How to Read an ECG

geekymedics.com/how-to-read-an-ecg/

Dr Matthew Jackson February 28,

2011

Introduction
This guide demonstrates how to read an ECG in a systematic and effective manner.

Confirm the name and date of birth of the patient matches the details on the ECG.

Confirm the date and time the ECG was performed.

Check out our ECG quiz on the new Geeky Medics quiz platform.

Step 1 – Heart rate

Heart rate can be calculated using the following method (if regular):

Count the number of large squares present within one R-R interval
Divide 300 by this number to calculate the heart rate

e.g. 4 large squares in an R-R interval: 300/4 = 75 beats per minute

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If the rhythm is irregular:

The first method of calculating the heart rate doesn’t work when the R-R interval
differs significantly throughout the ECG and therefore another method is required
Count the number of complexes on the rhythm strip (each rhythm strip is 10
seconds long)
Multiply the number of complexes by 6 (giving you the average number of
complexes in 1 minute)

e.g. 10 complexes on a rhythm strip X 6 = 60 beats per minute

What’s a normal adult heart rate?

Normal = 60 – 100 bpm
Tachycardia > 100 bpm
Bradycardia < 60 bpm

Hint: If there are obviously P-waves present, check the ventricular rate and the atrial
rate. The rates will be the same if there is 1:1 AV conduction.

Step 2 – Heart rhythm

The heart rhythm can be regular or irregular.

Irregular rhythms can be either:

Regularly irregular (i.e. a recurrent pattern of irregularity)

Irregularly irregular (i.e. completely disorganised)

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Mark out several consecutive R-R intervals on a piece of paper, then move them
along the rhythm strip to check if the subsequent intervals are the same.

Hint – if you are suspicious that there is some atrioventricular block, map out the atrial
rate and the ventricular rhythm separately (i.e. mark the P waves and R waves). As you
move along the rhythm strip, you can then see if the PR interval changes, if QRS
complexes are missing or if there is complete dissociation between the two.

Measure the R-R intervals to assess if the rhythm is

regular or irregular 1

Step 3 – Cardiac axis

Cardiac axis describes the overall direction of electrical spread within the heart.

In a healthy individual the axis should spread from 11 o’clock to 5 o’clock.

To determine the cardiac axis you need to look at leads I,II and III.

To get a better understanding of cardiac axis read this article.

Normal cardiac axis

In normal cardiac axis:

Lead II has the most positive deflection compared to Leads I and III

Normal Cardiac Axis

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Right axis deviation
In right axis deviation:

Lead III has the most positive deflection and Lead I should be negative
This is commonly seen in individuals with right ventricular hypertrophy

Right axis deviation 2

Left axis deviation

In left axis deviation:

Lead I has the most positive deflection

Leads II and III are negative
Left axis deviation is seen in individuals with heart conduction defects

Left axis deviation 2

Step 4 – P-waves
Next we look at the P-waves and answer the following questions:

Are P-waves present?

If so, is each P-wave followed by a QRS complex?
Do the P-waves look normal? (check duration, direction and shape)
If not present, is there any atrial activity e.g. sawtooth baseline → flutter waves /
chaotic baseline → fibrillation waves / flat line → no atrial activity at all?

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Hint – If P-waves are absent and there is an irregular rhythm it may suggest atrial fibrillation

P-waves 1

Step 5 – P-R interval

The P-R interval should be between 120-200 ms (3-5 small squares)

Prolonged PR interval (>0.2 seconds)

A prolonged PR interval suggests there is atrioventricular delay (AV block)

First degree heart block

First degree heart block involves a fixed prolonged PR interval (>200 ms)

First degree heart block

Second degree heart block (Mobitz type 1)

If the PR interval slowly increases then there is a dropped QRS complex (beat), this is
MOBITZ TYPE I SECOND DEGREE AV BLOCK (Wenckebach)

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 2nd degree AV block (Mobitz Type 1 – Wenckebach)

Second degree heart block (Mobitz type 2)

If the PR interval is fixed but there are dropped beats, this is MOBITZ TYPE 2 SECOND
DEGREE HEART BLOCK (clarify that by the frequency of dropped beats e.g 2:1, 3:1, 4:1)

Second degree heart block (Mobitz II)3

Third degree heart block (complete heart block)

If the P waves and QRS complexes are completely unrelated, this is THIRD DEGREE AV
BLOCK (complete heart block)

Complete heart block (3rd degree) 4

Tips for remembering types of heart block

To help remember these degrees of AV block, it is useful to remember the
anatomical location of the block in the conducting system:

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 First degree AV block:
Occurs between the SA node and the AV node (i.e. within the atrium)

Second degree AV block:

Mobitz I (Wenckebach) – occurs IN the AV node. This is the only piece of
conductive tissue in the heart which exhibits the ability to conduct at
different speeds
Mobitz II – occurs AFTER the AV node in the bundle of His or Purkinje fibres

Third degree AV block:

Occurs anywhere from the AV node down causing complete blockage of
conduction

Shortened PR interval
If the PR interval is short, this means one of two things:

Simply, the P-wave is originating from somewhere closer to the AV node so the
conduction takes less time (the SA node is not in a fixed place and some people’s
atria are smaller than others!)
The atrial impulse is getting to the ventricle by a faster shortcut instead of
conducting slowly across the atrial wall. This is an accessory pathway and can be
associated with a delta wave (see below which demonstrates an ECG of a patient with
Wolff Parkinson White syndrome)

Delta wave 5

Step 6 – QRS complex

There are several aspects of the QRS complex you need to assess:

Width
Height
Morphology

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 Various components of an ECG

Width
Width can be described as NARROW (< 0.12 seconds) or BROAD (> 0.12 seconds)

A narrow QRS complex occurs when the impulse is conducted down the bundle of
His and the Purkinje fibre to the ventricles. This results in well organised
synchronised ventricular depolarisation.
A broad QRS complex occurs if there is an abnormal depolarisation sequence – for
example, a ventricular ectopic where the impulse spreads slowly across the
myocardium from the focus in the ventricle. In contrast, an atrial ectopic would
result in a narrow QRS complex because it would conduct down the normal
conduction system of the heart. Similarly, a bundle branch block results in a broad
QRS because the impulse gets to one ventricle rapidly down the intrinsic
conduction system then has to spread slowly across the myocardium to the other
ventricle.

Height
Describe this as SMALL or TALL:

Small complexes are defined as < 5mm in the limb leads or < 10 mm in the chest
leads.
Tall complexes imply ventricular hypertrophy (although can be due to body habitus
e.g. tall slim people). There are numerous algorithms for measuring LVH, such as
the Sokolow-Lyon index or the Cornell index.

Morphology
You need to assess the individual waves of the QRS complex.

Delta wave
The mythical ‘delta wave’ is a sign that the ventricles are being activated earlier than
normal from a point distant to the AV node. The early activation then spreads slowly
across the myocardium causing the slurred upstroke of the QRS complex. Note – the

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presence of a delta wave does NOT diagnose Wolff-Parkinson-White syndrome. This
requires evidence of tachyarrhythmias AND a delta wave.

Delta wave 5

Q-waves
Isolated Q waves can be normal. A pathological Q wave is > 25% the size of the R wave
that follows it or > 2mm in height and > 40ms in width. A single Q wave is not a cause for
concern – look for Q waves in an entire territory (anterior / inferior) for evidence of
previous MI.

Q-waves (V2-V4), with T-wave inversion suggestive

of previous anterior MI 6

R and S waves
Look for R wave progression across the chest leads (from small in V1 to large in V6). The
transition from S > R wave to R > S wave should occur in V3 or V4. Poor progression (i.e.
S > R through to leads V5 and V6) can be a sign of previous MI but can also occur in very
large people due to lead position.

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 Poor R-wave progression 7

J point segment
The J point is where the S wave joins the ST segment

This point can be elevated resulting in the ST segment that follows it also being raised
(this is known as “High take off”)

High take off (or benign early repolarisation to give its full title) is a normal variant that
causes a lot of angst and confusion as it LOOKS like ST elevation

Key points:

Benign early repolarisation occurs mostly under the age of 50 (over age of 50,
ischaemia is more common and should be suspected first)
Typically, the J point is raised with widespread ST elevation in multiple territories
making ischaemia less likely
The T waves are also raised (in contrast to a STEMI where the T wave remains the
same size and the ST segment is raised)
The changes do not change! During a STEMI, the changes will evolve – in benign
early repolarisation, they will remain the same.

Step 7 – ST segment
The ST segment is the part of the ECG between the end of the S wave and start of
the T wave.

In a healthy individual it should be an isoelectric line (neither elevated or depressed).

Abnormalities of the ST segment should be investigated to rule out pathology.

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 Various components of an ECG

ST elevation
ST elevation is significant when it is greater than 1 mm (1 small square) in 2 or more
contiguous limb leads or >2mm in 2 or more chest leads.

It is most commonly caused by acute full thickness myocardial infarction.

ST elevation in the anterior leads

ST depression
ST depression ≥ 0.5 mm in ≥ 2 contiguous leads indicates myocardial ischaemia.

ST depression

Step 8 – T waves
The T waves represent repolarisation of the ventricles

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Tall T waves
T waves are tall if they are:

> 5mm in the limb leads AND

> 10mm in the chest leads (the same criteria as ‘small’ QRS complexes)

Tall T waves can be associated with:

Hyperkalaemia (“Tall tented T waves”)

Hyperacute STEMI

Tall tented T-waves 8

Inverted T waves
T waves are normally inverted in V1 and inversion in lead III is a normal variant.

Inverted T waves in other leads are a nonspecific sign of a wide variety of

conditions:

Ischaemia
Bundle branch blocks (V4 – 6 in LBBB and V1 – V3 in RBBB)
Pulmonary embolism
Left ventricular hypertrophy (in the lateral leads)
Hypertrophic cardiomyopathy (widespread)
General illness

Around 50% of ITU admissions have some evidence of T wave inversion during
their stay

Comment on the distribution of the T wave inversion e.g. anterior / lateral / posterior
leads

You must take this ECG finding and apply it in the context of your patient

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 Inverted T-wave

Biphasic T waves
Biphasic T waves have two peaks and can be indicative of ischaemia and
hypokalaemia

Biphasic t-wave 9

Flattened T waves
Another non-specific sign, this may represent ischaemia or electrolyte imbalance.

Flattened T-wave 9

U waves
Not a common finding.

The U wave is a > 0.5mm deflection after the T wave best seen in V2 or V3.

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These become larger the slower the bradycardia – classically U waves are seen in
various electrolyte imbalances or hypothermia, or antiarrhythmic therapy (such as
digoxin, procainamide or amiodarone).

U-wave 10

Document your interpretation

You should document your interpretation of the ECG in the patient’s notes (check
out our guide to documenting an ECG here).

References
1. Author: James Heilman, MD (Own work) – Fast atrial fibrillation – via Wikimedia
Commons – Licence: CC BY-SA 3.0

2. Author:Michael Rosengarten BEng, MD.McGill – Right axis deviation – via Wikimedia

Commons – Licence: CC BY-SA 3.0

3. Author: James Heilman, MD (Own work) – Mobitz type 2 AV block – via Wikimedia
Commons – Licence: CC BY-SA 3.0

4. Author: James Heilman, MD (Own work) – Complete heart block – via Wikimedia
Commons – Licence: CC BY-SA 3.0

5. Author: James Heilman, MD (Own work) – Delta wave – via Wikimedia Commons –
Licence: CC BY-SA 3.0

6. Author: Michael Rosengarten BEng, MD.McGill – Q-waves – via Wikimedia Commons –

Licence: CC BY-SA 3.0

7. Author: Michael Rosengarten BEng, MD.McGill – Poor R-wave progression – via

Wikimedia Commons – Licence: CC BY-SA 3.0

8. Author: Michael Rosengarten BEng, MD.McGill – Tall tented T-waves – via Wikimedia
Commons – Licence: CC BY-SA 3.0

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9. Author: CardioNetworks – T-wave morphology – via Wikimedia Commons – Licence: CC
BY-SA 3.0

10. Author: James Heilman, MD (Own work) – U-wave – via Wikimedia Commons –
Licence: CC BY-SA 3.0

11. Author: Michael Rosengarten BEng, MD.McGill – Left axis deviation – via Wikimedia
Commons – Licence: CC BY-SA 3.0

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