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ACYANOTIC

CONGENITAL HEART DISEASE

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

LA LV
Lungs

PA 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 (+) Heart failure (-)

Anti failure
Aortic valve Infundibular PH Spontaneous Smaller
prolaps stenosis closure

Fail Success PVD(-) PVD(+) Cath

PAB Cath FR<1.5 FR>1.5


Cath

Evaluate Reactive Non-


in 6 mths reactive

Conservative
Surgical closure/Transcatheter closure
VSD after occluded
VSD before occlusion
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 ASD

 Primary Atrial Septal Defect


ECG : LAD
 Partial Anomalous Pulmonary Vein
Drainage
 Pulmonary Stenosis
 Innocent Murmur

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

Small Shunt Large Shunt

Infants Children/Adults
Observation
Heart Heart PH (-) PH (+)
Evaluation Failure (-) Failure (+)
At age 5-8 yrs PVD PVD
Anti failure (-) (+)
Cath Hyperoxia
Success Fail

FR<1.5 FR>1.5 Age >1yrs Surgical Reac- Non


W >10kg Closure tive reactive

Conservative Transcatheter closure (Secundum ASD) / Conservative


Surgical Closure(others)
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

LA LV
Lungs

PA 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 Children/Adults

Heart failure (+) Heart failure (-) PH (-) PH (+)

Premature Full term


LR RL

Anti failure Anti failure


Indometacin Hyperoxia

Fail Success
Success Fail Reactive Non
Age >12wks reactive
W >4kg

Spontaneous Surgical Transcatheter closure Conservative


closure ligation
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
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

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