Dr. K.L. BARIK Professor, Dept. of Pediatrics Burdwan Medical College Acyanotic heart Disease Downloaded from: medicinehack.wordpress.com

ACYANOTIC HEART DISEASE- LEFT- TO -RIGHT SHUNT LESIONS:

NADA’S CRITERIA MINOR systolic murmur less than gr III abnormal S2abnormal ECGabnormal X-rayabnormal BP MAJOR systolic murmur gr III or more diastolic murmurcyanosisccf 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 cm 2 ) L to R persists.  Nonrestrictive VSDs (>1.0 cm 2 ) 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 P 2.

HEMODYNAMICS:  Shunting of oxygenated blood – L to R.  LV starts contraction before RV in systole  High pressure gradient- pan systolic murmur masking S 1. Usually syst. thrill.  Towards end of syst- LV pressure lower than aorta- produce A 2 but still LV pressure is >RV –murmur cont. - masking A 2.  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 P 2 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 III Ventricular septal defect iii

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

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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