2. SCOPE OF THIS TALK
Pediatric EGG:
Differences from adults
Developmental changes with age
ECG in some congenital heart diseases
2
3. MIND THESE POINTSâŚ
⢠Children are not small adults
⢠Small in size, small chest size
⢠Normal criteria which are for adultsď Cannot be followed in kids
⢠Z Scores
3
4. WHO AM I??
⢠Dutch physiologist
⢠Nobel Prize in Physiology: 1924
4
7. DEVELOPMENTAL CHANGES WITH AGE
⢠Decrease in HR
⢠Increase in P-wave duration, PR interval, QRS duration
⢠QRS Voltage: Low during 1st several months
⢠Mean QRS axis in frontal plane: Moves from right to left
⢠Increase in PR interval+ QRS duration: Changes in size of heart /AV node
7
8. VENTRICULAR DOMINANCE
⢠Newborn: QRS potentials result from RVď RV dominance
⢠Transition of ECG from RV dominance at birth to pattern of LV: Lags behind
hemodynamic changes
⢠Loss of RV dominance:
⢠Starts at 1 month of age
⢠LV dominance is well established by 1 year
8
9. VENTRICULAR DOMINANCE
⢠1st several weeks:
⢠Tall R+ small S in right and anterior precordium: V3R, V4R, and V1
⢠Deep S+ small R in left precordium: V6 and V7
⢠Corresponds to clockwise vector loop in horizontal plane
⢠2 months of age:
⢠Precordial leads progress to more adult pattern
⢠Deeper S waves in right and taller R waves in left leads
⢠Counterclockwise vector loop in horizontal plane
⢠1 year: Precordial R wave progression similar to adults
9
10. T WAVE CHANGES
⢠Rapid changes of RV pressure after birth: Great effect on T wave
⢠1st minutes after birth, T-wave vector: Anterior and to left i.e upright in V1+ V6
⢠May swing rightward in next several hours: Flattening/ inversion of T in left
lateral leads
10
11. T WAVE CHANGES
⢠Next 7 days:
⢠T-wave vector moves posterior+ leftward
⢠Inverted T in V1+ upright T in V6
⢠After 7- 8 years: Becomes upright again in V1
⢠May remain inverted throughout adolescence: Juvenile T-wave pattern
11
12. LETS THINKâŚ
⢠Neonates with CCHD have RAD+ RVH
⢠RAD+ RV dominance ď Rule in normal infants too
⢠SO, RVH WILL BE SUGGESTED BY??
⢠AXIS> +120 degrees
⢠Upright T in V1/ V3R
⢠Monophasic tall R in V1/ V3R
⢠RV strain pattern
12
13. PRE-TERM INFANTS: HOW R THEY DIFFERENT??
⢠Notable for its shorter QRS duration, PR interval and QT interval
⢠Less RV dominance at birth than ECG of full-term infant
⢠Precordial voltages: Lower in 1-year-old infant who was premature
⢠Intrinsic myocardial differences of premature or to altered cardiacâtorso
geometry: Unknown
13
16. FALLOTâS TETROLOGY
⢠P waves: Often normal/ May be peaked but not tall
⢠P wave duration: Shortď Under filled and relatively
small LA writes terminal force
⢠PR interval: Normalď Conduction system normal
⢠QRS complex: RAD, Normal duration
⢠LAD + Counterclockwise depolarization in Fallotâs
tetralogy??
ď TOF WITH AVCD 16
17. FALLOTâS TETROLOGY
⢠RV hypertrophy: Tall monophasic R wave confined to V1
⢠Abrupt change to an rS pattern in V2: Sudden transition
⢠Depth of Q waves+ amplitude of R waves in V5-6: Indicate LV filling
⢠Reduced PBF+ underfilled LV ď rS patterns in V2-6
⢠A balanced shunt accompanied by small q waves+ well-developed R waves in
V5-6
⢠Inverted right precordial T waves: Seldom occur, WHY??
⢠RVSP seldom exceeds systemic pressure 17
18. TOF WITH PA
⢠PA+ Abundant collateral arterial
circulationď P waves broad and bifid
⢠Q waves with well-developed R wavesď
Leads V5-6
⢠ST segment+ T wave abnormalitiesď
May be found in midprecordial leads
18
19. PROBLEM WITH DCRVâŚ
⢠Increase in RV pressure+ mass
confined to hypertensive
proximal compartment
⢠Hence, precordial leads display
normal QRS progression
from V1-6
ANY CLUE?? 19
20. SOâŚ
⢠Upright T wave in V3R
may be the only ECG
sign of right ventricular
hypertrophy
20
21. TOF WITH ABSCENT PULMONARY VALVE
⢠Tall monophasic R wave in
lead V1 extends to adjacent
precordial leads, in contrast
to Fallotâs Tetralogy
21
23. DORV, SUB AORTIC VSD AND NO PS
⢠P waves: Peaked
⢠Peaked RA P waves associated with bifid broad LA P waves when PBF increases
⢠PR prolongation: Due to prolonged course of AV bundle
⢠LAD with counterclockwise depolarization
⢠Elevated PVR associated with RAD and pure RVH
⢠LV volume overload indicated by large RS complexes in midprecordial leads and
tall R waves in left precordial leads
23
24. LETS TRY THIS (3)âŚ
⢠2 y, girl
⢠Cyanosis, No RD
⢠DIAGNOSIS⌠CLUEâŚ
⢠TOF PHYSIOLOGY, RAD,
CC-W LOOP
24
25. DORV, SUB AORTIC VSD WITH PS
MILD STENOSIS: SIMILAR TO NO PS
⢠Peaked and broad P waves
⢠Prolonged PR interval
⢠Left axis deviation
⢠As stenosis increasesď QRS axis
becomes vertical or rightward
⢠Distinctive feature: Persistence of
counterclockwise initial forces
⢠Terminal forces are deep and prolonged
with broad slurred S waves in leads 1,
aVL, and V5-6 and a broad R wave in
lead aVR
⢠DORV, PA: ECG similar to TOF with PA
25
26. TAUSSIG-BING ANOMALY
⢠PR interval prolongation:
Less frequent than DORV,
subaortic VSD
⢠Biatrial P wave
abnormalities: RV failure
⢠QRS axis: Vertical or
rightward with clockwise
depolarization
26
27. TAUSSIG-BING ANOMALY
⢠RV hypertrophy:
⢠Tall R waves in V1 and aVR and
⢠Deep S waves in left precordial leads
⢠Volume overload of LV: Well developed R waves in V5-6
27
28. TGA
⢠Tall peaked right atrial P
waves: Mean RA pressure
increased (systemic
circulation)
⢠LA P wave abnormalities:
Reserved for patients with
large ASD+ increased PBF
28
29. TGA CONTâŚ
QRS axis :
⢠RAD: Most striking when ASD occurs
with increased PBF, normal PA pressure
⢠RAD occurs when LV volume overload
is curtailed by pulmonary vascular
disease or PS
⢠BVH: Nonrestrictive VSD with low PVR+
both volume+ pressure overload of LV
29
30. TGA CONTâŚ
⢠Right precordial T waves seldom
deeply inverted, even the systemic
RV is volume-overloaded
⢠Not only positive but tend to be
distinctly taller than left precordial
T waves
30
31. LETS TRY THIS (4)âŚ
⢠24 year old, male
⢠Acyanotic, no respiratory
distress
⢠Presented with history of
palpitations
⢠DIAGNOSISâŚCLUESâŚ
⢠Abscent q in lt prec l
⢠QS pattern in rt prec leads
31
32. CC-TGA
Pathophysiology:
⢠Atrial septum is malaligned with inlet ventricular septum
⢠Anomalous anterior AV node instead of regular AV node makes contact with
right and left bundle branches
⢠Long penetrating A-V bundle
⢠Conduction fibres replaced with fibrous tissueď Responsible for AV block
32
33. CC-TGA CONTâŚ
Scalar ECG exhibits:
Disturbances in conduction and rhythm
QRS and T wave patterns that reflect ventricular inversion
AV Blocks:
⢠Varying degrees of AV block in how much percent of people??
⢠75%
⢠Overall incidence rate of CHB??
⢠30%
⢠Degree of block varies from time to time in same patient
33
34. CC-TGA CONTâŚ
⢠Absent Q waves in left sided
precordial leads
⢠QS pattern in Rt sided leads
⢠Marked LAD
⢠RAD in case of Ltď Rt shunts and PS
⢠Lt Ebsteins AV valve anamoly
associated with accessory pathways
⢠Lt AVVR associated with P wave
changes and AF
34
35. LETS TRY THIS (5)âŚ
⢠2 months old child
⢠Cyanosis
⢠No RD
⢠Left apex
⢠DIAGNOSISâŚCLUEâŚ
⢠LAD, LVH
35
36. TRICUSPID ATRESIA WITH NRGA
⢠Tall peaked RA P waves
⢠LA seldom represented, even it
receives entire return from
both systemic+ pulmonary
veins
⢠LAD+ LVH in cyanotic ď
Tricuspid atresia with
restrictive VSD, NRGA
36
37. TRICUSPID ATRESIA CONTâŚ
⢠Cause of LAD in tricuspid atresia: Not been firmly established
⢠Early arborization of left bundle accounts for LAD
⢠LVH ď
⢠Deep S waves in right precordial leads and
⢠Tall R waves with repolarization abnormalities i.e inverted T
waves in leads aVL and V5-6
37
38. TRICUSPID ATRESIA WITH TRANSPOSITION
⢠Typically occurs with a
nonrestrictive VSD and a well-
developed RV
⢠âPBF adds to LA volumeď Lt+ Rt
atria enlargement coexistď P
waves broad, bifid, peaked
⢠Relatively well-developed RV
contributes to normal QRS axis
38
39. TRUNCUS ARTERIOSUS
⢠Tall, bifid, broad P waves
⢠âPBF ď QRS axis rightward
and clockwise depolarisation
⢠âPBFď normal or Lt axis
⢠Precordial leads exhibit
biventricular hypertrophy
⢠(KATZ WACHTEL phenomenon)
39
41. SO IN TOF PHYSIOLOGYâŚ
⢠TOF: Cyanosis/ Murmur/No CHF/ RAD+
RVH/C-W loop/ Early transition from
V1ď V2 (RVH with strainď Strict NO NO)
⢠With LAD:
⢠AVCD with PS
⢠CC-TGA with PS
⢠TA
⢠With 1st deg AV block:
⢠AVCD with PS
⢠DORV, VSD, PS
⢠CC-TGA, VSD, PS
⢠No q in V5/V6: Single ventricle
⢠Q in V1, No Q in V6:
⢠CC-TGA, VSD, PS
⢠Extreme RAD:
⢠DORV, VSD, PS
⢠Associated ASD
41
42. LETS TRY THIS (6)âŚ
⢠1 month old child
⢠Acyonotic
⢠Severe respiratory distress
⢠DIAGNOSIS??
⢠LVH, LAD, CC-W LOOP
42
44. DEEP NARROW Q WAVES IN ALCAPAâŚ
⢠Sometimes q waves in lead aVL
can equal or exceed height of
R wave
⢠Q waves rare in rt precordial
leads
44
45. ALCAPA CONTâŚ
45
⢠Posterobasal region of LV selectively
increased in massď Capacity of
immature cardiomyocytes to replicate in
response to hypoxemiaď LVH + LAD
⢠Left atrial P wave abnormalities occur
because of mitral regurgitation
46. MI PATTERN IN ECG
⢠ALCAPA
⢠Kawasaki disease
⢠Myocarditis
⢠Pompe disease
46
48. WHO COINED THE TERM??
⢠1st female president of AHA
⢠Founder of Pediatric Cardiology
48
49. EBSTEINâS ANOMALY
Himalayan P waves: Prolonged aberrant conduction in enlarged RA
PR interval: Prolonged
Duration of PR interval and width of P wave correlate with prolonged conduction in
large RA
In presence of preexcitationď PR interval usually but not invariably short
However, a short PR interval occasionally occurs without a delta wave and without
a history of paroxysmal rapid heart action
49
50. EBSTEINâS ANOMALY CONTâŚ
⢠75% to 95%: QRS characterized by RV conduction defect of RBB type
⢠QRS prolongation: Result of prolonged activation of atrialized RV
⢠Conduction defect is therefore distal to RBB and is sometimes present despite a
septal accessory pathway
⢠A distinctive second QRS complex originates in atrialized RV according to
intracardiac mapping
50
51. EBSTEINâS ANOMALY CONTâŚ
⢠QRS axis is inferior: Although a splintered polyphasic QRS makes axis difficult to
determine
⢠LAD represents type B preexcitation
⢠Deep Q waves appear in leads 2, 3 and aVF but most important are right
precordial Q waves in lead V1 or in leads V1-4
⢠This distinctive Q wave pattern: Because precordial surface leads record RV
intracavitary potentials unusually far leftward as a result of large size of RA
⢠Prominent Q waves in right precordial leads can be misleading when adults with
Ebsteinâs anomaly present with chest pain 51
52. EBSTEINâS ANOMALY CONTâŚ
⢠W-P-W preexcitation: 5% to 25%
⢠Downward displacement of septal tricuspid leaflet is accompanied by
discontinuity between central fibrous body and septal A-V ringď Creates
substrate for preexcitation
⢠The only CCHD consistently associated with preexcitation, which is uniformly via
a right bypass tract (i.e., type B W-P-W)
⢠Combination of type B preexcitation+ cyanosisď Presumptive evidence
⢠Accessory pathway conduction can be permanent/ intermittent and can occur
without delta waves
⢠SVT, A fib, AF: 25%- 30%
⢠Prolonged PR interval may progress to CHB
52
54. VSD
Restrictive:
⢠Normal ECG
⢠Increased incidence of conduction disturbances if septal aneurysm
Moderately restrictive :
⢠Broad+ notched P wave in lead 1 and 2, Broad deep terminal force in lead V1
⢠Normal qrs axis
⢠LV overload: Tall R waves+ T waves in leads 2,3 and avF; Prominent q waves and
and R waves in V5-V6
54
55. VSD CONTâŚ
Large unrestrictive:
Both Rt and Lt atrial P wave i.e broad and notched, abnormalities seen in leads
2 and V1-V2
QRS axis moderately shifts to right
Biventricular hypertrophy: Tall R waves in both rt and lt sided leads, large
equidiphasic waves in mid precordial leads (KATZ WACHTEL phenomenon)
Eisenmengerisation:
Normal or peaked p waves
RAD
Monophasic R waves in V1 and prominent S wave in Lt precordial leads
55
56. VSD CONTâŚ
PERIMEMBRANOUS
VSD
INLET VSD MULTIPLE VSDs
With septal aneurysm-left
axis deviation
Counterclockwise loop,
LAD and prolonged PR
interval
Clockwise loop with left
axis deviation
56
59. WHAT DO YOU THINK???
⢠3 years old, asymptomatic kid, ESM pulmonary area, precordium:
Mildly hyperkinetic
⢠ECG: RAD+ Rsr in v1/ V3R
⢠DIAGNOSIS??
⢠Secundum ASD: RSR: 85-95%
59
60. SECUNDUM ASD
⢠Clockwise loop with vertical axis
⢠Right axis with PAH
⢠Left-axis deviation : Holt-Oram syndrome/LAHB
⢠RAE
⢠P wave axis-inferior and to left with upright p in inferior leads
⢠PR interval: May be prolonged, 1st degree AV block
60
61. SECUNDUM ASD CONTâŚ
⢠Wide QRS
⢠RBBB
⢠Râ In v1 and AVR is slurred
⢠Crochetage: Specific for ASD if present in all inferior leads
⢠Atrial fibrillation, Atrial flutter
61
63. FOLLOW UP
⢠PAH
⢠rsRâ gives way to R in v1
⢠Signs of PAH: RAD/RVH
⢠After surgery R may revert to rsRâ in 40% of patients
63
64. PRIMUM ASD
⢠Counterclockwise loop
⢠LAD
⢠PR prolongation
⢠RVH: Tall R in v1,deep s in v6
⢠Left A-V valve regurgitation: LVH
⢠Notching of s wave upstrokes in inferior leads
64
65. ASD HOW TO APPROACH
ASD
CLOCKWISE LOOP
SECUNDUM ASD: P -
wave axis
normal
Crochetage+
SV ASD: P- wave axis
superior
Crochetage+
COUNTER CLOCKWISE
LOOP
PRIMUM ASD: LAD
65
66. LETS SEE THIS CONDITIONâŚ
⢠Neonate with RDS, cyanosis, RVH with strain- Possibilities??
⢠TAPVC (Obstructed/ Unobstructed)
⢠PPHN
⢠Severe COA with BV dysfunction
66
67. A FEW WORDS ABOUT TAPVC
⢠Resembles secundum ASD
⢠PR interval tends to be prolonged
⢠A fib in older patients as it does with OS ASD
⢠Presence of pulmonary hypertension:
⢠Peaked right atrial P waves
⢠RAD
⢠Tall right precordial R waves
⢠Inverted T waves
⢠Deep left precordial S waves of RVH
67
68. LETS SEE THISâŚ
⢠Asymptomatic kid, prominent ESM over 2nd left space
⢠ECG: RVH, Tall R waves in V1/ V3R
⢠DIAGNOSIS??
⢠PS
⢠If ECG is: RSQ, THEN?????
⢠Dysplastic PV of Noonanâs Syndrome
68
69. DCM/ MYOCARDITIS
⢠Recent onset CHF, insignificant murmur
⢠DIAGNOSTIC TRIAD (50%):
⢠Low voltage QRS
⢠ST segment+ T wave changes
⢠Tachycardia
69