Dr. K.L . BARIK Professor, Dept. of Pediatrics Burdwan Medical College

1. Downloaded from: medicinehack.wordpress.com Dr. K.L. BARIKProfessor, Dept. of Pediatrics Burdwan Medical College Acyanoticheart Disease

2. ACYANOTIC HEART DISEASE-LEFT- TO -RIGHT SHUNTLESIONS:

3. NADA’S CRITERIA one major OR two minor are essential

4. COMMON ACYANOTIC CONGENITAL HEART DISEASES. FIVE TYPES OF LESIONS ARE COMMON.

5. VENTRICULAR SEPTAL DEFECT: • Most common CHD. • Accounts for 15% to 27% of all CHD. • Communication between the two ventricles. L-R shunt. • Septum consists of two parts: • Small membranous. • Large muscular part – a) Inlet. b) Trabecular. c) Outlet (Infundibular).

6. CLASSIFICATION OF VSD ACCORDING TO ANATOMICAL SITE: • Perimembranous defects most common 70%: i) Perimembranous inlet. ii) Perimembranous trabecular. iii) Perimembranous outlet (TOF). • Outlet defect 5% to 7%. Part of its rim by aortic/pul. Annulus.- subarterial/subpul. • Inlet defect -5% to 8%. • Trabecular defect -5%-20%: a)Marginal-multiple, small defects- Swiss cheese type. b) Central c) Apical defect. • Infundibular: Rt. Coronary cusp of aortic valve- herniates reduction of shunt –may cause AR.

7. CLASSIFICATION OFVSDACCORDING TO THE SIZE OF THE DEFECTS: • Restrictive VSD (<0.5 cm2) L to R persists. • Nonrestrictive VSDs (>1.0 cm2) equalized quickly. • Very small VSDs: Commonest cause of functional syst. murmur-ejection systolic. • Small VSDs: Pansystolic, no diastolic mur • Moderate VSDs: Long syt. murmur, diastolic murmur, cardiomegaly. • Large VSDs: Shorter & softer murmur, diastolic murmur, accentuated P2.

8. HEMODYNAMICS: • Shunting of oxygenated blood – L to R. • LV starts contraction before RV in systole • High pressure gradient- pan systolic murmur masking S1. Usually syst. thrill. • Towards end of syst- LV pressure lower than aorta-produce A2 but still LV pressure is >RV –murmur cont. - masking A2. • Due to both vent. contract- blood shunted directly to PA- no RV volume overload.

9. HEMODYNAMICS (Contd…) • Large VSDs- direct transmission of LV pressure and blood to RV through large shunt –pressure & volume overload of RV • LA enlargement and diastolic murmur – functional mitral stenosis. • Delayed P2 with wide & variable splitting • Shunt depend on defect size& pul.vas.res.(PVR). • Smaller shunt resist. offed. by size not PVR • Large VSD resistance offered by PVR not by size-called dependent shunt.

10. Ventricular Septal Defect III Ventricular septal defect iii

12. VENTRICULAR SEPTAL DEFECT - PATHOPHYSIOLOGY Normally pulmonary blood flow = systemic blood flow In VSD, pulmonary blood flow > systemic blood flow Normal heart QP:QS 1:1 Small VSD QP:QS 1.5:1, large VSD QP:QS >2:1

13. CLINICAL MENIFESTATIONS: • HISTORY: 1) Small VSD- asymptomatic with normal growth and development. 2)Moderate to large VSD-delayed growth & development/exercise intolerance/ repeated pulmonary infection and CCF. 3)Long- standing pulmonary hypertension. h/o cyanosis and decreased activity (Eisenmenger’s syndrome).

14. (C/F CONT….) 1)Infant with small VSD- well developed. 2)On 6 to 8 wk- with large VSD – poor wt. gain or signs of CCF. 3) Cyanosis & clubbing–(Eisenmenger’s syndrome) 4)Systolic thrill at LLSB. Precordial bulge large shunt VSD. 5)Pansyst./holosyt,/early syst.murmur. 6)Apical diastolic murmur. 7)Infundibular VSD –early diastolic murrm.ofAR. PHYSICAL EXAMINATION

15. VENTRICULAR SEPTAL DEFECT-SYMPTOMS • Small VSD – no symptoms, detection of heart murmur • Large VSD – heart failure • Breathing fast - tachypnea • Feeding difficulties • Excessive sweating • Inadequate growth

16. VENTRICULAR SEPTAL DEFECT-SIGNS • Small VSD – pansystolic murmur at mid left sternal border • Large VSD • Signs of heart failure –tachypnoea • Hyperdynamic precordium and LV apex • Systolic thrill along left sternal border • Pan systolic murmur at mid left sternal border • hepatomegaly

17. INVESTIGATIONS: • Electrocardiography: 1.Small VSD – Normal 2.Moderate VSD – LVH and LAH. 3.Large VSD – CVH with or LVH. 4.Pulmonary vas.obst. – Only RVH. • X-Ray Chest:- Cardiomegaly , Plethora , BVM Pul.obst,dis.- PA/hilarPA enlgd./ph.ichm. • ECHO: Number, size, location of shunts,PA pressure. • Complete blood count.

18. NATURAL HISTORY: • Spontaneous closure – 30%- 40% by 6m. Smaller membranous & muscular defect. • Almost 90% by 3yrs. Small mem.& muscl. • Inlet & Infundibular – do not close spnt. • CCF- with large VSD by 6 to 8 weeks. • VSD with R to L shunt by teenage years. • Infective endocarditis rarely occurs.

19. MANAGEMENT: • MEDICAL: 1. Rx of CCF – Digoxin & diuretics 2-4 m. 2. High calorie formula feeding. 3. Correction of anemia. 4. Good oral hygiene and antimicrobials for prophylaxis against SABE. 5. Medical closure – using Umbrella devices.

20. MANAGEMENT (contd): • SURGICAL: Indication- 1.CCF Rxed – growth failure- opn.by 6m. 2.Qp/Qs at least 2:1. (signifi. L-R shunt). 3.Older infant – incr. pul.vascular resist. Contraindication:- 1.Small VSD& no CCF by 6 months of age 2.VSD with Qp/Qs <1.5:1. 3.Pulmonary to syst. Vascular resis. ratio >.5. 4.Multiple small VSDs. 5.VSD with R to L shunt.

21. SURGICAL MANAGEMENT CONT.: • Direct closure of defects under cardiopulmonary bypass. • Complication: 1.RBBB. 2.Complete heart block. 3.Reopening of the shunt. 4.Infection.

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

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