1. Congenital Heart DiseasesCongenital Heart Diseases
CSN VittalCSN Vittal

3. Questions we face
1. Does the child have a heart
disease?
2. Is it congenital heart disease?
3. What type of lesion?
4. What is the severity of the lesion?

4. CHD
• DEFINITION
– PRESENT AT BIRTH
• INCIDENCE
– 6-8 PER 1000 LIVE BIRTHS IN
WESTERN COUNTRIES
• ETIOLOGY
– IN MAJORITY NOT KNOWN
– EQUAL IN BOTH SEXES

5. APPROACH TO CHD
• DOES THE PATIENT REALLY HAVE
CHD
• IS THE PATIENT CYANOTIC OR
ACYANOTIC
• IS PULM ARTERIAL BLOO FLOW
INC OR NOT
• LEFT OR RIGHT SIDE
• DOMINANT VENTRICLE
• PULM HTN PRESENT OR NOT

6. • HISTORY
– PRENATAL - DM,DRUG ABUSE,SLE
– INFANT - FEEDING DIFFICULTIES
• SYMPTOMS OF CHF
– POOR WEIGHT GAIN,DIFFICULTY IN FEEDING
– BREATHS TOO FAST & BREATHS BETTER
– WHEN HELD AGAIST THE SHOULDER
– PERSISTENT COUGH & WHEEZING
– IRRITABILITY,
– EXCESSIVE PERSPIRATION & RESTLESSNESS
– PUFFINESS OF FACE & PEDAL EDEMA.

7. Approach to CHD
• Does the child have Heart Disease?
NADAS Criteria
MAJOR
1. Systolic murmur Gr. III or
> intensity
2. Diastolic murmur
3. Cyanosis
4. CHF
MINOR
1. Systolic murmur Gr. II
intensity
2. Abnormal 2nd
Sound
3. Abnormal ECG
4. Abnormal Chest X Ray
5. Abnormal Blood Pressure
•Presence of 1 major or 2 minor criteria suggestPresence of 1 major or 2 minor criteria suggest
presence of Heart Diseasepresence of Heart Disease

8. Approach to CHD
• IS the Heart Disease Congenital?
CONGENITAL
1. Recognition early in age
2. Murmurs more
parasternally
3. Presence of central
cyanosis
4. Presence of extra-cardiac
anomalies
ACQUIRED
1. H/o. joint pains,
fever
2. Apical murmurs

9. Approach to Heart disease
Cyanotic CHDAcyanotic CHD
Patient
Apply NADAS’ Criteria
Heart Disease Present Heart Disease Absent
Re-evaluate after
Six months
L  R Shunts
Obstructive Lesions
Regurgitant lesions

10. CHDs
Shunting
Stenotic R - > L L - > R Mixing
Aortic
Stenosis
Tetrology of
Fallot
Patent
ducturs
Truncus
Pulmonic
Stenosis
Transposition VSD TAPVR
Coarctation Tricuspid
atresia
ASD HLH

11. Approach to CHD
• Is it Acyanotic or Cyanotic
CYANOTIC
1. Clinical cyanosis – Uniform or Differential
2. R/o. respiratory, CNS or metabolic causes
3. Presence of polycythemia
4. Fast regression of Thymus on X-Ray

12. Approach to CHD
• Pulmonary Blood Flow
Is it Normal / Increased / Decreased
INCREASED
1. Rec. respiratory infections
2. Cyanosis Mild in Cyanotic CHDs
3. Chest X- Ray
• Main pulmonary artery segment increased
in size
• Rt. And Lt. PA branches larger
• Plethoric lung fields

13. Second Heart Sound S2
S2
A2 P2
Accentuated
Diminished
Delayed
Early
SH, AR
Calc.AV, Aortic Atresia
AS, PDA, AR, LVF, LBBB
VSD, MR
PAH
PS, PA
PS, ASD, TAPVC, RBBB

14. Spliting of Second Heart Sound
Expiration InspirationSpliting
Normal
Wide & Variable
Paradoxical
Wide & Fixed
Single Second Sound
MR, VSD, PS
ASD, TAPVC, RBBB
AS, PDA, AR
TOF

16. Chief complaints
• Breathlessness
• Palpitation
• Chest pain
• Cough
• Edema
• Failure to thrive
• Joint pain / swelling
• Syncope

17. History
• Gestational and natal history
– Infections, (Rubella in 1st
trimester, Mumps, CMV,
HSV, Coxsackie virus B)
– Maternal Conditions
• Diabetes, advanced age, SLE, alcoholism,
cigarette smoking, etc.
– Medications
• Amphetamines, Phynetoin, trimethadone,
Progesterone – estrogen
– Birth weight
• IUGR, LGA

18. History
• Postnatal history
– Weight gain
• Feeding pattern
– Prolonged feeding time with multiple interruptions
– Dyspnoea during feeding
– Poor feeding
• Exercise Tolerance
– Fatigue while climbing, running, bicycle riding
• Cyanosis
– Onset, nature, spells
• Chest Pain
– Deep, heavy pressure, feeling of chocking, triggered by
exercise, not effected by respiration
• Palpitation
– PAT, MVP
• Syncope
– Differentiate from epilepsy, breath holding spells, hysterical
events

19. • Frequency of respiratory infections
– Rec. LRIs, Rec. wheezing or strider
• Joint symptoms
– Sore throat and joint symptoms
• Neurological symptoms
– Stroke – cyanotic CHDs, headache – hypoxia,
polycythemia, cerebral abscess
– Choreic movements
– Syncope – ventricular arrhythmias, long QT, MVP
• Medications
– Antihistamines, aminophylline
• Prior records
• Family History
– Hypertension, CHDs, Rh. fever
History

21. Physical Examination
• General examination
• Growth
• Respiration
• Excessive sweating
• Colour
– Cyanosis
– Pallor
– Jaundice
• Clubbing
• Edema
• Extracardiac anomalies

22. Pulse
• Peripheral pusles
– Lower limb pulses reduced in
coarctation of aorta
• Acyanosis with bradycardia
– AV canal defects
• Acyanosis with tachycardia
– VSD
• Acyanosis with wide pulse
pressure
– PDA, VSD with AR, AP window

23. JVP
• Prominent ‘a’ wave :
– Pulmonay stenosis
• Absent ‘a’ wave:
– Pulm. Hypertension due to L->R shunt
• V waves
– Tricuspid regurgitation

24. Signs & Symptoms of
Infective Endocarditis
• H/o CHD or any procedures
• Fever
• Chills
• Chest & abdominal pain
• Dyspnea
• Night sweats
• Weight loss
• CNS Manifestations
• Elevated temperature
• Tachycardia
• Embolic Phenomena –
Roth spot, osler nodes,
petechiae, splinter nail
bed hemorrages
• Janeway lesions
• New or changing
murmurs
• Splenomegaly
• Arthritis
• Heart failure
• Clubbing
• Metastatic infection

25. Signs & Symptoms of PHT
• History of Congenital Heart
disease
• Breathlessness, fatigue, syncope
on exertion
• Chest pain
• Hemoptysis

26. Signs & Symptoms of failure
• Feeding difficulty
• Hepatomegaly
• Edema on dependent parts
• Failure to thrive
• Feeding difficulty
• Forehead sweating
• Breathlessness

27. CHDs
• Specific lesions

28. Ventricular Septal Defects

29. Type of VSD
Anatomic location is important with regard to chance of
spontaneous closure, surgical approach, risk of conducting
system involvement and associated valvular dysfunction
1. Type I [5%] : Subarterial
(outlet, subpulmonic, supracristal or infundibular)
2. Type II [75-80%] : Perimembranous (subaortic)
3. Type III [9%] : Inlet (AV canal)
– Type IV [10%] : Muscular (Trabacular)
Anterior (marginal)
Swiss cheese type

33. Supracristal VSDs – Clinical
(subpulmonary, subarterial, conal defects)
• 5-7% of all VSDs in West, 30% in Far East
• Defect within outlet (conal) septum and part
of its rim is formed by aortic and pulm.
Annulus.
• Associated Aortic Incompetence Murmur
due to aortic leaflet prolapse
• Systolic murmur heard over pulmonic area
that radiates to the Lt. clavicle (similar to PS)

34. Perimembranous - Supracristal

35. Inlet (or AV canal) VSDs
• 5-8 % of all
VSDs
• Posterior and
inferior to the
perimembranou
s defect
• Beneath the
septal leaf let of
tricuspid valve

36. Muscular VSDs
• Representing 10% of isolated VSDs
• Completely surrounded by muscle
• May be in the
– inlet,
– trabecular, or
– outlet portion of the interventricular septum.
• Can be multiple, and have been described as
having a "swiss-cheese" appearance.
• Depicted by careful echocardiography,
particularly with color doppler imaging

37. Muscular VSDs - Clinical
• High frequency systolic murmur which
ends prior to systole

39. Clinical Manifestations
History
1. With a small VSD, the patient is asymptomatic with
normal growth and development.
2. With a moderate to large VSD, delayed growth and
development, decreased exercise tolerance, repeated
pulmonary infections, and CHF are relatively common
during infancy.
3. With long-standing pulmonary hypertension, a history
of cyanosis and a decreased level of activitymay be
present.

40. Clinical Manifestations
Physical Examination
Small VSD : Holosystolic murmur
Well developed and acyanotic

41. Clinical Manifestations
Physical Examination
Large VSD :
– Holosystolic murmur
– systolic thrill may be present at the lower left sternal border.
Precordial bulge and hyperactivity are present with a large-
shunt VSD.

42. Size of the Defect
1. Large : (nonrestrictive) >10mm
– Diameter of the defect equal to diameter of the aortic orifice;
– RV systolic pressure is systemic, &
– Degree of L-> R shunt depends on pulmonary vascular
resistance
1. Moderate (restrictive) 5 - 10mm
• Diameter of the defect < that of aortic orifice
• RV pressure is half to 2/3 systemic &
• L-R shunt is > 2:1
1. Small (restrictive) < 5 mm
• Diameter of the defect < 1/3 the size of aortic orifice
• RV pressure is normal &
• L-R shunt is < 2:1

43. Electrocardiography
1. With a small VSD, the ECG is normal.
2. With a moderate VSD, left ventricular hypertrophy
(LVH) and occasional left atrial hypertrophy (LAH)
may be seen.
3. With a large defect, the ECG shows biventricular
hypertrophy (BVH) with or without
4. If pulmonary vascular obstructive disease develops,
the ECG shows RVH only.

44. Electrocardiography
•Biventricular hypertrophy with left dominance.
•Note that V2 and V4 are in 1/2 standardization

45. X-Ray
• Heart size is moderately increased, with enlargement on both sides.
• Pulmonary vascular markings are increased, with a prominent main pulmonary artery
segment.
• In pulmonary vascular obstructive disease (PVOD), the main PA and the hilar PAs
enlarge noticeably, but the peripheral lung fields are ischemic

46. Echocardiogram
• Standard parasternal long-axis view
The ventricular septum consists of (from the aortic valve toward the
apex)
1. the infracristal outlet (Inf-C outlet)
2. septum (the VSD of TOF is seen here) and
3. the trabecular (middle and apical) septum.

47. Echocardiogram
• Parasternal RVOT view
The ventricular septum consists of (from the aortic valve toward the
apex)
1. supracristal outlet (Sup-C outlet) septum and
2. the trabecular septum

48. Echocardiogram
• Parasternal short-axis view showing the
aortic valve
1. the membranous septum is toward the 10 o'clock direction,
2. the infracristal outlet septum at the 12 o'clock direction, and
3. the supracristal outlet septum immediately adjacent to the pulmonary
valve

49. Echocardiogram
• Parasternal short-axis view showing the
aortic valve
1. the membranous septum is toward the 10 o'clock direction,
2. the infracristal outlet septum at the 12 o'clock direction, and
3. the supracristal outlet septum immediately adjacent to the pulmonary
valve

50. Echocardiogram
• Parasternal short-axis - The ventricular
septum at the mitral valve
1. the posterior muscular septum, is the inlet (INLET) septum.

51. Echocardiogram
• Parasternal short-axis - The ventricular
septum at at the papillary muscle (B3) is all
trabecular septum, so that one can easily classify
the defect into
1. Anterior (ANT),
2. middle (MID), and
3. posterior (POST) trabecular defects

52. Echocardiogram
• apical four-chamber view showing the
coronary sinus (C1),
• the ventricular septum is the posterior (POST)
trabecular septum.
In the standard apical four-chamber view, the membranous septum is not visible

53. Echocardiogram
In the apical four-chamber
view showing both AV
valves (C2),
1. the septum immediately beneath the
tricuspid valve is the inlet septum
(INLET) and the remainder is the
middle and apical septa.
2. The thin septum between the insertion
of the mitral and tricuspid valves is the
atrioventricular septum (C2), a defect
that can result in an LV-to-RA shunt.

54. Echocardiogram
• In the apical “five-chamber” view (C3),
• the membranous (MEMB) septum is seen beneath the
aortic valve and below it is the it is theinfracristal outlet
(Inf-C outlet) septum.

55. Echocardiogram
• Subcostal four-chamber view (D1)
• The ventricular septum seen similar to the apical
four-chamber view (C2).

56. Echocardiogram
• Subcostal four-chamber view
• With anterior angulation of the horizontal
transducer, the LVOT is seen (D2) and the
septum seen here is similar to the apical five-
chamber view (C3).

57. Echocardiogram
• Subcostal four-chamber view
• With further anterior angulation, the RVOT is seen
(D3). The superior part is the supracristal outlet
(Sup-C outlet) septum and the inferior part is the
anterior (ANT) trabecular septum (D3).

58. Echocardiogram
• The subcostal short-axis view showing
the RVOT (E1) is orthogonal to the
standard subcostal four-chamber view and
is an important view for evaluating the site
and size of a VSD.
• In this view both supracristal outlet (Sup-C outlet) and
infracristal outlet (Inf-C outlet) septa (in that order) are
seen beneath the pulmonary valve and the trabecular
septum (ANT and POST) is seen apical ward.
• The ventricular septum seen at the papillary muscle (E2)
is all trabecular septum and is similar to the parasternal
short-axis view (B3).

59. Echocardiogram

60. Echocardiogram
• The membranous septum is closely related to the
aortic valve.
• In the apical and subcostal “five-chamber” views,
it is seen in the LV outflow tract just under the
aortic valve
• In the parasternal short-axis view at the level of
aortic valve, it is seen adjacent to the tricuspid
valve
• These are the best views to confirm the membranous VSD.

61. Echocardiogram
• Two-dimensional echocardiogram showing membranous ventricular septal defect
(VSD). The membranous VSD
• is seen underneath the aortic valve in the left ventricular outflow tract (in the apical “five-
chamber” view).

64. Natural History
1. Spontaneous closure occurs in 30% to 40% of patients with
membranous VSDs and muscular VSDs during the first 6 months of
life. It occurs more frequently in small defects. These VSDs do not
become bigger with age; rather, they decrease in size. However, inlet
defects and outlet (infundibular) defects do not become smaller or
close spontaneously.
2. CHF develops in infants with large VSDs but usually not until 6 to
8 weeks of age.
3. Pulmonary vascular obstructive disease may begin to develop as
early as 6 to 12 months of age in patients with large VSDs, but the
resulting right-to-left shunt usually does not develop until the teenage
years.
4. Infundibular stenosis may develop in some infants with large
defects and result in a decrease in the magnitude of the left-to-right
shunt (i.e., acyanotic TOF), with an occasional occurrence of a right-
to-left shunt.
5. Infective endocarditis rarely occurs.

68. Atrial Septal
Defect
• An atrial septal defect (ASD) is anAn atrial septal defect (ASD) is an
opening in the atrial septum allowingopening in the atrial septum allowing
blood to shunt between left and rightblood to shunt between left and right
atria.atria.
• First described by Rokitansky inFirst described by Rokitansky in
18751875
• Clinical features first described byClinical features first described by
Bedford, Pepp and Parkinson inBedford, Pepp and Parkinson in
19411941

69. Atrial Septal Defects
1. Ostium Secundum: [most common CHD in adults]
Defect involves tissue of the septum primum at or
around the area of the foramen ovale
1. Sinus Venosus (sinoseptal defects):
Defects of the embryological origin of the junction of
superior and inferior vena cava into the right atrium
The latter defects are often associated with partial
anomalous pulmonary venous return.
1. Ostium Primum:
Defect involves endocardial cushion tissue.
4. Raghib type
Absent coronary sinus with Left SVC connection to
left atrium.
5. Multiple coalescent defects
Types:

70. Classification of ASD

73. Classification of ASDs
• Mild :
Pulm. Art. / Aortic flow ratio < 2:1
(QP – QS Ratio)
• Mod. to Large :
Pulm. Art. / Aortic flow ratio > 2:1
Depending upon Shunt Ratio :

74. Classification of ASDs
• Small : ASD area < 1 cm2
(Asymptomatic)
• Moderate : ASD area 1 - 3 cm2
(Asymptomatic or mild symptoms
due to thromboembolism, arrhythmias)
• Large : ASD area > 3 cm2
(Symptomatic, RV overload,
thromboembolism, arrhythmias)
Depending upon Size :

75. Hemodynamics
• Magnitude of L -> R shunt depends
upon
- Size of the defect
- Relative compliance of the ventricles
- Relative resistance in both the
pulmonary and systemic circulations

77.  RV Conduction delay (rSR’ pattern)

78. Sino-septal defects
• Involve the area of the atrial septum derived from the
sinus venosus.
• Most commonly this includes defects that occur at the
junction of the superior vena cava and the right atrium,
• The right upper pulmonary veins typically enter the left
atrium superiorly and just to the left of the atrial septum
and sinus venosus region. When a defect of the superior
sinus venosus exists, the flow from these veins may be
directed toward the right atrium through the sinus venosus
defect.
• Alternatively, these veins may truly be anomalous in their
drainage and enter the right atrium directly. These defects
are known as sinus venosus defects.

80. AVSD
• Atrioventricular septal defects (AVSD) result
from abnormal development of the membranous
and muscular atrioventricular septum.
Depending on severity, the defect can be
classified as complete or partial.
• The ventricular septal defect is located at the
'inlet' portion of the ventricle and the atrial septal
defect occurs as an ostium primum type (a
deficiency of the septum primum in its inferior
and anterior aspect).
• AVSD can accompany other complex congenital
heart disorders.

82. ASDs – Echocardiogram
• Secundum atrial defects are well defined on echo from
subcostal view and the defect can be sized.
• With use of color Doppler flow mapping, a qualitative
assessment of shunting and its direction can be
obtained.
• The four-chamber apical view can assess the shunt-
volume effects on size and wall thickness of the right
ventricle, but is less reliable for accurately measuring
the defect.
• The parasternal ventricular short axis view may
show a flattened interventricular septum during diastole
due to right ventricular volume overload.
• TEE can be extremely useful in diagnosis and
management since it accurately displays the region of
the atrial fossa where the secundum defects occur and
can determine eligibility for catheter-guided closure.

86. Course & Prognosis
• Most common CHD in adults (OS Type)
• Patients can pass through 3rd
or 4th
decade
with little hardship
• Life expectancy is shortened
• Recurrent respiratory infections due to shunt
• Effort intolerance and fatigue common
• Infective endocarditis rare –
• Lack of jet lesion
• Absence of turbulence because of low
velocity of flow across defect

87. Course & Prognosis
• Older patients – deteriorate rapidly
• Degeneration of coronary artery, systemic
hypertension leading to LVF
• Atrial arrhythmias : fibrillation, flutter, PAT
• Eisenmenger’s syndrome (seldom < 20
yrs)
• 5% infants with large ASDs succumb as
early as 1st
week of life
• Some symptomatic patients may improve
due to spontaneous closure

93. • Surgical or transcatheter device closure is advised for all
symptomatic patients and also for asymptomatic patients with a
Qp : Qs ratio of at least 2 : 1.

94. Patent Ductus Arteriosus
Types:Types:
1. Large PDA : significant LV overload, CHF, severe
PAH, murmur unlikely to be loud or continuous
2. Moderate PDA : some Lt heart overload, mild to
moderate PAH, no/mild CHF, murmur is continuous
3. Small PDA : minimal or no Lt heart overload, no
PAH or CHF, murmur may be continuous or only
systolic
4. Silent PDA : No murmur, no PAH. Diagnosed only
on echo Doppler

96. PDA - Anatomy

97. Clinical Features
1. Tachycardia and tachypnea - with CHF.
2. Bounding peripheral pulses with wide pulse pressure
3. The precordium is hyperactive.
4. A systolic thrill may be present at the upper left sternal
border
5. A grade 1 to 4/6 continuous (“machinery”) murmur is best
audible at the left infraclavicular area or upper left sternal
border.
6. If pulmonary vascular obstructive disease develops, a
right-to-left ductal shunt results in cyanosis only in the
lower half of the body (i.e., differential cyanosis).

98. ECG
• A normal ECG or LVH is seen with small to
moderate PDA.
• BVH is seen with large PDA.
• If pulmonary vascular obstructive disease
develops, RVH is present.

99. X-Ray
1. Chest x-ray films may be normal with a small-
shunt PDA.
2. Cardiomegaly of varying degrees occurs in
moderate- to large-shunt PDA with enlargement
of the LA, LV, and ascending aorta. Pulmonary
vascular markings are increased.
3. With pulmonary vascular obstructive disease,
the heart size becomes normal, with a marked
prominence of the PA segment and hilar vessels.

100. PDA
Diagnostic criteria
• Lumen of the
vessel visualized
along the entire
length.
• LAE
• LV dilatation

101. PDA - Hemodynamics

102. PDA - Echo
Note: The
Shunt
going from
below
upwards in
the
pulmonary
artery

103. PDA - Echo
• Parasternal short-axis view demonstrating patent ductus
arteriosus (PDA) that connects the main pulmonary
artery (MPA) and the descending aorta

104. Natural History of PDA
• Unlike PDA of prematures spontaneous
closure of PDA does not occur. PDA of
term are due to structural abnormality of
ductal smooth muscle.
• PVOD, CHF or recurrent pneumonia.
• Infective endocarditis may occur
• Rarely, aneurysm of PDA may develop
and possibly rupture in adult life.

107. DD
1. Coronary arteriovenous fistula
2. Systemic arteriovenous fistula
3. Pulmonary arteriovenous fistula
4. Venous hum
5. Collaterals in COA
6. VSD with AR
7. Absence of the pulmonary valve
8. Persistent truncus arteriosus
9. Aortopulmonary septal defect (aortopulmonary window):
10. Peripheral PA stenosis
11. Ruptured sinus of Valsalva aneurysm:
12. Total anomalous pulmonary venous return (TAPVR) draining into
the RA:

108. Management - Medical
1. Indomethacin is ineffective in term infants with
PDA and should not be used.
2. Standard anticongestive measures with digoxin
and diuretics are indicated when CHF develops.
3. No exercise restriction is needed in the
absence of pulmonary hypertension.
4. Prophylaxis for bacterial endocarditis is
indicated when indications arise.

109. Management - Nonsugical Closure
Small ductus less than 4 mm in diameter are closed by
Gianturco stainless coils and larger ones by an Amplatzer
PDA device.
Advantages
– no need for general anesthesia,
– Shorter hospital stay and convalescent period,
– Elimination of a thoracotomy scar
Disadvantages
– residual leaks,
– PA coil embolization,
– hemolysis,
– left PA stenosis,
– aortic occlusion with the Amplatzer device, and
– femoral vessel occlusion.

110. Timing of Closure
• Large/moderate PDA with CHF, PAH – Early
closure by 3-6 mo. (Class I)
• Moderate PDA, no CHF, PAH : 6 mo.- 1 yr –
(Class I). If failure to thrive – closure can be
earlier (class II)
• Small PDA – At 12 to 18 mo. (class I)
• Silent PDA – Closure not recommended (class
III)

111. Coarctation of Aorta (COA)
• 8- 10 % of all CHD.
• M:F = 2:1. 30% of Turners Syndrome.
• 85% of COA have bicuspid valve.
• Poor feeding, dyspnea & poor weight gain,
& acute circulatory shock in first 6 weeks .
• 20-30% of COA develop CHF by 3 months

112. Coarctation of the aorta
Diagnostic finding
Aortic lumen is narrowed,
typically distal to the left
subclavian artery.
Hypoplastic aortic arch
Post stenotic dilatation of
the aorta.
Bicuspid aortic valve.
Doppler will show the
severity of obstruction.

113. Coarctation of the aorta -
Hemodynamics

114. Coarctation of the aorta -
Types

115. Natural History of COA
• Bicuspid valve may cause stenosis or
regurgitation with age.
• SBE may occur on either aortic valve or
on coarctation.
• LV failure, rupture of aorta, ICH,
hypertensive encephalopathy may
develop during childhood.

116. Coractation of Aorta
• Diagnosis :
– Absent femoral pulses
– BP in upper and lower limbs
– X- Ray chest
– Echo
– CT angiography
– MRI

117. Coractation of Aorta
• Timing of Intervention :
– With LVH / CHF or severe upper limb hypertension :
Immediate intervention (Class I)
– Normal LVH, no CHF & mild upper limb
hypertension : Intervention beyond 3-6 mo. Age
(Class IIa)
– No hypertension, no heart failure, normal ventricular
function : Intervention at 1-2 yrs of age. (Class IIa)
– Intervention is not indicated if Doppler gradient across
coarct segment < 20 mm Hg with normal LV function.
(Class III)

118. Coractation of Aorta
• Mode of Intervention :
– Balloon dilatation of surgery for children> 6 mo. Age
– Surgical repair for infants < 6 mo. Age
– Balloon dilatation with stent development in children >
10 yrs age
– Elective endovascular stenting of aorta is
contraindicated for children < 10 yrs of age (class III)

119. Tetrology of Fallot

120. Infective Endocarditis Prophylaxis
• Every child with CHD must be advised to maintain
good oral hygiene and regular dental check up
• Unrepaired CCHDs are high risk conditions for IE.
So prophylaxis is mandatory
• ASD (secundum type) and valvular PS are low risk
conditions for IE – prophylaxis not recommended
• Other acyanotic CHDs including bicuspid aortic valve
are moderate risk & prophylaxis is recommended
• Repaired CHDs with prosthetic material need
prophylaxis for first 6 mo. after procedure
• Device placement by transcatheter route also require
prophylaxis for the first 6 mo.