Oxford Medical Education

ECG (EKG) Interpretation

oxfordmedicaleducation.com/ecgs/ecg-interpretation/

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 hearts 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).

The areas represented on the ECG are summarized below:
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.

What do the segments of the ECG represent?
P-wave: Atrial contraction
PR interval: Represents the time taken for excitation to spread from the sino-atrial (SA) node across the
atrium and down to the ventricular muscle via the bundle of His.
QRS: Ventricular contraction
ST segment: Ventricular relaxation
T-wave: Ventricular repolarisation

Normal duration of ECG segments:

PR interval: 0.12 0.2 secs (3-5 small squares)
QRS: <0.12 secs (3 small squares)
QTc: 0.38 0.42 secs

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How to read an ECG

There are many different systems to interpret the ECG. This system ensures you will never miss anything:
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
These components will now be explained in more detail.

1. Patient details
Patients name, date of birth and hospital number
Location
This becomes important as in the ED or acute medical setting doctors are often shown multiple ECGs.
You need to know where your patient is in order to ensure that they can be moved to a higher
dependency area if appropriate.

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 patients potassium level on the ECG.

3. Measuring the rate on an ECG

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Rate can be calculated in a number of ways:

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).

4. Assessing the rhythm on an ECG

Is the rhythm regular or irregular? If it is irregular is it regularly or irregularly irregular?
Rhythm can be difficult to assess especially in bradycardia or tachycardia. It may be helpful to use the paper
test.
To do this place a piece of scrap paper over the ECG and mark a dot next to the top of a QRS
complex, draw another dot next to the top of the next QRS then slide the paper along the ECG. If the
rhythm is regular you should see that your two dots match to the tops of the QRS complexes
throughout the ECG.

5. Assessing the axis on an ECG

Axis is the sum of all the electrical activity in the heart.
The contraction travels from the atria to the right and left ventricles. As the left ventricle is larger and more
muscular normal axis lies to the left (at -30 degrees to 90 degrees see Figure 5).
As a general rule if the net deflections in leads I and aVF are positive then the axis is normal.
If lead I has a net negative deflection whilst aVF is positive then there is right axis deviation.
If lead I has a positive deflection and aVF has a negative deflection then there is left axis deviation
If you want to work it out more precisely you can use the method below:
Count the number of small squares of positive or negative deflection in aVF and make a dot on the
aVF axis (see Figure 5) moving a mm for each small square counted (e.g. x mm up for negative and x
mm down for positive deflections).
Count the number of small squares of positive or negative deflection in lead 1 and make a dot on the
lead 1 axis moving a mm from the centre of the chart for each small square counted (e.g. x mm right
for negative and x mm left for positive deflections).
Draw a horizontal line through your lead 1 dot and a vertical line through your aVF dot then draw a line
from this intersection back through 0 and this will give you the accurate axis.

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Figure 5. The axis of the heart a useful diagram for assessing the cardiac axis using the method above.

Causes of axis deviation

Left axis deviation

Right axis deviation

Can be normal if the diaphragms are raised e.g. Ascites,

pregnancy

Normal in children or young thin

adults.

Left ventricular hypertrophy (LVH)

Right ventricular hypertrophy

(RVH)

Left anterior hemiblock (see notes on heart block)

Inferior myocardial infaction
Hyperkalaemia

Often due to respiratory

disease

Vertricular tachycardia (VT)

Pulmonary embolism (PE)

Paced rhythm

Anterolateral myocardial infarction

Left posterior hemiblock (rare)
Septal defect

6. P-wave and PR interval

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.

7. Assessing Q-wave and QRS complex

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).

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8. ST segment
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
A mimic of ST elevation is high-takeoff. High-takeoff is also known as benign early repolarization.
High-takeoff is where there is widespread concave ST elevation, often with a slurring of the j-point (start of
the ST segment). It is most prominent in leads V2-5, is usually in young health people and is benign.
The best ways to differentiate it from myocardial infarction are:
The ST segments are concave; they are most prominent in V2-5; they have a slurred start (j-point); the
ST elevation is usually minimal compared to the amplitude of the t-wave; there are no reciprocal
changes; the ST segments do not change over time.

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.

Causes of long QT:

Drugs

Metabolic

Familial

Other

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Tricyclic antidepressants
(TCAs)

Hypothermia

Long QT syndrome

IHD

Hypokalaemia

Brugada syndrome

Myocarditis

Terfenadine

Hypocalcaemia

Erythromycin

Hypothyroidism

Arrhythmogenic RV
dysplasia

Amiodarone
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
and click here for medical student OSCE and PACES exam questions
about ECGs
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