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ECG EKG Interpretation
ECG EKG Interpretation
29 July 2014
As with all investigations the most important things are your findings on history,
examination and basic observations. Having a good system will avoid making errors.
To start with we will cover the basics of the ECG, how it is recorded and the basic
physiology. The 12-lead ECG misleadingly only has 10 electrodes (sometimes also called
leads but to avoid confusion we will refer to them as electrodes).
The leads can be thought of as taking a picture of the heart’s electrical activity from 12
different positions using information picked up by the 10 electrodes. These comprise 4
limb electrodes and 6 chest electrodes.
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Figure 1. Electrode positions on an ECG (EKG).
When electrical activity (or depolarisation) travels towards a lead, the deflection is net
positive. When the activity travels away from the lead the deflection is net negative. If it is
at 90 degrees then the complex is ‘isoelectric’ i.e. the R and S wave are the same size.
This can often be seen in V4 (see Figure 3).
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Figure 2. The electrical activity on an ECG (EKG).
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Figure 3. The electrical activity on an ECG (EKG).
V1, V2 = RV
V3, V4 = septum
V5, V6 = L side of the heart
Lead I = L side of the heart
Lead II = inferior territory
Lead III = inferior territory
aVF = inferior territory (remember ‘F’ for ‘feet’)
aVL = L side of the heart
aVR = R side of the heart
The ECG can be broken down into the individual components. For the purpose of this we
will look at lead II (see Figure 4). All boxes are based on the assumption that the paper
speed is running at 25mm/sec, therefore 1 large square is equivalent to 0.2 secs and a
small square to 0.04 secs.
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Figure 4. The segments of the ECG.
1. Patient details
2. Situation details
3. Rate
4. Rhthm
5. Axis
6. P-wave and P-R interval
7. Q-wave and QRS complex
8. ST segment
9. QT interval
10. T-wave
1. Patient details
2. Situation details
When was the ECG done?
The time
The number of the ECG if it is one of a series
If you are concerned that there are dynamic changes in an ECG it is
helpful to ask for serial ECGs (usually three ECGs recorded 10 minutes
apart) so they can be compared. These should always be labelled 1, 2
and 3.
Did the patient have chest pain at the time?
Or other relevant clinical details. For example, if you are wanted an ECG to
look for changes of hyperkalaemia, note the patient’s potassium level on the
ECG.
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1. Count the number of QRSs on one line of the ECG (usually lead II – running along
the bottom) and multiply by six.
2. Count the number of large squares between R waves and divide 300 by this
number (if the patient is in atrial fibrillation it is more accurate to report a rate range
rather than a single value).
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Figure 5. The axis of the heart – a useful diagram for assessing the cardiac axis using the
method above.
Can you see a p-wave? If the rhythm is atrial fibrillation, atrial flutter or a junctional
tachycardia you may not be able to.
At this point you can also assess whether each p wave is associated with a
QRS complex. P-waves not in association with QRS complexes indicate
complete heart block.
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Assess p-wave morphology
In some cases there can be a notched (or bifid) p-wave known as “p mitrale”,
indicative of left atrial hypertrophy which may be caused by mitral stenosis.
There may be tall peaked p-waves. This is called “p-pulmonale” and is
indicative of right atrial hypertrophy often secondary to tricuspid stenosis or
pulmonary hypertension.
A similar picture can be seen in hypokalaemia (known as “pseudo p-
pulmonale”).
The PR interval may be prolonged in first degree heart block (described in more
detail later).
The PR interval may be shortened when there is rapid conduction via an accessory
pathway, for example in Wolff Parkinson White syndrome.
PR depression may be seen in pericarditis.
Q-wave
A q-wave is an initial downward deflection in the QRS complex. These are
normal in left-sided chest leads (V5, 6, lead I, aVL) as they represent septal
depolarization from left to right. This is as long as they are <0.04secs long (1
small square) and <2mm deep.
If q-waves are larger than this or present in other leads they are pathological.
QRS complex
Width
The QRS complex normally lasts for < 0.12 secs (3 small squares).
Causes of a wide QRS:
Bundle branch blocks (LBBB or RBBB)
Hyperkalaemia
Paced rhythm
Ventricular pre-excitation (e.g. Wolf Parkinson White)
Ventricular rhythm
Tricyclic antidepressant (TCA) poisoning
Shape and height
The QRS may be small (or low voltage) in pericardial effusion, high BMI,
emphysema, cardiomyopathy and cardiac amyloid.
The QRS is tall in left ventricular hypertrophy (LVH)
The criteria suggestive of LVH on the ECG is if the height of the R
wave in V6 + the depth of the S wave in V1. If this value is >35mm
this is suggestive of LVH.
The QRS can also be tall in young, fit people (especially if thin).
8. ST segment
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The ST segment can be normal, elevated or depressed. To be significant the S-T
segment must be depressed or elevated by 1 or more millimeters in 2 consecutive
limb leads or 2 or more millimeters in 2 consecutive chest leads. Look out for
reciprocal changes.
ST elevation indicates infarction.
ST depression is normally due to ischaemia.
ST segment depression may also be seen in digoxin toxicity. Here the ST
depression will be downsloping (sometimes known as the “reverse tick” sign).
NB: High-takeoff
9. QT interval
The QT interval is the time between the start of the q-wave and the end of the t-
wave.
The QT interval is corrected for heart rate giving the QTc.
As a quick check, if the t-waves occur over half way between the QRS
complexes the QTc may be lengthened
Not an accurate method but very quick!
A long QTc interval (known as “long QT”) is especially important to identify in
patients with a history of collapse or transient loss of consciousness.
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Tricyclic Hypothermia Long QT IHD
antidepressants Hypokalaemia syndrome Myocarditis
(TCAs) Hypocalcaemia Brugada
Terfenadine Hypothyroidism syndrome
Erythromycin Arrhythmogenic
Amiodarone RV dysplasia
Phenothiazines
Quinidine
10. T-wave
The t-wave can be flattened or inverted for a number of reasons:
Normal variant
Commonly inverted in aVR and V1 and often in V2 and V3 in people of afro-
Caribbean descent.
Ischaemia
Ventricular hypertrophy (strain pattern) usually in lateral leads
LBBB (t-wave inversion in the anterolateral leads)
Digoxin
Hypokalaemia (can cause flattened t-waves)
N.B. Hyperkalaemia causes peaked T waves. The classic changes in hyperkalaemia are:
Small p-wave
Tall, tented (peaked) t-wave
Wide QRS
Widening of the QRS indicates severe cardiac toxicity
Summary
Following steps 1-10 above give the ideal system for interpreting an ECG. If you work
through these steps you will be unlikely to miss anything significant.
Click here for the next section: how to identify bundle branch
blocks
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