ecg

1. THE ECG IN
CHAMBER ENLARGEMENT

2. Role of ECG
• ECG is a simple, readily available and
inexpensive tool for the detection of cardiac
chamber enlargement
• Can provide useful clues or arouse suspicion of
underlying cardiac condition
• Most ECG criteria have low sensitivity but high
specificity
• Clinical correlates and prognostic significance
• Screening and population based studies

3. General Principles
 Enlargement of a cardiac chamber may manifest
on the ECG as an alteration of:
 Wave form morphology
 Amplitude / voltage
 Axis
 Duration (widening)
 These apply to both the P wave and QRS
complex
 Atrial abnormality may suggest corresponding
ventricular hypertrophy

4. Fallacies / Limitations
 Enlargement ? Hypertrophy ? Dilatation ?
 Voltage criteria can vary significantly based
on
 Age
 Gender
 Race
 Habitus (chest wall thickness/ abnormalities)
 Pulmonary / pericardial pathology

5. Atrial abnormalities
 Atrial dilatation, hypertrophy, elevated atrial
pressure, impaired ventricular distensibility, and
delayed intraatrial conduction produce similar
changes on the ECG and cannot be
differentiated
 As such, the terms left atrial abnormality and
right atrial abnormality are preferable to
 left /right atrial enlargement,
 P mitrale/congenitale/pulmonale
J Am Coll Cardiol 2009;53:992–1002

6. P Wave
 P wave reflects atrial
depolarisation
 Right atrial activation
begins first.
 Proceeds from SAN in
inferior and anterior
direction and is
reflected by ascending
limb of P wave in
frontal plane leads.

7.  Left atrial activation
begins 0.03 sec after
right atrial activation
 Proceeds from high in
the IAS in a left,
inferior and posterior
direction
 Constitutes distal half
or descending limb of P
wave.

8. Normal P wave
Lead II LeadV1
Duration in lead II is 0.08 – 0.1 sec max.
0.11 sec.
Amplitude in lead II: Usually 2mm, max.
2.5 mm
Usually biphasic
Initial positive deflection < 1.5mm
Terminal negative deflection not exceeding
1 mm in depth and < 0.03 sec in duration.
Duration of P wave inV1 is 0.05 – 0.08 sec.

9. P wave axis
P wave axis in frontal plane: +45 to +65
Always positive in lead I, II, aVF,V4-V6 and
negative in lead AVR.

10. LEFT ATRIAL ABNORMALITY
3 basic ECG changes:
1. Prolongation and delay of the terminal or
left atrial component of atrial activation
(bachmann’s bundle)
2. Increased posterior deviation of left atrial
vector.
3. Left axis deviation of mean manifest frontal
plane P wave axis.

11. Criteria for LAA
 Ratio between the duration of the P wave in lead 2
and the PR segment of >1.6 (Marcuz index)
 Leftward shift of the P wave axis less than 15-30 o
V1 - PTerminal force
(MORRIS index)
Lead II

12. Echocardiographic evaluation of ECG
criteria for LAA
CRITERIA SENSITIVITY SPECIFICITY
Terminal negative P in V1 >
0.04 mm-sec
83 80
Duration between peak of P
wave notches > 0.04 s
15 100
P wave duration>0.11 s 33 88
Ratio of P wave duration to PR
segment > 1.6
31 64
Amplitude of terminal –ve P
wave deflection in V1 > 0.1mv
60 93
Munuswamy K et al Am J Cardiol 1984;53:829.

13. Causes of LA abnormality
 Valvular heart disease, mainly mitral and
aortic
 Hypertensive heart disease
 Cardiomyopathy (dilated / restrictive /
hypertrophic)
 CAD
 Constrictive pericarditis with AV groove
constriction (rare)

14. P mitrale
The term P mitrale refers to a P wave that is abnormally notched and
wide because this P wave is commonly seen in patients with mitral
valve disease, particularly mitral stenosis.

15. Right atrial abnormality
 Total P-wave duration is usually normal
 Peaked P waves with amplitudes in lead II >0.25 mV
(even a normal amplitude P wave if pointed )
 LeadV1:
 Prominent initial positivity of the P wave inV1 orV2
(>0.15 mV)
 Initial area under curve >0.06 mm-sec
 qR complex, namely a small q followed by a large R
wave, usually in tricuspid regurgitation
 Low-amplitude (< 0.6 mV) QRS complexes in leadV1
with a threefold or greater increase in leadV2

16. Change in P axis:
 In acquired heart disease (e.g. COPD), rightward
shift of the mean P wave axis to above +75
degrees – ‘P pulmonale’
 In congenital heart disease, the axis is normal or
to left (-40 to +70 degrees) – ‘P congenitale’

17. Kaplan criteria
 QRS axis > 90o
 P amplitude inV2> 0.15mv
 R/S > 1 inV1 in the absence of RBBB
 Combined sensitivity of 49% with specificity
of 100%
Kaplan JD, Evans GT et al. J Am Coll Cardiol 1994; 23: 747-52

18. Causes of RAA
 Congenital heart disease (Ebstein’s anomaly,
severe PS)
 Tricuspid valve disease
 Chronic cor pulmonale (COPD)
RAA is very uncommon in isolated ASD without
PH since mean RA pressure is usually normal

19. P Pulmonale
Tall, peaked (“gothic”) P wave in leads II, III, and aVF ,P axis > 70 degrees
No good overall correlation between P pulmonale and right atrial enlargement
Severity of COPD is more related to rightward P wave axis than to P wave amplitude

20. P Tricuspidale
 P wave in the frontal leads is notched and the first
component is increased in amplitude and taller than
the second component- reflects biatrial
enlargement

21. Himalayan P waves
Giant P waves-classically described in ebstein’s anomaly, also reported in
Tricuspid atresia, combined tricuspid and pulmonic stenosis
Best seen in leads II, III, aVF andV1

23. Pseudo-P pulmonale
 Tall peaked P waves in inferior leads in absence of right atrial enlargement
 Seen in hypertensive heart disease with/without heart failure
 Actually reflects Left atrial enlargement due to increase in the later P-
wave forces without prolongation of atrial depolarisation

24. Pseudo-P pulmonale
D- Pseudo P pulmonale pattern in left atrial enlargement.
The amplitude of the left atrial component is increased without increase in duration
of left atrial depolarization.
C- P mitrale –
increase in the left
atrial component in
amplitude and
duration.
Associated intraatrial
Conduction defect
- prolongation of P
wave duration

25. ECG evaluation of RAA & LAA is facilitated by differing times of
initiation of activation and by the differing directions of spread.
RAA- initial
component
of the P wave
is enlarged
leading to an
increase in
the height
of P wave
without any
widening.
LAA,
P-wave
widening with
an M-shaped
P wave in
lead II and
an increased
P terminal
force inV1
RAA LAA
Summary – LAA & RAA

26. Biatrial enlargement
 Large biphasic P wave inV1
 initial component > 1.5 mm in height and
 terminal component > 1 mm in depth and 0.04 sec in
duration.
 A P wave amplitude of more than 2.5 mm and
duration of more than 0.12 sec in lead II.
 The presence of a tall, peaked P wave (>1.5 mm)
in the right precordial lead and a wide, notched P
wave in the limb leads or left precordial leads (V5
andV6)

27. Biatrial enlargement
MS/ MR with PAH
MS/ MR withTS /TR
ASD with PAH
Lutembacher’s syndrome
DCM / RCM

28. Atrial abnormality in AF
 AF itself indicates possible dilatation of the
atria in most diseases
 Coarse f waves in leadV1 (>1 mm) were
associated with radiological and anatomic
evidence of atrial enlargement

29. Ventricular hypertrophy

30. Factors affecting QRS
voltage
 Age: QRS voltages decline with age.The
commonly used voltage criteria apply to
adults>35 yrs
 Gender: women have slightly lower voltages
 Race: Blacks have higher voltages, hispanics and
caucasians lower compared to whites
 Body Habitus:
 Large breasts insulating effect.
 Obesity increases LV mass but also distance of heart
from the electrodes. So QRS voltage is unaffected
JACC 2009;53:992–1002

31. Mechanisms of ECG changes
 Prolongation of action potential duration
 Increased transmural activation time
 Change in cardiac position with LV dilatation
 Brody effect
 Secondary ST-T chamges possibly due to
subendocardial ischemia ( the term ‘strain’ is
to be avoided)

32. Left Ventricular hypertrophy
V1 V5,6

33. Ventricular activation time
Indicator of transverse conduction time across
LV wall
Prolonged in LVH (normal <40ms in Left leads, <20ms in right leads)

34. Classification of LV enlargement
LV volume LV mass
Normal Abnormal
Comments
Normal
Normal Concentric
LVH
Abnormal
volume ≥
90ml/m2
Abnormal Isolated LV
volume
overload
Eccentric LVH
Comments Abnormal LV mass ≥ 131g/m2 in males, 108
g/m2 in females
Huwez FU, Pringle SD, Marcfarlane PW. Am J Cardiol 1992; 70: 687

35. Pressure / Systolic overload
 Increase in magnitude of QRS deflection.
 Attenuation of small initial q wave in left
oriented leads
 Increase inVAT (>40ms)
 Counterclockwise rotation of heart so that
the transition zone is shifted to right i.e. in
leadV3 orV2.

36. LVH with pressure overload
T wave inverted in left oriented leadsV5,V6, I,AVL and upright inV1,V2, AVR.
InvertedT wave - blunt apex, asymmetrical limb, the proximal limb is shallower
than distal limb.
Associated ST segment is minimally depressed with slight upward convexity.

37. LVH with diastolic overload
Deep and narrow Q waves in left oriented leadsV5,V6.
The tallT waves in left precardial leadsV5,V6 are symmetrical sharply
pointed.
ST segment inV5,V6 minimally elevated and concavity upwards.

38. Differentiating diastolic
overload of AR and MR
 Diastolic overload of MR can be distinguished
by ECG from AR.
 MR – Gaint LA will displace the heart forward,
 QRS vector is less aligned withV1 and more
aligned withV6. Hence S wave in leadVI will
be attenuated.
 In AR, the S wave inV1 is deep

39. CRITERIA
for LVH
Low
sensitivity
(50%)
high
specificity
(85-90%)
J Am Coll Cardiol
2009;53:992–1002

40. Selected criteria
 Sokolow Lyon criteria (1949):
S inV1 + R inV5/V6 > 3.5 mv or
R inV5 orV6 > 2.6O mv.
 Cornell voltage criteria (1987):
R in aVL + S inV3 > 2.80 mv for Males
> 2.00 mv for Females

41. Selected criteria
 Cornell voltage-duration product
QRS duration × Cornell voltage > 244 mVms
 QRS duration × sum of voltages in all leads
>1742 mm-sec
 R in aVL > 11 mm.
 R I + S III > 25 mm.
 Total 12 lead voltage >175 mm
 R-V6 > R-V5: Koito spodick criterion
 QTc interval combined with CVP

42. 4 points  Probable LVH, 5 points  Definite LVH

43. CRITERIA SENSITIVITY SPECIFICITY
SOKOLOW LYON 10-30% 85%-95%
ROMHILT ESTES 10-30% 85%-95%
CORNELL
VOLTAGE
35-50% 85%-95%

44. LVH in the presence of
conduction disorders: RBBB
 RBBB: reduces the S wave in the right precordial
leads (V1,V2) and thus reduces the sensitivity of
ECG for LVH
 Presence of LAA & LAD enhance possibility of
LVH

45. LVH in the presence of
conduction disorders: LAFB
 LAFB: QRS vector shifts in a posterior and
superior direction, resulting in larger R waves
in leads I and aVL and smaller R waves but
deeper S waves in leadsV5 andV6

46. LVH in the presence of
conduction disorders: LBBB
 LVH and LBBB share a number of common
features like prolonged QRS duration and
voltage.
 Criteria for LVH are most unreliable in the
presence of LBBB
 LBBB itself is indicative of LVH in most cases
 KLEIN et al, using echocardiograms, found that
in the presence of LBBB
 SV2 + RV6 >45mm.
 E/o LAE with QRS duration>0.16s

47. Significance
 LVH on ECG correlated with increased CV
mortality
 LIFE study showed improvement in survial
with LVH regression (Cornell criterion), also
HOPE trial (Sokolow Lyon criteria)
 Secondary ST-T changes and associated LAE
indicate worse prognosis

48.  Prominent STT changes in apical
hypertrophy (Yamaguchi syndrome)
 Cornell product is one of the best predictors
of overall outcome

49. Right ventricular hypertrophy
 The right ventricle is considerably smaller than
the left ventricle.
 For RV forces to be manifested on the ECG, they
must be severe enough to overcome the
concealing effects of the larger LV forces.
 In mild RVH, the ECG may be normal or there
may only be a shift of QRS axis.

50. ECG criteria for RVH
 The ECG is notoriously inadequate in
detecting RVH
 Its sensitivity is in the range of 2%–18% but it
is very specific (90%)

51.  Vectorial classification of RVH (Chou and
Helm, 1967)
 Type A: R inV1, S inV6 (CCW loop) - PS
 Type B: R/S>1 inV1 with R> 0.5mV (CW loop) – RHD
MS
 Type C: S inV5-6. with R/S<1 inV5, CW loop - COPD

52. RVH with pressure overload
Leads aVR,V1, andV2 – abnormally tall R waves.
I,aVL,V5,V6 – Deep S waves leading to RS or rS complex
Right axis deviation

53. J Am Coll Cardiol
2009;53:992–1002

54. Selected criteria
 Sokolow-Lyon criteria : R inV1 + S inV5/V6 >
1.10 mV
 R inV1 ≥ 0.7 mV
 S wave inV5 orV6 >0.7 mV
 qR inV1
 R/S ratio inV1 > 1 with R >0.5 mV
 R/S ratio of < 1 inV5 orV6
 SI SII SIII syndrome

55. BUTLER LEGGETT FORMULA
Direction ANTERIOR RIGHT POSTERIOR-
LEFTWARD
Amplitude Tallest R or
R’ in V1/V2
Deepest S in
I or V6
S in V1
RVH formula A + R - PL > 0.7mv

56. Criterion for RVH Sensitivity (%) Specificity (%)
R inV1 ≥ 0.7 mV <10 —
QR inV1 <10 —
R/S inV1 > 1 with R > 0.5
mV
<25 89
R/S inV5 orV6 < 1 <10 —
S inV5 orV6 > 0.7 mV <17 93

57. Right axis deviation ≥ + 90 degrees <14 99
S1Q3 pattern <11 93
S1S2S3 pattern <10 —
P pulmonale <11 97
Murphy ML,Thenabadu PN, de Soyza N, et al: Reevaluation of electrocardiographic criteria for
left, right and combined cardiac ventricular hypertrophy. Am J Cardiol 53:1140, 1984.
Criterion for RVH Sensitivity (%) Specificity (%)

58. Causes of RVH
 Systolic (pressure) overload
 Pulmonary Stenosis
 Pulmonary Hypertension
 TOF (unusual feature – no ‘strain’ pattern)
 Diastolic (volume) overload
 ASD /TAPVC / PAPVC
 SevereTR / PR

59. RVH with systolic overload
leadV1 –tall monophasic R wave or a diphasic RS, Rs, or qR complex.
T inversion in right precordial leads (‘strain’)
 rS pattern inV6
In pure valvular PS, age 2-20, height of R wave in mm multiplied by 5
gives RV systolic pressure

60. RVH with RBBB
Pattern of incomplete or complete RBBB
RVH is present if R' in the precordial leads is greater than 10 mm in height in
incomplete RBBB, and 15 mm in complete RBBB- Barker &Valencia criteria
Incomplete
RBBB

61. Other Causes of tall R wave in
V1
 Normal young adults
 True posterior infarction
 Dextrocardia
 LPFB
 Displacement of the heart due to pulmonary
disease
 Wolff-Parkinson-White pattern
 Muscular dystrophies

62.  Sinus tachycardia
 SI QIIITIII
 Recent axis shift
 “P pulmonale”
 Complete or incomplete RBBB
 NegativeT waves in two or more right precordial
leads
 Clockwise rotation
 Atrial arrhythmias
 May mimic inferior wall MI or rarely anterior MI
Acute Pulmonary embolism

64. BIVENTRICULAR HYPERTROPHY
 Hypertrophy of both ventricles produces
complex electrocardiographic patterns.
 Not the simple sum of the two sets of
abnormalities.
 The effects of enlargement of one chamber
may cancel the effects of enlargement of the
other.
 Sensitivity 20%, although the specificity was
high at 94%

65. BVH CRITERIA
 LVH + Prominent R waves in right precordial
leads.
 Voltage criteria for LVH + RAD
 LAE as sole criterion for LVH + RVH.
 ECG evidence of LVH with clockwise
rotation of heart.
 Large equiphasic QRS complex in mid
precordial leads.

66. Katz-Wachtel pattern
•Katz – wachtel phenomenon: Large equiphasic QRS complex in mid
precordial leads (V2-4).
•Seen in largeVSD with biventricular enlargement
•R+S > 45 in adults, > 60 in children

67. Chamber enlargement in
pediatric age group
 Related to changes in LV:RV mass.
 Birth : RV is thicker than LV.
 Large increase in LV weight during first month.
 LV:RV reaches 2:1 by 6 months of age.
At birth 0.8:1
1 month 1.5:1
6 months 2.0:1
Adult 2.5:1
LV:RVWEIGHT RATIO

68. Normal ECG
 New borns and infants < 2 month - RAD and RV dominance.
 > 3 years - Resembles adult ECG.
 1 month and 3 years – ECG’s are intermediate.
 T waves inV1 are almost always negative.
4 week infant

69. Atrial abnormality
RAA - Peaked P wave in leads II andV1
 3 mm in infants < 6 months
 >2.5 mm in infants > 6 months.
LAA- Prolongation of P wave duration
 12 mths->0.10 sec.
 < 12 mths ->0.08 sec.
 Terminal or deeply inverted P wave inV1 orV3R
 Broad and notched P wave in II, biphasic inV1.
[Emerg Med Clin N Am 24 (2006) 195–208,The Pediatric ECG]

70. RVH
 R wave greater than the 98th percentile in lead
V1.
 S wave greater than the 98th percentile in lead I
orV6.
 RSR’ pattern in leadV1,
 R’ height > 15 mm in infants <1 yr or
 R’ height > 10 mm in children >1 yr
 UprightT-wave inV1 (>7 days, upto 10 years)
 qR pattern in leadV1
 Overall Sensitivity 69%, specificity 82%

72. LVH
 R-wave amplitude greater than 98th percentile in
leadV5 orV6.
 R wave less than 5th percentile in leadV1 orV2
 S-wave amplitude greater than 98th percentile in
leadV1.
 Q wave greater than 4 mm in leadV5 orV6
 InvertedT wave in leadV6

74. Suggested reading / References
 An Introduction to Electrocardiography – Leo
Schamroth 7th ed
 Marriott’s Practical Electrocardiography 11th
ed
 Advanced 12-lead Electrocardiography;
Cardiology Clinics August 2006
 AHA/ ACCF / HRS recommendations for the
standardisation and interprertation of the
Electrocardiogram PartV. JACC 2009; 53:
992-1002

75. THANK YOU