Chamber Enlargement & Hypertrophy: ECG Criteria

Chamber
Enlargement &
Hypertrophy

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

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

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

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)

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

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.

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.

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.
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.

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.

Criteria for LAA
LEAD II
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°

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

CAUSES OF LA ABNORMALITY
• Valvular heart disease, mainly mitral and aortic
• Hypertensive heart disease
• Cardiomyopathy (dilated/ restrictive/hypertrophic)
• CAD

• 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.

• The mere presence of a twin-peaked P wave is not diagnostic of LA abnormality

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

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’

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%

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.

• 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

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.
‘P’ TRICUSPIDALE

• 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
HIMALAYAN ‘P’ WAVES

• 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.
PSEUDO ‘P’ PULMONALE

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

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.
 MS/ MR with PAH
 MS/ MR with TS/TR
 ASD with PAH
 Lutembacher's
syndrome
 DCM/RCM

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.

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

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)

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

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.

• 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
LVH WITH PRESSURE OVERLOAD

• 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.
LVH WITH DIASTOLIC OVERLOAD

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.

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

Cornell voltage criteria (1987)
R in aVL +S in V3 > 2.80 mv for Males
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

LVH IN THE PRESENCE OF
CONDUCTION DISORDERS:
RBBB (reduces the S wave in the precordial leads)

LAFB (QRS vector shifts posteriorly)

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 S V2 + R V6 > 45 mm.
• E/o LAE with QRS duration > 0.16.

Significance
• 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

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.

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

• 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
RVH WITH PRESSURE OVERLOAD

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

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

• 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

• 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
RVH WITH RBBB

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

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.
• 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.

• 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

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

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%.

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

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: ECG Criteria

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