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VENTRICULAR

SEPTAL
DEFECT

by
Dr.Amarnath BR
BMC
CONGENITAL
HEART DISEASE
(con-together,genitus-born)

The majority of congenital


anomalies of the heart are
present 6wks after
conception & most
anomalies compatible with
6mths of intrauterine life
permit live offspring at
term.
TYPES OF CHD

•Gr 1 Lt to Rt shunts
•Gr 2 Rt to Lt shunts
•Gr 3 Obsructive lesions
LEFT to RIGHT shunts
(acyanotic heart disease)

 Frequent chest infections (6-8 attacks first year of


life)
 Tendency for increased sweating with related
their tendency for developing CCF
 Precordial bulge
 Hyperkinetic precordium
 Tricuspid /mitral DDM
 X-ray plethoric +cardiomegaly
 VSD,ASD, PDA,AVcanal
RIGHT to LEFT shunts
(cyanotic heart disease)
 increased pulm. blood flow  decreased pulm.blood
* mildly cyanotic flow
* increased sweating * mod. to severe cyanosis
* CCF * ESM, delayed and
* FTT diminished P2 (PS)
* plethoric lung fields
* in PH ,accentuated &
* cardiomegaly palpable P2,ESM
*TGA,singlventricle,
* oligemic lung fields
* TOF,PA,TA,total
TA,total anomalous pulm. anomalous pulm. return
Return w/o obstruction w/ obstruction
Obstructive lesions
• absence of frequent chest infections
• absense of cyanosis
• absence of precordial bulge
• presence of forcible &heaving cardiac impulse

• systolic thrill +ESM & delayed corresponding
S2
•ECG shows obstructive lesions
•X-ray normal sized heart & pulm. Vasculature
•pulm.stenosis(rt side) & aortic
stenosis,coarctation of aorta(lt side)
NADA’S CRITERIA
MAJOR MINOR
• systolic murmur gr III or • systolic murmur less
more
than gr III
• diastolic murmur
• cyanosis • abnormal S2
• ccf • abnormal ECG
• abnormal X-ray
• abnormal BP
one major &two
minor are essential
VENTRICULAR SEPTAL
DEFECT
• most common ACHD
• 2nd most common CHD(32%)
• SYNONYMS
* Roger’s disease
* Interventricular septal defect
* congenital cardiac anomaly
PATHOPHYSIOLOGY
 primarily depends on size&status of pulm. vascular bed rather than
location
 Small communication (less than 0.5cm`) VSD is restrictive &
rt.ventricular pressure is normal – does not cause significant
hemodynamic derangement(Qp:Qs=1.75:1.0)
 Moderately restrictive VSD with a moderate shunt(Qp:Qs=1.5-
2.5:1.0) &poses hemodynamic burden on LV
 Large nonrestrictive VSDs(more than 1.0cm`) Rt&Lt ventricular
pressure are equalised(Qp:Qs is more than 2:1)
 Large VSDs at birth ,PVR may remain higher than normal and Lt to
Rt shunt may intially limited – involution of media of small
pulm.arterioles,PVR decreases—large Lt to Rt shunt ensues
 In some infants large VSDs ,pulm. arteriolar thickness never
decreases –pulm.obstructive disease develops .when Qp:Qs=1:1
shunt becomes bidirectional,signs of heart failure abate &pt.
becomes cyanotic. (Eisenmenger syndrome)
ANATOMICAL
CLASSIFICATION
typeI-MEMBRANOUS SEPTUM
paramembranous/perimembranous defect
(or infracristal,subaortic,conoventricular)
typeII-MUSCULAR SEPTUM
inlet,trabecular,central,apical,marginal or
swiss-cheese
typeIII-OUTLET SEPTUM deficient
supracristal,subpulmonary,infundibular or
conoseptal
SEPTAL DEFICIFNCY –AVseptal defect (AVcanal)
CLINICAL FEATURES
 Race : no particular racial predilection
 Sex :no particular sex preference
 Age :infants–
infants difficult in postnatal period,although ccf
during first 6mths is frequent,X-ray&ECG are normal.
children—after
children first year variable clinical picture
emerges.small VSD – asymptomatic
large VSD – common symptoms
-palpitation,dyspnoea on exertion,feeding
difficulties ,poor growth
-frequent chest infections
PHYSICAL FINDINGS
• Pulse pressure is relatively wide
• Precordium is hyperkinetic with a systolic thrill at LSB
• S1&S2 are masked by a PSM at Lt.sternal border ,max. intensity of
the murmur is best heard at 3rd,4th&5th Lt interspace.Also well heard at
the 2nd space but not conducted beyond apex
• Lt. 2nd space –widely split &variable accentuated P2
• Delayed diastolic murmur at the apex &S3
• Presence of mid-diastolic ,low pitched rumble at the apex is caused by
increased flow across the mitral valve &indicates Qp:Qs=2:1/greater
• Maladie de Roger –small VSD presenting in older children as a loud
PSM w/o other significant hemodynamic changes
INVESTIGATIONS
 ECHOCARDIOGRAPHY
two-dimensional &doppler colour flow
• CHEST RADIOGRAPHY
- normal
- biventricular hypertrophy
- pulmonary plethora
• ELECTROCARDIOGRAPHY
-smallVSD ~ normal tracing
-mod.VSD ~ broad,notched P wave characteristic of Lt. Atrial overload
as well as LV overload,namely,deep Q waves & tall R waves in leads
V5 and V6 and often AF
-large VSD ~RVH with rt. axis deviation. With further progression
biventricular hypertrophy;P waves may be notched/peaked.
Other investigations
 CAT SCAN
(Computed Axial Tomography)
• MRI
• ULTRASOUND
• ANGIOGRAPHY
(cardiac catheterization and angiography)
COMPLICATIONS
 Congestive cardiac failure
 Infective endocarditis on rt.ventricular side
 Aortic insufficiency
 Complete heart block
 Delayed growth & development (FTT) in infancy
 Damage to electrical conduction system during
surgery(causing arrythmias)
 Pulmonary hypertension
INTERVENTION
 3 MAJOR TYPES
 SMALL (less than 3mm
diameter)
- hemodynamically
insignificant
- b/w 80-85% of all VSDs
- all close spontaneously
* 50% by 2yrs
* 90% by 6yrs
* 10% during school yrs
- muscular close sooner than
membranous
 MODERATE VSDs
* 3-5mm diameter
* least common group of children(3-5%)
* w/o evidence of ccf/ pulm.htn can be
followed until spontaneous closure occurs.
• LARGE VSDs WITH NORMAL PVR
* 6-10mm in diameter
* usually requires surgery otherwise…
develop CCF & FTT by age of 3-6mths.
Conservative treatment
- treat CCF & prevent development of
pulm.vascular disease
- prevention & treatment of infective
endocarditis
INDICATIONS for SURGERY
 VSDs at any age where clinical symptoms and
FTT cannot be controlled medically.
 Infants b/w 6-12mths of age with large defects
ass. with PH ,even if symptoms are controlled by
medication.
 Pt.s older than 24mths of age with Qp:Qs is
greater than 2:1.
 Pt.s with supracristal VSD of any size, because of
high risk of development of AI.
CONTRAINDICATION –severe pulmonary
vascular disease.
Surgical
correction has
to be done
before
irreversible
damage to
pulmonary
vasculature
occurs.
Operative procedure
 Usually performed in second year.If symptoms are
not disabling ,procedure may be deffered to 4-
6yrs.
 Through a median sternotomy with the help of
extracorporeal circulation,a longitudinal
ventriculotomy is performed usually in the
infundibular part of the rt.ventricle & near the
ant.descending coronary artery.
 Alternate approach is through the rt.atrium,
particularly when PVR is increased .
 Defect is usually closed with an oval patch of
knitted dacron by mattress suture posteriorly and
continous suture anteriorly using prolene.
Much more to come

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all still
awake?

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