pem. cardiovaskular dr. mulyadi.ppt
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CURICULUM VITAE
Name : Mulyadi M. Djer, MD, SpA(K), PhDPlace / Date of Birth : Padang, 29 October 1964Adress : Jl. Taman Sari VIII/23, Jatinegara Baru, Buaran, Jakarta Timur 13940. Phone 021 48636322Current Position : Lecturer and Medical Staff, Department of Child Health FKUI-RSCM JakartaOrganization : Secretary of Indonesia Society of Pediatric Cardiology (Perkani)
Educational Qualifications:Year: 1989 Degree: Medical Doctor (MD)
Institution: FKUI 1997 Pediatric Specialist (SpA) FKUI
2003 Pediatric Cardiologist FKUI
2005 Consultant Pediatric Cardiologist [(SpA(K)] IDAI
2008 Doctor of Phylosophy (PhD) FKUI
Awards, Fellowship, Grants:2001-2002 Fellowship training in Pediatric Cardiology at Institut Jantung
Negara (National Heart Institute), Kuala Lumpur, Malaysia
2004 Live course in Pediatric Cardiac Intervention, Beijing, China2004 & 2006 Live course in Pediatric Catheter Intervention , Kuala Lumpur, Malaysia2004 Short course in Pediatric Cardiac Intensive Care, Miami, USA2005 & 2007 International Workshop on Interventional Pediatric Cardiology, Millan, Italy2005 Live course in Pediatric Interventional Cardiology and Emerging
New Technique in Cardiac Surgery, Buenos Aires, Argentina2006 Live course in Pediatric Interventional Cardiology and Adult
Congenital Heart Disease, Las Vegas, USA 2009 Live course in Pediatric and Adult Interventional Cardiac
Symposium, Cairns, Australia
Heart Disease in Infant and Children
Heart Disease in Infant and Children
Mulyadi M. Djer, MD, SpA(K), PhD
Mulyadi M. Djer, MD, SpA(K), PhD
Department of Child HealthMedical School University of Indonesia
Department of Child HealthMedical School University of Indonesia
Structures of the heart
Cardiac performanceCardiac performance
PreloadAfterloadContractilityRate
PreloadAfterloadContractilityRate
Normal Heart
Heart disease in childrenHeart disease in children Congenital heart disease
Acyanosis congenital heart disease Cyanosis congenital heart disease
Acquired heart disease Acute rheumatic fever Chronic rheumatic heart disease Kawasaki disease Cardiac involvement in systemic disease
Thalasemia Kidney disease etc
Congenital heart disease Acyanosis congenital heart disease Cyanosis congenital heart disease
Acquired heart disease Acute rheumatic fever Chronic rheumatic heart disease Kawasaki disease Cardiac involvement in systemic disease
Thalasemia Kidney disease etc
Heart disease in childrenHeart disease in children Congenital heart disease
Acyanosis congenital heart disease Cyanosis congenital heart disease
Acquired heart disease Acute rheumatic fever Chronic rheumatic heart disease Kawasaki disease Cardiac involvement in systemic disease
Thalasemia Kidney disease etc
Congenital heart disease Acyanosis congenital heart disease Cyanosis congenital heart disease
Acquired heart disease Acute rheumatic fever Chronic rheumatic heart disease Kawasaki disease Cardiac involvement in systemic disease
Thalasemia Kidney disease etc
Heart disease in childrenHeart disease in children Congenital heart disease
Acyanosis congenital heart disease Cyanosis congenital heart disease
Acquired heart disease Acute rheumatic fever Chronic rheumatic heart disease Kawasaki disease Cardiac involvement in systemic disease
Thalasemia Kidney disease etc
Congenital heart disease Acyanosis congenital heart disease Cyanosis congenital heart disease
Acquired heart disease Acute rheumatic fever Chronic rheumatic heart disease Kawasaki disease Cardiac involvement in systemic disease
Thalasemia Kidney disease etc
Congenital Heart DiseaseCongenital Heart Disease
Incidence of Congenital Heart DiseaseIncidence of Congenital Heart Disease The incidence: 8-10 in 1000 live birth
Indonesia: Total population : ± 235,000,000 Birth rate: 2.3 % Incidence CHD per year: 50,000
cases
The incidence: 8-10 in 1000 live birth Indonesia:
Total population : ± 235,000,000 Birth rate: 2.3 % Incidence CHD per year: 50,000
cases
Classification of CHDClassification of CHD Acyanosis
Normal pulmonary blood flow Pulmonary Stenosis (PS) Aortic Stenosis (AS) Coarctatio Aorta (CoA)
Increased pulmonary blood flow Patent Ductus Arteriosus (PDA) Atrial Septal Defect (ASD) Ventricular Septal Defect (VSD)
Cyanosis Normal pulmonary blood flow
TGA without PS Increased pulmonary blood flow
TGA with VSD Truncus arteriosus Total anomaly pulmonary vein drainage
Decreased pulmonary blood flow ToF Pulmonary atresia Ticuspid atresia
Acyanosis Normal pulmonary blood flow
Pulmonary Stenosis (PS) Aortic Stenosis (AS) Coarctatio Aorta (CoA)
Increased pulmonary blood flow Patent Ductus Arteriosus (PDA) Atrial Septal Defect (ASD) Ventricular Septal Defect (VSD)
Cyanosis Normal pulmonary blood flow
TGA without PS Increased pulmonary blood flow
TGA with VSD Truncus arteriosus Total anomaly pulmonary vein drainage
Decreased pulmonary blood flow ToF Pulmonary atresia Ticuspid atresia
Classification of CHDClassification of CHD Acyanosis
Normal pulmonary blood flow Pulmonary Stenosis (PS) Aortic Stenosis (AS) Coarctatio Aorta (CoA)
Increased pulmonary blood flow Patent Ductus Arteriosus (PDA) Atrial Septal Defect (ASD) Ventricular Septal Defect (VSD)
Cyanosis Normal pulmonary blood flow
TGA without PS Increased pulmonary blood flow
TGA with VSD Truncus arteriosus Total anomaly pulmonary vein drainage
Decreased pulmonary blood flow ToF Pulmonary atresia Ticuspid atresia
Acyanosis Normal pulmonary blood flow
Pulmonary Stenosis (PS) Aortic Stenosis (AS) Coarctatio Aorta (CoA)
Increased pulmonary blood flow Patent Ductus Arteriosus (PDA) Atrial Septal Defect (ASD) Ventricular Septal Defect (VSD)
Cyanosis Normal pulmonary blood flow
TGA without PS Increased pulmonary blood flow
TGA with VSD Truncus arteriosus Total anomaly pulmonary vein drainage
Decreased pulmonary blood flow ToF Pulmonary atresia Ticuspid atresia
PDA
Located between aorta and pulmonary arteryLocated between aorta and pulmonary artery
ASD
Defect between LA and RADefect between LA and RA
VSD VSD
Tetralogy Fallot
Syndrome consist of 4 items: VSD Pulmonary stenosis Aortic over-riding RVH
Syndrome consist of 4 items: VSD Pulmonary stenosis Aortic over-riding RVH
Transposition of Great arteryTransposition of Great artery
Fetal vs. Neonatal Circulation
Fetal vs. Neonatal Circulation
Changes in Pulmonary Vascular Resistance 7 weeks preceding birth, at birth and 7 weeks after birth
Changes in Pulmonary Vascular Resistance 7 weeks preceding birth, at birth and 7 weeks after birth
Park MK. Pediatric cardiology for practitioner. 5th Ed. Philadelphia: Elsevier, 2008
Pathophysiology Acyanotic and Cyanotic Pathophysiology Acyanotic and Cyanotic
Hemodynamic acyanoticHemodynamic acyanotic Hemodynamic cyanoticHemodynamic cyanotic
Critically Congenital Heart DiseaseCritically Congenital Heart Disease Complex CHD in which circulation to
lungs /systemic depend on PDA Duct dependent pulmonary circulation
Pulmonary Atresia Duct dependent systemic circulation
Hypoplastic left heart syndrom Duct dependent mixing circulation
Transposition of great artery
Complex CHD in which circulation to lungs /systemic depend on PDA Duct dependent pulmonary circulation
Pulmonary Atresia Duct dependent systemic circulation
Hypoplastic left heart syndrom Duct dependent mixing circulation
Transposition of great artery
Critically CHDCritically CHD
Duct Dependent PulmonaryCirculation
Duct Dependent Systemic Circulation
Duct Dependent Mixing Circulation
EtiologyEtiology
Genetic 10 % Chromosome 7 % Monogenic 3 %
Environment 3 % Multifactor 90 %
Genetic 10 % Chromosome 7 % Monogenic 3 %
Environment 3 % Multifactor 90 %
Sign and Symptom of CHDSign and Symptom of CHD Cyanosis Dyspneu Exercise intolerance
Infant Feeding problem Intermittent feeding Prolonged feeding
Big children Dyspneu on exertion Orthopneu Recurrent respiratory tract infection Poor weight gain Asymptomatic murmur
Cyanosis Dyspneu Exercise intolerance
Infant Feeding problem Intermittent feeding Prolonged feeding
Big children Dyspneu on exertion Orthopneu Recurrent respiratory tract infection Poor weight gain Asymptomatic murmur
No murmur does not exclude CHD
The presence of murmur does not mean that there is CHD
No murmur does not exclude CHD
The presence of murmur does not mean that there is CHD
DiagnosisDiagnosis Clinical finding Supporting examination
Level 1 Periphery blood examination Arterial blood gas analysis Chest X ray Electrocardiography
Level 2 Echocardiography
Level 3 Cardiac catheterization
Diagnostic Therapeutic
Others CT Scan MRI
Clinical finding Supporting examination
Level 1 Periphery blood examination Arterial blood gas analysis Chest X ray Electrocardiography
Level 2 Echocardiography
Level 3 Cardiac catheterization
Diagnostic Therapeutic
Others CT Scan MRI
History
A complete birth history: maternal history; prenatal, perinatal, and postnatal complications; history of labor and delivery;
Neonatal course should be obtained, especially the exact time when the cyanosis developed, because certain CHD present at birth, while others may take as long as one month to present themselves.
History
A complete birth history: maternal history; prenatal, perinatal, and postnatal complications; history of labor and delivery;
Neonatal course should be obtained, especially the exact time when the cyanosis developed, because certain CHD present at birth, while others may take as long as one month to present themselves.
Clinical Manifestations
General Physical examination
Initial physical examination should focus on vital signs and cardiac and respiratory examinations
Evaluate for rales, stridor, grunting, flaring, retractions, and evidence of consolidation or effusion on pulmonary examination.
General Physical examination
Initial physical examination should focus on vital signs and cardiac and respiratory examinations
Evaluate for rales, stridor, grunting, flaring, retractions, and evidence of consolidation or effusion on pulmonary examination.
Clinical Manifestations
Physical Extremities: strength and symmetry of
the pulses in the upper and lower extremities, edema, and cyanosis of the nail beds.
Hepatosplenomegaly may be consistent with right ventricular or biventricular heart failure.
Physical Extremities: strength and symmetry of
the pulses in the upper and lower extremities, edema, and cyanosis of the nail beds.
Hepatosplenomegaly may be consistent with right ventricular or biventricular heart failure.
Clinical Manifestations
Cardiac Physical examination…… Inspection: precordial impulse, Palpation: thrill, left precordial lift, right
ventricular heave Percussion Auscultation: S1, S2 systolic or diastolic
murmurs, splitting abnormalities, S3 or S4 gallop, ejection click, opening snap, or rub.
Cardiac Physical examination…… Inspection: precordial impulse, Palpation: thrill, left precordial lift, right
ventricular heave Percussion Auscultation: S1, S2 systolic or diastolic
murmurs, splitting abnormalities, S3 or S4 gallop, ejection click, opening snap, or rub.
Clinical Manifestations
CyanosisCyanosis Bluish discoloration of skin & mucous
membrane ↑ reduced Hb to 5 g/100 mL in cutaneous veins
Central cyanosis Associated with desaturation of arterial
blood Peripheral cyanosis
Normal arterial oxygen saturation Increased extraction of oxygen by
peripheral tissue Circulatory shock Hypovolemia Vasoconstriction from cold
Bluish discoloration of skin & mucous membrane ↑ reduced Hb to 5 g/100 mL in cutaneous veins
Central cyanosis Associated with desaturation of arterial
blood Peripheral cyanosis
Normal arterial oxygen saturation Increased extraction of oxygen by
peripheral tissue Circulatory shock Hypovolemia Vasoconstriction from cold
Cyanosis Acro vs. CentralCyanosis Acro vs. Central
Acrocyanosis part of normal
transition may last 72hr beware APGAR
of 10 hypoperfused severe anemia
Acrocyanosis part of normal
transition may last 72hr beware APGAR
of 10 hypoperfused severe anemia
Lefkowitz B, 2000
Types of CyanosisTypes of Cyanosis
Peripheral vs CentralPink Mucous membranes,
tongue, lips, trunk (?)Blue
Cool Extremities Warm cool
Decreased Perfusion Normal to decreased
Normal PaO2 Low
Usually benign Outcome Urgent management
(pulmonary, CHD*, sepsis, shock)
Differential cyanosis:•Pink right hand/head with blue feet-pulmonary hypertension; preductal coarctation with PDA or interrupted arch•Pink feet, blue hands-transposition with coarctation*CHD = congenital heart disease
Thompson TR, The Cyanotic Newborn Infant
http://www.med.umn.edu/img/assets/9223
CyanosisCyanosis Normally there are 2 g/100 mL
required another 3 g/100 ml reduced Hgb to produce cyanosis
Hgb X Desaturation = 3, so Desat = 3/Hgb
For example Hgb 15 g/dl cyanosis appear at
desaturation 3/15 = 20%, or cyanosis appears at SaO2 80%
Hgb 6 g/dL cyanosis appear at desaturation 3/6 = 50% or cyanosis appears at SaO2 50%
Normally there are 2 g/100 mL required another 3 g/100 ml reduced Hgb to produce cyanosis
Hgb X Desaturation = 3, so Desat = 3/Hgb
For example Hgb 15 g/dl cyanosis appear at
desaturation 3/15 = 20%, or cyanosis appears at SaO2 80%
Hgb 6 g/dL cyanosis appear at desaturation 3/6 = 50% or cyanosis appears at SaO2 50%
DiagnosisDiagnosis Clinical finding Supporting examination
Level 1 Periphery blood examination Arterial blood gas analysis Chest X ray Electrocardiography
Level 2 Echocardiography
Level 3 Cardiac catheterization
Diagnostic Therapeutic
Others CT Scan MRI
Clinical finding Supporting examination
Level 1 Periphery blood examination Arterial blood gas analysis Chest X ray Electrocardiography
Level 2 Echocardiography
Level 3 Cardiac catheterization
Diagnostic Therapeutic
Others CT Scan MRI
Sa O2 and pO2Sa O2 and pO2
100% pO2 ↑
100% pO2 ↑
70%
70%
80%pO2 ↓
80%pO2 ↓70%
70% 70%
70%
100% pO2 ↑
80%pO2 ↓
Central CyanosisLung disease Heart disease
100% pO2 ↑
100% pO2 ↑
70%
70%
80%pO2 ↓
Peripheral Cyanosis
80%pO2 ↓
80%pO2 ↓
70%
70%70%
70%
100% pO2 ↑↑
100% pO2 ↑↑
21% O2 -Room Air 100% O2-HyperoxiaLung disease
100% pO2 ↑
80%pO2 ↓
70%
70% 70%
70%
100% pO2 ↑↑
80%pO2 ↓
21% O2- Room air 100% O2-Hyperoxia
Heart Disease
Hyperoxia testHyperoxia testOxygen
Concentration (%)
Ventilation Status
PaCO2 Goal
PaO2 Values
PPHN Lung Disease
RL Cardiac
21 %-room air Spontaneous 40 40 40 40
100 %-hyperoxia Spontaneous or MV
40 40 >100 40
100 %-pre and postductal shunt
Spontaneous or MV
40 >10-15 <5 <5
100 %-hyperoxia, hyperventilation
MV
(Mechanical ventilation)
20-25 >100 >150 40
Thompson TR, The Cyanotic Newborn Infant
http://www.med.umn.edu/img/assets/9223
How to read chest X rayHow to read chest X ray
Ebstein anomaly
TAPVD
“Figure of eight”“Snowman Appearance”
ToF
“Boot shape”
“Egg on Side”
TGA
ElectrocardiographyElectrocardiography
Cardiac Potential Cardiac Potential action recording on action recording on ECC electrode placing ECC electrode placing on the surface of the on the surface of the bodybody
Reference value Reference value ageage
Cardiac Potential Cardiac Potential action recording on action recording on ECC electrode placing ECC electrode placing on the surface of the on the surface of the bodybody
Reference value Reference value ageage
DiagnosisDiagnosis Clinical finding Supporting examination
Level 1 Periphery blood examination Arterial blood gas analysis Chest X ray Electrocardiography
Level 2 Echocardiography
Level 3 Cardiac catheterization
Diagnostic Therapeutic
Others CT Scan MRI
Clinical finding Supporting examination
Level 1 Periphery blood examination Arterial blood gas analysis Chest X ray Electrocardiography
Level 2 Echocardiography
Level 3 Cardiac catheterization
Diagnostic Therapeutic
Others CT Scan MRI
EchocardiographyEchocardiography
DiagnosisDiagnosis Clinical finding Supporting examination
Level 1 Periphery blood examination Arterial blood gas analysis Chest X ray Electrocardiography
Level 2 Echocardiography
Level 3 Cardiac catheterization
Diagnostic Therapeutic
Others CT Scan MRI
Clinical finding Supporting examination
Level 1 Periphery blood examination Arterial blood gas analysis Chest X ray Electrocardiography
Level 2 Echocardiography
Level 3 Cardiac catheterization
Diagnostic Therapeutic
Others CT Scan MRI
Atrial septal defectAtrial septal defect
ASD ASD
DiagnosisDiagnosis Clinical finding Supporting examination
Level 1 Periphery blood examination Arterial blood gas analysis Chest X ray Electrocardiography
Level 2 Echocardiography
Level 3 Cardiac catheterization
Diagnostic Therapeutic
Others CT Scan MRI
Clinical finding Supporting examination
Level 1 Periphery blood examination Arterial blood gas analysis Chest X ray Electrocardiography
Level 2 Echocardiography
Level 3 Cardiac catheterization
Diagnostic Therapeutic
Others CT Scan MRI
MR-guided diagnostic and interventional proceduresMR-guided diagnostic and interventional procedures
Early diagnosis is important because: Management of disease and education to
parent depend on it Certain CHD has optimal age to undergo
definitive treatment TGA: 2 weeks Complete AVSD: 3-6 months Truncus arteriosus: < 6 months
Most CHD does not need intervention / surgery at time of diagnosis:
Intervention / surgery will be needed at any age in which the risk of intervention or surgery is low (usually above 1-2 year), but don’t late.
Early surgery / intervention is needed if conservative treatment fail.
Early diagnosis is important because: Management of disease and education to
parent depend on it Certain CHD has optimal age to undergo
definitive treatment TGA: 2 weeks Complete AVSD: 3-6 months Truncus arteriosus: < 6 months
Most CHD does not need intervention / surgery at time of diagnosis:
Intervention / surgery will be needed at any age in which the risk of intervention or surgery is low (usually above 1-2 year), but don’t late.
Early surgery / intervention is needed if conservative treatment fail.
Early diagnosis is important because: Management of disease and education to
parent depend on it Certain CHD has optimal age to undergo
definitive treatment Severe CoA / Interrupted Ao arch: as soon
as possible TGA: 2 weeks Complete AVSD: 3-6 months Truncus arteriosus: < 6 months
Most CHD does not need intervention / surgery at time of diagnosis:
Intervention / surgery will be needed at any age in which the risk of intervention or surgery is low (usually above 1-2 year), but don’t late.
Early surgery / intervention is needed if conservative treatment fail.
Early diagnosis is important because: Management of disease and education to
parent depend on it Certain CHD has optimal age to undergo
definitive treatment Severe CoA / Interrupted Ao arch: as soon
as possible TGA: 2 weeks Complete AVSD: 3-6 months Truncus arteriosus: < 6 months
Most CHD does not need intervention / surgery at time of diagnosis:
Intervention / surgery will be needed at any age in which the risk of intervention or surgery is low (usually above 1-2 year), but don’t late.
Early surgery / intervention is needed if conservative treatment fail.
Early diagnosis is important because: Management of disease and education to
parent depend on it Certain CHD has optimal age to undergo
definitive treatment TGA: 2 weeks Complete AVSD: 3-6 months Truncus arteriosus: < 6 months
Most CHD does not need intervention / surgery at time of diagnosis:
Intervention / surgery will be needed at any age in which the risk of intervention or surgery is low (usually above 1-2 year), but don’t late.
Early surgery / intervention is needed if conservative treatment fail.
Early diagnosis is important because: Management of disease and education to
parent depend on it Certain CHD has optimal age to undergo
definitive treatment TGA: 2 weeks Complete AVSD: 3-6 months Truncus arteriosus: < 6 months
Most CHD does not need intervention / surgery at time of diagnosis:
Intervention / surgery will be needed at any age in which the risk of intervention or surgery is low (usually above 1-2 year), but don’t late.
Early surgery / intervention is needed if conservative treatment fail.
Management of CHD Management of CHD
Transcatheter Intervention
HybridIntervention
Surgery
Palliative Definitive
Medical Treatment
Invasiveness
Effe
ctiv
enes
s
Good
Bad
State of ArtState of Art
Intervention
Minimal InvasiveSurgery
ConventionalSurgery
MedicalTreatment
Management of Congenital Heart DiseaseManagement of Congenital Heart Disease
Do not required treatment or intervention, some of defect closed spontaneously
Treatment Medical treatment
Initial treatment (PGE1, indomethacin) Complication treatment (anti failure, anti spell) Conservative treatment (Eisenmenger)
Palliative Intervention non-surgery (BAS, PDA stenting) Surgery (BT shunt, PA banding)
Definitive Intervention non-surgery Non-complex CHD Surgery Complex CHD
Do not required treatment or intervention, some of defect closed spontaneously
Treatment Medical treatment
Initial treatment (PGE1, indomethacin) Complication treatment (anti failure, anti spell) Conservative treatment (Eisenmenger)
Palliative Intervention non-surgery (BAS, PDA stenting) Surgery (BT shunt, PA banding)
Definitive Intervention non-surgery Non-complex CHD Surgery Complex CHD
Treatment of Congenital Heart DiseaseTreatment of Congenital Heart Disease
Medical treatment Initial treatment (PGE1, indomethacin) Complication treatment (anti failure, anti spell) Conservative treatment (Eisenmenger)
Palliative Intervention non-surgery (BAS, PDA stenting) Surgery (BT shunt, PA banding)
Definitive Intervention non-surgery Non-complex CHD Surgery Complex CHD
Medical treatment Initial treatment (PGE1, indomethacin) Complication treatment (anti failure, anti spell) Conservative treatment (Eisenmenger)
Palliative Intervention non-surgery (BAS, PDA stenting) Surgery (BT shunt, PA banding)
Definitive Intervention non-surgery Non-complex CHD Surgery Complex CHD
Treatment of Congenital Heart DiseaseTreatment of Congenital Heart Disease
Medical treatment Initial treatment (PGE1, indomethacin) Complication treatment (anti failure, anti spell) Conservative treatment (Eisenmenger)
Palliative Intervention non-surgery (BAS, PDA stenting) Surgery (BT shunt, PA banding)
Definitive Intervention non-surgery Non-complex CHD Surgery Complex CHD
Medical treatment Initial treatment (PGE1, indomethacin) Complication treatment (anti failure, anti spell) Conservative treatment (Eisenmenger)
Palliative Intervention non-surgery (BAS, PDA stenting) Surgery (BT shunt, PA banding)
Definitive Intervention non-surgery Non-complex CHD Surgery Complex CHD
Treatment of Congenital Heart DiseaseTreatment of Congenital Heart Disease
Medical treatment Initial treatment (PGE1, indomethacin) Complication treatment (anti failure, anti spell) Conservative treatment (Eisenmenger)
Palliative Intervention non-surgery (BAS, PDA stenting) Surgery (BT shunt, PA banding)
Definitive Intervention non-surgery Non-complex CHD Surgery Complex CHD
Medical treatment Initial treatment (PGE1, indomethacin) Complication treatment (anti failure, anti spell) Conservative treatment (Eisenmenger)
Palliative Intervention non-surgery (BAS, PDA stenting) Surgery (BT shunt, PA banding)
Definitive Intervention non-surgery Non-complex CHD Surgery Complex CHD
Medical TreatmentMedical Treatment1. Initial treatment: Prostaglandin E1
Critical CHD To open PDA Fast response Doses 10 nanogram/kg/minute Side effect:
Apneu Hypotension
1. Initial treatment: Prostaglandin E1
Critical CHD To open PDA Fast response Doses 10 nanogram/kg/minute Side effect:
Apneu Hypotension
...Medical treatment...Medical treatment
2. Complication treatmentCyanotic spella. Kneechest positionb. Acid-base correctionc. Sedation: Morphin sulphat 0,2 mg/kg
IM/SCd. Propranolol: 0,01-0,25 mg/kg
(average 0,05 mg/kg) IV slowly
2. Complication treatmentCyanotic spella. Kneechest positionb. Acid-base correctionc. Sedation: Morphin sulphat 0,2 mg/kg
IM/SCd. Propranolol: 0,01-0,25 mg/kg
(average 0,05 mg/kg) IV slowly
...Medical treatment...Medical treatmentHeart failure ↓ preload
Diuretic; Frusemide : 1-2mg/kg/day 2 X
Sprironolakton:
0-10 kg: 6,25mg/kg 12H; 11-20 kg: 12,5 12H mg/kg 2X; 21-40 kg: 25 mg/kg 12H; >40 kg: 25 mg/kg 12H
↓ afterload Vasodilator
Captopril: 0,3-6 mg/kg/day divided 2-3 dose
Heart failure ↓ preload
Diuretic; Frusemide : 1-2mg/kg/day 2 X
Sprironolakton:
0-10 kg: 6,25mg/kg 12H; 11-20 kg: 12,5 12H mg/kg 2X; 21-40 kg: 25 mg/kg 12H; >40 kg: 25 mg/kg 12H
↓ afterload Vasodilator
Captopril: 0,3-6 mg/kg/day divided 2-3 dose
...Medical treatment...Medical treatment ↑ Contractility
Dopamine : 5-10µg/kg/minute Dobutamine: 5-10 µg/kg/minute Digoxin (µg/kg/day)
Digitalization Maintenance
Premature 20 5 < 30 day 30 8 < 2 year 40-50 10-12 > 2 year 30-50 8-10
↑ Contractility Dopamine : 5-10µg/kg/minute Dobutamine: 5-10 µg/kg/minute Digoxin (µg/kg/day)
Digitalization Maintenance
Premature 20 5 < 30 day 30 8 < 2 year 40-50 10-12 > 2 year 30-50 8-10
↓ heart rate Adenosine: 0,1 mg/kg fastly Beta blocker: Propranolol: 0,01-0,25 mg/kg (average 0,05 mg/kg) IV slowly.
↓ heart rate Adenosine: 0,1 mg/kg fastly Beta blocker: Propranolol: 0,01-0,25 mg/kg (average 0,05 mg/kg) IV slowly.
PalliativePalliative
Aim: to release sign or symptom Non-surgery:
BAS PDA stenting
Surgery: BT Shunt PA banding
Aim: to release sign or symptom Non-surgery:
BAS PDA stenting
Surgery: BT Shunt PA banding
Balloon Atrial SeptostomiBalloon Atrial Septostomi
Transposition Great Artery
Balloon Atrial SeptostomyBalloon Atrial Septostomy
Balloon Atrial SeptostomyBalloon Atrial Septostomy
Balloon Atrial SeptostomyBalloon Atrial Septostomy
PDA stentingPDA stenting
Hypoplastic Left Heart Syndrome
PDA stenting
Pulmonary Artery Banding (PA banding)Pulmonary Artery Banding (PA banding)
VSD pada bayi
Blallock Tausig Shunt (BT shunt)Blallock Tausig Shunt (BT shunt)
Blallock Tausig Shunt (BT shunt)
Definitive TreatmentDefinitive Treatment
Non-surgery: Non-Complex CHD Surgery:
Bi-ventricular circulation Single-ventricular /univentricular
circulation One and half ventricle Heart transplantation
Non-surgery: Non-Complex CHD Surgery:
Bi-ventricular circulation Single-ventricular /univentricular
circulation One and half ventricle Heart transplantation
Biventricular Circulation
Transposition of Great arteryTransposition of Great artery
Uni / Single Ventricular Circulation
One and Half Ventricular Circulation
ComplicationsComplications Heart failure
preload afterload contractility heart rate
Cyanotic spell Endocarditis Eisenmenger syndrome etc
Heart failure preload afterload contractility heart rate
Cyanotic spell Endocarditis Eisenmenger syndrome etc
Patent Ductus ArteriosusPatent Ductus Arteriosus
PDA
Located between aorta and pulmonary arteryLocated between aorta and pulmonary artery
Patent Ductus Arteriosus Patent Ductus Arteriosus
Incidence + 10% Female : Male = 1.2 to 1.5 : 1 Premature and LBW higher
Embryology Fetus: ductus arteriosus connects PA and
aorta. If ductus does not closs Patent Ductus
arteriosus
Incidence + 10% Female : Male = 1.2 to 1.5 : 1 Premature and LBW higher
Embryology Fetus: ductus arteriosus connects PA and
aorta. If ductus does not closs Patent Ductus
arteriosus
RA
RV
LA
LV
RA LA
RV LV
Patent Ductus Arteriosus
Patent Ductus ArteriosusPatent Ductus Arteriosus
Clinical findings Small defect:
Symptom (-) Growth and development normal
Significant defect: Decreased exercise tolerant Weigh gained not good Frequent URTI
Specific case: pulsus seler at 4th extremities
Clinical findings Small defect:
Symptom (-) Growth and development normal
Significant defect: Decreased exercise tolerant Weigh gained not good Frequent URTI
Specific case: pulsus seler at 4th extremities
Patent Ductus ArteriosusPatent Ductus Arteriosus
Auscultation : continuous murmur at upper LSB 2Auscultation : continuous murmur at upper LSB 2
ECG LVH
ECG LVH
Patent Ductus ArteriosusPatent Ductus Arteriosus Chest X- Ray
Prominent PA segment LVH
Chest X- Ray Prominent PA segment LVH
EchocardiographyEchocardiography
Diagnosis Differential AP-window Arterio-venous fistulae
Management Medical treatment
Premature: indometacin Anti-failure
Definitive treatment PDA closure :
Transcatheter closure Surgery
Diagnosis Differential AP-window Arterio-venous fistulae
Management Medical treatment
Premature: indometacin Anti-failure
Definitive treatment PDA closure :
Transcatheter closure Surgery
Patent Ductus ArteriosusPatent Ductus Arteriosus
PDAPDA
Neonates/InfantsNeonates/Infants Children/AdultsChildren/Adults
Heart failure (+)Heart failure (+) Heart failure (-)Heart failure (-)
PrematurePremature Full termFull term
Anti failureIndomethacinAnti failure
Indomethacin
SuccessSuccess FailFail
Spontaneous closure
Spontaneous closure
Anti failureAnti failure
SuccessSuccessFailFail
Surgical ligation
Surgical ligation
Transcatheter closureTranscatheter closure
PH (-)PH (-) PH (+)PH (+)
LRLR RLRL
HyperoxiaHyperoxia
ReactiveReactive Nonreactive
Nonreactive
ConservativeConservative
Age >12wksW >4kg
Age >12wksW >4kg
FailFail
Transcatheter Closure of PDATranscatheter Closure of PDA
Plastic viseCombinationTouhy borst/hemostatis valve
Amplatzer occluder
Delivery cable
Delivery sheath
1 way stop cock
Amplatzer Ductal OccluderAmplatzer Ductal Occluder
ProcedureProcedure
Under general anesthesia
Access from femoral artery and vein
Under general anesthesia
Access from femoral artery and vein
Patent Ductus ArteriosusPatent Ductus Arteriosus
Amplatzer Ductal OccluderAmplatzer Ductal Occluder
PDA before occluded by device
PDA before occluded by device
Amplatzer Ductal OccluderAmplatzer Ductal Occluder
Device collapsed into catheter and pushed out to open distal disk
Device collapsed into catheter and pushed out to open distal disk
Amplatzer Ductal OccluderAmplatzer Ductal Occluder
Device and catheter withdrawn into PDA followed by opening proximal disk
Device and catheter withdrawn into PDA followed by opening proximal disk
Amplatzer Ductal OccluderAmplatzer Ductal Occluder
Immediateresults after occluded by ADO
Immediateresults after occluded by ADO
Amplatzer Ductal OccluderAmplatzer Ductal Occluder
10 minutes after occluded10 minutes after occluded
Amplatzer Ductal OccluderAmplatzer Ductal Occluder
During unscrewedthe device During unscrewedthe device
Amplatzer Ductal OccluderAmplatzer Ductal Occluder
PDA after occluded byADO
PDA after occluded byADO
Patent Ductus ArteriosusPatent Ductus Arteriosus
Patent Ductus Arteriosus
PDA before occludedusing coil
PDA before occludedusing coil
Patent Ductus Arteriosus
PDA after occludedusing coilPDA after occludedusing coil
PDA ligationPDA ligation
Atrial Septal DefectAtrial Septal Defect
ASD
Defect between LA and RADefect between LA and RA
Atrial Septal defect( ASD )Atrial Septal defect( ASD )
Incidence + 10 %♂: ♀ ratio = 1,5 to 2 : 1
Anatomy :Defect on foramen ovale : Secundum ASDDefect at SVC and RA junction: sinus venosus
ASDDefect at ostium primum : primum ASD
Incidence + 10 %♂: ♀ ratio = 1,5 to 2 : 1
Anatomy :Defect on foramen ovale : Secundum ASDDefect at SVC and RA junction: sinus venosus
ASDDefect at ostium primum : primum ASD
Atrial Septal Defect
Atrial Septal DefectAtrial Septal Defect
Diagram of ASDDiagram of ASD
RA
RV
LA
LV
RA
RV
LA
LV
Atrial septal Defect
Clinical findings Asymptomatic Auscultation :
Normal 1st HS or loudWide and fixed split 2nd HSEjection systolic murmur
Clinical findings Asymptomatic Auscultation :
Normal 1st HS or loudWide and fixed split 2nd HSEjection systolic murmur
Atrial septal DefectAtrial septal Defect
Normal Split 2nd Heart SoundNormal Split 2nd Heart Sound
ExpExp
InspInsp
A2 = P2A2 = P2
A2A2
P2P2
RARA
RARA LALA
RVRV
RVRV
LVLV
LALA
LVLV
Wide and Fixed Split 2nd Heart Sound in ASDWide and Fixed Split 2nd Heart Sound in ASD
ExpExp
InspInsp
A2A2
A2A2
P2P2
P2P2
RARA
RVRV
LALA
LVLV
RARA
RVRV
LALA
LVLV
Paradoxical Split 2nd Heart Sound in Aortic StenosisParadoxical Split 2nd Heart Sound in Aortic Stenosis
ExpExp
InspInsp
A2 = P2A2 = P2
A2A2P2P2
RARA
RARA LALA
RVRV
RVRV
LVLV
LALA
LVLV
Atrial Septal DefectAtrial Septal Defect
Auscultation :•1st HS N or loud•Wide and fixed split 2nd HS •Ejection systolic murmur
Auscultation :•1st HS N or loud•Wide and fixed split 2nd HS •Ejection systolic murmur
ECG : IRBB , right ventricular hypertrophyECG : IRBB , right ventricular hypertrophy
Atrial Septal DefectAtrial Septal Defect
•Right atrial enlargement•RVH•Prominence the MPA segment•Increased pulmonary vascular marking
•Right atrial enlargement•RVH•Prominence the MPA segment•Increased pulmonary vascular marking
Chest X-RayChest X-Ray
EchocardiographyEchocardiography
CatheterizationCatheterization
Atrial Septal DefectAtrial Septal Defect
Diagnosis Differential
Partial Anomalous Pulmonary Vein Drainage
Pulmonary Stenosis
Innocent Murmur
Diagnosis Differential
Partial Anomalous Pulmonary Vein Drainage
Pulmonary Stenosis
Innocent Murmur
Atrial Septal defectAtrial Septal defect
Management Medical treatment
Anti-failure Definitive treatment
Transcatheter closure using ASO (Amplatzer septal occluder)
Recent treatment Surgery : Preschool age
Management Medical treatment
Anti-failure Definitive treatment
Transcatheter closure using ASO (Amplatzer septal occluder)
Recent treatment Surgery : Preschool age
ASDASD
Small ShuntSmall Shunt Large ShuntLarge Shunt
ObservationObservation
EvaluationAt age 5-8 yrs
EvaluationAt age 5-8 yrs
CathCath
FR<1.5FR<1.5 FR>1.5FR>1.5
ConservativeConservative
InfantsInfants Children/AdultsChildren/Adults
Heart Failure (-)
Heart Failure (-)
Heart Failure (+)
Heart Failure (+)
Age >1yrsW >10kg
Age >1yrsW >10kg
Transcatheter closure (Secundum ASD) /Surgical Closure(other type of ASD)Transcatheter closure (Secundum ASD) /Surgical Closure(other type of ASD)
ConservativeConservative
Anti failureAnti failure
FailFailSuccessSuccess
PH (-)PH (-) PH (+)PH (+)
PVD (-)
PVD (-)
PVD (+)
PVD (+)
HyperoxiaHyperoxia
Reac-tive
Reac-tive
Nonreactive
Nonreactive
SurgicalClosureSurgicalClosure
Amplatzer Septal OccluderAmplatzer Septal Occluder
AMPLATZER Septal OccluderAMPLATZER Septal Occluder
Atrial septal defectAtrial septal defect
ASD before occlusionASD before occlusion
During balloon sizingDuring balloon sizing
Atrial septal defectAtrial septal defect
Atrial septal defectAtrial septal defect
ASD after occluded using ASOASD after occluded using ASO
….ASD Surgery….ASD Surgery
Ventricular Septal DefectVentricular Septal Defect
VSD VSD
Ventricular septal defectVentricular septal defect Incidence
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
Incidence 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
Ventricular Septal Defect
RA
RV
RA LALA
RV LVLV
Ventricular septal defect
Ventricular Septal Defect
Ventricular Septal DefectVentricular Septal Defect
Clinical findings Day 1st after birth: murmur (-) After 2-6 weeks : murmur (+) Murmur : pansystolic grade 3/6 or higher at
LLSB Small muscular defect: early systolic murmur Significant defect: Mid diastolic murmur at
apex
Clinical findings Day 1st after birth: murmur (-) After 2-6 weeks : murmur (+) Murmur : pansystolic grade 3/6 or higher at
LLSB Small muscular defect: early systolic murmur Significant defect: Mid diastolic murmur at
apex
Small VSD Small VSD
Large VSD Large VSD
Ventricular Septal DefectVentricular Septal Defect
Murmur: pansystolic grade 3/6 or higher at LSB 3
Murmur: pansystolic grade 3/6 or higher at LSB 3
ECG LVH
ECG LVH
Ventricular Septal DefectVentricular Septal Defect
•Cardiomegaly•Apex down ward•Prominence pulmonary artery segment•Increased pulmonary vascular marking
•Cardiomegaly•Apex down ward•Prominence pulmonary artery segment•Increased pulmonary vascular marking
Ventricular septal DefectVentricular septal Defect
Diagnosis Differential PDA with PH Tetralogy Fallot non cyanotic Innocent murmur
Diagnosis Differential PDA with PH Tetralogy Fallot non cyanotic Innocent murmur
Ventricular septal defectVentricular septal defect Management:
Medical treatment Anti-failure
Digoxin Diuretic
Palliative PA banding
Definitive : VSD closure
Surgery Transcatheter closure
Management: Medical treatment
Anti-failure Digoxin Diuretic
Palliative PA banding
Definitive : VSD closure
Surgery Transcatheter closure
DSVDSV
Heart failure (+)Heart failure (+) Heart failure (-)Heart failure (-)
Anti failureAnti failure
FailFail SuccessSuccess
PABPAB
Evaluate in 6 mothsEvaluate in 6 moths
Surgical closure/Transcatheter closureSurgical closure/Transcatheter closure
Aortic valve prolaps
Aortic valve prolaps
Infundibular stenosis
Infundibular stenosis
PHPH SmallerSmallerSpontaneousclosure
Spontaneousclosure
CathCath
PVD(-)PVD(-) PVD(+)PVD(+) CathCath
CathCath
ReactiveReactive Non-reactive
Non-reactive
ConservativeConservative
FR>1.5FR>1.5FR<1.5FR<1.5
….VSD Occlusion Amplatzer Perimembranous VSD Occluder
….VSD Occlusion Amplatzer Perimembranous VSD Occluder
Amplatzer Perimembranous VSD OccluderAmplatzer Perimembranous VSD Occluder
Ventricular septal defectVentricular septal defect
VSD before occlusionVSD before occlusion
Ventricular septal defectVentricular septal defect
Snaring wire at PA and pull it out to FV
Snaring wire at PA and pull it out to FV
Ventricular septal defectVentricular septal defect
VSD during deploying the deviceVSD during deploying the device
VSD after occludedusing ASOVSD after occludedusing ASO
…VSD Surgery…VSD Surgery
Tetralogy of FallotTetralogy of Fallot
Tetralogy Fallot
Syndrome consist of 4 items: VSD Pulmonary stenosis Aortic over-riding RVH
Syndrome consist of 4 items: VSD Pulmonary stenosis Aortic over-riding RVH
Tetralogy FallotTetralogy Fallot
Incidence5-8% from all CHD
AnatomyCaused: Left-anterior deviation of infundibular septum
Incidence5-8% from all CHD
AnatomyCaused: Left-anterior deviation of infundibular septum
What is the cause of ToFWhat is the cause of ToF Left deviation
Malalignment VSD Overriding aorta
Left deviation Malalignment VSD Overriding aorta
What is the cause of ToFWhat is the cause of ToF Anterior deviation
PS RVH VSD
Anterior deviation PS RVH VSD
Anterior Anterior
Tetralogy FallotTetralogy Fallot
DiagnosisClinically :
CyanosisSingle 2nd HS, ejection systolic murmur
DiagnosisClinically :
CyanosisSingle 2nd HS, ejection systolic murmur
Tetralogy FallotTetralogy Fallot
Single 2nd HS, ejection systolic murmurSingle 2nd HS, ejection systolic murmur
Tetralogi FallotTetralogi Fallot
CXR : Boot-shaped Concave
pulmonary segment
Apex upturned Decreased
pulmonary blood flow
CXR : Boot-shaped Concave
pulmonary segment
Apex upturned Decreased
pulmonary blood flow
Tetralogy FallotTetralogy Fallot
Tetralogy FallotTetralogy Fallot
ECG :
RAD
RVH
ECG :
RAD
RVH
Echocardiography: to confirm diagnosis
Echocardiography: to confirm diagnosis
Echocardiography: to confirm diagnosis
Echocardiography: to confirm diagnosis
Cardiac CatheterizationCardiac Catheterization
Cardiac CatheterizationCardiac Catheterization
Tetralogy FallotTetralogy Fallot
Diagnosis Differential Pulmonary Atresia Double outlet right ventricle and pulmonary stenosis Transposition of great artery and pulmonary
stenosis Management
Medical treatment Anti-spell
Palliative treatment: Blalock-Taussig shunt PDA stenting
Definitive: total correction
Diagnosis Differential Pulmonary Atresia Double outlet right ventricle and pulmonary stenosis Transposition of great artery and pulmonary
stenosis Management
Medical treatment Anti-spell
Palliative treatment: Blalock-Taussig shunt PDA stenting
Definitive: total correction
Tetralogy of FallotTetralogy of Fallot
< 1 yr< 1 yr > 1 yr> 1 yr
spell (+)spell (+) spell (-)spell (-)propranololpropranolol
failedfailed succeedsucceed
BTS or
PDA Stent
BTS or
PDA Stent
total correctiontotal correction
cath cath
small PAsmall PA good sized PAgood sized PA
• clinically• ECG
• clinically• ECG
• CXR• echo
• CXR• echo
age 1 yrage 1 yr
cathcath BTS/
PDA Stent
BTS/
PDA Stent
evaluationevaluation
Tetralogy FallotTetralogy Fallot
PDA stenting New alternative need for
palliative surgery in neonate
required
PDA stenting New alternative need for
palliative surgery in neonate
required
PDA stentingPDA stenting
Tetralogy FallotTetralogy Fallot
Interventional Treatment of Congenital Heart disease
Interventional Treatment of Congenital Heart disease
Invasiveness
Effe
ctiv
enes
s
Good
Bad
State of ArtState of Art
Intervention
Minimal InvasiveSurgery
ConventionalSurgery
Transcatheter treatment of CHD offers a number of advantages over surgery
Transcatheter treatment of CHD offers a number of advantages over surgery
Less invasive Fast recovery Eliminates thoracotomy No surgical complication No post surgical pain No chest scar Shortened hospitalization Minimal hospital service
requirements
Less invasive Fast recovery Eliminates thoracotomy No surgical complication No post surgical pain No chest scar Shortened hospitalization Minimal hospital service
requirements
SurgerySurgery InterventionIntervention
Interventional treatment in CHDInterventional treatment in CHDPalliative
Balloon atrial septectomy (BAS)PDA stenting
DefinitivePercutaneous occlusion of cardiac defect
PDA, ASD,VSDCollateralArtery-venous malformation
Balloon angioplasty / valvuloplasty Balloon valvuloplasty: PS, AS or MSBalloon dilatation / stent branch of pulmonary artery stenosisBalloon angioplasty Coarctation of aortaRadio frequency assisted valvotomi in PA-IVS
PalliativeBalloon atrial septectomy (BAS)PDA stenting
DefinitivePercutaneous occlusion of cardiac defect
PDA, ASD,VSDCollateralArtery-venous malformation
Balloon angioplasty / valvuloplasty Balloon valvuloplasty: PS, AS or MSBalloon dilatation / stent branch of pulmonary artery stenosisBalloon angioplasty Coarctation of aortaRadio frequency assisted valvotomi in PA-IVS
020406080
100120140160180
PDA ADO ASD VSD
RSCM RSJHK RS SOETOMO RS M HOESIN RS SARDJITO
020406080
100120140160180
PDA ADO ASD VSD
RSCM RSJHK RS SOETOMO RS M HOESIN RS SARDJITO
175
66
145 1
75
94
7 0 0
204 0 0 0
Interventional Pediatric Cardiology in IndonesiaInterventional Pediatric Cardiology in Indonesia
• Dr. Mazeni Alwi, MRCP (Kuala Lumpur)• Dr. Hasri Samion, MMed Paed (Kuala Lumpur)• Dr. Mulyadi M. Djer, SpAK (Jakarta)• Dr. Sukman T. Putra, SpAK, FACC, FESC (Jakarta)• Prof. Bambang Madiyono, SpJP, SpAK (Jakarta)• Prof. DR. Sudigdo Sastroasmoro, SpAK (Jakarta)• Dr. Ismet N Oesman, SpAK (Jakarta)• Dr. Najib Advani, SpAK, MMed Paed (Jakarta)• Dr. Syarif Rohimi, SpA (Jakarta)• Dr. Sasmito Nugroho, SpA (Yogyakarta)• Dr. Noormanto, SpAK (Yogyakarta)• Dr. Mahrus A. Rahman, SpAK (Surabaya)• Dr. Ria Nova, SpAK (Palembang)• All Fellow of School of Pediatric Cardiology
• Dr. Mazeni Alwi, MRCP (Kuala Lumpur)• Dr. Hasri Samion, MMed Paed (Kuala Lumpur)• Dr. Mulyadi M. Djer, SpAK (Jakarta)• Dr. Sukman T. Putra, SpAK, FACC, FESC (Jakarta)• Prof. Bambang Madiyono, SpJP, SpAK (Jakarta)• Prof. DR. Sudigdo Sastroasmoro, SpAK (Jakarta)• Dr. Ismet N Oesman, SpAK (Jakarta)• Dr. Najib Advani, SpAK, MMed Paed (Jakarta)• Dr. Syarif Rohimi, SpA (Jakarta)• Dr. Sasmito Nugroho, SpA (Yogyakarta)• Dr. Noormanto, SpAK (Yogyakarta)• Dr. Mahrus A. Rahman, SpAK (Surabaya)• Dr. Ria Nova, SpAK (Palembang)• All Fellow of School of Pediatric Cardiology
AcknowledgementAcknowledgement
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