VENTRICULAR SEPTAL DEFECT Powerpoint Presentation

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-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 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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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

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

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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)

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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-ray&ECG are normal. children—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 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

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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 hypertrophy;P 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 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.

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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

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CONGENITAL HEART DISEASE (con-together,genitus-born). The majority of congenital anomalies of the h more CONGENITAL HEART DISEASE (con-together,genitus-born). The majority of congenital anomalies of the heart are present 6wks after conception & most anomalies ... less