Module 1

Anatomy & Physiology

Anatomy of The Heart

Left Atrium

Right Atrium

Right Ventricle

Left Ventricle (3-4 times thicker than

the right)

HIS Bundle

Left Bundle

Branch (LBB)

Left Posterior

Fascicle (LPS)

Right Bundle

Branch (RBB)

Papillary Muscles

Chordae Tendinae

Mitral Valve

Tricuspid Valve

Septum

The passage of blood through

the heart

Superior vena cava

Inferior vena cava

Right atrium

Right ventricle Left ventricle

Left atrium

Pulmonary veins Pulmonary veins

Pulmonary artery Pulmonary artery

Aorta

Layers of The Heart

Pericardium

Myocardium

Endocardium

cardiac muscle cell

Intercalated discs

Coronary Artery

Acute Myocardial Infarction

15 minutes 2 hours 6 hours

% necrosis 0% 50% 90%

Fibrin Threads

A thrombus (darker red in the middle) forming a cap on a plaque of atheroma

Aorta

Right

Coronary

Artery

Left Main

Coronary

Artery

Left

Circumflex Branch

Left

Anterior

Descending

Marginal

Branch

Posterior

Interventricular

Anterior heart showing coronary vessels

Coronary Artery Anatomy

• Two coronary arteries arise from the aortic root.

–Left main coronary artery

–Right coronary artery

• These divide into smaller branches.

• There are general patterns of distribution, but

there is individual variation.

Left Main Coronary Artery (LCA)

• The main artery divides into the left anterior descending

(LAD) and the left circumflex branch (CX).

• The LAD supplies the anterior wall of the left ventricle,

most of the interventricular septum, the Bundle of His &

the bundle branches.

• The CX supplies the left atrium, posterior wall of the left

ventricle & high lateral portions of the left ventricle

• The CX may also supply the AV node and inferior wall of

the left ventricle.

• The left ventricle receives the most abundant blood

supply because of its greater work load.

Left Anterior Descending (LAD)

• Complications associated with an infarction of the anterior wall can be:

– Tachyarrythmias

– Bundle branch blocks (BBB)

– Complete heart block from bilateral BBB

– Cardiogenic shock

– Acute left ventricular failure

• Complete heart block associated with an occlusion of the LAD may not respond to treatment with atropine and will require pacing.

Right Main Coronary Artery (RCA)

• The RCA usually supplies the inferior & posterior wall of

the left ventricle, right ventricle, right atrium, the SA & AV

nodes.

• It sub-divides into the posterior interventricular branch

(PIB) and the marginal branch (MB).

• The PIB supplies the walls of both ventricles.

• The MB supplies the right ventricle.

Right Main Coronary Artery

• The RCA is associated typically with inferior / posterior

infarctions and right ventricular ischaemia.

• Complications associated with RCA occlusions may be:

– Atrial arrhythmias (Atrial Fibrillation / Flutter)

– Ventricular tachyarrythmias

– SA node disturbances (Sinus Bradycardia / Sinus

Arrest)

– AV blocks

– Cardiogenic shock

Coronary Veins

• Coronary veins run alongside the coronary

arteries and return deoxygenated blood from

the myocardium to the right atrium, principally

through the coronary sinus.

Cardiac Conduction System

Sinoatrial (SA)

Node

Atrioventicular (AV)

Node

Right Bundle

Branch

Left Bundle Branch

Bundle of His

Purkinje

Fibres

Left Posterior

Division

Left Anterior

Division

Depolarisation

1

2

2

First stage of

depolarisation

Second stage of

depolarisation

Depolarisation spreads

through the septum from left

to right (1)

Depolarisation then spreads

outwards through both ventricles

from the endocardium (2). The

left ventricle produces the larger

potential electrical force due to

the larger muscular mass

Potential Pacemaker sites of the Heart

1. The resting heart rate from the

SA node is usually 60 - 70 bpm

X

X X

2. The AV junctional

region intrinsic rate is

about 40 bpm

3. The intrinsic rate of

the Purkinje cells is

about 0 - 30 bpm

Narrow QRS (no preceding P wave)

Broad QRS

(no preceding P wave)

ECG: Wave pattern

atrial depolarisation

ventricular depolarisation

atrial/ventricular repolarisation

O

Millivolts

P T

R

S

Q Complete

cardiac diastole

0.4s

Ventricular

systole

0.3s

Atrial

systole

0.1s

Mechanical events at rest

Module 2

12 Lead ECG Theory

10 ECG Cables = 12 lead ECG

• A 12 lead ECG is obtained from the information collated

from 10 electrode cables.

• Using a central reference point, the ECG machine is able

to calculate the required information to produce 12 different

electrical views of the heart.

• This is achieved by two different methods:

– Bipolar leads I, II & III using 1 positive & 1 negative

lead.

– Unipolar leads (augmented leads & chest leads) using 1

positive electrode and calculating a notional central

reference point (central terminal) within the heart.

Lead Groups

Limb Leads Chest Leads

(precordial leads)

Lead I aVR V1 V4

Lead II aVL V2 V5

Lead III aVF V3 V6

Bipolar Unipolar Unipolar

Limb Leads

Right Arm

Right Leg

Left Leg

Left Arm • Limb leads are typically

placed on the inside of the

wrists and ankles

• To help reduce artifacts

you can use the upper

arms and thighs

• Do not place limb leads

on the torso

Standard Bipolar Leads

III II

I

Einthovens’

Triangle

- I +

III II

+ +

- -

Augmented Unipolar Leads

+

+ +

Augmented Voltage

Right (aVR) Augmented Voltage

Left (aVL)

Augmented

Voltage Foot (aVF)

aVR will always be

negative if the limb

leads are placed

correctly

Limb leads

-90° -60°

-30°

0°

+-30°

+60° +90°

+120°

+150°

+180°

-150°

-120°

aV R

aV L

aV F

I

II III Right axis

Left axis

Preparation

• In order to obtain a good quality diagnostic ECG it is

imperative to have good skin preparation prior to applying

the ECG electrodes.

• Remove excessive hair if this is necessary to maintain skin

contact from precordial leads.

• Rub the area of skin with a gauze pad to dry and remove

any skin oil or dead tissue.

• Make the patient as comfortable as possible. Keep them

warm, consider their modesty and try to get them to relax.

Chest Leads

(precordial leads)

V1 Fourth intercostal space to

the right of the sternum.

V2 Fourth intercostal space to

the left of the sternum.

V3 Directly between V2 & V4.

V4 Fifth intercostal space,

midclavicular line.

V5 Level with V4 at left anterior

axillary line

V6 Level with V5 at midaxillary

line (midpoint of the armpit).

V1

V2

V3 V4

V5 V6

Angle of

Louis

Artefact

• It is important that an ECG is free from any

artefact when using it to make a diagnosis.

• Causes of artefact can be:

– Poor application of ECG electrodes (Dried out gel, air trapped

under electrode & patient hair preventing good skin contact

– Patient’s movement

– Electrical interference

– Cable movement

– Vehicle movement

ECG Showing Artefact

The following ECG demonstrates what can happen with

poor preparation

This ECG has a wandering baseline in V1, V4 & V5

and no data from V6

12 Lead ECG Check List

“Remember” Always treat the patient - not the ECG.

1. The PR interval is between 0.12 & 0.2 sec (3 -5 small squares).

2. The QRS duration is <0.12 sec (<3 small squares).

3. Confirm that aVR is negative (if not check limb lead placement).

4. The ST segment should start isoelectric except in V1 & V2 where it

may be slightly elevated.

Chamberlain DA. Personal communication

Module 3

ECG Format

ECG Electrical Deflection

• When an electrical impulse travels towards an

electrode the ECG will record a positive or upward

deflection (A)

• When an electrical impulse travels away from an

electrode the ECG will record a negative or

downward deflection (B)

A

B Current Electrode Deflection

P,QRS & T Wave

Isoelectric line

P Wave

Q Wave

The septum depolarises from left to right

R Wave

S Wave

T Wave

Normal Intervals

PR

interval

QRS

complex

*P-R interval = 0.12 - 0.20 sec

(3 to 5 small squares)

QRS width = 0.08 - 0.12 sec

(2 to 3 small squares)

Q-T interval 0.35 - 0.43 sec

QT

interval

*The PR interval should really be referred to as

the PQ interval, however it is commonly

referred as the PR interval.

Variations to the QRS

R

QS

q s

R R

ST Segment

ST Segment

1 2 3

J Point

J Point Examples

1 2 3

4 5 6

Pathological Q Wave

> 0.04 sec wide

>25% of R wave

ECG Paper

Time

1 small box = 0.04

seconds

1 large box = 0.2 seconds

5 large boxes = 1 second

10 mm/1mv

Reference

Calculating Heart Rate

When The Rhythm is Regular

• There are 300 large squares per minute.

• If the rhythm is regular count the number of large

squares between two QRS complexes and divide it into

300

Heart Rate = 300 = 75 per minute

4

Calculating Heart Rate

When The Rhythm is Irregular

• 30 large squares correspond to 6 seconds.

• Count the number of QRS complexes in 30 large

squares and multiply by 10.

Number of QRS complexes in 30 squares = 9

Therefore, number of QRS complexes per minute = 9 X 10 = 90

Module 4

Cardiac Axis

Cardiac Conduction System

Sinoatrial (SA)

Node

Atrioventicular (AV)

Node

Right Bundle

Branch

Left Bundle Branch

Bundle of His

Purkinje

Fibres

Posterior Fascicles

Anterior Fascicles

What Is Cardiac Axis?

• The QRS axis is the sum total of all electrical currents

generated by the ventricular myocardium during

DEPOLARISATION.

• Cardiac axis is determined within the limb leads.

• An electrical impulse flowing

towards an electrode will record a

positive or upward deflection.

• An electrical impulse flowing away

from an electrode will record a

negative or downward deflection.

• The electrode situated at right angle

or perpendicular to the impulse will

record an equiphasic deflection.

ECG Electrical Deflection

Current

Deflection Electrode

Limb leads

-90° -60°

-30°

0°

+-30°

+60° +90°

+120°

+150°

+180°

-150°

-120°

aVR aVL

aVF

I

II III Right axis

Left axis

Normal axis

Extreme right

Normal QRS Axis

• The flow of electrical current through the heart

passes along a well defined pathway.

• Impulses originate in the sinoatrial node reaching the

ventricles via the atrioventricular node.

• The flow of electrical current is therefore, generally

from the ‘top right hand corner’ to the ‘bottom left

hand corner’.

• aVR should always be

negative.

• Lead II is predominantly

positive.

• Lead I is predominantly

positive.

Normal QRS Axis

• aVR is negative.

• Lead I is predominantly

positive.

• Lead II is predominantly

negative.

• Therefore the current flows

away from lead II, towards

aVL.

Left Axis Deviation

Causes of Left Axis Deviation

Left Axis Deviation is caused usually by either:

a) loss of conduction in the anterior division of

the left bundle (left anterior hemiblock) with

an ‘r S’ pattern or

b) loss of muscle elasticity (inferior myocardial

infarction) with a ‘Q r’ pattern.

• aVR is negative.

• Lead III is predominantly positive.

• Lead I is predominantly negative.

• Therefore the current flows away from Lead I, towards Lead III.

Right Axis Deviation

Causes of Right Axis Deviation

Right Axis Deviation is caused usually by right

ventricular hypertrophy.

It can also be a normal finding in the very young.

Module 5

ECG Rhythm Recognition

What to Look for on a rhythm strip

• Are all the P waves alike?

• Are all the QRS complexes alike?

• Are all the P waves and QRS complexes related or occurring independently?

• Is there a P wave in front of every QRS complex?

• Is the PR interval constant or does it vary?

• Is the PR interval too short (<0.12 s) or too long (>0.2 s)?

• Is the QRS complex widened (>0.12 s)?

Normal Sinus Rhythm

• NSR is a rate of between 60-100bpm.

• Each beat normally has one P wave, one corresponding QRS

complex and T wave.

• The R-R intervals should be regular and constant.

• The P-R interval is within normal range.

Sinus Bradycardia

• R-R intervals constant and regular.

• All waveforms are present, and there is 1 P-wave to each QRS

complex.

• The rate is <60bpm but not usually <40bpm.

• Patients usually asymptomatic and no treatment is required.

• Often caused by beta-blockers/calcium channel blockers.

• May also be seen in athletes and occur during sleep.

Sinus Tachycardia

• R-R intervals constant and regular.

• One P-wave per QRS complex.

• All waveforms present.

• Rate is >100bpm, but not usually >130bpm at rest.

• Occurs normally in exercise/stress. Patient is usually

asymptomatic.

• Other causes may be hypovolaemia/underlying medical

problems.

Muscle Tremor

• All waveforms are present, but are difficult to define due to the

wavering appearance on the isoelectric line.

• Common causes of muscle tremor are patient shivering or

anxiety.

• It may be difficult to accurately assess an ECG where muscle

tremor is present.

P P P P

Electrical Interference

• It may be difficult to make any assessment of an ECG where

there is electrical interference; none of the waveforms are

clearly defined.

• Common causes of this phenomenon are any electrical

appliances in close proximity to the ECG machine: i.e TV,

electrical beds, infusion pumps etc.

• Usually once all appliances are unplugged, a satisfactory quality

ECG can be carried out.

Atrial extrasystoles (AE)

• AE’s are a common form of supraventricular extrasystole.

• Cause is atrial beat arising outside the sinus node.

• Patients are generally asymptomatic and there is no treatment

indicated.

• A trial extrasystole falling on a critical time of atrial repolarisation

may trigger atrial fibrillation (AF) in some vulnerable patients.

x

Atrial Fibrillation

(AF)

• The atrial depolarisation is disorganised resulting in a chaotic ventricular rhythm.

• The ventricular response rate may be normal/fast/slow.

• This is a common arrhythmia, especially in the elderly; around 5-10% of whom experience AF.

• Treatment is usually with oral drug therapy, although may be successfully electrically cardioverted in patients with persisting AF of recent onset.

x x

x

x x x

Atrial Flutter

• A malfunction in the pattern of atrial depolarisation. A flutter usually gives atrial waves in the range of 280-320bpm.

• The AV node usually blocks 1/2 of these impulses and gives a ventricular response rate of 150bpm.

• Atrial flutter is usually regular in rhythm and displays a ‘saw-toothed’ appearance (especially V1) as above.

• Very responsive to DC electrical cardioversion.

x x

x

Supraventricular Tachycardia

(SVT)

• SVT is a general term for tachycardias that originate above the

ventricles.

• Rate may be in the range of - 150-250bpm

• Commonly starts in early adult life and is normally inconvenient

but benign.

• Adenosine to block AV response may slow the rate to determine

underlying atrial rhythm or may facilitate chemical cardioversion.

x

Paroxysmal Supraventricular Tachycardias

• May be SVT, AF, Atrial flutter.

• The term paroxysmal indicates that the arrhythmia is intermittent

and self-terminating.

• Atrial flutter carries a similar risk of thromboembolism as atrial

fibrillation and may require anticoagulation.

Wolff-Parkinson-White Syndrome (WPW)

• WPW is a syndrome with a characteristic

electrocardiogram - shortened PR interval (<0.12secs) and

a slurred upstroke on the QRS complex (delta wave)

together with a tendency to supraventricular arrhythmias.

• It is caused by an accessory conduction pathway which

bypasses the AV node.

Accessory

pathway

Delta

wave

PR

Normal

pathway

anterograde / retrograde

conduction

Paroxysmal

tachycardia

Junctional Rhythm (Nodal)

• When the electrical pathway originates further down in the conduction system, but is still coming from or near the AV node, a ‘nodal’ (junctional) rhythm occurs.

• If the pacemaker is high - an inverted P-wave may occur before the QRS complext.

• If the pacemaker is within the node - the P-wave is usually absent.

• If the conducting pathway is lower down, then the P-wave may have an inverted appearance and occur after the QRS and even resemble a S wave.

x High Mid Low

First-degree Heart Block

• The measurement from the start of the P-wave to the start of the

R-wave is prolonged to >5 sm squares (0.20secs).

• The P-waves and R-waves remain constant and regular.

• The heart rate is usually within normal parameters.

• Patient is not compromised and no treatment indicated.

• Caused by delay within the AV node.

P P

Second-degree Heart Block

Mobitz type I (Wenckebach)

• The P-R interval becomes progressively elongated with each heart beat; eventually conduction fails completely.

• The cycle then repeats itself once again.

• May be seen in individuals with high vagal tone especial during sleep.

• Where it occurs in complication of inferior MI, it does not usually require a pacemaker and often may be reversed with myocardial reperfusion.

? P R

P P P P

Second-degree Heart Block

Mobitz type II

• Most P-waves conducted as normal - followed by QRS.

• The P-R interval is normal and usually constant.

• Occasionally, the atrial conduction is not followed by a QRS

complex.

• Thought to be caused by an abnormality in the bundle of His.

• Considered more serious than type I block in that it can

progress to complete heart block without warning.

?

? ? ?

2:1 Heart Block

• Every alternate P-wave is not conducted.

• Cannot be classified as either Mobitz Type I or Mobitz Type II.

• Use of a pacemaker may be considered.

Third-degree Heart Block

(complete heart block)

• The P-P and R-R intervals are each usually regular but have no

relation to each other.

• This dissociation is due to a block at the AV junction.

x x

P P P P P P

Ventricular (Unifocal)

Extrasystole

• Occasional extrasystoles are common in healthy adults.

• 3 or more in a row may be described as VT, but shorter runs are

usually called salvoes.

• The morphology of each ectopic is unchanged if depolarisation

originates from a single focus.

x

Coupled Ventricular

Extrasystole

• This is the term used when every alternate beat is an

extrasystole.

• Treated only in exceptional circumstances.

• Coupled extrasystole may cause bigeminy: the condition in

which alternate ectopic beats of the heart are transmitted to the

pulse and felt as a double pulse beat followed by a pause.

x

Couplets

• A couplet is where there are 2 ventricular ectopics in a row.

• Not usually treated except in circumstances that make the

patient vulnerable to more serious arrhythmias

x

R on T Extrasystole

• When the ventricular extrasystole falls on the T-wave. This may

trigger serious ventricular arrhythmias.

x

• Where the origin of the ectopic beat originates from differing

foci within the ventricle.

• This may signify a high degree of ventricular excitability.

• Although extrasystoles may occasionally precipitate more

malignant arrhythmias, any decision on treatment should be

made only after considering the risk of anti-arrhythmic drugs.

x x x

Ventricular (Multifocal)

Extrasystole

Paced Beats

• A ventricular paced beat will display a broadened QRS complex.

• The slim, deflection immediately preceding the R-wave denotes

the pacing spike (arrowed above).

x Pacing

wire

Idioventricular Rhythm

• Often seen with reperfusion following acute MI, idioventricular

rhythm can be regarded as ‘slow VT’.

• The QRS is broad and bizarre, but uniform and regular.

• The rate is less than 100bpm.

• Usually no treatment is indicated.

x

Torsades de Pointes

• From the French ‘twisting of points’. This describes a form of VT where the cardiac axis twists round the isoelectric line.

• The rhythm may be intermittent and self-terminating. If it lasts more than a few seconds the patient will become symptomatic.

• Common causes are electrical imbalance - i.e K+ and/or Mg++ depletion or prolonged Q-T interval frequently caused by drugs such as Sotalol/Amiodarone or tricyclic antidepressants.

• The origin of the heartbeat is in the ventricles, producing a QRS

complex >0.12secs.

• 3 ventricular beats in succession may be called VT (or salvoes).

• VT can range in rate from 100-300bpm and the patient may be

conscious and asymptomatic, symptomatic, or unconscious.

Treatment will depend principally on the patients’ clinical status.

Ventricular Tachycardia

(VT) x

Ventricular Fibrillation

(VF)

• The ventricles are ‘quivering’, leading to a complete loss of cardiac

output.

• Bizarre complexes are characteristic, but are variable amplitude (course / fine VF).

• The most common arrhythmia causing cardiac arrest, but becomes

finer as minutes pass and soon becomes indistinguishable with

asystole.

• Patient will require immediate defibrillation (10% reduction in success

rate as each minute passes).

• Most common cause of death in early acute MI.

x x x

x x

x x x

x x

Ventricular Standstill

• No ventricular response to atrial depolarisation.

• There is no cardiac output and the patient is in cardiac arrest.

• Pacing is required. It is usually effective if atrial activity is

present.

Pulseless Electrical Activity (PEA)

•PEA describes a condition where QRS complexes continue but no cardiac output

can be detected.

•8 treatable causes: ‘4 Ts’ Tamponade ‘4 Hs’ Hypoxia

Toxicity Hypovolaemia

Tension pneumothorax Hypo/hyperkalaemia

Thrombo-embolic Hypothermia

•No cardiac output, although the rhythm displayed will be that of a non

life threatening nature.

•Treatment is life support as per non-VT/VF protocol until a cause is established.

Asystole

• Implies the absence of ventricular activity.

• No QRS complexes are present.

• Patient is in a state of full cardiac arrest.

• In asystole - always check patient, check leads, check

monitoring mode (? Paddles), increase the monitoring gain to

rule out fine VF.

Module 6

Bundle Branch Block

Bundle Branch Block

• Normally both bundle branches transmit a stimulus to the 2 ventricles simultaneously.

• The QRS duration will be less than 0.12 seconds (3 small squares).

• If one of the bundle branches is blocked, a ventricle may be depolarised through an abnormal pathway outside the main conduction system causing the QRS duration to be greater than 0.12 seconds.

ECG Leads

• To be able to identify which bundle branch is

blocked, you will need to know which leads best

show the resulting abnormality.

• The leads looking directly at the right ventricle are

V1 & V2.

• The leads looking at the left ventricle are V5,V6 &

lead I.

I V1 V2

V5

V6

V6 V3 Right Chest Leads

Left Chest

Leads Left Limb

Lead

Right Bundle Branch Block (RBBB)

• As the right ventricle depolarises after the left, caused by a block in the RBB, this will cause a widened notched rSR complex in the right chest leads (V1 & V2).

• RBBB can be a benign phenomenon and even congenitial.

r

R

S

V1

RBBB

• This can be a pre-existing condition but is always

pathological.

• Causes include either a new or old MI.

• It also causes ST / T wave changes, with T wave

inversion in the left ventricular leads.

A new LBBB caused by an Acute Coronary

Syndrome identifies a very high risk patient

associated with > 40% mortality without

treatment

Left Bundle Branch Block (LBBB)

LBBB

• LBBB produces a QS (negative complex) in V1 and wide notched complexes in the Left limb / chest leads (I, V5 & V6).

V1

QS

I V5 V6

LBBB

RBBB

LBBB

RBBB vs LBBB

R

R

S

VI-V2 V5-V6

Use V1 to identify the terminal force to determine if it

is positive or negative.

Bifasicular Block

• Uncomplicated RBBB indicates failure of

conduction in only one of the 3 main conducting

pathways in the ventricles.

• LBBB represents failure of conduction in two of

the conducting pathways (both ANTERIOR and

POSTERIOR fasicles); and is a form of

‘bifasicular’ block.

• RBBB with left axis deviation is another present-

ation of ‘bifasicular’ block: failure to conduct in

the anterior fascicle of the left bundle + the RBB

Identify which Bundle

Branch is blocked on the

following 6 ECGs which all

have a QRS > 0.12

ECG 1

ECG 2

ECG 3

ECG 4

ECG 5

ECG 6

Module 7

12 Lead ECG Diagnosis

Normal 12 Lead ECG

• All ST segments remain on the isoelectric line.

• aVR should always be negative.

• ST elevation in V1-V2 may be a normal variant.

• T wave inversion in V1-V2 may be a normal variant.

A normal 12-lead ECG

DOES NOT

rule out an

acute myocardial infarction

Ischaemia

• Inadequate myocardial oxygen supply.

• Can present with ST depression or T wave inversion.

Acute Myocardial Infarction

• ST elevation >2mm in V1-V3 and >1mm in all

other leads in >2 contiguous leads1.

• Myocardial injury presents as raised ST1.

• Infarction can present as Q wave1.

aVR

II Inferior

III Inferior aVF Inferior

V1 Septal

V2 Septal

I Lateral

aVL Lateral V5 Lateral

V6 Lateral

V4 Anterior

V3 Anterior

1. The Task Force on the management of acute myocardial infarction of the

European Society of Cardiology. Eur Heart J 2003;24:28-66

Evolution of an acute myocardial infarction

A. B. C.

D. E. F.

Onset > 1 Hour

Months

later > 24 Hours Days

Later

15 Minutes

Location of infarctions

Inferior AMI

II, III, AVF

Septal AMI

V1, V2

Anterior AMI

V3, V4

Lateral AMI

V5, V6 - ( I, AVL )

Caution

Atypical presentations of AMI can

be seen especially in

• Females

• Elderly

• Diabetics

Inferior AMI

aVF II III

II

I

aVL

V1

V6

V4

V2 V5

V3

aVR

III

II

aVF

Antero-septal AMI

V1 V2 V3

V4

aVR

III

I

aVF V5 II V6

aVL V1

V3

V4 V2

Antero-lateral AMI aVL

I

V1 V2 V3

V4 V5

V6

I V1

V6

V4

V2

V3

V5

V1

V2 V3

V4

V5 V6

aVR I II

III aVF

aVL

Lateral AMI

aVL

I I

aVL

V1

V6

V4

V3

II V2

aVF

V5

III

aVR

Reciprocal Changes

• If a lead is looking directly at the infarct site it will produce

ST segment elevation

• When a lead sees the infarct from the opposite

perspective, the ST segment may become depressed in

that lead

II, III aVF I, aVL, V leads

Infarction Overview

Site Indicative Leads Reciprocal Leads

Inferior II, III & aVF I & aVL

Septal V1 – V2 None

Anterior V3 – V4 None

Anteroseptal V1 – V4 None

Lateral I, aVL & V5 - V6 II, III & aVF

Anterolateral I, aVL & V3 –V6 II, III & aVF

Posterior None V1 – V4

? Posterior AMI V1-V4 Depression

Posterior - Lead Placement

V1 - V3 are moved round to

become V7 - V9.

They are placed on the same

horizontal plane as V4

V7 Posterior axillary line

V8 Midscapular line in between

V7 & V9

V9 To the left of the spine V7 V8 V9

V4 V4

Posterior ECG

Dynamic Changes in AMI

Pre-hospital ECG showing possible hyperacute

S-T changes in anterior leads

Dynamic Changes in AMI

2nd ECG taken 20mins later, showing established

antero-lateral S-T elevation

Identify the following 6 ECG

infarction sites

ECG 1

ECG 2

ECG 3

ECG 4

ECG 5

ECG 6

Summary

• A normal ECG does not rule out an AMI

• ST segment depression represents

ischaemia.

• ST segment elevation is a strong indicator

of an AMI.

Module 8

Imitators of ST Segment Abnormalities

AMI ECG Imitators

“Caution” The following ECGs can show

ST segment changes

– Left Bundle Branch Block

– Left Ventricular Hypertrophy

– Paced Rhythm

– Ventricular Rhythms

– Early Repolarisation

– Pericarditis

– Ventricular Aneurysm

This shows the importance of using an ECG along

with the clinical findings & not in isolation.

Left Bundle Branch Block

Left Ventricular Hypertrophy

Recognition:

• Compare V1 & V2, determine which has the deeper S

wave & measure the depth in mm (1mm = 1 small square).

• Compare V5 & V6, determine which has the taller R wave

& measure the height (mm).

• Add together the depth & height (mm). If the sum equals

35mm or more, then suspect LVH.

Paced Rhythm

Ventricular Rhythm

Early Repolarisation

Pericarditis

Ventricular Aneurysm

Summary

There are a number of ECGs that can

mimic ST segment changes as seen in

acute coronary syndrome (ACS). This

shows that it is important to evaluate the

clinical signs and symptoms first, then

follow up with confirmation from the ECG

Module 9

ECG Case Scenarios

54yr old woman who has been experiencing episodes of

chest ache for 4 days, worst episode this morning - 5hrs ago.

59yr old diabetic lady who has been experiencing some mild

chest and back ache for 5hrs today.

82yr old man with COPD has had chest ache for 2 days, worst

episode yesterday afternoon. He still has some residual pain.

44 year old male who has developed sudden onset of central

chest pain 1 hour following lunch.

77yr old lady with breathlessness; becoming worse late last

night; associated with some heaviness in her R arm.

67yr old lady, developed R arm pain 4hrs ago whilst hanging

out her washing.

29yr old female who admits to taking Cocaine on a regular

basis. Today, has developed severe crushing chest pain -

2hrs ago. She looks clammy and cyanosed.

45yr old man, who developed severe epigastric and back

pain today whilst at work. He has now had the pain for 2hrs.

44 year old lady, today was woken up by chest tightness,

similar to usual angina, at 6am (2hrs ago).

48yr old man who has had previous history of 2 MI’s. Today, was

at work at a call centre, when he experienced very severe chest tightness. Took GTN spray x 2 but pain has not alleviated.

42yr old man who has been feeling generally unwell for 1 week.

This evening, whilst eating a meal, developed sudden onset of severe central crushing chest pain (approx. 4hrs ago).

64yr old who is still in ICU following AAA repair yesterday.

Had been well overnight, but developed central chest

heaviness after lunch today - around 4hrs ago.

38yr old man playing football this evening, developed severe

chest tightness - not relieved by GTN in the ambulance.

63 year old lady who has presented with 3hrs retro-sternal

pain, which has worsened over the last 1hr.

80yr old lady, who has had angina (usually stable). Today her

pain has become worsened and is not relieved by GTN.

44 year old male who has developed severe crushing central

chest pain today whilst at work as an architect. Pain

commenced approx. 2 hrs ago.

67 year old man with no previous medical history. Awoke

4hrs ago with central crushing chest pain.

70yr old man who has been gardening today. Developed chest

ache and indigestion whilst mowing the lawn; approx. 3hrs ago.

80yr old man who has a long standing history of angina, was

watching TV this morning and experienced a sudden onset of

breathlessness and feeling of general malaise.

84yr old lady who has been admitted from a nursing home

today with breathlessness and palpitations.

90 year man who has been admitted today with episodes of

syncope.

78yr old man has been experiencing chest tightness for 1 wk;

becoming worse at lunchtime today approx. 3hrs ago.

28yr old man who has had 4wk history of viral illness - flu-like

in nature. Today, has experienced 3hrs chest pain.

59yr old man developed severe crushing chest pain 2hrs ago,

whilst making lunch. He collapsed after taking his GTN spray.

64yr old lady, was awoken from sleep 4hrs ago with central

chest discomfort.

79yr old lady who has history of SVT and takes beta-blocker.

Has come to outpatients for regular check-up and assessment.

78yr old man developed mild chest discomfort whilst playing

bowls. Indigestion remedies have not helped the discomfort.

72 year old lady, who has history of panic attacks and

depression. Today, has complained of feeling unwell, lethargic

and lightheaded.

44yr old lady, who has no previous medical history, but is

currently being investigated for thyroid problems. Just after breakfast, began to experience palpitations and dizziness.

56yr old lady, whilst watching TV this evening developed neck

and jaw pain like toothache, now lasting for 3hrs.

88yr old lady, finding it very hard to ‘catch her breath’. She

feels weak and dizzy and is visibly tachypnoeic.

50yr old man, who has previous history of hypertension. Has been

feeling unwell for 2 wks, experiencing tiredness and lethargy. Today, got up to use toilet and felt lightheaded and dizzy.

40yr old fit and well Ambulance man, presented at A/E with

concerns over his own ECG.

75yr old lady developed central chest and L arm pain today

(1hr 30mins ago), pain unresponsive to GTN.