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ECG ANALYSIS
“Absence Makes the Heart Grow Fonder”, oil on canvas, John William Godward, 1912.
The Great Nineteenth century Neo-Classicist painters such John William Godward were
able to beautifully illustrate the romantic inner “affairs of the heart”. In the medical field
we capture the inner “affairs of the heart” by the somewhat less romantic medium of the
electrocardiograph.
ECG ANALYSIS
INDEX
1.
Normal parameters.
2.
P Wave Abnormalities
3.
P-R Interval Abnormalities
4.
P-R Segment Abnormalities
5.
Q Wave Abnormalities
6.
QRS Abnormalities
7.
Q-T Interval Abnormalities
8.
T Wave Abnormalities
9.
U Waves Abnormalities
10.
Left Bundle Branch Block
11.
Right Bundle Branch Block
12.
Fascicular Block
13.
Left Axis Deviation
14.
Right Axis Deviation
15.
ST Segment Abnormalities
16.
Abnormalities of AVR
17.
Ventricular Hypertrophy
For paediatric considerations see separate guidelines
For ECG changes associated with specific conditions, see separate individual
guidelines for these conditions.
Normal Parameters
Standard tracing speed and ECG grid spacing:
ECG grid makings 1
1.
2.
3.
The standard ECG trace velocity is 25 mm per second.
●
One small square is 1 mm.
●
One large square is 5 mm.
The horizontal axis is a measure of time.
●
Each small square is 0.04 seconds
●
Each large square is 0.20 seconds.
The vertical axis is a measure of voltage and polarity.
●
Each small square is 0.1 mV.
●
Each large square is 0.5 mV.
●
1 millivolt is therefore 10 mm or 2 large squares.
Morphology of the Electrical Tracing:
P Wave
The P wave represents depolarization through both the atria.
Characteristics of the normal P wave include:
1.
Width:
●
2.
Amplitude:
●
3.
Duration is < 0.12 seconds, (< 3 small squares)
Amplitude is ≤ 3 mm (3 small squares)
Polarity:
●
Upright (ie positive) in I, II, AVF and V4-V6
4.
●
Inverted in AVR
●
May be positive, negative or biphasic in III, AVL, V1-V3
Morphology:
●
Shape, is normally smoothly curved (as opposed to an abnormal notched or
peaked)
PR Interval
●
This is measured from the beginning of the P wave to the beginning of the Q wave
(or the first ventricular deflection).
●
This represents the length of time taken for the electrical impulse to travel from the
atria to the ventricles.
●
The normal PR interval is 0.12 to 0.20 seconds, (or 3-5 small squares)
PR Segment
●
This is measured from the end of the P wave to the beginning of the QRS complex.
It is part of the PR interval.
●
The PR segment is normally isoelectric.
Q Wave
●
A normal q (usually expressed as a small letter) wave is often normally found in
leads in leads I, III, aVL, V5, and V6 2
1.
Width
●
2.
Amplitude:
●
3.
It is less than 0.04 seconds (1 small square) in duration.
It is less than 25% of the amplitude of the R wave.
Polarity
●
By definition a q wave has negative polarity.
QRS Interval
Nomenclature in QRS complexes:
●
Q wave: Any initial negative deflection
●
R wave: Any positive deflection
●
S wave: Any negative deflection after an R wave
1
Width:
2.
●
The normal QRS width is ≤ 3 mm (or 3 small squares.
●
Note that often there will not be a definite q wave at the beginning or a
definite S wave at the end of the complex. The “QRS” in these cases is
measured from the moment it leaves the iso-electric line to the moment it
returns.
●
The QRS represents the intra-ventricular conduction time.
Amplitude:
The QRS amplitude (voltage) can vary under normal circumstances.
It may be taller in:
●
The young
●
The thin
It may be smaller in:
●
The obese
●
COPD, (hyper-expanded lung) may cover the heart.
Its amplitude will also be affected in a number of pathological conditions, (see
below)
Normal Measurements
●
The upper limit of normal in a pre-cordial lead is 30 mm.
●
The upper limit of normal in a limb lead is 20 mm.
In the pre-cordial leads the voltage of the QRS complex should not be less than the
following: 1
3.
●
V1 and V6
6 mm
●
V2 and V5
8 mm
●
V3 and V4
10 mm
Polarity:
4.
●
Positive to equiphasic:
I, II, V3-V6
●
Positive, negative or equiphasic:
AVL and AVF
●
Negative:
AVR
Transitional zone:
●
The R wave in the precordial leads steadily increases in amplitude from lead
V1 to V6, with a corresponding decrease in S wave depth, culminating in a
predominantly positive complex in V6. Thus, the QRS complex gradually
changes from being predominantly negative in lead V1 to being
predominantly positive in lead V6
●
Around V3-V4 the R and S waves are roughly equiphasic and this defines
the transitional zone.
ST segment
●
This is the interval between the end of the QRS complex and the beginning of the T
wave.
●
It represents part of the re-polarization phase of the heart and is normally isoelectric but may slant slightly upward into the T wave.
●
Elevation or depression of this segment is highly significant, (see below) A nonpathological elevation of the ST segment may be seen with benign early
repolarisation which is particularly common in young males, athletes, and Africans.
2
QT Interval
●
This is an important measurement. It is the interval from the beginning of the Q
wave (or ventricular complex) to the end of the T wave.
●
It represents the sum of depolarization and re-polarization periods of the heart.
The normal QT interval is depended on the age of the patient and the heart rate. As
the heart rate increase the QT interval shortens and as it slows down the QT
lengthens.
The normal Q-T interval range: 0.35 – 0.43 seconds.
The normal QT interval can be corrected for variations in heart rate by using Bazzet’s
formula. The corrected QT is symbolized by Q-Tc.
Bazett’s formula:
●
Q-Tc = Q-T duration (in seconds) divided by the square root of the R-R interval.
●
The Q-Tc corresponds to Q-T duration (in seconds) at a heart rate of 60.
As a rough estimate:
●
Q-T should be < ½ the R-R interval (at rates of <90).
J point
●
The J point is defined as the end of the QRS complex and where the ST segment
begins, as shown below.
●
In leads V1 to V3 the rapidly ascending S wave often merges directly with the T
wave, making the J point indistinct and the ST segment difficult to identify. This
produces a pseudo-elevation of the ST segment, known as “high take-off.” 2
T wave
This is an upward or downward deflection that occurs at the end of the ST segment.
It represents re-polarization of the heart.
1
Width:
●
2.
3.
No widely accepted criteria exist regarding T wave width.
Amplitude:
●
No widely accepted criteria exist regarding T wave amplitude. 2
●
The T wave should generally be at least 1/8 but less than 2/3 of the
amplitude of the corresponding R wave. T wave amplitude rarely exceeds
10 mm. 2
Polarity:
T wave orientation usually corresponds with that of the QRS complex. 2
●
Positive in leads I, II, V3-V6
4.
●
Inverted in AVR
●
Positive or inverted in III, AVL, AVF, V1, V2
Shape:
●
The normal T wave is mildly asymmetrical, the first half having a more
gradual slope than the second half.
U Wave
The U wave is a small deflection that follows the T wave.
It results from repolarisation of the mid-myocardial cells, that is, those between the
endocardium and the epicardium and the His-Purkinje system. 2
1
Width and amplitude:
●
2.
It is often not seen because of its low voltage. Many electrocardiograms will
have no discernible U waves.
Polarity:
●
It is generally upright except in the aVR lead and is often most prominent in
leads V2 to V4. 2
The Vector Direction of the Electrical Axis:
The electrical vector axis of the heart can be determined by:
●
The 3 bipolar limb leads, I, II and III.
And
●
The 3 unipolar limb leads AVR, AVL and AVF
The electrical vectors of these leads can be represented by the following diagram:
The overall electrical vector or axis of the heart normally lies between -30 degrees
and +120 degrees.
The electrical axis of the heart can be determined by a number of different ways. The 2
commonest are presented below:
Axis at a glance
For examples of axis determination see appendix 3 below.
It should be remembered that:
The deflection will be greatest when the axis is in the same direction as the recording lead,
and that this deflection will be positive.
As the axis moves away from the recording lead the deflection will become progressively
smaller until at the perpendicular it will be zero. At this point there will be no sum
deflection (ie R =S)
Moving further away still the axis will change direction and become more and more
negative. If the axis is in the exact opposite direction the deflection will be maximally
negative.
Therefore:
Normal axis:
I and II are upright (first 3 examples in appendix 3
below)
Left axis deviation:
I is up and II is down.
Right axis deviation:
I is down and II is up.
Northwest (“No man’s land”)
I and II are down.
Two step method
This method makes use of the limb leads, which are all at 30 degrees to their neighbour.
Use 2 steps:
1.
Look for an equiphasic deflection. The axis (current flow vector) will be
perpendicular to this.
2.
Now that the plane of current flow is known, look for the lead whose axis is
parallel with the current flow to see whether current is flowing toward (positive
deflection) or away (negative deflection) from its positive electrode.
Estimating the Heart Rate
When the rhythm is regular the rate can be estimated by dividing the number of large
squares into 300.
When the rate is irregular an estimate can be made of the average heart rate by counting
the number of R waves in 6 seconds (30 large squares) and multiplying by 10.
P Wave Abnormalities
Abnormalities of the P wave include:
●
An increased width may indicate left atrial abnormality or right atrial hypertrophy.
●
An increased amplitude may indicate right atrial enlargement.
●
Abnormal shape: This suggests left atrial hypertrophy.
A notched P wave, (above left). Notched P waves result from a slight asynchrony
between right and left atrial depolarization.
Or
A biphasic P wave with a deep and broad terminal (inverted) “trough” seen in V1.
P-R Interval Abnormalities
●
A prolonged PR interval represents first degree heart block.
●
A short PR interval is seen in pre-excitation syndromes, such as Wolf Parkinson
White syndrome.
P-R Segment Abnormalities
●
This is normally isoelectric, it may be depressed in acute pericarditis.
Q Wave Abnormalities
●
Pathological q waves (see above) represent recent or old transmural myocardial
infarction.
QRS Abnormalities
Causes of a wide QRS complex:
1.
Ventricular rhythms:
●
Complete heart block
●
Premature ventricular contraction
●
IVR and AIVR
●
VT
●
2.
Pacemakers (ventricular paced).
Conduction abnormalities:
●
Pre-excitation syndromes, (eg WPW)
●
LBBB
●
RBBB
3.
Hyperkalemia
4.
Drugs and toxins
●
In particular TCAs and class I anti-arrhythmic agents.
Causes of an Increased Amplitude QRS
1.
LVH
2.
RVH
3.
Young age groups
4.
The thin.
Causes of a Decreased Amplitude QRS
1.
COPD
2.
Obesity
3.
Pericardial effusion.
4.
Dextrocardia.
Causes of a Dominant R Wave in V1
In pathological cases this usually implies there is an abnormal depolarization pattern in the
ventricles.
1.
Right bundle branch block (the most common cause)
2.
Right ventricular hypertrophy.
3.
Wolff Parkinson White syndrome (type A)
4.
True posterior myocardial infarction.
There are also 3 non-pathological causes:
5.
Incorrect lead placement.
6.
Dextrocardia.
7.
In pediatric ECGs, this may be a normal finding.
Causes of “notching” on the downstroke of the QRS
1.
Osborne (or J) waves of hypothermia
2.
BER
3.
Epsilon waves of ARVC, (but usually seen after the QRS)
Poor Anterior R Wave Progression
●
When the R wave is very small or absent in lead V1 and remains very small across
the chest leads, this is termed poor or abnormal R wave progression.
●
This is due usually due to loss ventricular muscle mass and is principally seen in
IHD after myocardial infarction.
Q-T Interval Abnormalities
Causes of a prolonged QT interval:
Congenital Syndromes:
1.
Lange-Neilson (autosomal recessive) associated with nerve deafness.
2.
Romano-Ward (autosomal dominant), no associated deafness.
Acquired Causes:
1.
Idiopathic
2.
Electrolyte disorders (all low)
3.
●
Decreased Ca
●
Decreased K
●
Decreased Mg
Drugs:
●
Class Ia anti-arrhythmics, eg. quinidine, procainamide, disopyramide
Including drugs with Ia or “quinidine like” effects, eg, TCAs,
phenothiazines
4.
●
Class Ic drugs, (eg flecainide)
●
Class III anti-arrhythmics, (eg, sotalol, amiodarone)
●
Others:
♥
Organophosphates
♥
Non-sedating antihistamines
♥
Antipsychotic agents, (both “typical” and “atypical”).
♥
Erythromycin
Certain clinical conditions:
●
Severe hypothermia
●
Raised intracranial pressure, especially with SAH, occasionally with severe
trauma.
●
Severe bradyarrythmias in general, eg, CHB with slow escape rhythms.
●
Rarely ischemia
T Wave Abnormalities
Causes of an Elevated T wave
1.
Normal variant in young and thin.
2.
BER
2.
Hyperacute myocardial infarction.
3.
Hyperkalemia
4.
Right sided chest leads in true posterior myocardial infarction
Causes of a depressed or inverted or biphasic T wave
1.
Myocardial ischemia
●
2.
In particular deep and symmetrical T wave inversion of the antero-septal
leads is suggestive of Wellen’s syndrome.
Pericarditis
3.
Drug effect, eg digoxin
4.
Hypokalemia.
5.
Intracerebral haemorrhage, including SAH.
Causes of an Inverted or Elevated T wave
1.
In association with a bundle branch block, (will be opposite to the terminal
deflection of the QRS complex)
2.
Pre-excitation syndromes, (will be opposite to the terminal deflection of the QRS
complex) and abnormal ventricular depolarization in general, (repolarization will
also be abnormal).
3.
LHV or RVH with strain pattern, (will be opposite to the terminal deflection of the
QRS complex)
U Wave Abnormalities
1.
Enhanced U waves are particularly seen in hypokalemia.
U waves seen in leads V1-3 in a patient with hypokalemia.
2.
Myocardial ischemia, (where it may be inverted).
3.
Hypertension, (where it may be inverted).
Left Bundle Branch Block
Morphology of LBBB
1.
QRS widened > 0.12 seconds (> 3 squares), (in complete blocks)
2.
V1 has:
●
A QS morphology, (without antero-septal MI)
Or
●
An rS morphology, (with antero-septal MI)
There may also be a notch within the complex (W-shaped)
3.
V6 has:
●
A monophasic R wave (no Q wave and no S wave) (without antero-septal
MI)
Or
●
A qR morphology, (with antero-septal MI)
There may also be a notch within the complex (M-shaped)
4.
T wave discordance:
●
5.
The T wave should be deflected opposite the terminal deflection of the QRS
complex. This is known as appropriate T wave discordance with bundle
branch block. A concordant T wave may suggest ischemia or myocardial
infarction.
Left axis deviation
Incomplete LBBB:
●
Incomplete LBBB looks like “normal” LBBB but the QRS duration is within
normal limits, with less ST-T wave changes. This is often a progression of LVH.
Causes of LBBB
1
Myocardial infarction
2.
Extensive CAD
3.
Hypertension
4.
Primary disease of the cardiac electrical conduction system
5.
Cardiomyopathy
Right Bundle Branch Block
Morphology of RBBB
1.
QRS widened > 0.12 seconds (> 3 squares), (in complete blocks)
2.
V1 has
A triphasic complex rSR/, (without antero-septal MI)
Or
A biphasic complex (QR), (with antero-septal MI)
3.
V6 has:
qRS (a deep terminal S wave), (without antero-septal MI)
Or
RS (a deep terminal S wave), (with antero-septal MI)
See below.
4.
T wave discordance:
●
The T wave should be deflected opposite the terminal deflection of the QRS
complex. This is known as appropriate T wave discordance with bundle
branch block. A concordant T wave may suggest ischemia or myocardial
infarction.
5.
Right axis deviation.
Incomplete RBBB looks like “normal” RBBB but has a QRS duration within normal limits
with the same terminal QRS features. This is often a normal variant.
Causes of RBBB
1.
May be a normal variant.
2.
Myocardial infarction
3.
Hypertension.
4.
Myocarditis
5.
Primary disease of the cardiac electrical conduction system
6.
Cardiomyopathy.
7.
Cor pulmonale due to chronic lung disease
8.
ASD
Fascicular Block
LAHB
1.
Normal QRS duration.
2.
Left axis deviation
3.
QRS morphology:
●
Small q in leads 1 and AVL
●
Small r waves in the inferior leads
LPHB
1.
Normal QRS duration.
2.
Right axis deviation
3.
QRS morphology:
●
q waves in II, III and AVF
●
r waves in leads I and AVL
Uni-fascicular Block
●
RBBB
●
LAHB
●
LPHB
●
1st Degree Heart Block
Bi- fascicular Block
●
RBBB and LAHB
●
RBBB and LPHB
●
LBBB
Tri- fascicular Block
●
RBBB and LAHB and 1st Degree Heart Block
●
RBBB and LPHB and 1st Degree Heart Block
●
LBBB and 1st Degree Heart Block
●
Alternating RBBB and LBBB
Left Axis Deviation
Causes
1.
LHV
2.
LAHB
3.
LBBB
Right Axis Deviation
Causes
1.
Body habitus:
●
Pregnancy
●
Obesity
2.
Infants and young children
3.
RVH
4.
LPHB
5.
RBBB
ST Segment Abnormalities
Causes of an Elevated ST Segment
Note that ST segment elevation is measured from the iso-electric line to the J point. The
iso-electric point (line) is taken as the ECG trace between beats, (ie the end of the T
wave to the beginning of the next P wave) 4
1.
ST segment elevation myocardial infarction
●
Persistent S-T elevation of > 2 small squares (2 mm) in 2 or more
contiguous pre-cordial leads.
●
Persistent S-T elevation of > 1 small square (1 mm) in 2 or more contiguous
limb leads.
●
Note the new LBBB is also considered evidence of STEMI
2.
Pericarditis
3.
Myocarditis
4.
Prinzmetal angina
5.
Brugada’s syndrome
6.
LBBB
7.
Ventricular aneurysm
8.
Benign Early Repolarization, (BER); (normal variant).
9.
Pseudo-ST elevation, such as may be seen in hyperkalemia.
Causes of a Depressed ST Segment
ST segment depression has a wide range of causes. The exact morphology of the depressed
segment can give important clues to aetiology.
1.
ST segment depression that is upward sloping:
This may be:
2.
●
A normal variant if the depression is mild. The normal ST segment curves
very slightly upward into the beginning of the T wave. 1
●
Seen in rapid tachyarrhythmias
ST segment depression with a horizontal base:
●
3.
4.
ST segment depression that is downward sloping:
●
Strain patterns in hypertrophy.
●
Digitalis effect, (the “reverse tick”).
ST segment depression that is sagging ie has a U shape with the nadir in the middle
of the segment.
●
5.
This pattern is seen with myocardial ischemia. In fact an absolutely
horizontal depressed ST segment, which forms a sharp angle with the T
wave is highly suggestive of ischemia.
Digitalis effect.
Non-specific ST segment depression:
●
Hypokalemia
●
Aortic dissection
●
Pulmonary embolism
●
Subarachnoid haemorrhage
Localization of STEMI infarction
(Source: Life in the fast lane Website)
Abnormalities of AVR
aVR has been described as the “forgotten lead” in ECG recordings.
ST segment elevation in aVR is often ignored as just being a “reciprocal change”; however
it does have two important diagnostic utilities:
●
In toxicology, where certain changes in the aVR lead may indicate fast sodium
channel blockade.
Diagnostic features of TCA poisoning (and sodium channel blockade in general) in
lead AVR include:
●
●
A large terminal R wave in aVR
●
An increased R/S ratio, (>0.7)
In cardiology where ST elevation in the aVR lead may indicate a left main
coronary artery critical stenosis.
Ventricular Hypertrophy
Ventricular hypertrophy can essentially be due to a pressure load (eg aortic stenosis or
hypertension) or a volume load, (eg mitral incompetence or dilated cardiomyopathies).
A pressure load results when myocardial fibers generate increased systolic force or
tension. This results in a concentric hypertrophy in which the ventricular wall thickness is
increased in relation to the ventricular cavity.
A volume load results when there is an increased end-diastolic wall stress.
This leads to eccentric hypertrophy, where the left ventricular wall thickness remains
normal relative to the increase in the radius of the left ventricle (chamber dilation). In this
situation the systolic pressure remains unchanged.
Diagram showing the patterns of hypertrophy, normal on the left, pressure loading in the
middle and volume loading on the right.
The gold standard of ventricular hypertrophy is echocardiography. However the ECG
remains an invaluable aid to diagnosis of ventricular hypertrophy. Its specificity is good
but sensitivity somewhat less.
Cardiac hypertrophy is an important finding as it has an association with a number of
cardiovascular complications including:
●
Myocardial infarction.
●
Stroke
●
Heart failure
●
Arrhythmias and sudden death.
Left Ventricular Hypertrophy
A number of different criteria and scoring systems exist for the determination of LVH on
the ECG.
A commonly used one is the Estes (or more correctly the Romhilt-Estes) system. It has
reasonable specificity (85-95%), but sensitivity is low.
Estes Scoring System for Left Ventricular Hypertrophy 3
This is scored o 6 criteria:
1.
Voltage criteria:
Any of:
2.
3.
●
R or S wave in limb leads = 20 mm
●
S wave in V1 or V2 = 30 mm
●
R wave in V5 or V6 = 30 mm
3 points
ST-T wave abnormalities (a strain pattern)
●
Without digitalis
3 points
●
With digitalis
1 point
Left atrial enlargement in V1
This refers to a biphasic P wave with a deep and
broad terminal (inverted) “trough” seen in V1.
3 points
4.
Left axis deviation.
2 points
5.
QRS duration> 0.9 seconds
1 point
6.
Instrinsicoid deflection in V5 and V6 ≥ 0.05 seconds
1 point
Instrinsicoid deflection is the distance from the onset of the QRS to the
peak of the R wave.
A total of 5 points is diagnostic of left ventricular hypertrophy.
A total of 4 points represents probable left ventricular hypertrophy.
See appendix 1 below.
Right Ventricular Hypertrophy
Right ventricular hypertrophy is associated with conditions that cause right ventricular
mass to begin competing with the left ventricle for the dominant overall effect on the ECG
Causes include:
1.
Pulmonary hypertension from any cause.
●
The most common will be COPD
2.
Pulmonary stenosis
3.
Some congenital heart conditions such as Tetralogy of Fallot.
ECG Changes of RVH:
ECG changes suggestive of RVH include:
1.
Right axis deviation, (>90 degrees)
2.
Tall or dominant R-waves in the RV leads, (V1-3)
3.
Deep or dominant S-waves in LV leads, (V4-6)
4.
Slight increase in QRS duration
5.
ST-T changes directed opposite to QRS direction in pre-cordial and inferior leads.
6.
Right atrial enlargement, (P pulmonale)
See appendix 2 below.
Appendix 1
Left ventricular hypertrophy:
Classic LVH with strain and left atrial enlargement.
Appendix 2
Right ventricular hypertrophy:
Classic RVH with strain and right atrial enlargement.
Appendix 3
Axis determination:
References
1.
Conover M.B Understanding Electrocardiography 7th ed 1996.
2.
Meek S. ABC of clinical electrocardiography. Introduction II - Basic terminology.
BMJ. 2002 February 23; 324(7335): 470–473.
3.
Romhilt DW, Estes EH Jr. A point-score system for the ECG diagnosis of left
ventricular hypertrophy. Am Heart J. 1968; 75(6):752-758.
4.
Hampton J.R, The ECG Made Easy, 4th ed. p. 48.
Dr J. Hayes
Reviewed 8 March 2012