ECG Analysis

ECGs
A systemic guide
Peter Watson

Objectives
• Electrical conduction in the heart
• Lead placement
• ECG settings
• ECG components
• ECG waves
• ECG complexes
• Abnormalies seen with ECG components
• Systemically work through an example

Cardiac conducting
system
Cardiac depolarisation
begins at the Sinoatrial
node, then spreads to the
Atrioventricular node,
before travelling to the
Bundle of HIS and the
Purkinje fibres to complete
an electrical cardiac cycle.

12 Lead ECG
Placement• 10 electrodes required to produce 12-lead ECG
• 4 Electrodes on all 4 limbs (RA, LL, LA, RL)
• 6 Electrodes on precordium (V1–6)
• Monitors 12 leads (V1–6), (I, II, III) and (aVR, aVF,
aVL)
• Allows interpretation of specific areas of the heart
◦ Inferior (II, III, aVF)
◦ Lateral (I, aVL, V5, V6)
◦ Anterior (V1–4)

Components of the
ECG• Rate
• Rhythm
• Axis
• P wave
• PR interval
• QRS
complex
• QT interval
& QTc
• ST segment
• T wave
• Other:
• Delta wave
• Epsilon
waves
• Osborne
waves
• U waves

Normal ECG
The normal ECG will display these characteristics:
• Rate
• 60- 99bpm
• Rhythm
• <10% variation in RR intervals)
• Cardiac Axis
• -30° – 90°
• P Waves
• 0.2-0.3mV
• 0.06 – 0.12s
• Upright in I, II, aVF, V2- V6
• Inverted in aVR
• Varies in III, aVLSinus origin
• PR Interval
• 0.12 – 0.2s
• Q Waves
• Small in I, II, aVL, V5, V6
• QRS Complex
• <0.12s
• ST Segment
• Isoelectric
• T Waves
• <2/3 height of preceding R wave
• 0.5mm in I, II, III
• <10mm in V1 – V6
• Same direction as preceding R wave
• U Waves
• <25% of T wave
• Same direction as T wave
• QTc
• <440ms in males
• <460ms in females

Standard ECG
Settings• Normal paper/monitor speed is 25mm/sec
• 1mm = 40msec (one small square)
• 5mm = 120msec (one big square)
• V = 10mm/mV
• V = 10mm/mV

Standard ECG
Settings• Normal paper/monitor speed is 25mm/sec
• Check the monitor/paper speed, this
should be displayed on the ECG

Step-by-Step
ECG Analysis
•Rate
• Rhythm
• Axis
• P wave
• PR interval
• QRS complex
• QT interval & QTc
• ST segment
• T wave
• Other waves

Rate
• Adults
• Bradycardia < 60bpm
• Normal 60-100bpm
• Tachycardia >100bpm
• Children
• Normal range of heart rate is age
dependent

Rate
• Calculating rate:
• one ECG paper page at 25mm/sec =
10sec duration, thus count complexes and
x6 = Rate
• OR
• For regular rhythms; Rate = 300 /(No.
large squares in-between the
complexes)
• For really fast rhythms; Rate =

Sinus Bradycardia
• Heart rate 35bpm

Sinus Tachycardia
• Heart rate 150bpm; Note P waves hidden in T
waves

Normal Sinus
Rhythm
• Heart rate 84

Step-by-Step
ECG Analysis
• Rate
•Rhythm
• Axis
• P wave
• PR interval
• QRS complex
• ST segment
• T wave
• Other waves

Rhythm
• Rhythms rate? Tachy/Brady/Normal
• Are P waves present?
• Are P waves regular?
• Is there always one P waves followed by one
QRS complex?
• Are QRS complexes regular morphology and
regular timing?
• Is the PR interval regular? Is there AV
association?

Rhythm
• Regular
OR
• Irregular
• Irregularly
Irregular
• Regularly
Irregular
• There are two parts of the rhythm
• Atrial: P waves
• Ventricular: QRS complex
• For each component, ?Is the rhythm;

Are P-waves Present?
ie. Is atrial activity present?
• Sinus P-waves are up in II and aVF
• P-wave duration <120ms
• Morphology - positive dome shaped in II an aVF
• If retrograde activation then P-waves in II and
aVF are inverted
• “Saw-tooth” flutter waves with a rate of 300/min
• No P-waves -> AF or atrial asystole

Rhythm
• If P-waves aren’t present it maybe:
• sinus arrest
• atrial fibrillation

Rhythm
• If P-waves are present it maybe:
• sinus
• atrial
• junctional,
• OR
• retrograde

Rhythm
- QRS complex
duration• If the rhythm originates above the AV node the QRS
complex will be narrow <120msec, it will be
propagated down the Bundles of His and through
the heart as normal.
• If the rhythm originates below the AV node it will be
propagated retrograde and antegrade and will
appear broad >120msec. The further away from the
AV node, the wider the QRS complex
• The exception to this is SVT with aberrant
conduction

Rhythm
• Is the atrial activity related to ventricular activity? Is there a
constant interval between p-waves and QRS complexes?
• Yes, then its likely the conduction between them is intact.
OR
• Yes, but not with every atrial depolarisation. ie Atrial flutter with
2:1 block
• No, there is a conduction delay i.e. 2nd degree heart block,
Mobitz I (Wenckebach) or Mobitz II

Bradycardia
QRS complex?
• Yes
• Sinus Bradycardia
• Sinus node exit block
• Sinus pause/arrest
• Junctional escape rhythm

Sinus arrest with a ventricular escape rhythm
Sinus pause / arrest (there is a single P wave visible on the 6-second rhythm strip).
Broad complex escape rhythm with a LBBB morphology at a rate of 25 bpm.
The LBBB morphology (dominant S wave in V1) suggests a ventricular escape
rhythm arising from the right bundle branch.

Bradycardia
QRS complex?
• No
• AV block:
• 2nd degree, Mobitz 1 (Wenkebach)
• 2nd degree, Mobitz 1I
• 2nd degree, Mobitz 1 or II with fixed ratio ie 2:1, 3:1
• 2nd degree, Mobitz 1 or II with high grade block ≥3:1
• 3rd degree/Complete Heart Block
• Ventricular escape rhythm

AV Block: 2nd degree, Mobitz I
(Wenckebach Phenomenon)
Progressive prolongation of the PR interval culminating in a non-conducted P wave
The PR interval is longest immediately before the dropped beat
The PR interval is shortest immediately after the dropped beat

AV Block: 2nd degree, Mobitz II
Intermittent non-conducted P waves without progressive prolongation of the PR
interval (compare this to Mobitz I).
The PR interval in the conducted beats remains constant.

AV block: 3rd degree
(complete heart block)
In complete heart block, there is complete absence of AV conduction – none of the supraventricular
impulses are conducted to the ventricles.
Perfusing rhythm is maintained by a junctional or ventricular escape rhythm. Alternatively, the patient may
suffer ventricular standstill leading to syncope (if self-terminating) or sudden cardiac death (if prolonged).

Ventricular escape rhythm in sinus arrest

Rhythm
- Narrow complex
tachycardia• Regular atrial
• Sinus tachycardia
• Atrial tachycardia
• Atrial flutter
• Inappropriate sinus
tachycardia
• Sinus node re-entrant
tachycardia
• Regular Atrioventricular
• Atrioventricular re-entry
tachycardia (AVRT)
• AV nodal re-entry tachycardia
• Automatic junctional
tachycardia
• Irregular atrial
• Atrial fibrillation
• Atrial flutter with variable
block
• Multifocal atrial tachycardia

Narrow complex
tachycardias
• AF
• Atrial flutter

AV nodal re-entry
tachycardia (AVNRT)
• AKA supraventricular tachycardia
• typically paroxysmal, may be spontaneous or provoked
• Rapid Palpitation, may have pre-syncopal symptoms
• Tachycardia 140-280bpm and regular
• Occurs via a functional re-entry circuit within the AV node

AV nodal re-entry
tachycardia (AVNRT)
• In AVNRT, there are two pathways within the AV node:
• The slow pathway (alpha): a slowly-conducting pathway with a short refractory period.
• The fast pathway (beta): a rapidly-conducting pathway with a long refractory period.
• If a premature atrial contraction (PAC) arrives while the fast pathway is still refractory,
the electrical impulse will be directed solely down the slow pathway (1). By the time the
premature impulse reaches the end of the slow pathway, the fast pathway is no longer
refractory (2) — hence the impulse is permitted to recycle retrogradely up the fast
pathway, thus creating a circus movement
Three Subtypes
1 Slow-Fast AVNRT (common type)
no visible p waves
2 Fast-Slow AVNRT (Uncommon AVNRT)
P waves visible after the QRS complexes
3 Slow-Slow AVNRT (Atypical AVNRT)
P waves visible before the QRS complexes

AV nodal re-entry tachycardia (AVNRT)
Slow-Fast (Typical) AVNRT: Narrow complex tachycardia at ~
150 bpm. No visible P waves. There are pseudo R’ waves in V1-
2.

Atrioventricular re-entry
tachycardia (AVRT)
• AVRT is a form of paroxysmal supraventricular tachycardia, occurring
in people with WPW syndrome.
• A reentry circuit is formed by the normal conduction system and the
accessory pathway (Bundle of Kent) resulting in circus movement.
• During tachyarrythmias the features of pre-excitation are lost as the
accessory pathway forms part of the reentry circuit. AVRT often
triggered by premature atrial or premature ventricular beats.
• Tachyarrhythmias can be fatal with AVRT
• AVRT are further divided in to orthodromic or antidromic conduction
based on direction of reentry conduction and ECG morphology.

Type A WPW
Delta wave, Dominant R wave in V1, associated with left
side accessory pathway

Type B WPW
Dominant S wave in V1, Delta wave, short PR interval,
associated with right side accessory pathway

Orthodromic Atrioventricular
re-entry tachycardia (AVRT)
• Orthodromic AVRT antegrade conduction is via the node
and retrograde via the accessory pathway
• Rate 200-300bpm
• P waves buried in QRS
• QRS alterans
• ST depression
• T wave inversion

Orthodromic AVRT
Narrow complex tachycardia 180bpm, no P waves

tachycardia (AVRT)
• Antidromic AVRT antegrade conduction via the accessory
pathway with retrograde conduction via the node
• Rate 200-300bpm
• Wide QRS
• Occurs in ~5% of WPW

Antidromic AVRT
Regular broad complex tachycardia,

Rhythm
- Broad complex
tachycardia• Regular
• Ventricular tachycardia
• Antidromic
tachycardia (AVRT)
• Supraventricular
tachycardia with
aberrant conduction
• Irregular
• Ventricular Fibrillation
• Polymorphic VT
• Torsades de Pointes
• AF with WPW
• SVT with aberrant
conduction; ie RBBB

AF/Atrial Flutter in
WPW• Atrial fibrillation can occur in up to 20% of patients with WPW.
Atrial flutter can occur in up to 7% of patients with WPW.
• The accessory pathway allows for rapid conduction directly to
the ventricles bypassing the AV node. Rapid ventricular rates
may result in degeneration to VT or VF.
• Rate > 200 bpm
• Irregular rhythm
• Wide QRS complexes due to abnormal ventricular
depolarisation via accessory pathway
• QRS Complexes change in shape and morphology
• Axis remains stable unlike Polymorphic VT

AF with WPW
Very rapid 300bpm, 2 conducted beats in V1-3, lack of
twisting seen in Torsades de Point

Monomorphic VT
• Ventricular Tachycardia (VT) is a broad complex
tachycardia originating in the ventricles.
• Monomorphic VT is the most common.
• Reenty pathway develops due to prior ischaemia or
infection causing abnormal myocardial scarring leading to
two distinct conduction pathways with a conduction block
and region of slow conduction, and is triggered by early or
late depolarisation and then accelerated abnormal
impulses generated in the ventricle
• >30sec sustained; <30sec non-sustained
• Patients maybe haemodynamically stable

Monomorphic VT
Uniform QRS complexes, indeterminate axis, Very broad QRS
~200ms, Josephsons sign, notching near the nadir of the S wave

Increased risk of VT
rather than SVT
Clinical features ECG features
Age >35years AV dissociation
Smoker Fusion beats
Ischaemic heart disease Captured beats
Previous VT Left axis variation >30° favours VT
Active angina QRS morphology in V1
Cannon “a” waves Variable intensity of S1
Unchanged intensity of S2
QRS with >140ms (<120ms SVT)
Concordance of QRS vectors in
pericardial leads
Brugada’s sign
Josephson’s sign

Brugada’s sign (red callipers) – The distance from the onset
of the QRS complex to the nadir of the S-wave is > 100ms.
Josephson’s sign (blue arrow) – Notching near the nadir of
the S-wave.

Polymorphic VT &
Torsades de Pointes
• Polymorphic ventricular tachycardia (PVT) is a form
of ventricular tachycardia in which there are multiple
ventricular foci with the resultant QRS complexes varying in
amplitude, axis and duration. The commonest cause of
PVT is myocardial ischaemia.
• Torsades de pointes (TdP) is a specific form of polymorphic
ventricular tachycardia occurring in the context of QT
prolongation; it has a characteristic morphology in which
the QRS complexes “twist” around the isoelectric line.

Causes of Torsades de Point
• Hypomagnesia
• Hypocalcaemia
• Class I and Class II antiarrhytmic drugs
• Phenothiaxine
• Tricyclic antidepressants
• Congenital long QT syndrome
• Organophosphates
• Complete heart block
• Drug interaction of terfenidine with erythromycin

Polymorphic VT-TdP
Sinus rhythm with inverted T waves, prominent U waves and
a long Q-U interval due to severe hypokalaemia (K+ 1.7)

Torsades de Pointes
“R on T” phenomenon causing Torsades de
Pointes, which subsequently degenerates to VF

Ventricular fibrillation
• Ventricular fibrillation (VF) is the the most important shockable
cardiac arrest rhythm.
• The ventricles suddenly attempt to contract at rates of up to 500
bpm. This rapid and irregular electrical activity renders the
ventricles unable to contract in a synchronised manner, resulting in
immediate loss of cardiac output. The heart is no longer an
effective pump and is reduced to a quivering mess.
• Unless advanced life support is rapidly instituted, this rhythm is
invariably fatal.
• Prolonged ventricular fibrillation results in decreasing waveform
amplitude, from initial coarse VF to fine VF and ultimately
degenerating into asystole due to progressive depletion of
myocardial energy stores.
• ECG Chaos, no P wave, no QRS, no T wave, Rate 150-500bpm

TdP to Ventricular
Fibrillation

Step-by-Step
ECG Analysis
• Rate
• Rhythm
•Axis
• P wave
• PR interval
• QRS complex
• ST segment
• T wave
• Other waves

Cardiac Axis
• Cardiac depolarisation begins
at the Sinoatrial node, then
spreads to the Atrioventricular
node, before travelling to the
Bundle of HIS and the Purkinje
fibres to complete an electrical
cardiac cycle.
• The biggest wave height
changes occur in leads inline
with the cardiac depolarisation.
• The smallest wave height
changes occur in those leads
perpendicular to the cardiac
depolarisation

Cardiac Axis
Normal Axis
= QRS axis between -30°&
+90°
Left Axis Deviation
= QRS axis <-30°.
Right Axis Deviation
= QRS axis >+90°.
Extreme Axis Deviation
= QRS axis between -90° &
180° (“Northwest Axis”).

How to calculate the
Cardiac Axis
• There are several ways to calculate the
cardiac axis:
• Quadrant Method - Leads 1 & aVF
• 3Lead analysis - Leads 1 & aVF
• Isoeletric Lead analysis
• Reaching and Leaving - Leads I & II
• Calculated method or Sam the Axis Man

Quadrant Method
• Using Leads I and aVF
• if positive in Lead I the axis is towards
Lead I
• if positive in Lead aVF the axis is towards
aVF
• This would be a normal axis between 0-
90°

Watsons’ Thumbs Up
Quadrant method
• Hold the ECG and look at it
• Your left hand should be closest to Lead I,
and right hand closer to Lead aVF than your
left hand
• Point you Left thumb up or down
corresponding to Lead I
• Point you Right thumb up or down
corresponding to Lead aVF

Watsons’ Thumbs Up
Quadrant method
• Both thumbs up - good ie. normal axis
• Left thumb up (+QRS in Lead I, -QRS in
aVF) Left axis deviation
• Right thumb up (-QRS in Lead I, +QRS in
aVF) Right axis deviation
• Both thumbs down - bad really bad ie. NW
axis

3 lead analysis
• Buy adding in Lead II to the Quadrant
method allows for more specific analysis of
axis

Isoelectric Lead
• The Lead with the least electric activity
(equaphasic) has an axis at 90° to the axis

Reaching and
Leaving• This is a quick glance technique only.
• Are Leads I & II Reaching towards each
other?
• ie the QRS of Lead I is predominately
negative and Lead II is predominately
positive = RAD
• Are Leads I & II Leaving each other?
• ie the QRS of Lead I is predominately
positive and Lead II is predominately
negative = LAD

Calculated Method
• Measure Lead I’s overall height = R-S (mm)
• Measure Lead aVF overall height = R-S
(mm)
• Place into this formula
• Axis = tan- (Lead I R-S)/(Lead aVF)*
*If both leads I and aVF are positive, this
figure stands works for the cardiac axis
If not, add 90° to the calculated figure

Sam- the Supper Axis
Man
• plot the net deflection (R-S) of Lead I
• plot the net deflection (R-S) of Lead aVF
• The intersection of these two lines is the
cardiac axis
• https://lifeinthefastlane.com/super-axis-man/

Normal Axis
Lead I and aVF positive (and Lead II); Not reaching Not leaving; Two thumbs up
aVL is isoelectric (-30°) thus axis is 60°
Tan- Lead I R-S (8-3=5) / Lead aVF R-S (8-0=8) =+55°

Lead I negative and aVF (and Lead II) positive; Reaching Not leaving; Right thumb up
aVR is isoelectric (-150°) thus axis is +120°
Tan- Lead I R-S (0-4=4) / Lead aVF R-S (12-1=11) [+90°] =-124°

• Right ventricular
hypertrophy
• Acute right ventricular strain,
e.g. due to pulmonary
embolism
• Lateral STEMI
• Chronic lung disease, e.g.
COPD
• Hyperkalaemia
• Sodium-channel blockade,
e.g. TCA poisoning
• Wolff-Parkinson-White
syndrome
• Dextrocardia
• Ventricular ectopy
• Secundum ASD – rSR’
pattern
• Normal paediatric ECG
• Left posterior fascicular
block – diagnosis of
exclusion
• Vertically orientated heart –
tall, thin patient
• Wrong limb leads

Left Axis Deviation
Lead I positive and aVF (and Lead II) negative; Not reaching but leaving; Left thumb up
aVR is isoelectric (-150°) thus axis is -60°
Tan- Lead I R-S (0-4=4) / Lead aVF R-S (12-1=11) [+90°]=-124°

Left Axis Deviation
• Left ventricular hypertrophy
• Left bundle branch block
• Inferior MI
• Ventricular pacing /ectopy
• Wolff-Parkinson-White Syndrome
• Primum ASD – rSR’ pattern
• Left anterior fascicular block – diagnosis of
exclusion
• Horizontally orientated heart – short, squat patient

Extreme Axis
Deviation
Lead I and aVF (and Lead II) negative; Not reaching and leaving; Both thumbs down
isoelectric?
Tan- Lead I R-S (5-15=10) / Lead aVF R-S (10-0=10) [+90°+90°]=-135°

Extreme Axis
Deviation• Ventricular rhythms – e.g.VT, AIVR,
ventricular ectopy
• Hyperkalaemia
• Severe right ventricular hypertrophy

Step-by-Step
ECG Analysis
• Rate
• Rhythm
• Axis
•P wave
• PR interval
• QRS complex
• ST segment
• T wave
• Other waves

Normal P waves
• Smooth contour
• Upright in lead II
• Inverted in aVR
• Biphasic in V1
• ≤120msec duration
• (≤ 3 small squares wide)
• ≤ 2.5 mm in limb leads
• <1.5mm in precordial leads
• Axis 0 to 75°; upright in Leads I, & II
and inverted in aVR
Atrial activity is best seen in leads II and V1

P wave abnormalities
• P mitrale (bifid P waves), seen with left atrial
enlargement.
• P pulmonale (peaked P waves), seen with right atrial
enlargement.
• P wave inversion, seen with ectopic atrial and junctional
rhythms.
• Variable P wave morphology, in multifocal atrial
rhythms.

Left atrial enlargement
(“P mitrale”)
• Bifid / notched P
waves in lead II
• P wave > 3 small
squares wide
Classically caused by
mitral stenosis

Right atrial
enlargement (“P
pulmonale”)• Peaked P waves in lead II
>2.5mm tall
Indicates right heart dilatation,
e.g. due to cor pulmonale

Biatrial atrial
enlargement (“P
pulmonale”)• Peaked P waves in
lead II > 2.5 mm tall
Indicates right heart
dilatation, e.g. due to cor
pulmonale

Flutter Waves
• Seen with atrial
flutter
• “Sawtooth” pattern at
300 bpm (one wave
per large square)
• Best appreciated by
turning the ECG
upside down

Fibrillatory Waves
• Seen with atrial fibrillation
• Irregular, chaotic
waveform
• May be coarse or fine
• Best seen in V1
• Not always visible (may
just have a irregular
baseline)
Coarse AF
Fine AF

Step-by-Step
ECG Analysis
• Rate
• Rhythm
• Axis
• P wave
•PR interval
• QRS complex
• ST segment
• T wave
• Other waves

PR interval
• The PR Interval indicates atrioventricular
conduction time. The interval is measured
from where the P wave begins until the
beginning of the QRS complex.
• This represents the conduction though the AV
node
• Normal duration 120-200msec
• <120msec suggests pre-excitation (eg.
WPW)or AV nodal (junctional rhythm)

How to interpret the PR
interval

Step-by-Step
ECG Analysis
• Rate
• Rhythm
• Axis
• P wave
• PR interval
• Q waves
•QRS complex
• ST segment
• T wave
• Other waves

QRS complex
• Composed of Q waves, R waves and S waves
• Normal duration 70-100ms
• QRS duration can indicate the origin of each
complex ie sinus, atrial, junctional, ventricular
• Narrow complexes originate above the ventricles
• Broad complexes originate from the ventricles or are
due to conduction delays.
• Large voltage? Hypertrophy
• Low voltage? Impedance (fat, fluid)

Normal Q waves
• Produced by depolarisation of the interventricular septum
• Any negative deflection prior to the R wave
• Features of normal (“septal”) Q waves:
• < 1 mm wide
• < 2 mm deep
• Absent in V1-3
NB. Larger Q waves are permitted in leads III and aVR as a normal
variant

Pathological Q
WavesIndicate previous myocardial infarction
Features:
• > 1 mm wide (>40msec)
• > 2 mm deep
• Seen in V1-3

Pathological Q
WavesDifferential Diagnosis include:
•Myocardial infarction
•Cardiomyopathies - HCM (“dagger Q waves”),
infiltrative myocardial disease
•Rotation of the heart - extreme
clock/anticlockwise rotation
•Lead placement errors

Pathological Q waves
This ECG demonstrates Q waves in the inferior leads
indicating a prior inferior infarct.

Dagger-like Q waves
Hypertrophic (Obstructive) Cardiomyopathy HCM (HOCM);
Dagger-like “septal Q waves” in the lateral leads.

R waves
• First positive deflection following the P wave
• Represents the early ventricular depolarisation
• R waves: Increase in height from V1-5 then
decrease in V6
• Abnormalities include:
• Dominant R Wave in V1
• Dominant R wave in aVR
• Poor R wave progression

Dominant R waves in
V1• Normal in children and young
adults
• Right Ventricular Hypertrophy
(RVH)
• Pulmonary Embolus
• Persistence of infantile
pattern
• Left to right shunt
• Right Bundle Branch Block
(RBBB)
• Posterior Myocardial Infarction
(ST elevation in Leads V7, V8,
V9)
• Wolff-Parkinson-White (WPW)
Type A
• Incorrect lead placement (e.g.
V1 and V3 reversed)
• Dextrocardia
• Hypertrophic cardiomyopathy
• Dystrophy
• Myotonic dystrophy
• Duchenne Muscular dystrophy

Paediatric ECG
Dominant R waves in V1

Right Bundle Branch Block
Dominant R waves in V1-6

Dominant R wave in
aVR• Poisoning with sodium-channel blocking drugs
(e.g. TCAs)
• Dextrocardia
• Incorrect lead placement (left/right arm leads
reversed)
• Commonly elevated in ventricular tachycardia
(VT)

Sodium Channel Blockade
Dominant ‘R wave in aVR.
Marked Tachycardia
R/S ratio ~0.7
This patient had taken 300 tablets of Amitryptaline 10mg, and had received IV
NaHCO3

Dextrocardia
Positive QRS complexes (with upright P and T waves) in aVR.
Negative QRS complexes (with inverted P and T waves) in lead I.
Marked right axis deviation. Absent R-wave progression in the chest
leads (dominant S waves throughout)

Poor R Wave
Progression
• Prior anteroseptal MI
• LVH
• WPW
• Dextrocardia
or left anterior fascicular
block
• Tension pneumothorax
with mediastinal shift
• Congenital heart disease
• Inaccurate lead
placement esp. in obese
women
• May be a normal variant

Left Bundle Branch Block
Note the poor R wave progression in the precordial leads

QRS Bundle Branch
Blocks
• Left BBB
• depolarised from RV
via the right bundle
then to the LV via the
left bundle
• Right BBB
• RV depolarisation is
delayed, and spreads
form left to right

Left Ventricular
Hypertrophy
• LV hypertrophies in response to pressure overload
such as AS, AR, hypertension, HCM, MR.
• This leads to:
• Increased R wave amplitude in the left-sided
(lateral) ECG leads (I, aVL and V4-6)
• Increased S wave depth in the right-sided leads
(III, aVR, V1-3).
• The thick LV wall leads to prolonged depolarisation
(increased R wave peak time) and delayed
repolarisation (ST and T-wave abnormalities) in the
lateral leads.

Left Ventricular Hypertrophy
• LVH criteria:
• Sokolov-Lyon criteria (S wave depth in V1 + tallest R wave height in V5-V6 > 35
mm).
• Increased R wave peak time >50msec in V5-6
• ST depression, T wave inversion, ‘strain’ pattern in I, aVL, and V5-6

Right Ventricular
Hypertrophy
• RV hypertrophies in response to pressure overload such
as pulmonary hypertension, PS, PR, MS, PE, Chronic
lung disease (cor pulmonale), Congential heart disease,
VSD, ARVD.
• This leads to:
• Right axis deviation
• Dominant R wave in V1 >7mm
• Dominant S wave in V6 >7mm
• QRS <120msec
• May see p pulmonale, RV strain pattern in V1-4, II, III, &
aVF, S1S2S3 pattern, Deep S waves in lateral leads (I,
aVL, V5-6)

Right Ventricular Hypertrophy
Right axis deviation, Dominant R in V1 (>7mm), Dominant S in
V6 (>7mm), Right ventricular strain pattern with ST depression
and T wave inversion in V1-4

Step-by-Step
ECG Analysis
• Rate
• Rhythm
• Axis
• P wave
• PR interval
• Q waves
• QRS complex
•QT interval &
QTc
• ST segment
• T wave
• Other waves

QT and QTc
• The QT interval indicates ventricular activity,
both depolarization and repolarization.
• QT is inversely proportional to heart rate.
• Measure the QT interval from the beginning of
the QRS complex to the end of the T wave.
• Males 440msec
• Females 460msec
• QT>500msec risk of Torsades de Pointes

QT and QTc
• Bazett’s formula: QTC = QT / √ RR
• Fredericia’s formula: QTC = QT / ∛RR
• Framingham formula: QTC = QT + 0.154 (1
– RR)
• Hodges formula: QTC = QT + 1.75 (heart
rate – 60)
• Guestimate: if the QT is less than half the
RR interval it’s probably normal

Prolonged QTc
• Hypokalaemia,
hypomagnesia,
hypocalcaemia
• Hypothermia
• Myocardial ischaemia
• Post cardiac arrest
• Raised ICP
• Congenital long QT
syndrome eg, Jervelle and
Lange–Neilson syndrome
(associated with deafness)
• Drugs:
• Antiarrhythmics;
flecainide, quinidine,
sotalol, procainamide,
amiodarone
• Gastric motility promoter;
cisapride, domperidone
• Antibiotics;
clarithromycin,
erythromycin
• Antipsychotics;
chlorpromazine,
haloperidol

QT Normogram
• Risk of TdP is determined by considering both the
absolute QT interval and the simultaneous heart rate
• A QT interval-heart rate pair that plots above the line
indicates that the patient is at risk of TdP.

Quetiapine toxicity
QT 560msec, HR 120
Despite the QT prolongation, the risk of TdP is decreased
due to the concurrent tachycardia.

Short QTc
• Hypercalcaemia
• Short QT syndrome
• Short QT syndrome is a recently-
discovered arrhythmogenic disease
associated with paroxysmal atrial
and ventricular fibrillation, syncope
and sudden cardiac death. Due to a
potassium channelopathy
• Digoxin effect

Congenital Short QTc
Very short QTc (280ms) with tall, peaked T waves

Digoxin effect
QT 260msec QTc 310msec
Note the reverse tick appearance in the lateral leads

Step-by-Step
ECG Analysis
• Rate
• Rhythm
• Axis
• P wave
• PR interval
• Q waves
• QRS complex
•ST segment
• T wave
• Other waves

ST segment
• The ST segment begins at the end of the QRS
complex and continues to beginning of the T wave.
• The ST segment is the flat, isoelectric section of
the ECG between the end of the S wave (the J
point) and the beginning of the T wave.
• It represents the interval between ventricular
depolarization and repolarization.
• The most important cause of ST segment
abnormality (elevation or depression) is myocardial
ischaemia or infarction.

ST segment changes
and Coronary arteries

ST Elevation
• Causes of ST elevation
•Acute myocardial infarction
•Coronary vasospasm (Printzmetal’s
angina)
•Pericarditis
•Benign early repolarization
•Left bundle branch block
•Left ventricular hypertrophy
•Ventricular aneurysm
•Tako-Tsubo cardiomyopathy
•Brugada syndrome
•Ventricular paced rhythm
•Raised intracranial pressure
•Less Common Causes of ST segment
Elevation
•Pulmonary embolism and acute cor
pulmonale (usually in lead III)
•Acute aortic dissection (classically
causes inferior STEMI due to RCA
dissection)
•Hyperkalaemia
•Sodium-channel blocking
drugs (secondary to QRS widening)
•J-
waves (hypothermia, hypercalcaem
ia)
•Following electrical cardioversion
•Others: Cardiac tumour,
myocarditis, pancreas or
gallbladder disease

Benign Early Repolarisation
Widespread modest (<25% Twave height) STE, Notching at the J point,
Concordant T waves, No reciprocal changes, Fish-hook pattern in V4

Extensive Anterior
AMI
ST elevation in V1-6 plus I and aVL (most marked in V2-4). Minimal reciprocal ST depression in III and aVF.
Q waves in V1-2, reduced R wave height (a Q-wave equivalent) in V3-4.
There is a premature ventricular complex (PVC) with “R on T’ phenomenon at the end of the ECG; this puts
the patient at risk for malignant ventricular arrhythmias.

Pericarditis
Generalised ST elevation, Presence of PR depression, Normal T wave
amplitude, ST segment / T wave ratio > 0.25, Absence of “fish hook”
appearance in V4

ST Depression
•ST depression can be either upsloping, downsloping, or
horizontal.
•Horizontal or downsloping ST depression ≥ 0.5 mm at the J-
point in ≥ 2 contiguous leads indicates myocardial ischaemia
(according to the 2007 Task Force Criteria).
•Upsloping ST depression in the precordial leads with
prominent “De Winter’s” T waves is highly specific for
occlusion of the LAD.
•Reciprocal change has a morphology that resembles “upside
down” ST elevation and is seen in leads electrically opposite
to the site of infarction.
•Posterior MI manifests as horizontal ST depression in V1-3
and is associated with upright T waves and tall R waves.

ST Depression
• Myocardial ischaemia / NSTEMI;
LMCA, Triple vessel disease.
• Reciprocal change in STEMI;
• Inferior STEMI produces reciprocal
ST depression in aVL (± lead I).
• Lateral or anterolateral
STEMI produces reciprocal ST
depression in III and aVF (± lead II).
• Reciprocal ST depression in V1-3
occurs with posterior infarction
• Posterior MI
• De Winters T waves
• Digoxin effect
• Hypokalaemia: widespread
downsloping ST depression with T-
wave flattening/inversion, prominent U
waves and a prolonged QU interval.
• Supraventricular tachycardia
• Right bundle branch block (RBBB):
• Right ventricular hypertrophy:
• Left ventricular hypertrophy
• Ventricular paced rhythm
• Supraventricular Tachycardia(e.g.
AVNRT) rate-related widespread
horizontal ST depression, most
prominent in the left precordial leads
(V4-6). resolves with treatment.

Posterior MI
ST depression in V2-3. Tall, broad R waves (> 30ms) in V2-3. Dominant R
wave (R/S ratio > 1) in V2, Upright terminal portions of the T waves in V2-3

Sgarbossa Criteria for
LBBB/paced rhythms
Modified Sgarbossa Criteria:
• ≥ 1 lead with ≥1 mm of
concordant ST elevation
• ≥ 1 lead of V1-V3 with ≥ 1 mm of
concordant ST depression
• ≥ 1 lead anywhere with ≥ 1 mm
STE and proportionally
excessive discordant STE, as
defined by ≥ 25% of the depth of
the preceding S-wave.
These criteria are specific, but not
sensitive for myocardial infarction.
•A total score of ≥ 3 is reported to
have a specificity of 90% for
diagnosing myocardial infarction.
•But Low sensitivity (20%)

Step-by-Step
ECG Analysis
• Rate
• Rhythm
• Axis
• P wave
• PR interval
• Q waves
• QRS complex
• ST segment
•T wave
• Other waves

T wave
• The T wave is the positive deflection after each
QRS complex and represents ventricular
repolarisation.
• Upright in all leads except aVR and V1
• Amplitude < 5mm in limb leads, < 15mm in
precordial leads

T wave Abnormalities
• Hyperacute “Peaked" T waves:
• Early STEMI, (De Winters T waves), Prinzmetal angina
• Inverted T waves:
• Paediatric, MI, BBB, Ventricular Hypertrophy “strain pattern”, PE, HCM,
Raised ICP
• Biphasic T waves:
• MI, Hypokalaemia
• Wellens’ Syndrome; type I, and type II (LAD critical stenosis)
• ‘Camel Hump’ T waves;
• prominent U waves, hidden P waves
• Flattened T waves;
• Ischaemia, hypokalaemia

De Winters T waves
T waves are tall and peaked , and preceded by an area of up-sloping ST segment depression in most
of the precordial leads (esp V2 – V5). There is no ST elevation in these leads but there is subtle ST
elevation in aVR. strongly suggestive of an acute left anterior descending coronary artery occlusion.

Wellens Syndrome
Note the Biphasic T wave in V2

Hypertrophic Cardiomyopathy
Deep T-waves in all of the precordial leads.

Bilateral Pulmonary Embolism
T wave inversion in the inferior and right pericardial leads

U waves
•The U wave is a small (0.5 mm up to 2mm)
deflection immediately following the T wave
•Inversely proportional to the heart rate, more
visible when HR <65 bpm.
•U wave is usually in the same direction as the
T wave.
•U wave is best seen in leads V2 and V3.

Prominent U waves
•U wave >2mm or >25% of the T wave
•Prominent with bradycardia, severe hypokalaemia
•Maybe seen with:
•hypocalcaemia, hypomagnesia, hypothermia
•Raised ICP
•LVH
•HCM
•Drugs: Digoxin, Phenothiazides, Class Ia (quinidine,
procainamide) and Class III (sotalol, amiodarone)
antiarrhythmics

Inverted U waves
•U wave inversion in leads with upright T wave
•A negative U wave is highly specific for the presence of heart
disease
•The main causes of inverted U waves are:
•Coronary artery disease
•Hypertension
•Valvular heart disease
•Congenital heart disease
•Cardiomyopathy
•Hyperthyroidism Unstable angina

Sinus Bradycardia
Prominent U waves in this patient with anorexia nervosa

NSTEMI
Subtle U wave inversion the lateral leads (I, V5-6)

Step-by-Step
ECG Analysis
• Rate
• Rhythm
• Axis
• P wave
• PR interval
• Q waves
• QRS complex
• ST segment
• T wave
•Other waves

Other Waves
• Delta Wave
• Epsilon Waves
• Osborne Waves

Delta Waves
• Slurred upstroke of the QRS complex
• Often associated with a short PR interval
• <120msec
• Most commonly seen in WPW syndrome
• Broad QRS (>100msec)

Wolff-Parkison-White
Syndrome
Delta Waves (slurred upstroke of her QRS) are the cardinal sign of WPW, and
most obvious in leads V1 & V2. The minor ST changes seen resolved promptly.

Epsilon Waves
• The epsilon wave is a small positive
deflection (‘blip’) buried in the end of the
QRS complex.
• Characteristic finding in arrhythmogenic right
ventricular dysplasia (ARVD).

Osborne Waves
• Osborne Waves (J wave) is a positive deflection at the J point
(negative in aVR and V1)
• It is usually most prominent in the precordial leads
• Most commonly seen in hypothermia
• Also seen in hypercalcaemia, Head injury, raised ICP, secondary to
medications, idiopathic VF.

Hypothermia
The ECG rhythm is slow and irregularly irregular.Atrial fibrillation. The other marked ECG
feature is an extra positive deflection immediately after the main QRS seen most
obviously in leads V3-V6 and leads II & III. These are J or Osborne waves. Put together
with slow AF the ECG pattern is one of moderate to severe hypothermia. This patient’s
temperature measured at 29.50C

Work through this
example, step-by-
step?

39 year old man with chest pain after going to the gym
Rate= 9-10/10seconds
= 54-60/min

Rhythm
=
Sinus
Every QRS is preceded by a P-wave
P-waves appear normal; normal axis normal
morphology

Axis +QRS in Lead 1 -QRS in aVF
+/-QRS in Lead II = 60° Normal Axis ~ 60°

P waves
present, regular, followed by a
QRS
duration = 60-80ms,morphology = normal

PR interval ≤200ms

Q waves None visible

QRS duration ≤120ms

LV Hypertrophy if, SV1 + (RV5 or RV6) > 35mm
SV1 + RV5 19mm
X

RV Hypertrophyif R/S ratio V5 or V6 < 1
X
Or R/S ratio V1 > 1
Or S1S2S3 pattern
R/S ratio V5 or V6 < 1
X
R/S ratio V1 > 1
X
S1S2S3 pattern
X

STDuration & morphology appear normal

T wavesDuration & morphology appear normal

QT Duration ~400ms QTc =QT / ∛RR
RRQT
=0.4/∛1.2 =376ms

Additional WavesHmm.....Is that a U wave?
And that? And that?

Interpretation: Sinus Bradycardia with associated U waves
No signs of acute ischaemia or dysrhythmia

Implication:Not uncommon ECG finding in healthy
individuals
Look for other source of pain

Objectives Covered
• Electrical conduction in the heart
• Lead placement
• ECG settings
• ECG components
• ECG waves
• ECG complexes
• Abnormalies seen with ECG components

References
• http://www.newhealthadvisor.com/Tachycardia-in-Children.html
• https://prepgenie.com.au/gamsat/importance-of-graphs-and-data-
tables-in-gamsat-biology-questions/
• https://thephysiologist.org/study-materials/the-normal-ecg/
• https://lifeinthefastlane.com/ecg-library/accelerated-junctional-rhythm/
• https://ekg.academy
• http://www.ems12lead.com/2010/12/23/why-learn-axis/
• http://alstrainingresources.com/education/ecg-image-library/junctional-
rhythm/
• http://www.dallasheart.com/page2/page42/page43/page43.html
• http://hqmeded-ecg.blogspot.com.au/2012/04/is-this-simple-right-
bundle-branch.html

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