ACYANOTIC CONGENITAL HEART DISEASE

Muhammad Ali Pediatric Cardiology Division University of Sumatera Utara

Structures of the heart

Ventricular Septal Defect (VSD)

Insidence 20 % of all CHD No sex influenced Anatomy Subarterial defect : below pulmonary and aortic valve Perimembranous defect: below aortic valve at pars membranous septum Muscular defect

VSD

VSD

Lungs
PA

LA

LV

AO

RV

RA

Systemic

Qp > Qs

VSD

RA

LA

RA

LA

RV

LV

RV

LV

VSD

VSD

Clinical findings Day 1st after birth: murmur (-) After 2-6 weeks : murmur (+) Murmur : pansystolic grade 3/6 or higher at LSB 3 Small muscular defect: early systolic murmur Significant defect: Mid diastolic murmur at apex

VSD

Murmur: pansystolic grade 3/6 or higher at LSB 3

Small VSD

Large VSD

VSD

Cardiomegaly Apex down ward Prominence pulmonary artery segment Increased pulmonary vascular marking

VSD
Diagnosis Differential PDA with PH Tetralogy Fallot non cyanotic Inoscent murmur

Management: Definitive : VSD closure Surgery Transcatheter closure

VSD

Heart failure (+)

Anti failure

Heart failure (-)

Aortic valve prolaps

Fail Success PAB Evaluate in 6 mths

Infundibular stenosis

PH Spontaneous closure PVD(+)

Smaller

PVD(-) Cath

Cath

Cath
Reactive

FR<1.5 FR>1.5

Nonreactive Conservative

Surgical closure/Transcatheter closure

VSD before occlusion

VSD after occluded using ASO

Atrial Septal Defect ( ASD )

Insidence : + 10 % : ratio = 1,5 to 2 : 1 Anatomy : Defect on foramen ovale : Secundum ASD Defect at SVC and RA junction: sinus venosus ASD Defect at ostium primum: primum ASD

ASD

ASD

Clinical findings Asymptomatic Auscultation : Normal 1st HS or loud Widely split and fixed 2nd HS Ejection systolic murmur

ASD

Auscultation :1st HS N or loud widely split and fixed 2nd HS Ejection Systolic Murmur ECG : IRBB , right ventricular hypertrophy

Chest X-Ray

Right atrial enlargement Prominence the MPA segment Increased pulmonary vascular marking

Diagnosis Differential
Primary Atrial Septal Defect ECG : LAD Partial Anomalous Pulmonary Vein Drainage Pulmonary Stenosis Innocent Murmur

ASD

Management
Surgery : Preschool age Recent treatment: transcatheter closure using ASO (Amplatzer septal occluder)

ASD

Small Shunt
Infants Observation Evaluation At age 5-8 yrs Cath Heart Failure (-)

Large Shunt Children/Adults

PH (-) Heart Failure (+) PVD (-) Anti failure

Fail

PH (+)
PVD (+) Hyperoxia

Success

FR<1.5

FR>1.5

Age >1yrs W >10kg

Surgical Closure

Reactive

Non reactive

Conservative

Transcatheter closure (Secundum ASD) / Surgical Closure(others)

Conservative

ASD

ASD after occluded using ASO

Patent Ductus Arteriosus (PDA)

Insidence
+ 10% Female : Male = 1.2 to 1.5 : 1 Premature and LBW higher

Anatomy
Fetus: ductus arteriosus connects PA and aorta. If ductus does not closs Patent Ductus arteriosus

PDA

PDA

Lungs PA

LA

LV

AO Systemic RV RA

Qp > Qs

PDA

Clinical findings Small defect: Symptom (-) Growth and development normal Significant defect: Decreased exercise tolerant Weigh gained not good Frequent URTI Specific case: pulsus seler at 4th extremities

PDA

Diagnosis
Pulsus seler and continuous murmur heard

Auscultation : continuosus murmur at upper LSB 2

Chest X- Ray: Similar to VSD

PDA

Diagnosis Differential AP-window Arterio-venous fistulae Management premature: indometasin PDA closure : surgery transcatheter closure (ADO and coil)

PDA Neonates/Infants Heart failure (+) Premature Anti failure Indometacin Success Heart failure (-) Full term Anti failure Fail Success Children/Adults PH (-) LR PH (+) RL

Hyperoxia
Non reactive

Fail

Reactive
Age >12wks W >4kg

Spontaneous closure

Surgical ligation

Transcatheter closure

Conservative

PDA

Pulmonary Stenosis (PS)

Incidence : 8-10%
Anatomy: Pulmonary stenosis valvular : Bicuspid pulmonary valve Valve leaflet thickening and adhession Pulmonary stenosis infundibular : Hyperthropy infundibulum

PS

Clinical findings Valvular stenosis

Mild : Ejection systolic Wide 2nd HS ejectiin click Moderate: ejection systolic, early systolic click Severe : ejecstion systolic, ejection click (-) Stenosis infundibular Ejection click ( - ) 1st HS normal, 2nd HS weak, ejection systolic Pulmonary stenosis periphery 1st & 2nd HS normal, ejection systolic

PS

Mild

: ejection systolic 2nd HS wide split ejection click Moderate: ejecsi systolic , early ejection click Severe : ejection systolic, click ejection (-)

Diagnosis Asymptomatic patient: click systolic (stenosis valvular) systolic murmur wide split 2nd HS vary with respiration

PS

Normal or mild cardiomegaly Marked pulmonary valve post stenotic dilatation Normal pulmonary vascularity

ECG : RAD
Echocardiograhhy : confirmation diagnosis Catheterization: increased RV pressure without increased oxygen saturation

PS

Management
Medicamentosa : useless Mild stenosis: intervention (-) Moderate stenosis: observation Severe stenosis: balloon valvuloplasty

Coarctation of Aorta (CoA)

Incidence In Western country 5 % of all CHD In Asian Country incidence lower under diagnose? Anatomy Stenosis at any where in the aorta (from aortic valve to abdominalis aorta) More frequent at ductus arteriosus Botalli and pulmonary artery junction

CoA

Clinical findings Severe coarctation in neonates period can cause heart failure in 1st weeks of life Clinical manifestation in children: arterial hypertension commonly asymptomatic Different pulses felt at upper and lower extremities Examination : increased left ventricular activity, thrill systolic, 1st and 2nd HS normal, ejection systolic murmur

CoA

Diagnosis Clinically : lower extremities pulses are weak CXR : Mild cardiomegaly Prominence of aortic knob Normal pulmonary blood flow ECG : normal or LVH Echocardiography: a discrete shelf-like membrane Cardiac catheterization and angiography: to confime diagnosis

 Management
Neonates : PGE1 to maintain PDA Diuretic Correction acid-base imbalance Prepared to undergo surgery Big children: Surgery should be done as soon as diagnosis made Balloon angioplasty

CoA

CoA