Acyanotic Defect
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Transcript of Acyanotic Defect
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dr.Meriah Sembiring,Sp.Adr.Meriah Sembiring,Sp.ASubDivisionSubDivision Cardiology Cardiology Pediatric Pediatric DepartmentDepartmentOf the General Ulin HospitalOf the General Ulin HospitalBANJARMASIN – SOUTH OF BANJARMASIN – SOUTH OF KALIMANTANKALIMANTAN
ACYANOTIC DEFECTACYANOTIC DEFECT
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Acyanotic defects
PBF Normal PBF
LVH/CVH RVH LVH RVH
- AS or AR - PS - VSD - ASD - COA - COA - PDA (often RBBB) - Primary (in infants) - ECD - PAPVR myocardial - MS - PVOD disease (second to L – R (EFE) Shunt lesions) MR
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VENTRIKEL SEPTAL DEFEK
(VSD)
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VENTRIKEL SEPTAL DEFEK (VSD)
Insidensi
PJB Paling banyak ditemukan (20-30%)
Perempuan Laki – laki
Klasifikasi
VSD Perimembrane :
- INLET
- OUTLET
- Trabekular
VSD Muskular :
- Muskuler INLET
- Muskuler Trabekular
- Muskuler OUTLET
VSD Subarterial (Doubly Commited Sub Arterial Defect)
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Hemodinamik
VSD Kecil ( <5 mm2 ) = Peny. Rober :
- Hemodinamik tidak terganggu = Normal - Menutup Spontan 2 thn pertama
VSD Sedang – besar ( 5-10, > 10 mm2 ) :
- Pirau yang bermakna
- Menyebabkan PVR (PULM VAS. RESIST)
- Dapat terjadi :
1. Defek mengecil : – pasien baik
2. Defek menutup
3. Defek bertambah besar :
a. PVR
b. Tek. VENT. Kanan > Vent Kiri Pirau kanan kiri
SYND Eisenmenger (Pasien Sianotik)
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Manifestasi Klimis
VSD Kecil :Asimtomatik tumbuh dan kembang anak normal
Auskultasi :
Bising sistolik (early sistlnik mur-mur)
Pan sistolik mur-mur LSB – ICR III – IV
VSD Sedang : Bayi :
- Minum/ menyusui butuh waktu lebih lama/tidak mampu menghabiskan susu/makannya
- Susah nafas waktu minum/ makan
- Peningkatan BB
- Infeksi Paru berulang
- Gagal jantung (3bln)
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P. Fisik - Insp :
a. Tampak kurus b. Dispnu, Takinoe, Retraksi
- Aust : a. Bising pansistolik/ LSB IOR III - IV b. Getaran/TRILL
VSD Besar ( 10 m2 ) : Tanda2 Gagal Jantung :
- Dispnu saat istirahat - Sianosis - Organ gagal tumbuh
Ausku : Pansistolik
Pem. Penunjang Ro” :
- VSD Kecil : Normal/ Vask Paru - Sedang/ besar : a. Kardiomegali dengan conus polmunal menonjol b. Vaskulansasi paru
EKG Echocardiografi
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Penata Laksanaan Gagal Jantung
• Digoxin• Atasi Inf. Saluran pernapasan• Diuretik
Bedah :• Bergantung klinis• Amplazer kateter
Prognosis :• Menutup dalam 2 thn pertama spontan• >6 tahun tidak menutup
Komplikasi :• Endokarditis• Synd. Esinmenger• Prolap kat Aorta
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ARTERIAL SEPTAL DEFEK
(ASD)
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ATRIAL SEPTAL DEFEK
Insidens
10% dari PJB
Remaja >> bayi
Defek sekat atrium, dibagi 3 :
ASD Primum
ASD sekundum (80%)
ASD Sinus Venosus (10%)
ASD Sekundum
Defek fossa ovalis
Beban volume atr/vent kanan
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Gejala Klinis
Bergantung besar defek
Asimtomatis bayi/ anak
Defek besar :
Inf. Saluran nafas berulang
Tumbuh – kembang normal
Gagal jantung jarang (CHF)
P. Fisik :
INSP Dalam batas normal
AUSKUL :
- Bising injeksi sistolik LSB ICR II di pulmoNal
- Bj II Split
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PEM. Penunjang
Ro” Defek Besar : PBF Sedikit kardiomegali Atrum kanan >> Conus Pulmo >>
EKG RBBB (95g) RAD Sekundum
LAD Primum
Block Derajat 1 (PR memanjang) Echo
Penata laksanaan
Bedah
Ket. Amplazer
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DUKTUS ARTERIOUS PERSISTEN
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DUKTUS ARTERIOUS PERSISTEN(PDA)
Hubungan menetap art. Pul – aorta
7 % dari PJB
>> Bayi premature
>> Bayi prematur dengan ventilator
Bila Duktus menetap – resistensi vask. Paru pirau aorta ke A.pulmo
(L to R shunting)
Klinis PDA dibagi menjadi 3 :
Kecil
Sedang
Besar
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Gejala klinis
Bergantung pada besarnya defek
PDA kecil :
Seperti anak normal
Pada ausk. LSB ICR II – bising kontinyu (Machine mur-mur)
PDA sedang :
Gejala usia 2-5 bulan:
Kesulitan makan
Inf. Sal. Nafas
Mudah lelah
Nafas cepat
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PDA Besar :
Gejala muncul pd mgg pertama
Takipnoe, dispnoe
Banyak keringat
Sulit makan & minum pertama
BB
Inf. Sal. Nafas berulamg
Ro” :
Vask. Paru
Kardiomegali
EkG :
Tanda LVH
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Penata laksanaan
A. Mendikamen :
Bayi Prematur < minggu I :
- Indometacin IV 0,2 mg/kg BB/12 jm
Bayi Mature :
- Tidak Efektif
Gagal Jantung : - Digoxcin
- Diuretik
B. Bedah :
Ind : - Gagal Medik
- Endokarditis
Non bedah :
Kateter Amplazer
Prognosis :
Kecil : Menutup Spontan