ACYANOTIC CONGENITAL HEART

DISEASE

Muhammad AliPediatric Cardiology

DivisionUniversity 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

LA LV

RV RA

PA AO

Systemic

Lungs

Qp > Qs

VSD

RA

RV

RA LALA

RV LVLV

VSD

VSD

VSD

• Clinical findingsDay 1st after birth: murmur (-)After 2-6 weeks : murmur (+)Murmur : pansystolic grade 3/6 or higher

at LSB 3 Small muscular defect: early systolic murmurSignificant defect: Mid diastolic murmur at apex

Small VSD

Large VSD

VSD

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

VSD

CardiomegalyApex down wardProminence pulmonary artery segmentIncreased pulmonary vascular marking

VSDDiagnosis Differential

PDA with PH Tetralogy Fallot non cyanotic Inoscent murmur

Management:

Definitive : VSD closure Surgery Transcatheter closure

VSD

Heart failure (+) Heart failure (-)

Anti failure

Fail Success

PAB

Evaluate in 6 mths

Surgical closure/Transcatheter closure

Aortic valve prolaps

Infundibular stenosis

PH SmallerSpontaneousclosure

Cath

PVD(-) PVD(+) Cath

Cath

Reactive Non-reactive

Conservative

FR>1.5FR<1.5

VSD before occlusion VSD after occludedusing 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 findingsAsymptomaticAuscultation :

Normal 1st HS or loudWidely split and fixed

2nd HSEjection systolic

murmur

ASD

Auscultation :1st HS N or loudwidely split and fixed 2nd HS Ejection Systolic Murmur

ECG : IRBB , right ventricular hypertrophy

Right atrial enlargementProminence the MPA segmentIncreased pulmonary vascular marking

Chest X-Ray

ASDDiagnosis Differential

Primary Atrial Septal DefectECG : LAD Partial Anomalous Pulmonary Vein Drainage Pulmonary Stenosis Innocent Murmur

ManagementSurgery : Preschool ageRecent treatment: transcatheter closure using ASO (Amplatzer septal occluder)

ASD

Small Shunt Large Shunt

Observation

EvaluationAt age 5-8 yrs

Cath

FR<1.5 FR>1.5

Conservative

Infants Children/Adults

Heart Failure (-)

Heart Failure (+)

Age >1yrsW >10kg

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

Conservative

Anti failure

FailSuccess

PH (-) PH (+)

PVD (-)

PVD (+)

Hyperoxia

Reac-tive

Nonreactive

SurgicalClosure

ASD

ASD after occluded using ASO

Patent Ductus Arteriosus (PDA)

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

AnatomyFetus: ductus arteriosus connects PA and aorta.

If ductus does not closs Patent Ductus arteriosus

PDA

LA LV

RV RA

PA AO

Systemic

Lungs

Qp > Qs

PDA

PDA

• Clinical findings

Small defect: Symptom (-) Growth and development normal

Significant defect:Decreased exercise tolerantWeigh gained not goodFrequent 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

Diagnosis DifferentialAP-windowArterio-venous fistulae

Management premature: indometasin

PDA closure : surgery transcatheter closure

(ADO and coil)

PDA

PDA

Neonates/Infants Children/Adults

Heart failure (+) Heart failure (-)

Premature Full term

Anti failureIndometacin

Success Fail

Spontaneous closure

Anti failure

SuccessFail

Surgical ligation

Transcatheter closure

PH (-) PH (+)

LR RL

Hyperoxia

Reactive Nonreactive

Conservative

Age >12wksW >4kg

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 findingsValvular stenosis

Mild : Ejection systolic Wide 2nd HS ejectiin click

Moderate: ejection systolic, early systolic clickSevere : ejecstion systolic, ejection click (-)

Stenosis infundibular Ejection click ( - )1st HS normal, 2nd HS weak, ejection systolic

Pulmonary stenosis periphery1st & 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 (-)

• DiagnosisAsymptomatic patient:

click systolic (stenosis valvular)systolic murmurwide split 2nd HS vary with respiration

PS

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

ECG : RADEchocardiograhhy : confirmation diagnosisCatheterization: increased RV pressure without increased oxygen saturation

PS

• Management

Medicamentosa : uselessMild stenosis: intervention (-)Moderate stenosis: observationSevere stenosis: balloon valvuloplasty

Coarctation of Aorta (CoA)Incidence• In Western country 5 % of all CHD• In Asian Country incidence lower

under diagnose?

AnatomyStenosis at any where in the aorta (from aortic valve to abdominalis aorta)More frequent at ductus arteriosus

Botalli and pulmonary artery junction

• Clinical findingsSevere coarctation in neonates period can cause heart failure in 1st weeks of life

Clinical manifestation in children: arterial hypertensioncommonly 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 weakCXR : Mild cardiomegaly

Prominence of aortic knob Normal pulmonary blood flow

ECG : normal or LVHEchocardiography: a discrete shelf-like membraneCardiac catheterization and angiography: to confime diagnosis

CoA

• 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