VENTRICULAR SEPTAL DEFECT by Dr.Amarnath BR BMC. CONGENITAL HEART DISEASE...

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VENTRICULAR SEPTAL DEFECT by Dr.Amarnath BR BMC

Transcript of VENTRICULAR SEPTAL DEFECT by Dr.Amarnath BR BMC. CONGENITAL HEART DISEASE...

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VENTRICULAR SEPTAL DEFECT

by

Dr.Amarnath BRBMC

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CONGENITAL CONGENITAL HEART DISEASE HEART DISEASE

(con-together,genitus-born)(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.

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TYPES OF CHDTYPES 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 shuntsLEFT to RIGHT shunts(acyanotic heart disease)(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 shuntsRIGHT to LEFT shunts (cyanotic heart disease)(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 lesionsObstructive 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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NADA’S CRITERIANADA’S CRITERIA

MAJORMAJOR• systolic murmur gr III

or more• diastolic murmur• cyanosis• ccf

one major &two minor are essential

MINORMINOR • systolic murmur less

than gr III• abnormal S2• abnormal ECG• abnormal X-ray• abnormal BP

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VENTRICULAR SEPTAL VENTRICULAR SEPTAL DEFECTDEFECT

• most common ACHD

• 2nd most common CHD(32%)

• SYNONYMS

* Roger’s disease

* Interventricular septal defect

* congenital cardiac anomaly

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PATHOPHYSIOLOGYPATHOPHYSIOLOGY 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)

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ANATOMICALANATOMICALCLASSIFICATIONCLASSIFICATION

typeI-MEMBRANOUS SEPTUMMEMBRANOUS SEPTUM paramembranous/perimembranous defect (or infracristal,subaortic,conoventricular)typeII-MUSCULAR SEPTUMMUSCULAR SEPTUM inlet,trabecular,central,apical,marginal or swiss-cheesetypeIII-OUTLET SEPTUMOUTLET SEPTUM deficient supracristal,subpulmonary,infundibular or

conoseptalSEPTAL DEFICIFNCYSEPTAL DEFICIFNCY –AVseptal defect (AVcanal)

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CLINICAL FEATURESCLINICAL FEATURES

Race : no particular racial predilection Sex :no particular sex preference Age :infantsinfants– difficult in postnatal period,although ccf

during first 6mths is frequent,X-ray&ECG are normal. childrenchildren—after 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 FINDINGSPHYSICAL 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 RogerMaladie de Roger –small VSD presenting in older children as a loud PSM w/o other significant hemodynamic changes

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INVESTIGATIONSINVESTIGATIONS ECHOCARDIOGRAPHYECHOCARDIOGRAPHY two-dimensional &doppler colour flow

• CHEST RADIOGRAPHYCHEST RADIOGRAPHY - normal - biventricular hypertrophy - pulmonary plethora

• ELECTROCARDIOGRAPHYELECTROCARDIOGRAPHY -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.

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Other investigationsOther investigations

CAT SCAN

(Computed Axial Tomography)

• MRI

• ULTRASOUND

• ANGIOGRAPHY

(cardiac catheterization and angiography)

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COMPLICATIONSCOMPLICATIONS

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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INTERVENTIONINTERVENTION

3 MAJOR TYPES SMALL (less than 3mm SMALL (less than 3mm

diameter)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 VSDsMODERATE 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 PVRLARGE 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 SURGERYINDICATIONS 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.

CONTRAINDICATIONCONTRAINDICATION –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 procedureOperative 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 comeMuch more to come

Are we all still awake?

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