dr. k.l . barik professor, dept. of pediatrics burdwan medical college

Dr. K.L. BARIKProfessor, Dept. of Pediatrics Burdwan Medical CollegeAcyanotic heart Disease

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ACYANOTIC HEART DISEASE-LEFT- TO -RIGHT

SHUNT LESIONS:

NADA’S CRITERIA

MINOR

systolic murmur less than gr III

abnormal S2

abnormal ECG

abnormal X-ray

abnormal BP

MAJOR

systolic murmur gr III or more

diastolic murmur

cyanosis

ccf

one major OR two minor are essential

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

1)Venticular septal defect (VSD).

2)Atrial septal defect (ASD).

3)Patent ductus arteriosus (PDA).

4)Endocardial cushion defect (ECD).

5)Partial anomalous pulmonary venous return (PAPVR).

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:

i. Small membranous.ii. Large muscular part –

a) Inlet. b) Trabecular. c) Outlet (Infundibular).

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.

CLASSIFICATION OF VSD ACCORDING 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.

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.

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.

Ventricular Septal Defect IIIVe

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VENTRICULAR SEPTAL DEFECT - PATHOPHYSIOLOGY

Normally pulmonary blood flow = systemic blood flowIn VSD, pulmonary blood flow > systemic blood flow

Normal heart QP:QS 1:1Small VSD QP:QS 1.5:1, large VSD QP:QS >2:1

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).

(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

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

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

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.

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.

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.

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.

SURGICAL MANAGEMENT CONT.:

Direct closure of defects under cardiopulmonary bypass.

Complication:

1.RBBB.

2.Complete heart block.

3.Reopening of the shunt.

4.Infection.

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

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