ECG IN CONGENITAL HEART DISEASE

LEAVE SOME SPACE FOR GREEN

ECG IN CHD

• ACYANOTIC CHD

• CYANOTIC CHD

AcyanoticCHD

Without shunt(normal or decreased pulmonary flow)

Right side of heart

Left side of heart

↑ PBF

AtrialVentricularAortic root

right side of heartAortopulmonary level

II° ASD• Sinus arrhythmia

• 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,intra-atrial/H-V conduction delay-first-degree AV block

• Wide QRS

• RBBB

• R’ In v1 and AVR is slurred

•Crochetage-specific for ASD if present in all

inferior leads

• SND occurs as early as 2 years of age

• Atrial fibrillation,Atrial flutter

• PAT

CROCHETAGE SIGN:R WAVE NOTCH IN ALL INFERIOR LEADS

FOLLOW UP

• PAH

rsR’ gives way to R in v1

Signs of PAH: RAD/RVH

• After surgery R may revert to rsR’ in 40% of patients

ORIGINAL AND MODIFIED METHODS OF DEFINING THE BUTLER-LEGGETT SCORE

I°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

I° ASD

ASD ALOGARITHM

A S D

Clockwise loop

II° ASD P -wave axis normal

Crochetage+

SV ASDP- wave axis superior

Crochetage+

CounterclockwiseLoop

I° ASDLAD/Notching of s in inf leads

LVH/LAE

VSD

•Location

•Hemodynamic burden

•Associated anomalies

•Typical features

LV volume overload

Progressing to BVH

LOCATION

PERIMEMBRANOUS VSD

INLET VSD MULTIPLE VSD

With septal aneurysm-left axis deviation

Counterclockwise loop, LAD and prolonged PR interval

Clockwise loop with left axis deviation

HEMODYNAMICS

• Accurately reflects underlying hemodynamics

• Restrictive & small-no changes

• Deep s in right precordial leads,R in v5,v6-lv volume overload

• Moderately restrictive-LVH+LAE

• Non restrictive-BVH and Katz -Wetchel,RAD

• EISENMENGER-Moderately peaked p waves,RAD,tall monophasic R in v1,deep S in left precordial leads

ASSOCIATED ANAMOLIES• PS-early transition

• AR-marked LVH in presence of restrictive VSD-DEEP Tall Deeply inverted T and coved ST segments in left precordial leads

• DORV,L-TGA-Similar to VSD

CONDUCTION DEFECTS• PR prolongation

Inlet VSD

ECDS

DORV

L-TGA

• Septal aneurysm-AF,AFLU,PAT,CHB/Axis change

• POST OP-RBBB(ventricular approach)

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 arrhythmias

• Pathognomonic-RAE with LV volume overload

CONGENITALLY CORRECTED TRANSPOSITION

• The AV node is displaced outside of Koch’s triangle, anterior and slightly more laterally

• An elongated His bundle extends toward the site of fibrous continuity between the right-sided mitral valve and pulmonary artery(posterior)

• It courses across the anterior rim of the pulmonary valve and continues along the superior border of VSD

• Conduction system

• QRS patterns

• Modifications of P,QRS,ST,T segments

TYPICAL • 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

• 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

• In even in prescence of left AV valve regurgitation and volume overload-no Q waves in left precordial leads

VSD

LEFT AXIS

Clockwise loop-L-TGA

MULTIPLE MUSCULAR

Counter clockwise-DORV

INLET VSDTRICUSPID ATRESIA

RAD

Severe PAH

VSD

LVH

MODERATELY RESTRICTIVE

WITH RAE-GERBODES

BVH

NONRESTRICTIVE

NONRESTRICTIVE-BVH

Q IN LATERAL LEADS

PRESENT-simple VSD

ABSENT-LTGA

PDA• SIMILAR TO VSD

• QRS axis

• RAD- infants with respiratory distress

• Superior/extreme left-Rubella syndrome

AP WINDOW• SIMILAR TO non restrictive VSD

D-MALPOSED GA• P wave abnormality- if RA recieves shunt or TR develops

• PR prolongation is seen

• CHB can develop

• QRS axis is normal or rightward

• All 4 chambers enlarged-into RA

• RVH,LAE,LVH-into RV

• Only LA,LV-rupture into LA

• LVH is seen,RVH is seen ,but it occyurs alone it is due to RVOT obstruction by unruptured aneurysm

WITHOUT SHUNT: NORMAL OR DECREASED PULMONARY FLOW

• Right side of heart

Valvular PS

DCRV

Peripheral PS

VALVULAR PSTall monophasic R or qR in v1

Right axis deviation

Strain pattern in right precordial leads

SEVERITY OF PS

MILD MODERATE SEVERE

Normal in 30%-60% of cases

Right axis deviation<100°

R in v1<10-15mm Upright right precordial T

waves after 4 days of age maybe only sign

Gradient of 40mm mmHg RVSP<50% of LVSP

r/s in v1>4:1 rsR’ or a small r is

present on upstroke of R’ R in v1 <20mm 50%-upright T aves Gradient>40 mm Hg RVSP>50% of LVSP

RAD>150° Monophasic R or Qr R >20mm P in lead 2 tall and

peaked,in v1 terminal force is written by right atrial dilatation

P maybe negative RVSP=LVSP or more Gradient >80 mm Hg Deep inverted T

waves ,ST depression beyond v2 and R in v1 >20mm-RVSP>LVSP

PS SPECIAL

• PS with extreme right axis deviation with splintered QRS and QS in inferior leads-dysplastic PS of Noonan syndrome.

• 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

DCRV

• RVH can be present

• But in 40% of cases upright T in v3R can be the only finding

ASD WITH PS

• Non restrictive ASD and mild PS

• like ASD

• RVH will be disproportionate

• QRS axis is vertical or rightward

• rsR’ in v1-R’will be taller than that due to isolated ASD

• Severe PS with PFO-resembles isolated severe PS

NORMAL OR ↓ PBF

• Left side of heart

Coarctation of aorta

Cortriatriatum

Congenital MS

Congenital AS

COARCTATION

• 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

• LV strain pattern in infancy is indication for surgery

INTERRUPTION OF AORTIC ARCH

• Peaked right atrial p waves and RVH-infants

• BVH gradually develops

COR TRIATRIATUM

SHONES COMPLEX

ALOGARITHM FOR ACYANOTIC CHD:STEP I

• Which chamber is enlarged

• Step -2-suppose it is RV

• Step-3-is it volume overload(rsr’/rsR’)or pressure overload(monophasic R/qR)

• Step-4-volume overload-ASD/RSOV

• Pressure overload-PS

DCRV

Infantile coarctation

• Cortriatriatum-broad left atrial P waves

• Cogenital MS-LAE

STEP II

Suppose it is LV

Is it LVH alone/BVH?

LVH alone?

volume/pressure?

volume overload Moderately restrictive VSD

PDA

Pressure overload Coarctation of aorta

Congenital AS

Interrupted .aortic arch

Critical PS of infancy

• BVH

Nonrestrictive VSD

Large PDA

AP window

RSOV

L-TGA

• q in lateral leads/v1 : lateral leads-simple VSD,PDA,RSOV

• q in v1,2:L TGA

• RA enlargement is present-RSOV

DORV

DORV

• Left axis deviation with counter clockwise loop

• QRS duration is normal

• RVH is obligatory-tall R in v1

• Deep s in V6

• LV volume overload –tall RS complexes in mid precordial leads and tall R in v5/v6

• PAH-clockwise loop with right axis deviation

CYANOTIC AND ↑ PBF

Transposition physiology

D-TGA

• D-TGA nonrestrictive VSD with tricuspid atresia

• DORV with sub pulmonary VSD with NO PS

• Tausig Bing

• Admixture physiology

Common atrium

Truncus arteriosus

TAPVC

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

• D-TGA: conal inversion

• right and anterior aorta

• TGA (IVS or small VSD) with increased PBF and small ICSa

• TGA (VSD large) with increased PBF and large ICS

• TGA (VSD and LVOTO), with restricted PBF

• TGA (VSD and PVOD), with restricted PBF

• 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

TGA WITH SUB PULMONIC OBSTRUCTION

• Pure RAD with RVH

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 v5,6,1,avl and broad R in avr 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

TRICUSPID ATRESIA

VAN PRAAGH AND ASSOCIATES- 1971

tricuspid atresia First classification

morphology of the tricuspid valve

(a) muscular type, (b) fibrous (membranous) type, and (c) Ebstein’s type

modified by him”’ and by Weinberg

muscular type constituted 84%

membranous type n 8%

The Ebstein’s type in 8%

TRIUSPID ATRESIA BY KUHNE

ECG

• Cyanotic child

• LAD

• Left ventricular hypertrophy

• Type1- adult pattern of progression

• RAE

TYPE -2• Usually non restrictive VSD

• Normal or vertical axis

• LAE and RAE

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• BVH common

• RVH

• LVH

• Stereotype QRS

90% ARE LV MORPHOLOGY INVERTED OUT LEFT 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

BVH

• Biventricular Hypertrophy (difficult ECG diagnosis to make)

• R/S ratio in V5 or V6 < 1

• S in V5 or V6 > 6 mm

• RAD (> 90 degrees)

ESTES CRITERIA FOR LVH>5 SURE,>4 PROBABLY

I AM NOT BE 100% ENTERTAINING