Kuliah CHD

128
Burhanuddin Iskandar Pediatric Cardiology Pediatric Department,Medical Faculty, Hasanuddin University/ WS Hospital Makassar

Transcript of Kuliah CHD

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Burhanuddin IskandarPediatric Cardiology

Pediatric Department,Medical Faculty, Hasanuddin University/ WS Hospital Makassar

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Telur TGAManusia salju/angka 8 TAPVDKarpet Ebstein anomaliSepatu both TF

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Structures of the heart

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Normal Heart

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Atrial Septal defect( ASD )

• Insidence : + 10 %• ♀: δ ratio = 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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Atrial Septal Defect

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LA LV

RV RA

PA AO

Systemic

Lungs

Qp > Qs

Atrial septal defect

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Atrial Septal Defect

Diagram of ASD

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RA

RV

LA

LV

RA

RV

LA

LV

Atrial septal Defect

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Clinical findingsAsymptomaticAuscultation :

Normal 1st HS or loudWidely split and

fixed 2nd HSEjection systolic murmur

Atrial septal Defect

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Atrial Septal Defect

Auscultation :1st HS N or loud

widely split and fixed 2nd HS

Ejection Sistolic Murmur

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ECG : IRBB , right ventricular hypertrophy

Atrial Septal Defect

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Right atrial enlargementProminence the MPA segmentIncreased pulmonary vascular marking

Atrial Septal DefectChest X-Ray

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Atrial Septal Defect

Diagnosis Differential

Primary Atrial Septal Defect

ECG : LAD

Partial Anomalous Pulmonary Vein Drainage

Pulmonary Stenosis

Innocent Murmur

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Atrial Septal defect

Management

Surgery : Preschool age

Recent 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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Atrial septal defect

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Atrial septal defect

ASD before occlusion

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During balloon sizing

Atrial septal defect

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Atrial septal defect

ASD after occluded using ASO

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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

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VSD

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Ventricular Septal Defect

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LA LV

RV RA

PA AO

Systemic

Lungs

Qp > Qs

Ventricular Septal defect

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RA

RV

RA LALA

RV LVLV

Ventricular septal defect

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Ventricular Septal Defect

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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

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Small VSD

Large VSD

Ventricular Septal Defect

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

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Ventricular Septal Defect

CardiomegalyApex down wardProminence pulmonary artery segmentIncreased pulmonary vascular marking

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Ventricular septal Defect

Diagnosis Differential

PDA with PH Tetralogy Fallot non cyanotic Inoscent murmur

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Ventricular septal defect

Management:

Definitive : VSD closure

Surgery

Transcatheter closure

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DSV

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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Ventricular septal defect

VSD before occlusion

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Ventricular septal defect

VSD during deploying the device

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Ventricular septal defect

VSD after occludedusing ASO

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Patent Ductus Arteriosus

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

Patent Ductus Arteriosus

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RA

RV

LA

LV

RA LA

RV LV

Patent Ductus Arteriosus

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Patent Ductus Arteriosus

• 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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Patent Ductus Arteriosus

DiagnosisPulsus seler and continuous murmur heard

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Patent Ductus Arteriosus

• Chest X- Ray– Similar to VSD

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Patent Ductus Arteriosus

Auscultation : continuosus murmur at upper LSB 2

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Diagnosis Differential

AP-window

Arterio-venous fistulae

Management

premature: indometasin

PDA closure : surgery

transcatheter closure

Patent Ductus Arteriosus

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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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Patent Ductus Arteriosus

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Patent Ductus Arteriosus

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Patent Ductus Arteriosus

PDA before occludedusing ADO

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Patent Ductus Arteriosus

PDA after occludedusing ADO

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Patent Ductus Arteriosus

PDA before occludedusing coil

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Patent Ductus Arteriosus

PDA after occludedusing coil

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Pulmonary Stenosis

• Incidence : 8-10%

• Anatomy:

Pulmonary stenosis valvular :

Bicuspid pulmonary valve

Valve leaflet thickening and adhession

Pulmonary stenosis infundibular :

Hyperthropy infundibulum

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Pulmonary Stenosis

• 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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Pulmonary Stenosis

Mild : ejection systolic 2nd HS wide split ejection click

Moderate: ejecsi systolic , early ejection click Severe : ejection systolic, click ejection (-)

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Poulmonary Stenosis

• DiagnosisAsymptomatic patient:

click systolic (stenosis valvular)systolic murmurwide split 2nd HS vary with respiration

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Poulmonary Stenosis

Normal or mild cardiomegaly Marked pulmonary valve post stenotic dilatationNormal pulmonary vascularity

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ECG : RAD

Echocardiograhhy : confirmation diagnosis

Catheterization: increased RV pressure without increased oxygen saturation

Pulmonary Stenosis

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Pulmonary Stenosis

• Management

Medicamentosa : useless

Mild stenosis: intervention (-)

Moderate stenosis: observation

Severe stenosis: balloon valvuloplasty

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Pulmonary Stenosis

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Pulmonary Stenosis

Before ballooning

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Pulmonary Stenosis

During ballooning

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Pulmonary Stenosis

After ballooning

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Coarctation AortaIncidence• In Western country 5 % of all CHD• In Asian Country incidence lower

underdiagnosis ?

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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Coarctation Aorta

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• Clinical findings

Severe coarctation in neonates period can cause heart failure in 1st weeks of life

Clinical manifestation in children:

arterial hypertension

commonly asymptomatic

Different pulses felt at upper and lower extremities

Examination : increased left ventricular activity, thrill systolic, 1st and 2nd HS normal, ejection systolic murmur

Coarctation Aorta

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• Diagnosis

Clinically : lower extremities pulses are weak

CXR : Mild cardiomegaly

Prominence of aortic knob

Normal pulmonary blood flow

ECG : normal or LVH

Echocardiography: a discrete shelf-like membrane

Cardiac catheterization and angiography: to confime diagnosis

Coarctation Aorta

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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

madeBalloon angioplasty

Coarctation Aorta

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Coarctation Aorta

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Coarctation Aorta

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Coarctation Aorta

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Coarctation Aorta

Before ballooning

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Coarctation Aorta

During ballooning

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Coarctation Aorta

After ballooning

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Tetralogy FallotInsidence

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

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Tetralogy Fallot

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Tetralogy Fallot

Hemodynamic acyanotic Hemodynamic cyanotic

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Tetralogy Fallot

• Diagnosis

Clinically : cyanosis

Single 2nd HS, ejection systolic murmur

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Tetralogy Fallot

Single 2nd HS, ejection systolic murmur

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Tetralogi Fallot

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CXR : Boot-shapedConcave pulmonary

segmentApex upturnedDecreased pulmonary

blood flow

Tetralogy Fallot

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Tetralogy Fallot

ECG : RAD

Echocardiography : to confirm diagnosis

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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

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Tetralogy of Fallot

< 1 yr > 1 yr

spell (+) spell (-)propranolol

failed succeed

BTS

total correction

cath

small PA good sized PA

• clinically• ECG

• CXR• echo

age 1 yr

cath BTS/

PDA Stent

evaluation

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Tetralogy Fallot

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Tetralogy Fallot

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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

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Transposition of Great artery

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Hemodynamic normal Hemodynamic of TGA

“series” “parallel”

Transposition of Great artery

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TGA without VSD

In adequate Mixing Adequate Mixing

Transposition of Great artery

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TGA with large VSD TGA with VSD and PS

Transposition of Great artery

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• Clinical aspects

More frequent in maleBirth weight usually normal or biggerCyanotic vary from mild to severeAuscultation : single 2nd HS and loudMurmur vary from silent to pansystolic murmur or continuous murmur

Transposition of Great artery

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• DiagnosisClinically :

Suspicious if neonates presents with cyanotic with birth weight normal or bigger

Murmur (-)Single 2nd HS and loud

Transposition of Great artery

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Murmur (-)Single 2nd HS and loud

Transposition of Great artery

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Transposition of Great artery

CXR :

Cardiomegaly

Egg-on-side heart

Increased pulmonary vascular marking

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Transposition of Great artery

ECG :

RAD

RVH

BVH

Echocardiography : to confirm diagnosis

Cardiac catheterization: usually is not needed

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Diagnosis Differential

trunkus arteriosus

trikuspid atresia

pulmonary atresia

Management

Surgery: arterial switch

Paliative : Blalock-Taussig shunt

Transposition of Great artery

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Transposition of Great Artery

PGE1

VSD(-) VSD(+)

1mth > 1mth

Cath

LV2/3 syst LV<2/3 syst

PAB

Arterial Switch

LVOTO(-) LVOTO(+)

>3 mths3 mths

Cath

PARI<8 PARI8

Arterial Switch and Perforated VSD

Dynamic &resectable

Un-resectable

BTS/PDA stent

Cath

Rastelli

Senning

BAS/Blallock Hanlon

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Transposition of Great artery

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Truncus ArteriosusInsidence

around 1 % of CHD

Anatomy

Failure of septation of truncus arteriosus form aorta and

pulmonary artery

There are 3 type:

Type 1 : MPA arises from the truncus and then divides into the RPA and LPA

Tipe 2 : The PAs arise from the posterior aspect of the truncus

Tipe 3 : The PAs arise from the lateral aspects of the truncus

Tipe 4: Arteries arising from the descending aorta supply the lungs

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Truncus Arteriosus

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Truncus Arteriosus

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Truncus Arteriosus

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• Diagnosis

Clinically suspected if:

neonates present with cyanotic and single 2nd HS

murmur vary

CXR: cardiomegaly

increased pulmonary vascular marking

ECG: biventricular hypertrophy

Echocardiografhy: to confirm diagnosis

Catheterization: decreased oxygen saturation at right heart and aorta

Truncus Arteriosus

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Diagnosis Differential

Transposisi of great artery

Total anomalus pulmonary vein drainage

Management

Medicamentosa : temporary

Surgery: Rastelli

Palliative: pulmonary artery banding

Truncus Arteriosus

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Truncus Arteriosus

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Tricuspid Atresia

• Incidence– 1 % from all CHD

• Embriology– Valve formed at 5th weeks– Fussion of part of endocardial

cushion, ventricular septum and miocardium

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• Anatomy– Valve leaflet adhession one to another,

difficult to open– ASD essentially required to drain blood

from RA to LA – Classified into 2 group

• Normal related great artery• Transposed grat artery

Tricuspid Atresia

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Tricuspid Atresia with normal related great artery

Tricuspid atresia with transposed geat artery

Tricuspid Atresia

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• Manifestasi klinis– Cyanosis early after birth– Increased RV activity– Increased LV activity– Auscultation

• Single 1st and 2 nd HS

Tricuspid Atresia

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• Clinical manifestation

– In almost all patients murmur is silent

– If murmur present

• Diastolic murmur due to relative MS

• Pansystolic murmur due to VSD

Tricuspid Atresia

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Tricuspid Atresia

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• Diagnosis and diagnosis differential– Clinically: Cyanosis with or without murmur

Tricuspid Atresia

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CXR: Heart minimally EnlargedThe PVMs are DecreasedThe MPA segment is concave

Tricuspid Atresia

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– ECG: • LAD• Left ventricular hypertrophy• With or without LAE

Tricuspid Atresia

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• Echocardiography: Essential to make diagnosis

• Catheterization– Catheter can not be passed from RA to RV– Increased RA and LA pressure– Decreased oxygen saturation in LA– Angiography: definitive diagnosis

Tricuspid Atresia

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• Diagnosis differential

– Transposition of great artery

– Truncus arteriosus

– Tetralogy of Fallot

– Total Anomalous pulmonary vein drainage

Tricuspid Atresia

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• Management

– Fontan operation

Tricuspid Atresia

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Tricuspid Atresia

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Tricuspid Atresia

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Tricuspid Atresia

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Tricuspid Atresia

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Tricuspid Atresia

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Modification of Fontan operation

Tricuspid Atresia