ECG IN CONGENITAL HEART

DISEASE
 Significance of ECG
• ECG is a simple non invasive tool to assist in
the diagnosis of congenital heart disease.
• In arrhythmias-no substitute
• In CHD assists in –
1. Diagnosis
2. Severity of the condition
3. Complications
4. Associated conditions
 OVERVIEW

• Normal ECG changes in children

• Situs & Ventricular position identification
• Common acyanotic heart disease
• Common cyanotic heart disease
• Others
 NORMAL ECG CHANGES IN
CHILDREN
• A positive correlation between ECG and
hemodynamic findings has been
described.
• ECG changes appear to be determined
largely by the load imposed on the
ventricles
 At birth –PVR > SVR; the pressure in both ventricles is
presumably equal.

With expansion of the lungs and ligation of the cord, PVR falls
rapidly ,SVR rises, right to left shunt across ductus ceases

RV thickness remains higher than left

initially

Thus ,at birth Tall R waves are recorded in right and

especially mid-precordial leads and deep S waves in left leads
Changes in hemodynamics at birth are better reflected by T wave
variability than changes in QRS complex

Positive on day 0 to Day 5-7,It becomes negative by

day 5 and remains so throughout infancy and early
childhood
 During first 72 hrs – RV forces more prominent than LV.
Loop is usually clockwise

By 6 weeks to 2 months –loop changes to counterclockwise

loop

Loop is most anterior by 2 months age, by 1 – 2 yrs becomes

more posterior

ECG Change from RV dominance to LV dominance lags behind

the changes in ventricular weight ratio.
LV:RV weights = equal by 1 month age,2.5-3:1 by 3 to 6 months
age,
But ECG changes to normal adult LV dominance by 1 to 3 yrs age
• NEW BORN

• FIRST 72 hrs

• 1 WEEK TO 1
MONTH
• 1 MONTH TO 6
MONTHS

• 6 MONTHS TO 3 YRS

• 3 YRS TO 8 YRS

• 8 TO 16 YRS
IDENTIFICATION OF SITUS AND
VENTRICULAR POSITION BY
ECG
 IDENTIFYING SITUS
• In situs solitus,Right atrial focus-P wave
axis is normal, approx +60 degrees
Positive P in I and AVF ,Inverted in avR
• In situs inversus,left atrial focus – P wave
axis is shifted Rightwards,approx +120
degrees
Negative in I,positive in avF
I

AVF

V1
• Situs solitus with ectopic left atrial focus –
negative P in I,dome and dart P in V1
• Situs inversus with ectopic left atrial
focus-normal P wave axis,dome and dart P
in V1
• Situs ambiguus –
• Asplenia syndrome – 2 sinus nodes may
occur,competition between them may
occur. 2 p waves,one positive in lead I and
other negative in Lead I
• Polysplenia syndrome-absent SAN,Low
atrial pacemaker,giving p wave axis of -90
degrees
 VENTRICULAR POSITION
• Ventricular position is independent of
atrial situs
• 4 patterns –
1. Normal or levocardia
2. Mirror image dextrocardia
3. Dextro rotation
4. Ventricular inversion
 Normal Dextrocardia Dextro Ventricular
rotation inversion

Biphasic V3 or V4 One of the V1,V3R,V4R,

voltages right chest V3 resembles
leads(V3R,V4 V6
R)
Initial forces Superior and Superior & Same as Superior and
right(Q in left(No deep q normal left (Q in
I,V6) in I,AVF) V1,absent Q in
I,AVL,V6)
Major forces Inferior & Inferior & Same as
left(tall R in Right(rS or QS normal
I,AVF,V6) in I,V6;tall R
in AVF)
Terminal Superior & Superior & Same as
forces left(small s in right (S in normal
AVF,Tall R in I,AVF,V6)
I,V6)
 DEXTROCARDIA
AVR and AVL reversed
Lead I predominantly negative
Right precordial leads should be recorded in
suspected dextrocardia
• D loop of heart tube – RV to Right of LV
and septal depolarisation from left to right
• Thus,Q in left precordial leads

• L loop- Q in right precordial leads

Ventricular
Inversion
 CARDIAC MALPOSITIONS
• 4 Combinations can occur-
• Situs solitus with levocardia
• Situs solitus with dextrocardia
• Situs inversus with dextrocardia
• Situs inversus with levocardia

• Mesocardia
 Normal ECG
• Important in the identification of
• 1.atrial situs,2.ventricular position,3.D/L loop
SITUS INVERSUS WITH DEXTROCARDIA
ACYANOTIC CHD
ECG
 With shunt
• ASD:
• Secundum Atrial Septal Defects:
• Clockwise loop with vertical axis. right
axis with pulmonary hypertension or
young females with pulmonary vascular
disease
• left-axis deviation is rare but has been
described in hereditary forms such as
Holt-Oram syndrome and in older adults
with presumably acquired left anterior
fascicular block
• Pwave-tall right atrial p wave
• P wave axis-inferior and to left with upright p in
inferior leads
• PR interval:may be prolonged, -intra-atrial and
H-V conduction delay-first-degree AV block
• QRS: duration may be prolonged
• terminal QRS is directed rightward
,superior and anterior-rsR’ in v1 and
widening of s in v6
• R’ In v1 and AVR is slurred
• Crochetage-specific for ASD if present in
all inferior leads
• Arrhythmias:
• SND occurs as early as 2 years of age
• Atrial fibrillation,flutter,PAT are common
in 4th decade
 CROCHETAGE
• In inferior leads, a notch near the apex of the R
wave,coined “crochetage,” has been correlated with ASD
• Seen in 73.1%, specificity - 92% (all 3 inf
leads),86.1%(atleast 1 inf lead)
 Evolution
• As PAH develops rsR’ gives way to R in v1
• Signs of PAH like RAD develop
• RVH signs develop
• After surgery R may revert to rsR’ in 40%
of patients
 Sinus venosus ASD
• P wave axis is superior and left-inverted p
in inferior leads,isoelectric in v1 and
positive in AVR
 TYPES OF ASD
OS OP Sinus venosus

P wave Axis Normal Normal Superior axis in

SVC type
QRS Axis Vertical LAD Vertical
LAD – assoc
MVP/MR
Loop Clockwise Anticlockwise Clockwise

Crochetage + _ +

Notch in upstroke
of S in Inf leads
Arrhythmias First degree AV
block more
common,Atrial
arrhythmias more
 Severity of shunt
Size of Shunt Mild Moderate Severe

Qp/Qs <1.4 1.4 – 2 >2

RAE No Yes Yes

RV volume No Yes Yes

overload

N rsr’ rsR’/evidence of
PAH

Crochetage No No Yes

Evidence of PAH No No Yes

R’ > 7mm in V1
 ASSOCIATED CONDITIONS

• Lutembacher’s syndrome – LAE,RVH

more common,Atrial arrhythmias more
common
• TAPVR-resembles OS ASD,PR prolonged,
AF in older persons
• PFO – no hemodynamic changes
ECG is normal or shows crochetage
• Common Atrium –
Absent atrial septum
ECG shows features of combination
of
OS, OP, Sinus venosus ASD
 PRIMUM ASD
• Counterclockwise loop
• Left axis deviation(extreme in downs)
• PR prolongation
• RVH- tall R in v1,,deep s in v6-pul.htn –left
A-V valve regugitation
• Notching of s wave upstokes in inferior
leads
 analysis
ASD-clockwise loop
with rsR’,right atrial
P wave

Clockwise loop counterclockwise

Secundum-pwave Sinus venosus-p primum-leftaxis

axis wave axis Notching of s waves
normal,crochetage superior,crochetage LVH/LAE
 GERBODES DEFECT
• Tall peaked p waves and RAE from infancy,
• PR prolongation
• rsr’ in v1,terminal r in avr and V3r –RV
volume overload
• LV volume overload
• Increased incidence of arrythmias
• Pathognomonic-RAE with LV volume
overload
 VSD
• Site
• Hemodynamic status
• Associated anomalies
• Typical features are LV volume overload -
gradually progressing to BVH.
 site

• Usually normal axis

Left axis deviation –seen in 3 – 15%

• Inlet VSD
• Large Peri membranous VSD with Inlet extension
• Ventricular septal aneurysm
• Multiple muscular VSDs
• DORV VSD
• L TGA VSD

• RAD-VSD with PAH

• L TGA with VSD-LAD Clockwise
• DORV with VSD-LAD Counter clockwise
 hemodynamics

• Accurately reflects underlying

hemodynamics

• Restrictive,small-no changes,only deep s

in right precordial leads,R in v5,v6-Lv
volume overload
• Moderately restrictive-LVH+,LAE

• Non restrictive-BVH- katz wachtel , RAD

• EISENMENGER-moderately peaked
p waves, RAD , tall monophasic R in v1,
deep S in left precordial leads
• Katz- Wachtel phenomenon
• High amplitude RS complexes in mid
precordial leads
• R + S waves in mid precordial lead >
60mm
• Classically described in VSD
 COMPLICATIONS
• PAH
• RAD
• RVH
• R/S >1 in V1
• ST depression,T inversion in Right leads
 Conduction defects
• PR prolongation-inlet vsd
• ECDS
• DORV
• L-TGA
• Septal aneurysm-AF,AFLU,PAT,CHB
• POST OP-RBBB(ventricular approach)
• ARRHYTHMIAS
• First-degree AV block occurs in about 10% of
patients, with a 1% to 3% incidence of complete
heart block on long-term follow-up.
• PR interval prolongation – Inlet VSD,Endocardial
cushion defects, DORV, L TGA
• Right bundle branch block +/- LAFB is found in 30%
to 60% of patients, independent of whether the VSD
was repaired through an atrial or ventricular
incision
• CHB is a recognized complication of transcatheter
device closure.
• Isolated VPC, couplets, and multiform
premature ventricular contractions may be
noted.
• Nonsustained or sustained VT occurs in
5.7% of patients, particularly with higher
pulmonary artery pressures.
• Endocardial cushion defects – LAD,
prolonged PR interval
• RAE + LV & RV volume overload =
Gerbode defect
• DORV with VSD –LAD,Increased PR
interval, Notched and broad S in II III aVF,
notch R in I AVL,V5,V6,counterclockwise
loop
• L TGA – LAD, q in V1/V2 with absent q in
lateral leads, heart block
• Associated with PS – RVH dominates,
RAD, T inversion in right leads
• Associated with AR
• CoA LVH dominates
• PDA
 GERBODES DEFECT
• Tall peaked p waves and RAE from infancy,
• PR prolongation
• rsr’ in v1,terminal r in aVR and V3R –RV
volume overload
• LV volume overload
• Increased incidence of arrythmias
• Pathognomonic-RAE with LV volume
overload
VSD CWLOOP VSD CCWL
LAD LAD

TRICUSPID
L-TGA
ATRESIA

MULTIPLE
INLET VSD
MUSCULAR

DORV
VSD RAD

SEVERE
PAH
 CCTGA
• The atrial septum is mal aligned with the
inlet ventricular septum, the regular AV node
does not make contact with infra nodal right
and left bundle branches.
• The AV node is displaced outside of Koch’s
triangle, anterior and slightly more laterally.
• Anomalous anterior AV node with a bundle
penetrates the atrioventricular fibrous
annulus and descends onto the anterior aspect
of the ventricular septum.
• The long penetrating atrioventricular
bundle is well formed in the hearts of
young children, but in adolescence, the
conduction fibers are replaced by fibrous
tissue, which is responsible for
atrioventricular block
• The right bundle branch is concordant with
the morphologic right ventricle, and the left
bundle branch is concordant with the
morphologic left ventricle.
• An Ebstein anomaly of the left
atrioventricular valve with left-sided
accessory pathways provides the substrate
for pre-excitation between the morphologic
left atrium and the morphologic right
ventricle.
• 75% have AV conduction abnormalties
• 30% have complete heart block
• Incidence of complete heart block increases
by 2% /yr
• Long bundle length –difficult to localise site
of block
• Sub pulmonic stenosis develops-axis will be
right
• Even in prescence of left AV valve
regurgitation and volume overload-no Q
waves in left precordial leads.
 3 MAJOR ECG FEATURES OF
CCTGA
• (1) Disturbances in conduction and
rhythm

• (2) QRS and T-wave patterns that reflect

ventricular inversion

• (3) Modifications of the P wave, QRS, ST

segment, and T wave caused by coexisting
congenital heart disease
 Typical features
• Reversal of the normal Q-wave pattern in
the precordial leads: Q waves are present in
the right precordial leads but are absent in
the left precordial leads
• Clockwise loop
• Left axis deviation
• Upright T waves in all precordial leads –
side by side orientation of both ventricles
• P wave usually normal.
• Occasionally broad in cases of non
restrictive VSD and left AV valve
regurgitation.
• Peaked p waves in cases of PAH/PS.
 AV SEPTAL DEFECTS
• Extreme form is when atria and ventricles
are connected by a common opening-
called common AV canal.
• It permits shunt between –
• LA to RA
• LV to RA
• RV to LA
• LV to RV
 AV SEPTAL DEFECTS
• Marked left to right
shunt
• Early development of
PAH
• Associated MR
determines outcomes
• Ostium primum ASD
• Cleft mitral valve-MR
• Cleft septal leaflet tricuspid valve-TR
• Malformation or lack of development of
left anterior fascicle-LAD
• Small high membranous vsd
 AV SEPTAL DEFECTS
• Characteristic finding :
• - left axis deviation
• - QRS vector counter clockwise loop
Mech : due to posterior and inferior displacement
of the AV node and the left bundle
• S waves in leads II, III, and aVF have a
characteristically
notched upstroke
• QRS pattern in right leads resembles OS-ASD-Due
to longer than normal Rt bundle
• The atrioventricular conduction axis
penetrates only at the crux, and the
penetrating bundle is displaced posteriorly,
lying on the posteroinferior rim of the
ventricular component of the defect.
• The His bundle is shorter than normal and is
posteriorly positioned. The left bundle
branch is displaced posteriorly and arises
from the common bundle immediately after
it enters the ventricular septum.
 The left anterior division of the left bundle
branch has fewer fibers than normal and is
increased in length. The left posterior
division is shorter than normal and
provides small branches to the
posterobasal wall of the left ventricle.
• The right bundle branch is abnormally
long.
• Short HV intervals are in accordance with
elaborate studies that show early
activation of the posterobasal left
ventricular wall in atrioventricular septal
defects.
• These anatomic and electrophysiologic
observations provide acceptable
explanations for left axis deviation and for
the depolarization Pattern.
 COMPLICATIONS
• PAH –
1. Complete AV canal defects with marked
left to right shunt
2. Ostium primum ASD with left AV valve
regurgitation
3. Pulmonary vascular disease of down’s
syndrome
• ARRHYTHMIAS
• PR prolongation also commonly seen (>50%)
Mech: secondary to intra atrial and
atrioventricular nodal conduction delay
• Rarely CHB-in immediate post op in 1-
7%,~2% thereafter
• Atrial flutter/fibrillation-with increase in age,
after surgical repair in >5%
• VPC-30%,Complex ventricular arrhythmia-
those with LV dysfunction
 ASSOCIATED CONDITION
• Extreme LAD,early development of PAH –
Down’s syndrome
• Sub aortic obstruction – further increases
left to right shunt,early PAH
 PDA
• Diagnosis by -
• LV Volume overload
• LAE
• +/- RV pressure overload
• QRS axis – normal
 SHUNT SEVERITY
• Small –normal
• Moderate – LAE + LV Vol overload
q & Tall R in V5-6,deep S in
V1-2,
T remain upright
• Large – Biatrial enlargement + BV
hypertrophy
• Eisenmenger – RAE + RVH
 COMPLICATIONS
• PAH
• BUT Q IN V5-V6 PERSIST EVEN AFTER
DEVELOPMENT OF PAH
• PR interval prolongation -10 – 20%
• AF – in older persons with large shunt
 ASSOCIATED CONDITIONS
• RAD – Neonates ,
LAD- Rubella,sometimes superior axis
• CoA – LVH with secondary ST- T changes
STENOTIC LESIONS
 Without shunt:
normal or decreased pulmonary flow

• Right side of heart

Valvular PS
DCRV
Peripheral PS
 Pulmonary stenosis

• Obstruction to RVOT increases afterload

on RV – RV systolic overload
• RVH With or without RAE
• Good correlation with hemodynamics and
ECG
• Normal ht of R in V1 =<8 mm in infancy,
<10 mm in children
• Persistent upright T waves in V1 & V2
after 4 days age indicates RVH
MILD MODERATE SEVERE

1 Normal in 30%-60% 1 r/s in v1>4:1 1 RAD>150°

of cases 2 rsR’ or a small r is 2 Monophasic R or Qr
2 Right axis present on upstroke 3 R >20mm in V1
deviation<100° of R’ 4 P in lead 2 tall and
3 R in v1<10-15mm 3 R in v1 <20mm peaked
4 Upright right 4 50%-upright T
precordial T waves waves 5 RVSP=LVSP or more
after 4 days of age 5 Gradient>40 mm Hg 6 Gradient >80 mm Hg
maybe only sign 6 RVSP>50% of LVSP 7 Deep inverted T
5 Gradient of waves ,ST depression
40mmHg beyond v2
6 RVSP<50% of LVSP -RVSP>LVSP
MILD PS -RVSP<50% of LVSP
MODERATE -RVSP>50% of LVSP
SEVERE – RVSP >LVSP
 RVSP MEASUREMENTS
• Ht of R in V1/V4R x 5,between 2 – 20 yrs age, if
pure R wave is present.
• Ht of R in V1 x 3 + 47
 TYPES OF PS
• Valvular PS – As described
• Sub/Supra valvular –same
• Sub infundibular PS/DCRV –Degree of RVH
in V1-3 less than anticipated,
Upright T in V3R may be the only finding in
40% cases
• Dysplastic Pulmonary valvular stenosis as a
part of Noonan syndrome –Extreme axis
deviation,QRS prolonged and splinteredQRS
in inferior and left precordial leads
 ASSOCIATED CONDITIONS
• Extreme RAD –may indicate pulmonary
valve dysplasia
• LAD – PS + Rubella syndrome
• PS as a part of TOF – RV pressures less
than in pure PS
• PS with large ASD- resembles OS-
ASD+RVH
Pure PS TOF(VSD + PS)
• RAD, marked • Not Marked RAD
• Tall R in Rt precordial • Tall R only in V1,with
leads sudden transition
• Less deeply inverted T
• Deeply inverted waves/upright T in V1 &
symmetric T waves V2
• Infants with severe stenosis, in whom the
right ventricle may be hypoplastic, have a
more leftward axis than expected (in the
range of +30 to +70 degrees) as well as
evidence of left ventricular hypertrophy
 CONGENITAL AS
• LVOT OBSTRUCTION
• LVH with T inversions,ST depression and
absent q waves
 SEVERITY OF AS
• ECG of valvular aortic stenosis is a poor
predictor of the severity of stenosis
• A completely or nearly normal ECG does
not exclude severe stenosis
• SCD can occur inspite of normal ecg
• Severity may progress without change in
ECG
 TYPES OF AS
• ECG is similar in valvular,sub and supra
valvular AS
• Evidence of subendocardial ischemia –
Severe AS,Supravalvular AS with
coronary ostial narrowing
 COARCTATION OF AORTA
• LAE in adults, LVH-tall R waves and low
flat inverted T waves
• Deeply coved ST segments-AS –bicuspid
aortic valve
• Q waves in left precordial leads suggests
AR
• Symptomatic infants-RAE ,RAD with
RVH
 COARCTATION OF AORTA

• LV pressure overload
• LAE
• Normal Axis
 ASSOCIATED CONDITIONS
• AS due to bicuspid aortic valve –
prominent ST depressions and deeply
inverted T waves
• AR due to bicuspid aortic valve –
Prominent q in left precordial leads
• RVH – Infants,Assoc PAH
• RV volume overload – Associated PFO
with left to right shunt
CONGENITAL MITRAL STENOSIS

• The electrocardiogram exhibits right atrial

P waves, right axis deviation,
and right ventricular hypertrophy.
Shones complex
 COR TRIATRIATUM
• RAE, RVH,RAD are common
• LAE may be seen due to prolonged
conduction in proximal accessory chamber
 Endocardial Fibroelastosis

• The electrocardiogram records a variety of

disturbances in rhythm and conduction,
including paroxysmal atrial, junctional or
ventricular tachycardia, and neonatal
atrial fibrillation.
• Complete heart block has been detected in utero and
raises the question of a relationship between maternal
antibodies.
• P waves show left atrial, biatrial, or right atrial
abnormalities.
• The QRS axis is normal, although rightward or
leftward axes occasionally occur.
• Left ventricular hypertrophy is an important
electrocardiographic feature of primary endocardial
fibroelastosis of the dilated type.
• An infarct pattern is a feature of
endocardial fibroelastosis associated with
anomalous origin of the left coronary
artery from the pulmonary trunk . If an
infarct pattern occurs in primary
endocardial fibroelastosis, the Q waves are
in right precordial leads, not in leads 1
and aVL
 REGURGITANT LESIONS
• CONGENITAL PR
• Normal in mild-mod cases
• RV volume overload in severe cases

• CONGENITAL AR
• LV volume overload with LV q waves
ALGORITHM FOR ACYANOTIC
CHD:
STEP 1
Which chamber is enlarged
RV LV

volume Pressureoverload
overload(rsr’/rs (monophasic
R’) R/qR
PS
•ASD DCRV
•RSOV Infantile
coarctation
Cortriatriatum-broad
left atrial P waves
Congenital MS-LAE
 LVH alone/BVH?

volume overload Nonrestrictive VSD

Moderately
restrictive VSD Large PDA
PDA AP Window
Pressure overload RSOV
Coarctation of aorta LTGA
Congenital AS
Interrupted .aortic
arch
Critical PS of infancy
• q in lateral leads : -simple
VSD,PDA,RSOV
• q in v1,2:L TGA
• RA enlargement if present-RSOV
 SMALL VSD
MILD PS
NORMAL AXIS COA(ADULT)
AS

VSD WITH PAH

(MUSCULAR ,OULET)
RIGHT AXIS ASD WITH PAH
CLOCKWISE LOOP PDA WITH PAH
CONGENITAL MS
CORTRIATRIUM

ACHD MULTIPLE MUSCULAR

LEFT AXIS
VSD
L TGA +VSD

COUNTERCLOCKWISE INLET VSD

LEFT AXIS
LOOP AV CANAL DEFECT
CYANOTIC HEART DISEASES
 Cyanotic and ↓ PBF
• Dominant RV
TOF
DORV+VSD+PS
SINGLE VENTRICLE(RV)+PS
 Cyanotic and ↓ PBF
• Dominant LV
Tricuspid atresia
Ebstein’ anomaly
Single ventricle –LV type with PS
• TGA (VSD and LVOTO), with restricted
PBF
• TGA (VSD and PVOD), with restricted
PBF
 Cyanotic and ↑ PBF
 Transposition physiology
D-TGA
• DORV with sub pulmonary VSD with NO PS
Tausig Bing
• Admixture physiology
Common atrium
Truncus arteriosus
TAPVC
 Cyanotic and ↓ PBF
• Dominant RV
TOF
DORV+VSD+PS
SINGLE VENTRICLE(RV)+PS
 Tetralogy of fallot
• P waves usually normal.
• Duration of P wave may be narrow due to underfilled LA.
• The QRS axis is the same as the axis of a normal newborn.

• The QRS axis and the direction of ventricular

depolarization do not change as the neonate matures
because the functional demands on the right ventricle do
not change.

• RVH is characterized by a tall monophasic R wave

confined to lead V1 with an abrupt change to an rS pattern
in lead V2.
• Presence and depth of Q waves and the
amplitude of R waves in leads V5-6 are
sensitive signs of the magnitude of
pulmonary blood flow and left ventricular
filling.
• Reduced pulmonary flow with an
underfilled left ventricle is accompanied
by rS patterns in leads V2_6.
• RBBB is common after surgical repair of
tetralogy of Fallot, even when the repair is
performed from a transatrial approach.
• This is probably due to delayed activation
of the right ventricular outflow tract
caused by disruption of the right
ventricular conduction system during
resection of infundibular stenosis.
• All patients with ventricular
tachycardia or sudden death had QRS
duration >180 ms.
 Cyanotic and ↓ PBF
• Dominant LV
Tricuspid atresia
Ebstein’ anomaly
Single ventricle –LV type with PS
• d-TGA (VSD and LVOTO), with restricted
PBF
• d-TGA (VSD and PVOD), with restricted
PBF.
 ECG
• Counter clockwise loop
• LAD
• Left ventricular hypertrophy
• Little or No RV forces
• RAE
 Type -2
• Usually non restrictive VSD
• Normal or vertical axis
• LAE and RAE
Ebsteins anomaly
 Hypoplastic left heart
• Always RVH
• qR pattern
• Left precordial R waves are diminutive
• Deep S waves are usually seen in lead V6
• Right atrial enlargement
• Right axis deviation
• ST segment changes
may reflect inadequate coronary perfusion from restriction
of retrograde flow through a hypoplastic ascending
aortic arch
 Single Ventricle

• RVH
• LVH
• Stereotype QRS
90% are LV morphology inverted outlet
chamber
Non inverted outlet chamber include left
axis deviation, left ventricular
hypertrophy, QRS complexes of great
amplitude, and stereotyped precordial
patterns
• Inverted outlet chamber include PR
interval prolongation, an inferior or
rightward QRS axis, absent left precordial
Q waves, RS complexes of great
amplitude, and stereotyped precordial
patterns
• Right ventricular morphology:Precordial
QRS complexes are stereotyped with right
ventricular hypertrophy patterns of
increased amplitude
 Cyanotic and ↑ PBF
 Transposition physiology
D-TGA
Tausig Bing
• Admixture physiology
Common atrium
Truncus arteriosus
TAPVC
 TGA
• Typical feature is RAD with RVH/BVH
• one third of infants with large VSD have
normal QRS axis for age.
• Left-axis deviation - typical in TGA with
AV canal types of VSD
TGA with non restrictive ASD

• Initial normal ECG

• Developing into RAD with RVH
• LV not prominent
 TGA nonrestrictive VSD

• RAD
• Biventricular hypertrophy
• As PAH increases it evolves into
pure RVH
DORV
DORV with subaortic VSD with no PS

• Left axis deviation with counterclockwise

depolarization is an important feature .

• PR interval prolongation is common -unusually

long course of the common atrioventricular
bundle.

• Peaked right atrial P waves are associated with

bifid broad left atrial P waves when pulmonary
blood flow is increased.

• Mechanism of left axis deviation is unknown.

• Right ventricular hypertrophy -obligatory and is
manifested by tall R waves in leads V1 and aVR
with deep S waves in left precordial leads .
• Left ventricular volume overload is indicated by
large RS complexes in mid-precordial leads and
by tall R waves in left precordial leads .
• Elevated pulmonary vascular resistance is
associated with right axis deviation and püre right
ventricular hypertrophy
 DORV with sub aortic VSD with PS
• Peaked right atrial P waves
• Right ventricular hypertrophy
• Important
– Distinction from TOF is presence of
counterclockwise loop with slurred s in II III
aVF and broad R in aVR I V5 V6 and
presence of PR prolongation
Taussig bing anamoly
 Truncus
• Tall peaked right atrial p waves
• Bifid left atrial p waves
• Left axis deviation-increased pulmonary
blood flow
• Right axis deviation-decreased pulmonary
blood flow
• Biventricular hypertrophy
Common atrium
 TAPVC
• Resembles secundum ASD
• Vertical/right axis
• RVH-common feature
• RAE-present only in non
obstructive type
 TOF(PINK
NORMAL
TOF,
D-TGA VSD PS ,
L-TGA VSD PS ,
SV(LV) INV
OULET
SV(RV)
CLOCKWISE RIGHT AXIS
LOOP TAPVC
EISENMENGERS
SEVERE PS WITH
ASD

LEFT AXIS ADULT TOF

CCHD

TA
COUNTERCLOCK SV(LV)NI OUT
WISE LOOP LEFT AXIS AV CANAL/EISE
COMMON
ATRIUM

RIGHT AXIS

DORV VSD PS

TA TYPE II C
NORMAL AXIS