VENTRICULAR SEPTAL DEFECT

by Dr.Amarnath BR
BMC

CONGENITAL HEART DISEASE
(con-together,genitus(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

PDA.ASD.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.AVcanal .

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delayed and diminished P2 (PS) * in PH .singlventricle.blood flow * mod. return w/ obstruction .RIGHT to LEFT shunts (cyanotic heart disease)  increased pulm.ESM * oligemic lung fields * TOF.PA.accentuated & palpable P2.total anomalous pulm. to severe cyanosis * ESM.total anomalous pulm. TA.TA. blood flow * mildly cyanotic * increased sweating * CCF * FTT * plethoric lung fields * cardiomegaly *TGA. Return w/o obstruction  decreased pulm.

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stenosis(rt side) & aortic stenosis.coarctation of aorta(lt side) . Vasculature ‡pulm.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.

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NADA¶S 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 .

VENTRICULAR SEPTAL DEFECT ‡ most common ACHD ‡ 2nd most common CHD(32%) ‡ SYNONYMS * Roger¶s disease * Interventricular septal defect * congenital cardiac anomaly .

PVR decreases²large Lt to Rt shunt ensues  In some infants large VSDs .75:1.0cm`) Rt&Lt ventricular pressure are equalised(Qp:Qs is more than 2:1)  Large VSDs at birth .0) &poses hemodynamic burden on LV  Large nonrestrictive VSDs(more than 1. (Eisenmenger syndrome) .5cm`) VSD is restrictive & rt.obstructive disease develops .signs of heart failure abate &pt.5:1.pulm. arteriolar thickness never decreases ±pulm.PVR may remain higher than normal and Lt to Rt shunt may intially limited ± involution of media of small pulm.ventricular pressure is normal ± does not cause significant hemodynamic derangement(Qp:Qs=1. vascular bed rather than location  Small communication (less than 0.arterioles.0)  Moderately restrictive VSD with a moderate shunt(Qp:Qs=1.PATHOPHYSIOLOGY  primarily depends on size&status of pulm.when Qp:Qs=1:1 shunt becomes bidirectional. becomes cyanotic.52.

marginal or swiss-cheese typeIII-OUTLET SEPTUM deficient OUTLET supracristal.infundibular or conoseptal SEPTAL DEFICIFNCY ±AVseptal defect (AVcanal) .trabecular.subaortic.ANATOMICAL CLASSIFICATION typeI-MEMBRANOUS SEPTUM MEMBRANOUS paramembranous/perimembranous defect (or infracristal.conoventricular) typeII-MUSCULAR SEPTUM MUSCULAR inlet.central.subpulmonary.apical.

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although ccf during first 6mths is frequent. children²after first year variable clinical children picture emerges.poor growth -frequent chest infections .dyspnoea on exertion.feeding difficulties .X-ray&ECG are normal.CLINICAL FEATURES  Race : no particular racial predilection  Sex :no particular sex preference  Age :infants difficult in postnatal infants± period.small VSD ± asymptomatic large VSD ± common symptoms -palpitation.

intensity of the murmur is best heard at 3rd.sternal border .4th&5th Lt interspace.max.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 .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.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 .

With further progression biventricular hypertrophy.P waves may be notched/peaked. Atrial overload as well as LV overload.pulmonary plethora ‡ ELECTROCARDIOGRAPHY -smallVSD ~ normal tracing -mod.INVESTIGATIONS  ECHOCARDIOGRAPHY two-dimensional &doppler colour flow ‡ CHEST RADIOGRAPHY .notched P wave characteristic of Lt.deep Q waves & tall R waves in leads V5 and V6 and often AF -large VSD ~RVH with rt.normal .biventricular hypertrophy .namely.VSD ~ broad. axis deviation. .

Other investigations  CAT SCAN (Computed Axial Tomography) ‡ MRI ‡ ULTRASOUND ‡ ANGIOGRAPHY (cardiac catheterization and angiography) .

ventricular side Aortic insufficiency Complete heart block Delayed growth & development (FTT) in infancy Damage to electrical conduction system during surgery(causing arrythmias)  Pulmonary hypertension       .COMPLICATIONS Congestive cardiac failure Infective endocarditis on rt.

all close spontaneously * 50% by 2yrs * 90% by 6yrs * 10% during school yrs .INTERVENTION  3 MAJOR TYPES  SMALL (less than 3mm diameter) .hemodynamically insignificant .b/w 80-85% of all VSDs .muscular close sooner than membranous .

Conservative treatment .vascular disease . MODERATE VSDs * 3-5mm diameter * least common group of children(3-5%) * w/o evidence of ccf/ pulm. ‡ LARGE VSDs WITH NORMAL PVR * 6-10mm in diameter * usually requires surgery otherwise« develop CCF & FTT by age of 3-6mths.prevention & treatment of infective endocarditis .htn can be followed until spontaneous closure occurs.treat CCF & prevent development of pulm.

 Infants b/w 6-12mths of age with large defects ass.even if symptoms are controlled by medication. with PH . because of high risk of development of AI.s older than 24mths of age with Qp:Qs is greater than 2:1. .  Pt.  Pt.s with supracristal VSD of any size. CONTRAINDICATION ±severe pulmonary vascular disease.INDICATIONS for SURGERY  VSDs at any age where clinical symptoms and FTT cannot be controlled medically.

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

atrium.ventricle & near the ant.  Alternate approach is through the rt. 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.descending coronary artery.a longitudinal ventriculotomy is performed usually in the infundibular part of the rt.  Through a median sternotomy with the help of extracorporeal circulation.procedure may be deffered to 4-6yrs. .If symptoms are not disabling .Operative procedure  Usually performed in second year.

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Much more to come Are we all still awake? .