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VENTRICULAR SEPTAL DEFECT

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.

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VENTRICULAR SEPTAL DEFECT

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  1. VENTRICULAR SEPTAL DEFECT by Dr.Amarnath BR BMC

  2. 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.

  3. TYPES OF CHD Gr 1 Lt to Rt shunts Gr 2 Rt to Lt shunts Gr 3 Obsructive lesions

  4. 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

  5. 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 RIGHT to LEFT shunts(cyanotic heart disease)

  6. 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)

  7. 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 NADA’S CRITERIA

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

  9. 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)

  10. 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)

  11. 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

  12. 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

  13. 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.

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

  15. 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

  16. 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

  17. 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

  18. 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.

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

  20. 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.

  21. Much more to come Are we all still awake?

  22. THANK YOU

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