VENTRICULAR SEPTAL DEFECT

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VENTRICULAR SEPTAL DEFECT

• by
• Dr.Amarnath BR
• BMC

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CONGENITAL HEART DISEASE (con-together,genitus-b
orn)

• 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.

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TYPES OF CHD

• Gr 1 Lt to Rt shunts
• Gr 2 Rt to Lt shunts
• Gr 3 Obsructive lesions

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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

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RIGHT to LEFT shunts (cyanotic heart disease)

• increased pulm. blood flow
• mildly cyanotic
• increased sweating
• CCF
• FTT
• plethoric lung fields
• cardiomegaly
• TGA,singlventricle,
  
  
• TA,total anomalous pulm. Return w/o
  obstruction

• decreased pulm.blood flow
• mod. to severe cyanosis
• ESM, delayed and diminished P2 (PS)
• in PH ,accentuated palpable P2,ESM
• oligemic lung fields
• TOF,PA,TA,total anomalous pulm. return w/
  obstruction

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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)

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NADAS CRITERIA

• MAJOR
• systolic murmur gr III or more
• diastolic murmur
• cyanosis
• ccf
  
• one major two minor are essential

• MINOR
• systolic murmur less than gr III
• abnormal S2
• abnormal ECG
• abnormal X-ray
• abnormal BP

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VENTRICULAR SEPTAL DEFECT

• most common ACHD
• 2nd most common CHD(32)
• SYNONYMS
• Rogers disease
• Interventricular septal defect
• congenital cardiac anomaly

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PATHOPHYSIOLOGY

• primarily depends on sizestatus 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(QpQs1.751.0)
• Moderately restrictive VSD with a moderate
  shunt(QpQs1.5-2.51.0) poses hemodynamic
  burden on LV
• Large nonrestrictive VSDs(more than 1.0cm) RtLt
  ventricular pressure are equalised(QpQs is more
  than 21)
• 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
  decreaseslarge Lt to Rt shunt ensues
• In some infants large VSDs ,pulm. arteriolar
  thickness never decreases pulm.obstructive
  disease develops .when QpQs11 shunt becomes
  bidirectional,signs of heart failure abate pt.
  becomes cyanotic. (Eisenmenger syndrome)

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ANATOMICALCLASSIFICATION

• 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)

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CLINICAL FEATURES

• Race no particular racial predilection
• Sex no particular sex preference
• Age infants difficult in postnatal
  period,although ccf during first 6mths is
  frequent,X-rayECG are normal.
• childrenafter first year variable
  clinical picture emerges.small VSD asymptomatic
• large VSD common symptoms
• -palpitation,dyspnoea on
  exertion,feeding difficulties ,poor growth
• -frequent chest infections

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PHYSICAL FINDINGS

• Pulse pressure is relatively wide
• Precordium is hyperkinetic with a systolic thrill
  at LSB
• S1S2 are masked by a PSM at Lt.sternal border
  ,max. intensity of the murmur is best heard at
  3rd,4th5th 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 QpQs21/greater
• Maladie de Roger small VSD presenting in older
  children as a loud PSM w/o other significant
  hemodynamic changes

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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 hypertrophyP
  waves may be notched/peaked.

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Other investigations

• CAT SCAN
• (Computed Axial Tomography)
• MRI
• ULTRASOUND
• ANGIOGRAPHY
• (cardiac catheterization and angiography)

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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

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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

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• 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

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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 QpQs is
  greater than 21.
• Pt.s with supracristal VSD of any size, because
  of high risk of development of AI.
• CONTRAINDICATION severe pulmonary vascular
  disease.

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Surgical correction has to be done before
irreversible damage to pulmonary vasculature
occurs.
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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.

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Much more to come
Are we all still awake?
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THANK YOU