Structures of the heart

Normal Heart
 KLASIFIKASI
• PJB ASIANOTIK
– ASD - AVSD
– VSD - PS
– PDA
• PJB SIANOTIK
– TOF - TRIKUSPID ATRESIA
– TGA - TRUNKUS ARTERIOSUS
– TAPVD - ATRESIA PULMONAL
 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
ANATOMY
ASD
 Atrial Septal Defect

Diagram of ASD
 Clinical Features
Symptoms
 Most infants : asymptomatic …..undetected
 The first present at age 6 to 8 weeks with a soft
murmur and possibly a fixed and somewhat widely
split S2
 Infant with large ASD may present with poor
growth, recurrent lower respiratory tract
infection and heart failure
 Atrial septal defect

LA LV
Lungs

PA AO

Systemic
RV RA

Qp > Qs
 Atrial septal Defect

RA LA

RA LA

RV LV
RV LV
 Atrial Septal Defect

Auscultation :1st HS N or loud

widely split and fixed 2nd HS
Ejection Sistolic Murmur
 Atrial Septal Defect

Diagnosis Differential

 Primary Atrial Septal Defect

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

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(other tipe of ASD)
Transchateter closure of ASD
Atrial septal defect
 Ventricular septal defect
• 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
 Ventricular Septal defect

LA LV
Lungs

PA AO

RV RA Systemic

Qp > Qs
 Ventricular septal defect

RA
LA
RA LA

RV LV RV LV
 Ventricular Septal Defect

• 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
 Ventricular Septal Defect

Murmur: pansystolic
grade 3/6 or higher at
LSB 3 Small VSD

Large VSD
 Ventricular Septal Defect

Cardiomegaly
Apex down ward
Prominence pulmonary
artery segment
Increased pulmonary vascular
marking
 Ventricular septal Defect

Diagnosis Differential

 PDA with PH
 Tetralogy Fallot non cyanotic
 Inoscent murmur
 Ventricular septal defect

Management:

Definitive : VSD closure

 Surgery

 Transcatheter closure
 DSV

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
 Patent Ductus Arteriosus

Anatomy

Fetus: ductus arteriosus connects PA and aorta

If ductus does not closs  Patent Ductus

arteriosus
PDA
 Patent Ductus Arteriosus

RA LA
RA LA

RV LV
RV LV
 Patent Ductus Arteriosus

LA LV
Lungs

PA AO

Systemic
RV RA

Qp > Qs
• 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 Arteriosus

• Clinical findings

Small defect:
Symptom (-)
Growth and development normal
Moderate and large defect:
Decreased exercise tolerant
Weigh gained not good
Frequent URTI
 DIAGNOSIS
• Medical history : asphyxia,preterm,congenital
rubella, chromosomal aberrations

• Physical examination : bounding pulse, wide blood

pressure, hyperactive precordium, present of
murmur
Supported by CXR, ECG

Confirmed by Echocardiography
 Patent Ductus Arteriosus

Auscultation : continuosus murmur

at upper LSB 2
 Chest X-Ray

Large PDA:
Prominence of the left
atrium,
left ventricle, ascending
aorta,
Pulmonary vascular
marking 
ECG
• Small PDA : normal
• Moderate PDA : LVH
• Large PDA : BVH
• PDA with PVOD : RVH
 Patent Ductus Arteriosus

Diagnosis Differential
AP-window
Arterio-venous fistulae

Management
premature: ibuprofen
PDA closure : surgery
transcatheter closure
 MANAGEMENT
• Medical treatment : prostaglandin synthesis inhibitor
Preterm neonates : usefull
Aterm neonates : useless

• Transcatheter closure : mostly choice treatment

• Surgical closure :
Infant < 5 kg with large PDA
Preterm neonates : medical treatment unsuccessful
or contraindicated
 PDA IN PRETERM NEONATES

• Special 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 Fallot
Incidence
5-8% from all CHD

Anatomy
Cause: Left-anterior deviation of infundibular septum

Sindroma consist of 4 items:

 VSD
 pulmonary stenosis
 aortic over-riding
 RVH
Tetralogy Fallot
Central cyanosis
Central cyanosis
 Pathophysiology
• Cyanosis is a bluish discoloration of the
skin and mucous membranes resulting
from an increased concentration of
reduced hemoglobin
• Clinical cyanosis occurs when the amount
of reduced hemoglobin in the cutaneous
vein may result 5 g/100ml
• The 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 cyanosis
• Inadequate pulmonary blood flow (severe
cyanosis)
– Tricuspid atresia
– Pulmonary atresia
– Tetralogy 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 Shaped

ECG: RAD, RVH
 Tetralogy Fallot

Single 2nd HS, ejection systolic murmur

CXR :
Boot-shaped
Concave pulmonary segment
Apex upturned
Decreased pulmonary blood flow
 Tetralogy Fallot

ECG : RAD, RVH

Echocardiography : to confirm diagnosis
 Tetralogy Fallot

• Diagnosis 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
 • clinically • CXR
• ECG Tetralogy of Fallot • echo

< 1 yr > 1 yr

spell (+) spell (-)

propranolol
age 1 yr
cath
failed succeed

BTS
evaluation

cath BTS/ small PA good sized PA

PDA Stent

total correction
 Transposition of Great
Artery
Insidence
5% of CHD

Anatomy
Abnormality of formation of trunkal septum that cause
aorta arising from RV and PA arising from LV
Transposition of Great artery
 Transposition of Great artery

Hemodynamic normal Hemodynamic of TGA

“series” “parallel”
 Transposition of Great artery

• Clinical aspects

More frequent in male

Birth weight usually normal normal or bigger
Cyanotic vary from mild to severe
Auscultation : single 2nd HS and loud
Murmur vary from silent to pansystolic murmur or
continuous murmur
 Transposition of Great artery

• Diagnosis
Clinically :
Suspicious if neonates presents with cyanotic
with birth weight normal or bigger
Murmur (-)
Single 2nd HS and loud
 Transposition of Great artery

Murmur (-)
Single 2nd HS and loud
 Transposition of Great artery

ECG :
RAD
RVH
Echocardiography : to confirm diagnosis
Cardiac catheterization: usually is not
needed
 Transposition of Great artery

Diagnosis Differential

 trunkus arteriosus
 trikuspid atresia
 pulmonary atresia

Management

Surgery: arterial switch

Paliative : Blalock-Taussig shunt
Transposition of Great artery
TERIMA KASIH