ECG Made Extra Easy [PDF]

ElectroCardioGraphy (ECG) made extra easy

ElectroCardioGraphy (ECG) made extra easy


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ECG made extra easy …

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Objectives for this tutorial What is an ECG?

Overview of performing

electrocardiography on a patient Simple physiology

Interpreting the ECG

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By the end of this tutorial the student should be able to:

State a definition of electrocardiogram

Perform an ECG on a patient, including explaining to the patient what is involved

Draw a diagram of the conduction pathway of the heart Draw a simple labelled diagram of an ECG tracing

List the steps involved in interpreting an ECG tracing in an ord erly way

Recite the normal limits of the parameters of various parts of t he ECG

Interpret ECGs showing the following pathology:

MI, AF, 1st 2 nd and 3 rd degree heart block, p pulmonale , p mitrale , Wolff – Parkinson – White syndrome, LBBB, RBBB, Left and Right axis deviation, LVH, pericarditis , Hyper – and hypokalaemia , prolonged QT.

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What is an ECG?


Tracing of heart ’ s electrical activity

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Recording an ECG

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Overview of procedure


Greet, rapport, introduce, identify, privacy, explain procedure, permission

Lay patient down

Expose chest, wrists, ankles

Clean electrode sites

May need to shave

Apply electrodes

Attach wires correctly

Turn on machine

Calibrate to 10mm/mV Rate at 25mm/s

Record and print Label the tracing

Name, DoB , hospital number, date and time, reason for recording

Disconnect if

adequate and remove electrodes

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Electrode placement

10 electrodes in total are placed on the patient

Firstly self – adhesive ‘ dots ’ are attached to the patient. These have single electrical contacts on them

The 10 leads on the ECG machine are then clipped onto the contacts of the ‘ dots ’

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Electrode placement in 12 lead


6 are chest electrodes

Called V1 – 6 or C1 – 6

4 are limb electrodes

Right arm Left arm Left leg

Right leg


R ide Y our

G reen B ike

The right leg electrode is a neutral or “ dummy ” !

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Electrode placement

For the chest electrodes

V1 4 th intercostal space right sternal edge V2 4 th intercostal space left sternal edge

(to find the 4 th space, palpate the manubriosternal angle (of Louis)

Directly adjacent is the 2 nd rib, with the 2 nd intercostal space directly below. Palpate inferiorly to find the 3 rd and then 4 th space

V 4 over the apex (5 th ICS mid – clavicular line)

V 3 halfway between V2 and V4

V5 at the same level as V4 but on the anterior axillary line

V6 at the same level as V4 and V5 but on the mid – axillary line

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Recording the trace

Different ECG machines have different buttons that you have to press.

Ask one of the staff on the ward if it is a machine that you are unfamiliar with.

Ask the patient to relax completely. Any skeletal muscle activity will be picked up as interference.

If the trace obtained is no good, check that all the dots are stuck down properly – they have a tendency to fall off.

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Pacemaker = sinoatrial node

Impulse travels across atria

Reaches AV node

Transmitted along interventricular septum in Bundle of His

Bundle splits in two (right and left branches)

Purkinje fibres

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direction of

cardiac impulse

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How does the ECG work?

Electrical impulse (wave of depolarisation) picked up by placing electrodes on patient

The voltage change is sensed by measuring the current change across 2 electrodes – a positive electrode and a negative electrode

If the electrical impulse travels towards the positive electrode this results in a positive deflection

If the impulse travels away from the positive electrode this results in a negative deflection

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Away from






= negative

= positive



Direction of impulse (axis)

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Types of Leads

Coronal plane (Limb Leads)

1. Bipolar leads — l , l l , l l l

2. Unipolar leads — aVL , aVR , aVF

Transverse plane

V 1 — V 6 (Chest Leads)

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Electrodes around the heart

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How are the 12 leads on the

ECG (I, II, III, aVL , aVF , aVR , V1 – 6) formed

using only 9 electrodes (and a neutral)?

Lead I is formed using the right arm electrode (red) as the negative electrode and the left arm (yellow) electrode as the positive

– Lead I +

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– Lead I +

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Lead II is formed

using the right arm

electrode (red) as the negative electrode and the left leg electrode as the positive

Lead II

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Lead II

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Lead III is formed using the left arm

electrode as the negative electrode and the left leg electrode as the positive

aVL , aVF , and aVR are composite leads , computed using the information from the other leads

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Leads and what they tell you

Limb leads

Limb leads look at the heart in the coronal


aVL , I and II = lateral II, III and aVF = inferior

aVR = right side of the heart

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Leads look at the heart from

different directions


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Leads and what they tell you

Each lead can be thought of as ‘ looking at ’ an area

of myocardium

Chest leads

V 1 to V 6 ‘ look ’ at the heart on the transverse plain V 1 and V 2 look at the anterior of the heart and R


V 3 and V 4 = anterior and septal

V 5 and V 6 = lateral and left ventricle

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Elements of the trace

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What do the components


P wave =



atrial depolarisation

ventricular depolarisation

repolarisation of the ventricles

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Interpreting the ECG

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Interpreting the ECG


Name DoB

Time and date

Indication e.g. “ chest pain ” or “ routine pre – op ” Any previous or subsequent ECGs

Is it part of a serial ECG sequence? In which case it may be numbered

Calibration Rate

Rhythm Axis

Elements of the tracing in each lead

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Check that your ECG is calibrated correctly


10mm = 1mV

Look for a reference pulse which should be the rectangular looking wave somewhere near the left of the paper. It should be 10mm (10 small squares) tall

Paper speed


25 mm (25 small squares / 5 large squares) equals one second

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If the heart rate is regular

Count the number of large squares between R waves

i.e. the RR interval in large squares

Rate = 300


e.g. RR = 4 large squares 300/ 4 = 75 beats per minute

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If the rhythm is irregular (see next slide on rhythm to check whether your rhythm is regular or not) it may be better to estimate the rate using the rhythm strip at the bottom of the ECG (usually lead II)

The rhythm strip is usually 25cm long (250mm i.e.

10 seconds)

If you count the number of R waves on that strip

and multiple by 6 you will get the rate

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Is the rhythm regular?

The easiest way to tell is to take a sheet of paper and line up one edge with the tips of the R waves on the rhythm strip.

Mark off on the paper the positions of 3 or 4 R wave tips

Move the paper along the rhythm strip so that your first mark li nes up with another R wave tip

See if the subsequent R wave tips line up with the subsequent marks on your paper

If they do line up, the rhythm is regular. If not, the rhythm i s irregular

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Sinus Rhythm



Cardiac impulse originates from the sinus node. Every QRS must be preceded by a P wave.

(This does not mean that every P wave must be followed by a QRS – such as in 2 nd degree heart block where some P waves are not followed by a QRS, however every QRS is preceded by a P wave and the rhythm originates in the sinus node, hence it is a sinus rhythm. It could be said that it is not a normal sinus rhythm)

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Sinus arrhythmia

There is a change in heart rate depending on the phase of respiration

Q. If a person with sinus arrhythmia inspires, what happens to t heir heart rate?

A. The heart rate speeds up. This is because on inspiration th ere is a decrease in intrathoracic pressure, this leads to an increased venous return to the right atrium. Increased stretching of the right atrium sets off a brainstem reflex (Bainbridge ’ s reflex) that leads to sympathetic activation of the heart, hence it speeds up)

This physiological phenomenon is more apparent in children and young adults

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Sinus bradycardia

Rhythm originates in the sinus node Rate of less than 60 beats per minute

Sinus tachycardia

Rhythm originates in the sinus node

Rate of greater than 100 beats per minute

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The axis can be though of as the overall direction of the cardiac impulse or wave of depolarisation of the heart

An abnormal axis (axis deviation) can give a clue to possible pathology

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An axis falling

outside the normal range can be left

or extreme axis


axis deviation

right axis deviation

A normal axis can lie


between -30 and +90 degrees or +120 degrees

according to some

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Axis deviation – Causes

Wolff – Parkinson – White

syndrome can cause both Left and Right axis deviation

A useful mnemonic:

“ RAD RALPH the LAD from VILLA ”

R ight A xis D eviation

R ight ventricular hypertrophy A nterolateral MI

L eft P osterior H emiblock

L eft A xis D eviation

V entricular tachycardia I nferior MI

L eft ventricular hypertrophy L eft A nterior hemiblock

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The P wave

The P wave represents atrial


It can be thought of as being

made up of two separate

waves due to right atrial

depolarisation and left atrial depolarisation.

Which occurs first?

Right atrial depolarisation

Sum of

right and

left waves

right atrial depolarisation left atrial depolarisation

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The P wave


No hard and fast rules


a P wave over 2.5mm should arouse suspicion


a P wave longer than 0.08s (2 small squares) should arouse suspicion

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The P wave


A tall P wave (over

2.5mm) can be called P pulmonale

Occurs due to R atrial hypertrophy

Causes include:

pulmonary hypertension, pulmonary stenosis tricuspid stenosis

normal P pulmonale


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The P wave


A P wave with a length >0.08 seconds (2 small squares) and a bifid

shape is called P mitrale

It is caused by left atrial hypertrophy and delayed left atrial depolarisation

Causes include:

Mitral valve disease LVH

normal P mitrale

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The PR interval

The PR interval is measured between the start of the P wave to the start of the QRS complex

(therefore if there is a Q wave before the R wave the PR interval is measured from the start of the P wave to the start of the Q wave, not the start of the R wave)

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The PR interval

The PR interval corresponds to the time period between depolarisation of the atria and ventricular depolarisation.

A normal PR interval is between 0.12 and 0.2 seconds ( 3 – 5 small squares)

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The PR interval

If the PR interval is short (less than 3 small

squares) it may signify that there is an accessory electrical pathway between the atria and the ventricles, hence the ventricles depolarise early giving a short PR interval.

One example of this is Wolff – Parkinson – White syndrome where the accessory pathway is

called the bundle of Kent. See next slide for an animation to explain this

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Depolarisation begins at

the SA node

The wave of

depolarisation spreads

across the atria

It reaches the AV node

and the accessory bundle

Conduction is delayed as

usual by the in-built delay

in the AV node

However, the accessory

bundle has no such delay

and depolarisation begins

early in the part of the

ventricle served by the


As the depolarisation in this part of the ventricle
Until rapid depolarisation

does not travel in the high speed conduction
resumes via the normal

pathway, the spread of depolarisation across the ventricle is slow, causing a slow rising delta wave
pathway and a more normal

complex follows

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The PR interval

If the PR interval is long (>5 small squares or 0.2s):

If there is a constant long PR interval 1 st degree heart block is present

First degree heart block is a longer than normal delay in conduction at the AV node

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The PR interval

If the PR interval looks as though it is widening every beat and then a QRS complex is missing, there is 2 nd degree heart block, Mobitz type I . The lengthening of the PR interval in

subsequent beats is known as the Wenckebach phenomenon

(remember ( w )one, W enckebach , w idens)

If the PR interval is constant but then there is a missed QRS complex then there is 2 nd degree heart block, Mobitz type II

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The PR interval

If there is no discernable relationship between the P waves and the QRS

complexes, then 3 rd degree heart block is present

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Heart block (AV node block)


1 st degree

constant PR, >0.2 seconds

2 nd degree type 1 ( Wenckebach )

PR widens over subsequent beats then a QRS is dropped

2 nd degree type 2

PR is constant then a QRS is dropped

3 rd degree

No discernable relationship between p waves and QRS complexes

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The Q wave

Are there any pathological Q waves?

A Q wave can be pathological if it is:

Deeper than 2 small squares (0.2mV)


Wider than 1 small square (0.04s) and/or

In a lead other than III or one of the leads that look at the heart from the left (I, II, aVL , V5 and V6) where small Qs (i.e. not meeting the criteria above) can be normal

Normal if in


Pathological anywhere

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The QRS height

If the complexes in the chest leads look very tall, consider left ventricular hypertrophy (LVH)

If the depth of the S wave in V 1 added to the height of the R wave in V 6 comes to

more than 35mm, LVH is present

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QRS width

The width of the QRS complex should be less than 0.12 seconds (3 small squares)

Some texts say less than 0.10 seconds (2.5 small squares)

If the QRS is wider than this, it suggests a

ventricular conduction problem – usually right or left bundle branch block (RBBB or LBBB)

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If left bundle branch block is present, the QRS

complex may look like a

‘ W ’ in V 1 and/or an ‘ M ’ shape in V 6.

New onset LBBB with chest pain consider Myocardial infarction

Not possible to interpret the ST segment.

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It is also called RSR pattern

If right bundle branch block is present, there may be an ‘ M ’ in V1 and/or a ‘ W ’ in V6.

Can occur in healthy

people with normal QRS width – partial RBBB

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QRS width

It is useful to look at leads V 1 and V 6

LBBB and RBBB can be remembered by the mnemonic:

W i LL ia M M a RR o W

Bundle branch block is caused either by infarction or fibrosis (related to the ageing process)

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The ST segment

The ST segment should sit on the isoelectric line

It is abnormal if there is planar (i.e. flat) elevation or depression of the ST segment

Planar ST elevation can represent an MI or Prinzmetal ’ s ( vasospastic ) angina

Planar ST depression can represent ischaemia

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Myocardial infarction

Within hours:

T wave may become peaked ST segment may begin to rise

Within 24 hours:

T wave inverts (may or may not persist)

ST elevation begins to resolve

If a left ventricular aneurysm forms, ST elevation may persist

Within a few days:

pathological Q waves can form and usually persist

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Myocardial infarction

The leads affected determine the site of the infarct

Inferior II, III, aVF Anteroseptal V1 – V4

Anterolateral V4 – V6, I, aVL

Posterior Tall wide R and ST ↓ in V1

and V2

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Acute Anterior MI

ST elevation

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Inferior MI

ST elevation

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The ST segment

If the ST segment is elevated but slanted, it may not be significant

If there are raised ST segments in most of the leads, it may indicate pericarditis – especially if the ST segments are saddle shaped. There can also be PR segment depression

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The T wave

Are the T waves too tall?

No definite rule for height T wave generally shouldn ’ t be taller than half the size of the preceding QRS



Acute myocardial infarction

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The T wave

If the T wave is flat, it may indicate hypokalaemia

If the T wave is inverted it may indicate ischaemia

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The QT interval

The QT interval is measured from the start of the QRS complex to the end of the T wave.

The QT interval varies with heart rate

As the heart rate gets faster, the QT interval gets shorter

It is possible to correct the QT interval with respect to rate by using the following formula:

QTc = QT/ √ RR ( QTc = corrected QT)

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The QT interval

The normal range for QTc is 0.38 – 0.42

A short QTc may indicate hypercalcaemia

A long QTc has many causes

Long QTc increases the risk of developing an arrhythmia

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The U wave

U waves occur after the T wave and are often difficult to see

They are thought to be due to

repolarisation of the atrial septum

Prominent U waves can be a sign of hypokalaemia , hyperthyroidism

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Supraventricular tachycardias

These are tachycardias where the impulse is initiated in the atria ( sinoatrial node, atrial wall or atrioventricular node)

If there is a normal conduction pathway when the

impulse reaches the ventricles, a narrow QRS complex is formed, hence they are narrow complex tachycardias

However if there is a conduction problem in the

ventricles such as LBBB, then a broad QRS complex is formed. This would result in a form of broad complex tachycardia

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Atrial Fibrillation


There maybe tachycardia

The rhythm is usually irregularly irregular No P waves are discernible – instead there is a shaky baseline

This is because there is no order to atrial depolarisation, different areas of atrium depolarise at will

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Atrial Fibrillation

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Atrial flutter

There is a saw – tooth baseline which rises above and dips below the isoelectric line. Atrial rate 250/min

This is created by circular circuits of depolarisation set up in the atria

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Ventricular Tachycardia

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Ventricular Tachycardia

QRS complexes are wide and irregular in shape Usually secondary to infarction

Circuits of depolarisation are set up in damaged myocardium

This leads to recurrent early repolarisation of the ventricle leading to tachycardia

As the rhythm originates in the ventricles, there is a broad QRS complex

Hence it is one of the causes of a broad complex tachycardia

Need to differentiate with supraventricular tachycardia with aberrant conduction

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Ventricular Fibrillation

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Ventricular fibrillation

Completely disordered ventricular depolarisation

Not compatible with a cardiac output

Results in a completely irregular trace consisting of broad QRS complexes of varying widths, heights and rates

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Elements of the tracing

P wave

Magnitude and shape,

e.g. P pulmonale , P mitrale

PR interval (start of P to start of QRS)

Normal 3 – 5 small squares, 0.12 – 0.2s

Pathological Q waves?

QRS complex

Magnitude, duration and shape

≤ 3 small squares or 0.12s duration

ST segment

Should be isoelectric

T wave

Magnitude and direction

QT interval (Start QRS to end of T)

Normally < 2 big squares or 0.4s at 60bpm

Corrected to 60bpm

( QTc ) = QT/ √ RR interval

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Further work

Check out the various quizzes / games available on the Imperial Intranet

Get doctors on the wards to run through a patient ’ s ECG with you

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