k3 acyanotic chd
TRANSCRIPT
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ACYANOTIC CONGENITAL HEART
DISEASE
Muhammad AliPediatric Cardiology
DivisionUniversity of Sumatera
Utara
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Structures of the heart
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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
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VSD
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LA LV
RV RA
PA AO
Systemic
Lungs
Qp > Qs
VSD
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RA
RV
RA LALA
RV LVLV
VSD
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VSD
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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
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Small VSD
Large VSD
VSD
Murmur: pansystolic grade 3/6 or higher at LSB 3
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VSD
CardiomegalyApex down wardProminence pulmonary artery segmentIncreased pulmonary vascular marking
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VSDDiagnosis Differential
PDA with PH Tetralogy Fallot non cyanotic Inoscent murmur
Management:
Definitive : VSD closure Surgery Transcatheter closure
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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
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VSD before occlusion VSD after occludedusing ASO
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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
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ASD
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ASD
Clinical findingsAsymptomaticAuscultation :
Normal 1st HS or loudWidely split and fixed
2nd HSEjection systolic
murmur
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ASD
Auscultation :1st HS N or loudwidely split and fixed 2nd HS Ejection Systolic Murmur
ECG : IRBB , right ventricular hypertrophy
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Right atrial enlargementProminence the MPA segmentIncreased pulmonary vascular marking
Chest X-Ray
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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)
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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
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ASD
ASD after occluded using ASO
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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
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PDA
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LA LV
RV RA
PA AO
Systemic
Lungs
Qp > Qs
PDA
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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
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PDA Diagnosis
Pulsus seler and continuous murmur heard
Auscultation : continuosus murmur at upper LSB 2
• Chest X- Ray: Similar to VSD
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Diagnosis DifferentialAP-windowArterio-venous fistulae
Management premature: indometasin
PDA closure : surgery transcatheter closure
(ADO and coil)
PDA
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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
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PDA
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Pulmonary Stenosis (PS)• Incidence : 8-10%
• Anatomy:Pulmonary stenosis valvular : Bicuspid pulmonary valve Valve leaflet thickening and adhession Pulmonary stenosis infundibular : Hyperthropy infundibulum
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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
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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
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PS
Normal or mild cardiomegaly Marked pulmonary valve post stenotic dilatationNormal pulmonary vascularity
ECG : RADEchocardiograhhy : confirmation diagnosisCatheterization: increased RV pressure without increased oxygen saturation
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PS
• Management
Medicamentosa : uselessMild stenosis: intervention (-)Moderate stenosis: observationSevere stenosis: balloon valvuloplasty
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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
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• 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
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• 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
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• 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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CoA