Module 1
Anatomy & Physiology
Anatomy of The Heart
Left Atrium
HIS Bundle
Mitral
Valve
Left Bundle
Branch (LBB)
Right Atrium
Chordae Tendinae
Left Posterior
Fascicle (LPS)
Papillary Muscles
Right Bundle
Branch (RBB)
Tricuspid Valve
Left Ventricle
Right Ventricle
(3-4 times thicker than
the right)
Septum
The passage of blood through
the heart
Aorta
Pulmonary artery
Pulmonary artery
Pulmonary veins
Pulmonary veins
Superior vena cava
Left atrium
Right atrium
Inferior vena cava
Right ventricle
Left ventricle
Layers of The Heart
Coronary Artery
Pericardium
Myocardium
Endocardium
Intercalated discs
cardiac muscle cell
Acute Myocardial Infarction
A thrombus (darker red in the middle) forming a
cap on a plaque of atheroma
Fibrin Threads
15 minutes
% necrosis
0%
2 hours
50%
6 hours
90%
Anterior heart showing coronary vessels
Aorta
Right
Coronary
Artery
Left Main
Coronary
Artery
Left
Circumflex Branch
Posterior
Interventricular
Marginal
Branch
Left
Anterior
Descending
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
Bundle of His
Sinoatrial (SA)
Node
Left Bundle Branch
Atrioventicular (AV)
Node
Left Anterior
Division
Right Bundle
Branch
Left Posterior
Division
Purkinje
Fibres
Depolarisation
First stage of
depolarisation
Second stage of
depolarisation
2
1
2
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
3. The intrinsic rate of
the Purkinje cells is
about 0 - 30 bpm
X
X
2. The AV junctional
region intrinsic rate is
about 40 bpm
Narrow QRS
(no preceding P wave)
X
Broad QRS
(no preceding P wave)
ECG: Wave pattern
atrial
depolarisation
ventricular
depolarisation
atrial/ventricular
repolarisation
O
Millivolts
R
T
P
Q
S
Atrial
systole
Complete
cardiac
diastole
0.4s
0.1s
Ventricular
systole
0.3s
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
Arm
Left
Leg
• 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
I
-
I
+
- Einthovens’ Triangle
III
II
II
III
+
+
Augmented Unipolar Leads
+
+
Augmented Voltage
Right (aVR)
aVR will always be
negative if the limb
leads are placed
correctly
Augmented Voltage
Left (aVL)
+
Augmented
Voltage Foot (aVF)
Limb leads
Left axis
-90°
-120°
-60°
-30° aV L
-150°
aV R
0° I
+180°
+-30°
+150°
Right axis
+120°
III
+90°
aV F
+60°
II
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)
Angle of
Louis
V1
V2
V3
V4
V5
V6
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).
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.
4.
Confirm that aVR is negative (if not check limb lead placement).
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
*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
PR
interval
QT
interval
QRS
complex
*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
R
q
R
s
QS
ST Segment
ST Segment
1
2
3
J Point
J Point Examples
1
4
2
3
5
6
Pathological Q Wave
> 0.04 sec wide
>25% of R wave
ECG Paper
1 large box = 0.2 seconds
5 large boxes = 1 second
1 small box = 0.04
seconds
10 mm/1mv
Reference
Time
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
Bundle of His
Left Bundle Branch
Atrioventicular (AV)
Node
Anterior Fascicles
Right Bundle
Branch
Posterior Fascicles
Purkinje
Fibres
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.
ECG Electrical Deflection
• 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.
Current
ElectrodeDeflection
Limb leads
Left axis
-90°
Extreme right
-120°
-60°
aVR-150°
-30°
aVL
0° I
+180°
+-30°
+150°
Normal axis
Right axis
+120°
III
+90°
aVF
+60°
II
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’.
Normal QRS Axis
• aVR should always be
negative.
• Lead II is predominantly
positive.
• Lead I is predominantly
positive.
Left Axis Deviation
• aVR is negative.
• Lead I is predominantly
positive.
• Lead II is predominantly
negative.
• Therefore the current flows
away from lead II, towards
aVL.
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.
Right Axis Deviation
• aVR is negative.
• Lead III is predominantly
positive.
• Lead I is predominantly
negative.
• Therefore the current flows
away from Lead I, towards
Lead III.
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
P
P
P
P
• 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.
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.
x
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
x x x
xx
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
xx
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 ‘sawtoothed’ appearance (especially V1) as above.
• Very responsive to DC electrical cardioversion.
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.
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)
Normal
pathway
Accessory
pathway
Paroxysmal
tachycardia
Delta
wave
anterograde / retrograde
conduction
PR
• 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.
Junctional Rhythm (Nodal)
x
•
•
•
•
High
Mid
Low
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.
First-degree Heart Block
P
P
• 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.
Second-degree Heart Block
Mobitz type I (Wenckebach)
P
P
P
R
P
P
?
• 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.
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)
x x
P
P
P
P
P
P
• 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.
Ventricular (Unifocal)
Extrasystole
x
• 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.
Coupled Ventricular
Extrasystole
x
• 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.
Couplets
x
• 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
R on T Extrasystole
x
• When the ventricular extrasystole falls on the T-wave. This may
trigger serious ventricular arrhythmias.
Ventricular (Multifocal)
Extrasystole
x
x
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.
Paced Beats
Pacing
wire
x
• A ventricular paced beat will display a broadened QRS complex.
• The slim, deflection immediately preceding the R-wave denotes
the pacing spike (arrowed above).
Idioventricular Rhythm
x
• 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.
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.
x
Ventricular Tachycardia
(VT)
• 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.
x
x x
x
x
x
x xx
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.
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
V6
V5
Left Chest
Leads
Left Limb
I
Lead
V1 V2
Right Chest Leads
V3
V6
• 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.
Right Bundle Branch Block (RBBB)
R
V1
r
S
• 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.
RBBB
Left Bundle Branch Block (LBBB)
• 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
LBBB
V1
QS
• LBBB produces a QS (negative complex) in
V1 and wide notched complexes in the Left
limb / chest leads (I, V5 & V6).
I
V5
V6
LBBB
RBBB vs LBBB
VI-V2
V5-V6
R
R
RBBB
S
LBBB
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 presentation 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.
I
Lateral
aVR
V1 Septal
V4 Anterior
II Inferior aVL Lateral
V2 Septal
V5 Lateral
III Inferior aVF Inferior
V3 Anterior
V6 Lateral
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.
Onset
D.
C.
F.
E.
> 24 Hours
> 1 Hour
15 Minutes
Days
Later
Months
later
Location of infarctions
Septal AMI
V1, V2
Anterior AMI
V3, V4
Lateral AMI
Inferior AMI
II, III, AVF
V5, V6 - ( I, AVL )
Caution
Atypical presentations of AMI can
be seen especially in
• Females
• Elderly
• Diabetics
Inferior AMI
I
aVR V1
II aVL V2
III aVF V3
II
V4
V5
V6
III
aVF
II
Antero-septal AMI
V1 V2
V3
V4
I
II
III
aVR V1
aVL V2
aVF V3
V4
V5
V6
Antero-lateral AMI
aVL
V6
V5
V4
V1 V2V3
I
II
I
III
aVR V1 V4
aVL V2 V5
V1 V4
aVF V3 V6
V2 V5
V3
V6
I
Lateral AMI
aVL
I
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
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
V4
V4
V7 V8 V9
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.