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Materi kuliah blok 15
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Structures of the heart
Normal Heart
Atrial Septal defect( ASD )Insidence : + 10 % : ratio = 1,5 to 2 : 1Anatomy : Defect on foramen ovale : Secundum ASD Defect at SVC and RA junction: sinus venosus ASD Defect at ostium primum : primum ASD
ANATOMY
ASD
Atrial Septal DefectDiagram of ASD
Clinical FeaturesSymptomsMost infants : asymptomatic ..undetectedThe first present at age 6 to 8 weeks with a soft murmur and possibly a fixed and somewhat widely split S2Infant with large ASD may present with poor growth, recurrent lower respiratory tract infection and heart failure
LALVRVRAPAAOSystemicLungsQp > QsAtrial septal defect
RARVLALVRARVLALVAtrial septal Defect
Atrial Septal DefectAuscultation :1st HS N or loudwidely split and fixed 2nd HS Ejection Sistolic Murmur
Atrial Septal DefectDiagnosis Differential
Primary Atrial Septal DefectECG : LADPartial Anomalous Pulmonary Vein DrainagePulmonary StenosisInnocent Murmur
Atrial Septal defect
ManagementSurgery : Preschool ageRecent treatment: transcatheter closure using ASO (Amplatzer septal occluder)
ASDSmall ShuntLarge ShuntObservationEvaluationAt age 5-8 yrsCathFR1.5ConservativeInfantsChildren/AdultsHeart Failure (-)Heart Failure (+)Age >1yrsW >10kgTranscatheter closure (Secundum ASD) /Surgical Closure(other tipe of ASD)ConservativeAnti failureFailSuccessPH (-)PH (+)PVD (-)PVD (+)HyperoxiaReac-tiveNonreactiveSurgicalClosure
Transchateter closure of ASD
Atrial septal defect
Ventricular septal defectInsidence 20 % of all CHD No sex influencedAnatomy Subarterial defect : below pulmonary andaortic valve Perimembranous defect: below aortic valve at pars membranous septum Muscular defect
VSD
SystemicLungsQp > QsVentricular Septal defect
LA
LV
RV
RA
PA
AO
RARVRALALARVLVLVVentricular septal defect
Ventricular Septal DefectClinical 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 Ventricular Septal DefectMurmur: pansystolic grade 3/6 or higher at LSB 3
Ventricular Septal DefectCardiomegalyApex down wardProminence pulmonary artery segmentIncreased pulmonary vascular marking
Ventricular septal DefectDiagnosis Differential
PDA with PHTetralogy Fallot non cyanoticInoscent murmur
Ventricular septal defectManagement:
Definitive : VSD closure Surgery Transcatheter closure
Patent Ductus Arteriosus Anatomy
Fetus: ductus arteriosus connects PA and aorta
If ductus does not closs Patent Ductus arteriosus
PDA
RARVLALVRALARVLVPatent Ductus Arteriosus
LALVRVRAPAAOSystemicLungsQp > QsPatent Ductus Arteriosus
PDA is more common in : Premature infants BW < 1750 g : 45% BW < 1200 g : 80% Genetic abnormalities Infants whose mother had German measles (Rubella)PDA in preterm haemodynamic instability co-morbidity & mortality EARLY DIAGNOSIS
Patent Ductus ArteriosusClinical findings
Small defect: Symptom (-) Growth and development normalModerate and large defect:Decreased exercise tolerantWeigh gained not goodFrequent URTI
DIAGNOSIS
Patent Ductus ArteriosusAuscultation : continuosus murmur at upper LSB 2
Chest X-RayLarge PDA:Prominence of the left atrium,left ventricle, ascending aorta,Pulmonary vascular marking
ECGSmall PDA : normalModerate PDA : LVHLarge PDA : BVHPDA with PVOD : RVH
Patent Ductus ArteriosusDiagnosis DifferentialAP-windowArterio-venous fistulae
Management premature: ibuprofenPDA closure : surgery transcatheter closure
MANAGEMENT
Medical treatment : prostaglandin synthesis inhibitorPreterm neonates : usefullAterm neonates : useless
Transcatheter closure : mostly choice treatment
Surgical closure :Infant < 5 kg with large PDAPreterm neonates : medical treatment unsuccessful or contraindicated
PDA IN PRETERM NEONATESSpecial problem : haemodynamic instability
Treatment should be started as soon as PDA suspected Once a significant shunt is present increased pulmonary blood flow damage to premature lungs
PDA can be closed with prostaglandin synthesis inhibitors
TRANSCATHETER CLOSURE *Transcatheter occlusion is effective with a high rate of complete occlusion
*Complication rare
Tetralogy FallotIncidence5-8% from all CHD
AnatomyCause: Left-anterior deviation of infundibular septum
Sindroma consist of 4 items: VSD pulmonary stenosis aortic over-riding RVH
Tetralogy Fallot
Central cyanosis
Central cyanosis
PathophysiologyCyanosis is a bluish discoloration of the skin and mucous membranes resulting from an increased concentration of reduced hemoglobinClinical cyanosis occurs when the amount of reduced hemoglobin in the cutaneous vein may result 5 g/100mlThe critical level of reduced hemoglobin in the cutaneous vein may result from either desaturation of arterial blood or increased extraction of oxygen by peripheral tissue
Cardiac causes of cyanosisInadequate pulmonary blood flow (severe cyanosis)Tricuspid atresiaPulmonary atresiaTetralogy of Fallot
Independent pulmonary and systemic circulation (severe cyanosis)Tranpose great artery
Mixing (moderate cyanosis)Truncus arteriosus
Diagnosis
Clinically : cyanosis Single 2nd HS, ejection systolic murmur
X Ray : Boot ShapedECG: RAD, RVH
Tetralogy FallotSingle 2nd HS, ejection systolic murmur
CXR : Boot-shapedConcave pulmonary segmentApex upturnedDecreased pulmonary blood flow
Tetralogy FallotECG : RAD, RVHEchocardiography : to confirm diagnosis
Tetralogy FallotDiagnosis Differential Pulmonary Atresia Double outlet right ventricle and pulmonary stenosis Transposisi of great arteri and pulmonary stenosis
Management Paliative treatment: Blalock-Taussig shunt Definitive: total correction
Tetralogy of Fallot< 1 yr> 1 yrspell (+)spell (-)propranololfailedsucceedBTStotal correction cathsmall PAgood sized PA clinically ECG CXR echoage 1 yrcathBTS/PDA Stentevaluation