The document discusses the role of ECG in detecting cardiac chamber enlargement. Some key points: - ECG can detect chamber enlargement through changes in waveform morphology, amplitude/voltage, axis, and duration. These changes apply to both P waves and QRS complexes. - Common ECG criteria for left atrial enlargement include prolonged/notched P waves in lead II and terminal negative deflection in lead V1. For right atrial enlargement, criteria include tall peaked P waves in leads I, II, III and V1. - Common ECG patterns of left ventricular hypertrophy include tall R waves in left chest leads, ST-T wave changes, and prolonged QRS duration

1. Chamber
Enlargement &
Hypertrophy

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 ECCG criteria have low sensitivity but high specificity
• Clinical correlates and prognostic significance
• Screening and population based studies
Chamber Enlargement & Hypertrophy 2

3. General Principles
• Enlargement of the cardiac Chambers may manifest on the ECG as
an alteration of
• Waveform morphology
• Amplitude / Voltage
• Axis
• Duration (widening)
• These applied to both the p waves and the QRS complex
• Atrial abnormalities may suggest corresponding ventricular
hypertrophy
Chamber Enlargement & Hypertrophy 3

4. Limitations
• Enlargement? hypertrophy? dilatation?
• Voltage criteria can carry significantly based on
• Age
• Gender
• Race
• Habitus (chest wall thickness/abnormalities )
• Pulmonary/pericardial pathology
Chamber Enlargement & Hypertrophy 4

5. Before commenting
• Assess technical quality of ECG
• Placement of the electrolytes (especially precordial)
• Voltage standardisation (1 mm=0.1 millivolt)
• SPEED of recording (can affect measurement of duration)
• Preferable to express voltage in millivolts (mV) rather than millimeter (mm)
Chamber Enlargement & Hypertrophy 5

6. Atrial abnormalities
Atrial dilatation, hypertrophic, elevated atrial pressures, impaired ventricular
distensibility, and delayed intra-atrial conduction produced similar changes
on ECG and cannot be differentiated
As such, the terms of left atrial abnormality in right atrial abnormality or
preferably to left / right atrial enlargement, the mitrale / congenitale /
pulmonale
Chamber Enlargement & Hypertrophy 6

7. ‘P’ wave

8. Chamber Enlargement & Hypertrophy 8
P wave reflects atrial
depolarisation
Right atrial activation begins first.
Proceeds from the SAN into
(sinoatrial node) in the inferior
and the anterior direction and is
reflected by ascending limb of the
p wave in the frontal plane leads.

9. Chamber Enlargement & Hypertrophy 9
Left atrial activation begins 0.03
seconds after the right atrial
activation.
Proceeds from high in the
interatrial septum (IAS) in a left,
inferior and posterior direction.
Constitute distal half of the
descending limb of the p wave.

10. Normal ‘P’ wave
LEAD II
Duration in lead II is 0.08 - 0.1 second,
Max 0. 11 second.
Amplitude in lead: Usually 2 mm, max
2.5 mm.
Chamber Enlargement & Hypertrophy 10
LEAD V1
Usually biphasic.
Initial positive movement deflection < 1.5
mm
Terminal negative deflection not exceeding 1
mm in-depth and < 0.03 seconds in duration.
Duration of p wave in V1 is 0.05-0.08
second.

11. Left atrial abnormalities
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 main manifest frontal plane p wave axis.
Chamber Enlargement & Hypertrophy 11

12. Criteria for LAA
LEAD II
Chamber Enlargement & Hypertrophy 12
LEAD V1 – P terminal force (MORRIS
Index)
• Ratio between the duration of p wave in lead II and the PR
segment of >1.6 (Marcuz Index)
• Leftward shift of the p wave axis less than 15-30°

13. ECHOCARDIOGRAPHIC
EVALUATION
OF ECG CRITERIA FOR LAA
CRITERA 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 31 64
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
Chamber Enlargement & Hypertrophy 13

14. CAUSES OF LA ABNORMALITY
• Valvular heart disease, mainly mitral and aortic
• Hypertensive heart disease
• Cardiomyopathy (dilated/ restrictive/hypertrophic)
• CAD
Chamber Enlargement & Hypertrophy 14

15. • 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.
Chamber Enlargement & Hypertrophy 15

16. • The mere presence of a twin-peaked P wave is not diagnostic of LA abnormality
Chamber Enlargement & Hypertrophy 16

17. Right atrial abnormalities
LEAD II
• Total p wave duration is usually normal.
• Peaked p waves with amplitudes in lead to more than 0.25 millivolts
(even a normal amplitude p wave if pointed)
LEAD V1
• Prominent initial positivity of the P wave in V1 or V2 (>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 lead V1 with a threefold
or greater increase in lead V2
Chamber Enlargement & Hypertrophy 17

18. 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’
Chamber Enlargement & Hypertrophy 18

19. Kaplan Criteria
• QRS axis> 90°
• P amplitude in V2> 0.15mv
• R/S> 1 in V1 in the absence of RBBB
• Combined sensitivity of 49% with specificity of 100%
Chamber Enlargement & Hypertrophy 19

20. CAUSES OF RA ABNORMALITY
• Congenital heart disease (Ebstein's anomaly, severe PS)
• Tricuspid valve disease
• Chronic cor pulmonale (COPD)
RAA is very uncommon in isolated ASD without PH.
Chamber Enlargement & Hypertrophy 20

21. • Tall, peaked ("gothic") P wave in leads IIL, IIL, 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
Chamber Enlargement & Hypertrophy 21

22. 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.
Chamber Enlargement & Hypertrophy 22
‘P’ TRICUSPIDALE

23. • 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 and V1
Chamber Enlargement & Hypertrophy 23
HIMALAYAN ‘P’ WAVES

24. • 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.
Chamber Enlargement & Hypertrophy 24
PSEUDO ‘P’ PULMONALE

25. • (C) P mitrale - increase in the left atrial component in
amplitude and duration. Associated intraatrial
Conduction defect - prolongation of P wave duration
Chamber Enlargement & Hypertrophy 25
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.

26. BIATRIAL ENLARGEMENT
• Large biphasic P wave in V1 initial component> 1.5 mm in height
and terminal component >1 mm in depth and 0.04 sec in duration.
• ‘P’ wave amplitude of more than 2.5 m and duration of more than
0.12 sec in lead II.
Chamber Enlargement & Hypertrophy 26
 MS/ MR with PAH
 MS/ MR with TS/TR
 ASD with PAH
 Lutembacher's
syndrome
 DCM/RCM

27. Atrial Fibrillation, itself indicates possible dilatation of the
atria in most disease.
Course ‘f’ waves in lead V1 (>1 mm) were associated with
radiological and anatomical evidence of atrial enlargement.
Chamber Enlargement & Hypertrophy 27

28. Ventricular Hypertrophy
• Age: QRS voltages decline with age. The commonly used voltage criteria
apply to adults > 35 years
• Gender: women have slightly lower voltages Race: Blacks have higher
voltages, hispanics and caucasians lower compared to whites
• Body Habitus
Chamber Enlargement & Hypertrophy 28

29. 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)
Chamber Enlargement & Hypertrophy 29

30. Chamber Enlargement & Hypertrophy 30
Ventricular Activation Time
• Indicator of transverse conduction
time across LV wall
• Prolonged in LVH (normal <4Oms
in Left leads, <20ms in right leads)

31. CLASSIFICATION OF LV
ENLARGEMENT
LV VOLUME
LV MASS
COMMENT
S
NORMAL
ABNORMA
L
NORMAL NORMAL
CONCENTRIC
LVH
Abnormal
Volume >
90ml/m2
ABNORMAL
ISOLATED LV
VOLUME
OVERLOAD
ECCENTRIC
COMMENTS
Abnormal LV mass > 131g/ m2 in males,
108 g/m2 in females.
Chamber Enlargement & Hypertrophy 31

32. • T wave inverted in left oriented leads V5, V6, I, AVL and upright in V1, V2, AVR.
• Inverted T wave - blunt apex, asymmetrical limb, the proximal limb is shallower than distal limb.
• Associated ST segment is minimally depressed with slight upward convexity
Chamber Enlargement & Hypertrophy 32
LVH WITH PRESSURE OVERLOAD

33. • Deep and narrow Q waves in left oriented leads V5, V6.
• The tall T waves in left precordial leads V5, V6 are symmetrical sharply pointed.
• ST segment in V5, V6 minimally elevated and concavity upwards.
Chamber Enlargement & Hypertrophy 33
LVH WITH DIASTOLIC OVERLOAD

34. DIASTOLIC OVERLOAD IN AR &
MR
• Diastolic overload of MR can be distinguished by ECG from AR.
• In MR, Giant LA will displace the heart forward, QRS vector is
less aligned with V1 and more aligned with V6. Hence S wave in
lead V1 will be attenuated.
• In AR, the S wave in V1 is deep.
Chamber Enlargement & Hypertrophy 34

35. Sokolow Lyon Criteria (1949)
S in V1 + R in V5/V6 > 3.5 mv
OR
R in V5 or V6 > 2.60 mv.
Chamber Enlargement & Hypertrophy 35

36. Cornell voltage criteria (1987)
R in aVL +S in V3 > 2.80 mv for Males
Chamber Enlargement & Hypertrophy 36
Cornell voltage-duration product
• QRS duration x Cornell voltage >244 mVms
• QRS duration x sum of voltages in all leads >1742 mm-
sec
• R in aVL >11 mm.
• RI+SIII > 25 mm.
• Total 12 lead voltage >175 mm

37. LVH IN THE PRESENCE OF
CONDUCTION DISORDERS:
RBBB (reduces the S wave in the precordial leads)
Chamber Enlargement & Hypertrophy 37

38. LVH IN THE PRESENCE OF
CONDUCTION DISORDERS:
LAFB (QRS vector shifts posteriorly)
Chamber Enlargement & Hypertrophy 38

39. LVH IN THE PRESENCE OF
CONDUCTION DISORDERS:
LBBB
Chamber Enlargement & Hypertrophy 39
• 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 S V2 + R V6 > 45 mm.
• E/o LAE with QRS duration > 0.16.

40. Significance
Chamber Enlargement & Hypertrophy 40
• LVH on ECG correlated with increased CV mortality
• LIFE study showed improvement in survival with LVH regression
(Cornell criterion), also HOPE trial (Sokolow Lyon criteria)
• Secondary ST-T changes and associated LAE indicate worse
prognosis
• Prominent ST T changes in apical hypertrophy (Yamaguchi
syndrome)
• Cornell product is one of the best predictors of overall outcome

41. 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.
Chamber Enlargement & Hypertrophy 41

42. 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%)
• Vectorial classification of RVH (Chou and Helm, 1967)
• Type A: R in V1, S in V6 (CCW loop) - PS
• Type B: R/S>1 in Vi with R> 0.5m V (CW loop) - RHD MS
• Type C :S in V5-6. with R/S<1 in V5, CW loop - COPD
Chamber Enlargement & Hypertrophy 42

43. • Leads aVR, V1, and V2- abnormally tall R waves.
• I, aVL, V5, V6- Deep S waves leading to RS or rS complex
• Right axis deviation
Chamber Enlargement & Hypertrophy 43
RVH WITH PRESSURE OVERLOAD

44. Sokolow Lyon Criteria (1949)
• R in V1 + S in V5/V6 > 1.10 mV
• R in V1 > 0.7 mV
• S wave in V5 or V6 > 0.7 mV
• qR in V1
• R/S ratio in V1 > 1 with R >0.5 mV
• R/S ratio of < 1 in V5 or V6
Chamber Enlargement & Hypertrophy 44

45. CAUSES OF RVH
• Systolic (pressure) overload
• Pulmonary Stenosis
• Pulmonary Hypertension
• TOF (unusual feature - no ‘strain’ pattern)
• Diastolic (volume) overload
• ASD/ TAPVC/ PAPVC
Chamber Enlargement & Hypertrophy 45

46. • In lead V1 -tall monophasic R wave or a diphasic RS, Rs, or qR Compleex.
• Inversion in right precordial leads ('strain)
• S pattern in V6
• In pure valvular PS, age 2-20, height of R wave in mm multiplied by 5gives RV systolic pressure
Chamber Enlargement & Hypertrophy 46

47. • 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
Chamber Enlargement & Hypertrophy 47
RVH WITH RBBB

48. V1
• Normal young adult
• True posterior infarction
• Dextrocardia
• LPFB
• Displacement of the heart due to pulmonary disease
• Wolff Parkinson White pattern
• Muscular dystrophy
Chamber Enlargement & Hypertrophy 48

49. 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.
Chamber Enlargement & Hypertrophy 49
• 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.

50. • 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.
• LV:RV WEIGHT RATIO
o At birth - 0.8:1
o 1 month - 1.5:1
o 6 months - 2.0:1
o Adult - 2.5:1
Chamber Enlargement & Hypertrophy 50

51. ATRIAL ABNORMALITY
• RAA - Peaked P wave in leads II and V1
• 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 waves in V1 or V3R
Chamber Enlargement & Hypertrophy 51

52. RVH
R wave greater than the 98th percentile in lead V1.
S wave greater than the 98th percentile in lead I or V6.
RSR' - pattern in lead V1,
R' height > 15 mm in infants less than 1 year or
R' height > 10 mm in Children's more than 1 year.
Upright T waves in V1 (> 7 days, up to 10 years)
qR pattern in V1
Overall sensitivity 69%, specificity 82%.
Chamber Enlargement & Hypertrophy 52

53. LVH
• R-wave amplitude greater than
98th percentile in lead V5 or V6.
• R wave less than 5th Percentile
in lead V1 or V2.
• S-wave amplitude greater than
98th percentile in lead V1.
• Q wave greater than 4 mm in
lead V5 or V6 Inverted T wave in
lead V6 Chamber Enlargement & Hypertrophy 53

54. Suggested Reading
An Introduction to
Electrocardiography -Leo
Schamroth 7th ed
AHA/ ACCF/ HRS
recommendations for the
standardisation and
interpretation of the
Electrocardiogram Part V.
JACC 2009; 53: 992-1002
Marriott's Practical
Electrocardiography 11thed
Cardiology Clinics August
2006
Advanced 12-lead
Electrocardiography;
Chamber Enlargement & Hypertrophy 54

55. Thank you.