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HEART DISEASES
SASMITO
CONGENITAL HEART DISEASE
INCIDENCE : 4-8 / 1000 LIVE BIRTH
ETYOLOGIC FACTORS :
ENVIROMENT
GENETIC /CHROMOSSOMAL ABNORMALITY
BASED ON ANATOMY
1. DEFECT AT THE VENTRICLE LEVEL
2. DEFECT AT THE ATRIAL LEVEL
3. DEFECT AT THE ARTERIAL LEVEL
4. DEFECT AT THE VALVE
Systolic Diastolic
Systolic Diastolic
Mitral ins Mitral stenotic
Tricuspid ins Tricuspid stenotic
Bayangan jantung
CTR = Ka +Ki
Posterior Anterior
Th
Mengukur rasio Kardio Thorax (CTR)
a a = cekungan pulmonal
Oxygen
saturation
CLINICAL SYMPTOM :
Ussually asimptomative
Management:
No activity limitation
Not need prophylaxis SBE unless associated MVP
Heart failure infant anti congestive is recomended
ASD closure by ASDOS or surgical after 4 years
old
VSD ( Ventricular septal defect)
15-20 % CHD
Clinical symptom :
PS infundibular
Endocarditis infective
Defect closure:
- non surgical
- surgical : as soon as possible if not respond with ant
congestive
> 1 year if respond to anti congestive
> 4 years if not closure spontaneously
PDA( ductus arteriosus persistent)
5-10% CHD
M :FM : 1 : 3
Very common in premature baby
Clinical symptom:
Small defect asymptomative
Large defect : repeated lung infection, H failure
Physical examination:
tachycardia, dyspnea on effort
cyanotic differential in PH
hyperactive precordial
. Continuous machinery murmur inL infra clavicle
Bounding pulse
ECG : small sz normal, moderate/large : LVH/BVH
Natural history :
Spontaneous closure in premature baby with small defect
heart failure in large defect, pneumonia
PH
endocarditis
Management:
Indomethacin in premature baby
SBE prophylaxis
ADO
Ligation : in 6 months - 2 years, as soon as posible in H.fail