernoulli(Simplied Bernoulli
equation)equation)
 VSD gradient = LV systolic pressure – RVVSD gradient = LV systolic pressure – RV
systolic pressuresystolic pressure
 RVSP = LVSP - VSD gradientRVSP = LVSP - VSD gradient
 RVSP = cuff systolic BP - VSD gradient (orRVSP = cuff systolic BP - VSD gradient (or
4 x v4 x v22
))
 Assuming no aortic outflow tract obstructionAssuming no aortic outflow tract obstruction
 PASP = RVSPPASP = RVSP
 Assuming no pulmonary outflow tractAssuming no pulmonary outflow tract

VENTRICULARVENTRICULAR
SEPTAL DEFECTSEPTAL DEFECT
Dolly mathewDolly mathew

 AA VSDVSD is a defect in the ventricular septumis a defect in the ventricular septum
 The ventricular septum consists of an inferiorThe ventricular septum consists of an inferior
muscular and superior membranous portionmuscular and superior membranous portion
 The membranous portion -most commonly affectedThe membranous portion -most commonly affected
in adults and older childrenin adults and older children
 most common congenital cardiac anomalies.most common congenital cardiac anomalies.
 3-3.8 per 1000 live births3-3.8 per 1000 live births
 30-60% of all newborns with a CHD30-60% of all newborns with a CHD
 Prospective studies give a prevalence of 2-5 perProspective studies give a prevalence of 2-5 per
100 births of trabecular VSDs that closes shortly100 births of trabecular VSDs that closes shortly
after birth in 80-90% of the casesafter birth in 80-90% of the cases

Location of VSDsLocation of VSDs
Swiss cheese
Muscular
Inlet
outlet
perimembranous

Small VSD in infancySmall VSD in infancy
 <1/3<1/3rdrd
size of aortic rootsize of aortic root
 shunt limited by size of the defectshunt limited by size of the defect
 Shunt entirely during ventricular systoleShunt entirely during ventricular systole
 LL R shunt <50% LV outputR shunt <50% LV output
 Pulmonary:systemic flow ratio < 2:1Pulmonary:systemic flow ratio < 2:1

Medium sized VSDMedium sized VSD
 VSD size about half –VSD size about half –
equal to the size ofequal to the size of
the aortic orificethe aortic orifice
 When PA & RVSPWhen PA & RVSP
are > 50% ofare > 50% of
systemic arterialsystemic arterial
pressurepressure
 mod-large Lmod-large L RR
shunt developsshunt develops
 p218p218

Large VSDLarge VSD
 Size equal to the aorticSize equal to the aortic
rootroot
 Equalization of pressuresEqualization of pressures
in RV& LVin RV& LV
 Increased LA pressureIncreased LA pressure
opening of foramen ovaleopening of foramen ovale

Cardiac catheterizationCardiac catheterization
Hemodynamic assessmentsHemodynamic assessments
cardiac indexcardiac index
oximetryoximetry
quantification of shuntquantification of shunt
To assess pulmonary vascular resistanceTo assess pulmonary vascular resistance
 Pts with increased PVR, with mod or large LPts with increased PVR, with mod or large LRR
shuntshunt
 If PVR is increased, response to 100% oxygen,NOIf PVR is increased, response to 100% oxygen,NO
testedtested

Other imaging modalitiesOther imaging modalities
 Cardiac CT-Cardiac CT- assess VSD anatomy inassess VSD anatomy in
suboptimal echo imgessuboptimal echo imges
No information about shuntNo information about shunt
fractionfraction
 MRIMRI
 delineate vsd location& shunt fraction indelineate vsd location& shunt fraction in
complex associated lesionscomplex associated lesions

 Observation & follow upObservation & follow up
Small VSDsSmall VSDs
 Medical managementMedical management
Medium sized vsdMedium sized vsd
CCF- treat with diuretics & digitalis,CCF- treat with diuretics & digitalis,
ACEIACEI
failure ppted by LRTI- Treat bothfailure ppted by LRTI- Treat both
2-3 months follow up2-3 months follow up
RV & PA pressures assessedRV & PA pressures assessed
Failure to thriveFailure to thrive
 SurgicalSurgical
Large vsdLarge vsd

LVLV  RA shuntRA shunt
 Gerbode defectGerbode defect
 Shunt begins inuteroShunt begins inutero
 Usually restrictiveUsually restrictive
 Rightward thoracicRightward thoracic
position of murmurposition of murmur
 X ray – RAX ray – RA
enlargementenlargement
disproportionate todisproportionate to
the size of pulmonarythe size of pulmonary
trunktrunk

Ventricular SeptalVentricular Septal
DefectsDefects
Tate Gisslen, MDTate Gisslen, MD
Mentor: Bradley S. Marino,Mentor: Bradley S. Marino,
MD, MPP, MSCEMD, MPP, MSCE
May 6, 2011May 6, 2011

PhysiologyPhysiology
 Blood flow (which way and how much)Blood flow (which way and how much)
dependent on multiple factorsdependent on multiple factors
 Small and restrictiveSmall and restrictive
 Lesion sizeLesion size
 Large and non-restrictiveLarge and non-restrictive
 Balance between pulmonary andBalance between pulmonary and
systemic vascular resistancesystemic vascular resistance

Lesion SizeLesion Size
• Restrictive VSDRestrictive VSD
– < 0.5 cm< 0.5 cm22
(Smaller than Ao valve orifice area)(Smaller than Ao valve orifice area)
– Small L to R shuntSmall L to R shunt
– Normal RV outputNormal RV output
– 75% spontaneously close < 2yrs75% spontaneously close < 2yrs
• Non-restrictive VSDNon-restrictive VSD
– > 1.0 cm> 1.0 cm22
(Equal to or greater than to Ao valve(Equal to or greater than to Ao valve
orifice area)orifice area)
– Equal RV and LV pressuresEqual RV and LV pressures
– Large hemodynamically significant L to R shuntLarge hemodynamically significant L to R shunt

Vascular ResistanceVascular Resistance
• Pulmonary resistance may remain high longer in infantsPulmonary resistance may remain high longer in infants
with large VSDwith large VSD
– Minimal L to R shuntMinimal L to R shunt
• Decreasing pulmonary resistance leads to significant L toDecreasing pulmonary resistance leads to significant L to
R shuntR shunt
– Clinical symptoms of CHFClinical symptoms of CHF
• Persistent L to R shunt leads to hypertrophy of the medialPersistent L to R shunt leads to hypertrophy of the medial
smooth muscle layer of the pulmonary arteries whichsmooth muscle layer of the pulmonary arteries which
increases PVR and potential R to L shuntingincreases PVR and potential R to L shunting
• Long-standing L to R shunting that results in chronicallyLong-standing L to R shunting that results in chronically
increased PVR may lead to persistent R to L shuntingincreased PVR may lead to persistent R to L shunting
described as “Eisenmenger Physiology”described as “Eisenmenger Physiology”

Clinical Features-Small LesionsClinical Features-Small Lesions
 MurmurMurmur
 4 to 10 days, early with rapid4 to 10 days, early with rapid
decrease in PVRdecrease in PVR
 AsymptomaticAsymptomatic
 normal feeding, growth andnormal feeding, growth and
developmentdevelopment

MurmursMurmurs
 Restrictive VSD - HolosystolicRestrictive VSD - Holosystolic
murmurmurmur
 correlates with continuouscorrelates with continuous
pressure gradientpressure gradient
 Non-restrictive large VSD – noNon-restrictive large VSD – no
murmur (no turbulence if nomurmur (no turbulence if no
gradient)gradient)

Clinical Features-Large LesionsClinical Features-Large Lesions
 Accentuated precordial activityAccentuated precordial activity
 More prominent as LV volume increasesMore prominent as LV volume increases
 Signs/symptoms of CHFSigns/symptoms of CHF
 DiaphoresisDiaphoresis
 TachypneaTachypnea
 Fatigue with feedingFatigue with feeding
 HepatomegalyHepatomegaly
 RalesRales
 Duskiness with cryingDuskiness with crying
 May develop as early as 2 weeksMay develop as early as 2 weeks
 Severity increases as PVR decreasesSeverity increases as PVR decreases

EvaluationEvaluation
 Chest RadiographyChest Radiography
CardiomegalyCardiomegaly
Increased pulmonaryIncreased pulmonary
vasculaturevasculature
Pulmonary edemaPulmonary edema

EvaluationEvaluation
 EKGEKG
 Small: normal or LVHSmall: normal or LVH
 Prominent Q, R, and T waves in II, III,Prominent Q, R, and T waves in II, III,
aVF and V6aVF and V6
 Large: Biventricular hypertrophyLarge: Biventricular hypertrophy
 RVH- rsR’ in V1, S wave in V6RVH- rsR’ in V1, S wave in V6

EchocardiographyEchocardiography
 Assess indication in consultation withAssess indication in consultation with
CardiologyCardiology
 Assess location, size, and multiplicityAssess location, size, and multiplicity
 RV and PA pressureRV and PA pressure
 Assess for LA and LV dilationAssess for LA and LV dilation
 Assess LV functionAssess LV function
 Note relation to great vessels, AV valvesNote relation to great vessels, AV valves

Cardiac CatheterizationCardiac Catheterization
 Able to documentAble to document
 Number of defectsNumber of defects
 Presence of associated defectsPresence of associated defects
 Magnitude of shuntMagnitude of shunt
 Estimate PVREstimate PVR
 Not used if information apparent byNot used if information apparent by
other meansother means
 Most information available throughMost information available through

PrevalencePrevalence
 Most common congenital heartMost common congenital heart
lesionlesion
 Occurs in 50% of children withOccurs in 50% of children with
heart lesionsheart lesions
 15-20% in isolation15-20% in isolation
 5-50 per 1000 live births5-50 per 1000 live births
 56% female56% female

Chromosomal DisordersChromosomal Disorders
associated with VSDassociated with VSD
 Trisomy 21: 40% of T21 will have VSDTrisomy 21: 40% of T21 will have VSD
 Trisomy 13, 18: 18% of T13, 31% of T18 will haveTrisomy 13, 18: 18% of T13, 31% of T18 will have
VSDVSD
 22q11 deletion:22q11 deletion:
 Tetrology of Fallot is most common anomalyTetrology of Fallot is most common anomaly
 VSD with or without aortic arch anomaly is second mostVSD with or without aortic arch anomaly is second most
commoncommon
 Holt-Oram (Hand-heart syndrome): TBX5 gene foundHolt-Oram (Hand-heart syndrome): TBX5 gene found
on Chromosome 12on Chromosome 12
 Recurrence risk for VSD based on parental VSDRecurrence risk for VSD based on parental VSD
 Paternal 2%Paternal 2%


Treatment for Small VSDTreatment for Small VSD
 No medication or surgery ifNo medication or surgery if
asymptomaticasymptomatic
 75-80% close by 2 years75-80% close by 2 years
 ObservationObservation
 No antibiotic prophylaxis forNo antibiotic prophylaxis for
proceduresprocedures

CHF TreatmentCHF Treatment
 High-calorie formulaHigh-calorie formula
 MedicationMedication
 DiureticsDiuretics
 Furosemide with or withoutFurosemide with or without
spironolactonespironolactone
 Afterload reductionAfterload reduction
 Enalapril or CaptoprilEnalapril or Captopril
 Digoxin (maybe)Digoxin (maybe)
 Symptoms of CHF improve as L to RSymptoms of CHF improve as L to R
shunt decreasesshunt decreases

Indications for InterventionIndications for Intervention
 Decompensated CHFDecompensated CHF
 Compensated CHF with:Compensated CHF with:
 Large hemodynamically significantLarge hemodynamically significant
VSD - L to R shunting with Qp/QsVSD - L to R shunting with Qp/Qs >>
2:1, even if asymptomatic, ideally2:1, even if asymptomatic, ideally
before 1 yearbefore 1 year
 Growth failure, unresponsive toGrowth failure, unresponsive to
medical therapy is an indication formedical therapy is an indication for
surgerysurgery

Post-InterventionPost-Intervention
 Most infants have normal growth andMost infants have normal growth and
developmentdevelopment
 Early closure (< 1 year) associated withEarly closure (< 1 year) associated with
better LV function and regression ofbetter LV function and regression of
hypertrophyhypertrophy
 Residual VSD is not commonResidual VSD is not common
 RBBB is common following surgeryRBBB is common following surgery
 Rare complete heart blockRare complete heart block

Part IPart I
Fetal Circulation, ASD, VSDFetal Circulation, ASD, VSD

 Most common CHD in children (25%)Most common CHD in children (25%)
 Isolated VSD found in only 10% ofIsolated VSD found in only 10% of
adults with CHDadults with CHD
 75-80% of small VSD’s close75-80% of small VSD’s close
spontaneously by late childhoodspontaneously by late childhood
 10-15% of large VSD’s close10-15% of large VSD’s close
 60% of defects close before age 3, and60% of defects close before age 3, and
90% before age 890% before age 8
 Risk factors for decreased survival forRisk factors for decreased survival for
unoperated patients include:unoperated patients include:
 Cardiomegaly on CXR, Elevated PASPCardiomegaly on CXR, Elevated PASP
(>50 mmHg), and CV symptoms(>50 mmHg), and CV symptoms

Ventricular SeptumVentricular Septum
 Partitioning begins as aPartitioning begins as a
muscular ridge near themuscular ridge near the
apexapex
 Ridge undergoes activeRidge undergoes active
growth which forms thegrowth which forms the
muscular septum (inlet,muscular septum (inlet,
trabecular, and outlet)trabecular, and outlet)
 Concomitantly endocardialConcomitantly endocardial
cushions fuse and the twocushions fuse and the two
regions meetregions meet Inlet
Trabecular
Outlet

Types of VSD’sTypes of VSD’s
 Perimembranous defect (70-80%)Perimembranous defect (70-80%)
 Less likely to be associated with other defectsLess likely to be associated with other defects
 Highest rate of spontaneous closureHighest rate of spontaneous closure
 Muscular or apical defects (5-20%)Muscular or apical defects (5-20%)
 Typically occur in isolationTypically occur in isolation
 High spontaneous closure rates unless multipleHigh spontaneous closure rates unless multiple
 AV-Canal type (5-8%)AV-Canal type (5-8%)
 Rarely close spontaneously, commonly seen in Trisomy 21Rarely close spontaneously, commonly seen in Trisomy 21
 Usually large & associated with abnormal AV valveUsually large & associated with abnormal AV valve
 Supracristal or subaortic defects (5-7%)Supracristal or subaortic defects (5-7%)
 Often small but need closure due to associated AROften small but need closure due to associated AR

VSDVSD
 Arterial pulse is often normalArterial pulse is often normal
 There may be a systolic thrill on palpation ofThere may be a systolic thrill on palpation of
the precordium (maximal in 3the precordium (maximal in 3rdrd
or 4or 4thth
ICS)ICS)
 Holosystolic, high frequency murmur (gradeHolosystolic, high frequency murmur (grade
4-6/6) with small VSD and normal PAP4-6/6) with small VSD and normal PAP
 Once PAP increases above the systemicOnce PAP increases above the systemic
pressures the holosystolic murmurpressures the holosystolic murmur
disappearsdisappears
 Increase flow across pulmonary valve causesIncrease flow across pulmonary valve causes
a SEMa SEM
 A loud P2 component is heard in this settingA loud P2 component is heard in this setting

ECG in VSDECG in VSD May be normal but often shows LVH and LAEMay be normal but often shows LVH and LAE
 Presence of RAD represents elevated RVP and PAPPresence of RAD represents elevated RVP and PAP
 Postoperative RBBB is commonPostoperative RBBB is common

CXR in VSDCXR in VSD
 Cardiomegaly with LAE and LVE will be seen with large L to RCardiomegaly with LAE and LVE will be seen with large L to R
shuntsshunts
 A large defect associated with a small heart and oligemic lung fieldsA large defect associated with a small heart and oligemic lung fields
should raise the suspicion of pulmonary vascular diseaseshould raise the suspicion of pulmonary vascular disease

VSDVSD
 Hemodynamic severity grading of isolated VSDs inHemodynamic severity grading of isolated VSDs in
adults:adults:
 Small: Qp:Qs <1.4, and pulmonary to aortic systolicSmall: Qp:Qs <1.4, and pulmonary to aortic systolic
pressure <0.3pressure <0.3
 Moderate: Qp:Qs = 1.4-2.2, and systolic pressure ratio >0.3Moderate: Qp:Qs = 1.4-2.2, and systolic pressure ratio >0.3
 Large: Qp:Qs >2.2, and systolic pressure ratio >0.3Large: Qp:Qs >2.2, and systolic pressure ratio >0.3
 Eisenmenger: Qp:Qs <1.5 and systolic pressure ratio >0.9Eisenmenger: Qp:Qs <1.5 and systolic pressure ratio >0.9
 Physiologic classification:Physiologic classification:
 Restrictive: RV pressure < LV pressure in absence ofRestrictive: RV pressure < LV pressure in absence of
RVOTORVOTO
 Nonrestrictive: RV pressure = LV pressure in absence ofNonrestrictive: RV pressure = LV pressure in absence of
RVOTORVOTO

VSDVSD
 Clinical severity grading:Clinical severity grading:
 Small: Causes negligible hemodynamic changes. LV sizeSmall: Causes negligible hemodynamic changes. LV size
normal w/o PHTNnormal w/o PHTN
 Moderate: Causes LV and LA enlargment, and usually someModerate: Causes LV and LA enlargment, and usually some
PHTN (reversible)PHTN (reversible)
 Large: Results in pulmonary vascular obstructive diseaseLarge: Results in pulmonary vascular obstructive disease
and Eisenmenger physiology unless there is coexistentand Eisenmenger physiology unless there is coexistent
RVOTORVOTO
 Pathologic and surgical classification:Pathologic and surgical classification:
 Perimembranous: bordered by fibrous continuity of an AVPerimembranous: bordered by fibrous continuity of an AV
valve and an arterial valve, usually with inlet or outletvalve and an arterial valve, usually with inlet or outlet
extensionextension
 Muscular: bordered by muscular rim, usually trabecularMuscular: bordered by muscular rim, usually trabecular
 Doubly committed: bordered by fibrous continuity of both theDoubly committed: bordered by fibrous continuity of both the
aortic and pulmonary valvesaortic and pulmonary valves

VSD RepairVSD Repair
 When repair is performed in the first two years ofWhen repair is performed in the first two years of
life, asymptomatic adult survival with normal growthlife, asymptomatic adult survival with normal growth
and development can be anticipatedand development can be anticipated
 When surgery is undertaken in older children, aWhen surgery is undertaken in older children, a
late postopeartive increase in LV chamber size,late postopeartive increase in LV chamber size,
together with decreased systolic function is seentogether with decreased systolic function is seen
 Development of late postoperative PHTN is largelyDevelopment of late postoperative PHTN is largely
determined by the age at surgery and preoperativedetermined by the age at surgery and preoperative
PVRPVR
 Risk of SBE persists and requires prophylaxisRisk of SBE persists and requires prophylaxis

 The initial workup at a minimum shouldThe initial workup at a minimum should
include:include:
 A through clinical assessmentA through clinical assessment
 ECGECG
 CXRCXR
 TTE/Doppler evaluationTTE/Doppler evaluation

 The diagnostic workup may require:The diagnostic workup may require:
 OxymetryOxymetry
 Right heart Cath (PAP and PVR determination, to assessRight heart Cath (PAP and PVR determination, to assess
pulmonary vascular reactivity)pulmonary vascular reactivity)
 Coronary angio (in high risk pts or in pts >40 y if surgicalCoronary angio (in high risk pts or in pts >40 y if surgical
repair is planned)repair is planned)
 MRI to prove existence of VSD or to assess for otherMRI to prove existence of VSD or to assess for other
anomalie if doubt remains after other imaging modalities.anomalie if doubt remains after other imaging modalities.
Also can calculate Qp:QsAlso can calculate Qp:Qs
 Oxygen saturation with exercise if there is any suggestion ofOxygen saturation with exercise if there is any suggestion of
PHTN. Do not exercise if there is severe PHTN or restingPHTN. Do not exercise if there is severe PHTN or resting
oxygen Sat is <85%oxygen Sat is <85%
 Open lung Bx should be considered when the reversibility ofOpen lung Bx should be considered when the reversibility of
PHTN is uncertain from hemodynamic dataPHTN is uncertain from hemodynamic data

 Indications for intervention: Geade C, Level IVIndications for intervention: Geade C, Level IV
 Presence of a significant VSD (symptomatic QP/QS = 2/1,Presence of a significant VSD (symptomatic QP/QS = 2/1,
PASP > 50 mmHg), deteriorating ventricular fx due toPASP > 50 mmHg), deteriorating ventricular fx due to
volume (LV) or pressure (RV) overloadvolume (LV) or pressure (RV) overload
 Significant RVOTO (pk to pk gradient of > 50 mmHg, orSignificant RVOTO (pk to pk gradient of > 50 mmHg, or
instantaneous gradient >70 mmHg)instantaneous gradient >70 mmHg)
 Perimembranous or doubly committed VSD with more thanPerimembranous or doubly committed VSD with more than
mild ARmild AR
 In presence of severe PHTN (PAP >2.3 SABP, or PVR >2/3In presence of severe PHTN (PAP >2.3 SABP, or PVR >2/3
SVR), there must be a net L to R shunt of >1.5 or evidenceSVR), there must be a net L to R shunt of >1.5 or evidence
of PA reactivity when challenged with pulmonary vasodilator,of PA reactivity when challenged with pulmonary vasodilator,
or lung Bx evidence of PA changes are potentially reversibleor lung Bx evidence of PA changes are potentially reversible
(Heath Edwards grade II-III or less)(Heath Edwards grade II-III or less)
 Hx of endocarditis especially if recurrentHx of endocarditis especially if recurrent

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