COLLECTED BY:

DR.MOHAMMAD MUNIR MOSHARRAF KHAN

MBBS, MPH, MSS, MPRHGD,
CPEM (Emergency Medicine-DMCH and University of Pennsylvania),
DEM-Emergency Medicine (RLA-UK), CCD (BIRDEM)
Cambridge Advance Course on CNCDs Epidemiology (IEDCR).

Clinical Care Coordinator and In-Charge Emergency Dept, USBMCH.

Executive Member & Academic Secretary – Bangladesh Society of
Emergency Medicine (BSEM).

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 ECG
ECG Rate Interpretation:

The usual paper speed is 25mm/sec:

• 1mm (small square) = 0.04 sec

• 5mm (big square) = 0.2 sec

Estimate the rate:

There are multiple methods to estimate the rate:

• Regular rhythms:
• Rate = 300 / number of large squares in between each consecutive R wave.
• Very fast rhythms:
• Rate = 1500 / number of small squares in between each consecutive R wave.
• Slow or irregular rhythms:
• Rate = number of complexes on the rhythm strip x 6 (this gives the average rate
over a ten-second period).

Interpretation (adults):

• 60–100 beats/min
• Normal
• >100 beats/min
• Tachycardia
• <60 beats/min
• Bradycardia

Normal Heart Rates in Children

• Newborn: 110 – 150 bpm

• 2 years: 85 – 125 bpm
• 4 years: 75 – 115 bpm
• 6 years+: 60 – 100 bpm

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ECG Rhythm:
The rhythm is best analyzed by looking at a rhythm strip. On a 12 lead ECG this is usually a 10 second
recording from Lead II. Confirm or corroborate any findings in this lead by checking the other leads. A
longer rhythm strip, recorded perhaps recorded at a slower speed, may be helpful.
A useful 7 step approach to ECG rhythm analysis is described.

1. Rate

• Tachycardia or bradycardia?
• Normal rate is 60-100/min.

2. Pattern of QRS complexes

• Regular or irregular?
• If irregular is it regularly irregular or irregularly irregular?

3. QRS morphology

• Narrow complex — sinus, atrial or junctional origin.

• Wide complex — ventricular origin, or supraventricular with aberrant conduction.

4. P waves

• Absent — sinus arrest, atrial fibrillation

• Present — morphology and PR interval may suggest sinus, atrial, junctional or even retrograde
from the ventricles.

5. Relationship between P waves and QRS complexes

• AV association (may be difficult to distinguish from isorhythmic dissociation)

• AV dissociation
• Complete — atrial and ventricular activity is always independent.
• Incomplete — intermittent capture.

6. Onset and termination

• Abrupt — suggests re-entrant process.

• Gradual — suggests increased automaticity.

7. Response to vagal maneuvers

• Sinus tachycardia, ectopic atrial tachydysrhythmia — gradual slowing during the vagal
maneuver, but resumes on cessation.

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 • AVNRT or AVRT — abrupt termination or no response.
• Atrial fibrillation and atrial flutter — gradual slowing during the maneuver.
• VT — no response.

Differential Diagnosis
1. Narrow Complex (Supraventricular) Tachycardias
Regular Irregular

Atrial • Sinus tachycardia • Atrial fibrillation

• Atrial tachycardia • Atrial flutter with variable block

• Atrial flutter • Multifocal atrial tachycardia

• Inappropriate sinus tachycardia

• Sinus node re-entrant tachycardia

Atrioventricular • Atrioventricular re-entry tachycardia

(AVRT)

• AV nodal re-entry tachycardia

(AVNRT)

• Automatic junctional tachycardia

2. Broad Complex Tachycardias

a) Regular

Ventricular tachycardia
Antidromic Atrioventricular re-entry tachycardia (AVRT).
Any regular supraventricular tachycardia with aberrant conduction — e.g. due to bundle
branch block, rate-related aberrancy.

All regular BCTs should be considered to be VT until proven otherwise.

b) Irregular

• Ventricular fibrillation
• Polymorphic VT

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 • Torsades de Pointes
• AF with Wolff-Parkinson-White syndrome
• Any irregular supraventricular tachycardia with aberrant conduction — e.g. due to bundle
branch block, rate-related aberrancy.

Bradycardias:
a. P waves present:

Each P wave is followed by a QRS complex (= sinus node dysfunction)

• Sinus bradycardia
• Sinus node exit block
• Sinus pause / arrest

Not every P wave is followed by a QRS complex (= AV node dysfunction)

• AV block: 2nd degree, Mobitz I (Wenckebach)

• AV block: 2nd degree, Mobitz II
• AV block: 2nd degree, “fixed ratio blocks” (2:1, 3:1)
• AV block: 2nd degree, “high grade AV block”
• AV block: 3rd degree (complete heart block)

b. P waves absent:
➢ Narrow complexes
Junctional escape rhythm

➢ Broad complexes
Ventricular escape rhythm

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 ECG leads coronary artery territories

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ECG Axis Interpretation:
The diagram below illustrates the relationship between QRS axis and the frontal leads of the
ECG.

• Normal Axis = QRS axis between -30° and +90°.

• Left Axis Deviation = QRS axis less than -30°.
• Right Axis Deviation = QRS axis greater than +90°.
• Extreme Axis Deviation = QRS axis between -90° and 180° (AKA “Northwest Axis”).

Methods of ECG Axis Interpretation:

There are several complementary approaches to estimating QRS axis, which are summarized
below:

1. The Quadrant Method – (Lead I and aVF)

2. Three Lead analysis – (Lead I, Lead II and aVF)
3. Isoelectric Lead analysis
4. Super SAM the Axis Man

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 ❖ Method 1 – The Quadrant Method

The most efficient way to estimate axis is to look at LEAD I and LEAD aVF.

Examine the QRS complex in each lead and determine if it is Positive, Isoelectric
(Equiphasic) or Negative:

• A positive QRS in Lead I puts the axis in roughly the same direction as lead I.
• A positive QRS in Lead aVF similarly aligns the axis with lead aVF.
• Combining both coloured areas – the quadrant of overlap determines the axis. So If Lead
I and II are both positive, the axis is between 0° and +90° (i.e. normal axis).

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Now estimate the AXIS using the Lead I and aVF – Quadrant Method:

AXIS: QRS Positive Lead I – QRS Negative Lead aVF

AXIS: QRS Negative Lead I – QRS Positive Lead aVF

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 AXIS: QRS Negative Lead I – QRS Negative Lead aVF

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Method 2: Three Lead analysis – (Lead I, Lead II and aVF)
Next we add in Lead II to the analysis of Lead I and aVF

• A positive QRS in Lead I puts the axis in roughly the same direction as lead I.
• A positive QRS in Lead II similarly aligns the axis with lead II.
• We can then combine both colored areas and the area of overlap determines the axis. So
If Lead I and II are both positive, the axis is between -30° and +90° (i.e. normal axis).

• The combined evaluation of Lead I, Lead II and aVF – allows rapid and accurate QRS
assessment. The addition of Lead II can help determine pathological LAD from normal
axis/physiological LAD
• Note: Lead III or aVF can both be used in three lead analysis

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QRS Positive Lead I – QRS Equiphasic Lead II – QRS Negative Lead aVF

QRS Positive Lead I – QRS Negative Lead II – QRS Negative Lead aVF

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QRS Negative Lead I – QRS Positive Lead II – QRS Positive Lead aVF

QRS Negative Lead I – QRS Negative Lead II – QRS Negative Lead aVF

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Summary Table:

Method 3 – The Isoelectric Lead

This method allows a more precise estimation of QRS axis, using the axis diagram below

Key Principles

• If the QRS is POSITIVE in any given lead, the axis points in roughly the same direction as this
lead.

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 • If the QRS is NEGATIVE in any given lead, the axis points in roughly the opposite direction to this
lead.
• If the QRS is ISOELECTRIC (equiphasic) in any given lead (positive deflection = negative
deflection), the axis is at 90° to this lead.

Step 1: Find the isoelectric lead.

The isoelectric (equiphasic) lead is the frontal lead with zero net amplitude. This can be either:

• A biphasic QRS where R wave height = Q or S wave depth.

• A flat-line QRS with no discernible features.

Step 2: Find the positive leads.

• Look for the leads with the tallest R waves (or largest R/S ratios)

Step 3: Calculate the QRS axis.

• The QRS axis is at 90° to the isoelectric lead, pointing in the direction of the positive leads.

❖ Example 1:

Answer – Lead I, II, aVF

• Lead I = POSITIVE
• Lead II = POSITIVE
• aVF = POSITIVE

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 • This puts the axis in the left lower quadrant (LLQ) between 0° and +90° – i.e. normal axis

+ Answer – Isoelectric Lead Method

• Lead aVL is isoelectric, being biphasic with similarly sized positive and negative deflections
(no need to precisely measure this).
• From the diagram above, we can see that aVL is located at -30°.
• The QRS axis must be ± 90° from lead aVL, either at +60° or -120°
• With leads I (0), II (+60) and aVF (+90) all being positive, we know that the axis must lie
somewhere between 0 and +90°.
• This puts the QRS axis at +60° – i.e. normal axis

❖ Example 2:

Answer – Quadrant Method

• Lead I = NEGATIVE
• Lead II = Equiphasic
• Lead aVF = POSITIVE
• This puts the axis in the left lower quadrant, between +90° and +180°, i.e. RAD

+ Answer – Isoelectric Lead Method

• Lead II (+60°) is the isoelectric lead.

• The QRS axis must be ± 90° from lead II, at either +150° or -30°.
• The more rightward-facing leads III (+120°) and aVF (+90°) are positive, while aVL (-30°) is
negative.
• This puts the QRS axis at +150°.

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 This is an example of right axis deviation secondary to right ventricular hypertrophy.

❖ Example 3:

+ Answer – Quadrant Method

• Lead I = POSITIVE
• Lead II = Equiphasic
• Lead aVF = NEGATIVE
• This puts the axis in the left upper quadrant, between 0° and -90°, i.e. normal or LAD.
• Lead II is neither positive nor negative (isoelectric), indicating physiological LAD.

+ Answer – Isoelectric Lead Method

• Lead II (+60°) is isoelectric.

• The QRS axis must be ± 90° from lead II, at either +150° or -30°.
• The more leftward-facing leads I (0°) and aVL (-30°) are positive, while lead III (+120°) is
negative.
• This confirms that the axis is at -30°.

This is an example of borderline left axis deviation due to inferior MI.

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 ❖ Example 4:

+ Answer – Quadrant Method

• Lead I = NEGATIVE
• Lead II = NEGATIVE
• Lead aVF = NEGATIVE
• This puts the axis in the upper right quadrant, between -90° and 180°, i.e. extreme axis
deviation.

NB. The presence of a positive QRS in aVR with negative QRS in multiple leads is another clue to the
presence of extreme axis deviation.

+ Answer – Isoelectric Lead Method

• The most isoelectric lead is aVL (-30°).

• The QRS axis must be at ± 90° from aVL at either +60° or -120°.
• Lead aVR (-150°) is positive, with lead II (+60°) negative.
• This puts the axis at -120°.

This is an example of extreme axis deviation due to ventricular tachycardia.

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 ❖ Example 5:

Reveal Answer

• Lead I = isoelectric.
• Lead aVF = positive.
• This is the easiest axis you will ever have to calculate. It has to be at right angles to lead I and in
the direction of aVF, which makes it exactly +90°!

This is referred to as a “vertical axis” and is seen in patients with emphysema who typically have
a vertically orientated heart.

Vertical Heart in Emphysema

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Causes of Axis Deviation

I. Right Axis Deviation

• Right ventricular hypertrophy

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

RAD: leads II, III and aVF are POSITIVE; Leads I and aVL are NEGATIVE

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 II. 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

Example ECG of LAD

• • Left Axis Deviation: leads I and aVL are positive; leads II and aVF are
negative

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 lll. Extreme Axis Deviation

• Ventricular rhythms – e.g. VT, AIVR, ventricular ectopy

• Hyperkalemia
• Severe right ventricular hypertrophy

Lead positioning

➢ 3-electrode system
• Uses 3 electrodes (RA, LA and LL)
• Monitor displays the bipolar leads (I, II and III)
• To get best results – Place electrodes on the chest wall equidistant from the heart
(rather than the specific limbs)

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 ➢ 5-electrode system:

• Uses 5 electrodes (RA, RL, LA, LL and Chest)

• Monitor displays the bipolar leads (I, II and III)
• AND a single unipolar lead (depending on position of the brown chest
lead (positions V1–6)

➢ 12-lead ECG:

• 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)

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Electrodes

• LA = left arm
• RA = right arm
• LL = left leg
• RL/N = right leg (neutral electrode)

Leads

• Bipolar leads: I, II, III

• Augmented unipolar leads: aVL, aVF, aVR
• Wilson’s central terminus (WCT): the ‘zero’ lead, produced by averaging signals from the
limb electrodes

• Einthoven’s Triangle

The relationship between the limb leads and electrodes is described by Einthoven’s triangle.

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Each lead has a specific quantity and direction (vector) produced by adding or subtracting
voltages from the recording electrodes.

Bipolar leads

• Lead I is the voltage difference between the LA and RA electrodes (LA – RA), directed
towards LA at zero degrees.
• Lead II is the voltage difference between the LL and RA electrodes (LL – RA), directed
towards LL at +60 degrees.
• Lead III is the voltage difference between the LL and LA electrodes (LL – LA), directed
towards LL at +120 degrees.

Augmented Unipolar leads

• Lead aVL is directed towards the LA electrode (-30 degrees), calculated as follows: aVL =
LA – (RA + LL)/2.
• Lead aVF is directed towards the LL electrode (+90 degrees), calculated as follows: aVF =
LL – (LA + RA)/2.
• Lead aVR is directed towards the RA electrode (-150 degrees), calculated as follows: aVR
= RA – (LA + LL)/2.

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The P wave
• The P wave is the first positive deflection on the ECG
• It represents atrial depolarization

Characteristics of the Normal Sinus P Wave

Morphology

• Smooth contour
• Monophasic in lead II
• Biphasic in V1

Axis

• Normal P wave axis is between 0° and +75°

• P waves should be upright in leads I and II, inverted in aVR

Duration

• < 120 ms

Amplitude

• < 2.5 mm in the limb leads,

• < 1.5 mm in the precordial leads

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Atrial abnormalities are most easily seen in the inferior leads (II, III and aVF) and
lead V1, as the P waves are most prominent in these leads.
Normal P-wave Morphology – Lead II

• The right atrial depolarization wave (brown) precedes that of the left atrium (blue).
• The combined depolarization wave, the P wave, is less than 120 ms wide and less than

2.5 mm high.

Right Atrial Enlargement – Lead II

• In right atrial enlargement, right atrial depolarization lasts longer than normal and its
waveform extends to the end of left atrial depolarization.
• Although the amplitude of the right atrial depolarization current remains unchanged, its
peak now falls on top of that of the left atrial depolarization wave.
• The combination of these two waveforms produces a P waves that is taller than normal
(> 2.5 mm), although the width remains unchanged (< 120 ms).

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Left Atrial Enlargement – Lead II

• In left atrial enlargement, left atrial depolarization lasts longer than normal but its
amplitude remains unchanged.
• Therefore, the height of the resultant P wave remains within normal limits but its
duration is longer than 120 ms.
• A notch (broken line) near its peak may or may not be present (“P mitrale”).

Normal P-wave Morphology – Lead V1

The P wave is typically biphasic in V1, with similar sizes of the positive and negative deflections.

Right Atrial Enlargement – Lead V1

Right atrial enlargement causes increased height (> 1.5mm) in V1 of the initial positive deflection of the
P wave.

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Left Atrial Enlargement – Lead V1
Left atrial enlargement causes widening (> 40ms wide) and deepening (> 1mm deep) in V1 of the
terminal negative portion of the P wave.

Biatrial Enlargement
Biatrial enlargement is diagnosed when criteria for both right and left atrial enlargement are present on
the same ECG.
The spectrum of P-wave changes in leads II and V1 with right, left and bi-atrial enlargement is

summarized in the following diagram:

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Common P Wave Abnormalities
• Common P wave abnormalities include:
• 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, seen in multifocal atrial rhythms.
P mitrale

The presence of broad, notched (bifid) P waves in lead II is a sign of left atrial enlargement,
classically due to mitral stenosis.

Bifid P waves (P mitrale) in left atrial enlargement

P PulmonaleThe presence of tall, peaked P waves in lead II is a sign of right atrial enlargement, usually
due to pulmonary hypertension (e.g. cor pulmonale from chronic respiratory disease).

Peaked P waves (P pulmonale) due to right atrial enlargement

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Inverted P Waves P-wave inversion in the inferior leads indicates a non-sinus origin of the P
waves. When the PR interval is < 120 ms, the origin is in the AV junction (e.g. accelerated junctional
rhythm):

Accelerated Junctional Rhythm

When the PR interval is ≥ 120 ms, the origin is within the atria (e.g. ectopic atrial rhythm):

Ectopic Atrial Rhythm

Variable P-Wave Morphology
The presence of multiple P wave morphologies indicates multiple ectopic pacemakers within the atria
and/or AV junction.
If ≥ 3 different P wave morphologies are seen, then multifocal atrial rhythm is diagnosed:

Multifocal Atrial Rhythm If ≥ 3 different P wave morphologies are seen and the rate is ≥
100, then multifocal atrial tachycardia (MAT) is diagnosed:

Multifocal Atrial Tachycardia

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The Q wave
A Q wave is any negative deflection that precedes an R wave.
Origin of the Q Wave

• The Q wave represents the normal left-to-right depolarization of the interventricular septum
• Small ‘septal’ Q waves are typically seen in the left-sided leads (I, aVL, V5 and V6)

Normal Q wave in V6
Q waves in different leads

• Small Q waves are normal in most leads

• Deeper Q waves (>2 mm) may be seen in leads III and aVR as a normal variant
• Under normal circumstances, Q waves are not seen in the right-sided leads (V1-3)

Pathological Q Waves

Q waves are considered pathological if:

• > 40 ms (1 mm) wide

• > 2 mm deep
• > 25% of depth of QRS complex
• Seen in leads V1-3

Pathological Q waves usually indicate current or prior myocardial infarction.

Differential Diagnosis

• Myocardial infarction
• Cardiomyopathies — Hypertrophic (HCM), infiltrative myocardial disease
• Rotation of the heart — Extreme clockwise or counter-clockwise rotation
• Lead placement errors — e.g. upper limb leads placed on lower limbs

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ECG Examples
Example 1

• Inferior Q waves (II, III, aVF) with ST elevation due to acute MI

Example 2

• Inferior Q waves (II, III, aVF) with T-wave inversion due to previous MI

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Example 3

• Lateral Q waves (I, aVL) with ST elevation due to acute MI

Example 4

• Anterior Q waves (V1-4) with ST elevation due to acute MI

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Example 5

• Anterior Q waves (V1-4) with T-wave inversion due to recent MI

Loss of normal Q waves

The absence of small septal Q waves in leads V5-6 should be considered abnormal.
Absent Q waves in V5-6 is most commonly due to LBBB.

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R wave Overview

• The R wave is the first upward deflection after the P wave

• The R wave represents early ventricular depolarization
Abnormalities of the R wave
There are three key R wave abnormalities:

1. Dominant R wave in V1
2. Dominant R wave in aVR
3. Poor R wave progression

Dominant R wave in V1
• Causes of Dominant R wave in V1
• Normal in children and young adults
o Right Ventricular Hypertrophy (RVH)
o Pulmonary Embolus
o 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
o Myotonic dystrophy
o Duchenne Muscular dystrophy

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Examples of Dominant R wave in V1
Normal pediatric ECG (2 yr old)

Right Ventricular Hypertrophy (RVH)

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Right Bundle Branch Block

Right Bundle Branch Block MoRRoW

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Posterior MI

WPW (type A)

Leads V1 and V3 reversed

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 Leads V1 and V3 reversed

• Note biphasic P wave (typically seen in only in V1) in lead “V3”

Muscular dystrophy

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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)
Examples of Dominant R wave in aVR<

Poisoning with sodium-channel blocking drugs

• Causes a characteristic dominant terminal R wave in aVR

• Poisoning with sodium-channel blocking agents is suggested if:
• R wave height > 3mm
• R/S ratio > 0.7

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Dextrocardia

This ECG shows all the classic features of 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)

Left arm/right arm lead reversal

Lead reversal

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 Lead reversal reversed

The most common cause of a dominant R wave in aVR is incorrect limb lead placement, with
reversal of the left and right arm electrodes. This produces a similar pattern to dextrocardia in
the limb leads but with normal R-wave progression in the chest leads.
With LA/RA lead reversal:

• Lead I becomes inverted

• Leads aVR and aVL switch places
• Leads II and III switch places

Ventricular Tachycardia

Poor R wave progression

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Poor R wave progression is described with an R wave ≤ 3 mm inV3 and is caused by:
• Prior anteroseptal MI
• LVH
• Inaccurate lead placement
• May be a normal variant

Poor R wave progression

Note that absent R wave progression is characteristically seen in dextrocardia (see previous
ECG).

T wave:
• The T wave is the positive deflection after each QRS complex.
• It represents ventricular repolarization

Characteristics of the normal T wave

• Upright in all leads except aVR and V1

• Amplitude < 5mm in limb leads, < 15mm in precordial leads
• Duration

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T wave abnormalities

• Hyper acute T waves

• Inverted T waves
• Biphasic T waves
• ‘Camel Hump’ T waves
• Flattened T waves

Peaked T waves

• Tall, narrow, symmetrically peaked T-waves are characteristically seen in hyperkalemia.

Hyper acute T waves

• Broad, asymmetrically peaked or ‘hyper acute’ T-waves are seen in the early stages of ST-
elevation MI (STEMI) and often precede the appearance of ST elevation and Q waves.
• They are also seen with Prinzmetal angina.

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 Hyperacute T waves due to anterior STEMI

Loss of precordial T-wave balance

Loss of precordial T-wave balance occurs when the upright T wave is larger than that in V6. This
is a type of Hyperacute T wave.

• The normal T wave in V1 is inverted. An upright T wave in V1 is considered abnormal —

especially if it is tall (TTV1), and especially if it is new (NTTV1).
• This finding indicates a high likelihood of coronary artery disease, and when new implies acute
ischemia.

Inverted T waves

Inverted T waves are seen in the following conditions:

• Normal finding in children

• Persistent juvenile T wave pattern
• Myocardial ischaemia and infarction
• Bundle branch block
• Ventricular hypertrophy (‘strain’ patterns)

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 • Pulmonary embolism
• Hypertrophic cardiomyopathy
• Raised intracranial pressure

T wave inversion in lead III is a normal variant. New T-wave inversion (compared with prior
ECGs) is always abnormal. Pathological T wave inversion is usually symmetrical and deep
(>3mm).

Pediatric T waves

• Inverted T-waves in the right precordial leads (V1-3) are a normal finding in children,
representing the dominance of right ventricular forces.

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Persistent Juvenile T-wave Pattern

• T-wave inversions in the right precordial leads may persist into adulthood and are most
commonly seen in young Afro-Caribbean women.
• Persistent juvenile T-waves are asymmetric, shallow (<3mm) and usually limited to leads V1-3.

Myocardial Ischaemia and Infarction

T-wave inversions due to myocardial ischaemia or infarction occur in contiguous leads based on
the anatomical location of the area of ischaemia/infarction:

• Inferior = II, III, aVF

• Lateral = I, aVL, V5-6
• Anterior = V2-6

NOTE:

• Dynamic T-wave inversions are seen with acute myocardial ischaemia.

• Fixed T-wave inversions are seen following infarction, usually in association with pathological Q
waves.

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 Inferior T wave inversion due to acute ischaemia

Inferior T wave inversion with Q waves due to prior inferior MI

T wave inversion in the lateral leads due to acute ischaemia

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 Anterior T wave inversion with Q waves due to recent anterior MI
Bundle Branch Block

Left Bundle Branch Block

• Left bundle branch block produces T-wave inversion in the lateral leads I, aVL and V5-6.

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Right Bundle Branch Block

• Right bundle branch block produces T-wave inversion in the right precordial leads V1-3.

Ventricular Hypertrophy

Left Ventricular Hypertrophy

• Left ventricular hypertrophy produces T-wave inversion in the lateral leads I, aVL, V5-6 (left
ventricular ‘strain’ pattern), with a similar morphology to that seen in LBBB.

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Right Ventricular Hypertrophy

• Right ventricular hypertrophy produces T-wave inversion in the right precordial leads V1-3 (right
ventricular ‘strain’ pattern) and also the inferior leads (II, III, aVF).

Pulmonary Embolism

• Acute right heart strain (e.g. secondary to massive pulmonary embolism) produces a similar
pattern to RVH
• T-wave inversions in the right precordial (V1-3) and inferior (II, III, aVF) leads.

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 T wave inversion in the inferior and right precordial leads – bilateral PEs

Deep T wave inversion in V1-3 with RBBB in a patient with massive PE

SI QIII TIII
• Pulmonary embolism may also produce T-wave inversion in lead III as part of the SI QIII TIIIpattern
• S wave in lead I, Q wave in lead III, T-wave inversion in lead III

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 SI QIII TIII pattern in acute PE

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Hypertrophic Cardiomyopathy (HCM)

• Hypertrophic Cardiomyopathy is associated with deep T wave inversions in all the precordial
leads.

Raised intracranial pressure (ICP)

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 • Events causing a sudden rise in intracranial pressure (e.g. subarachnoid haemorrhage) produce
widespread deep T-wave inversions with a bizarre morphology.

Biphasic T waves

There are two main causes of biphasic T waves:

• Myocardial ischaemia
• Hypokalaemia

The two waves go in opposite directions:

• Ischaemic T waves go up then down

• Hypokalaemic T waves go down then up

Ischaemia – up then down

Biphasic T waves due to ischaemia

Hypokalaemia – down then up

Biphasic T waves due to hypokalaemia

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Wellens’ Syndrome
Wellens’ syndrome is a pattern of inverted or biphasic T waves in V2-3 (in patients presenting with
ischaemic chest pain) that is highly specific for critical stenosis of the left anterior descending artery.
There are two patterns of T-wave abnormality in Wellens’ syndrome:

• Type 1 Wellens’ T-waves are deeply and symmetrically inverted

• Type 2 Wellens’ T-waves are biphasic, with the initial deflection positive and the terminal
deflection negative

Wellens’ Type 1

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Wellens’ Type 2

‘Camel hump’ T waves

‘Camel hump’ T waves is a term used by Amal Mattu to describe T-waves that have a double peak. There
are two causes for camel hump T waves:

• Prominent U waves fused to the end of the T wave, as seen in severe hypokalaemia
• Hidden P waves embedded in the T wave, as seen in sinus tachycardia and various types of
heart block

Prominent U waves due to severe hypokalaemia

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 Hidden P waves in sinus tachycardia

Hidden P waves in marked 1st degree heart block

Hidden P waves in 2nd degree heart block with 2:1 conduction

Flattened T waves

Flattened T waves are a non-specific finding, but may represent

• ischaemia (if dynamic or in contiguous leads) or

• electrolyte abnormality, e.g. hypokalaemia (if generalised).

Ischaemia

Dynamic T-wave flattening due to anterior ischaemia (above). T waves return to normal once
the ischaemia resolves (below).

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Dynamic T wave flattening due to anterior ischaemia

T waves return to normal as ischaemia resolves

Hypokalaemia

Note generalized T-wave flattening with prominent U waves in the anterior leads (V2 and V3).

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 T wave flattening due to hypokalemia

U wave:
• The U wave is a small (0.5 mm) deflection immediately following the T wave
• U wave is usually in the same direction as the T wave.
• U wave is best seen in leads V2 and V3.

Source of the U wave

The source of the U wave is unknown. Three common theories regarding its origin are:

• Delayed repolarization of Purkinje fibers

• Prolonged repolarization of mid-myocardial “M-cells”
• After-potentials resulting from mechanical forces in the ventricular wall

Features of Normal U waves

• The U wave normally goes in the same direction as the T wave

• U -wave size is inversely proportional to heart rate: the U wave grows bigger as the heart rate
slows down
• U waves generally become visible when the heart rate falls below 65 bpm
• The voltage of the U wave is normally < 25% of the T-wave voltage: disproportionally large U
waves are abnormal
• Maximum normal amplitude of the U wave is 1-2 mm

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 Normal U Wave
Abnormalities of the U wave

• Prominent U waves
• Inverted U waves

Prominent U waves

U waves are prominent if >1-2mm or 25% of the height of the T wave.

• The most common cause of prominent U waves is bradycardia.

• Abnormally prominent U waves are characteristically seen in severe hypokalaemia.

Prominent U waves may also be seen with:

• Hypocalcaemia
• Hypomagnesaemia
• Hypothermia
• Raised intracranial pressure
• Left ventricular hypertrophy
• Hypertrophic cardiomyopathy

The following drugs may cause prominent U waves:

• Digoxin
• Phenothiazines (thioridazine)
• Class Ia antiarrhythmics (quinidine, procainamide)
• Class III antiarrhythmics (sotalol, amiodarone)

Note that many of the conditions causing prominent U waves will also cause a long QT.

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Prominent U waves due to sinus bradycardia

• Prominent U waves in a patient with marked sinus bradycardia due to anorexia nervosa

U waves associated with hypokalaemia

• Prominent U waves in a patient with a K+ of 1.9

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 U waves associated with digoxin use

• Prominent U waves in a patient taking digoxin

U waves associated with quinidine use

• Prominent U waves in a patient receiving quinidine

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Inverted U waves

• U-wave inversion is abnormal (in leads with upright T waves)

• 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

In patients presenting with chest pain, inverted U waves:

• Are a very specific sign of myocardial ischaemia

• May be the earliest marker of unstable angina and evolving myocardial infarction
• Have been shown to predict a ≥ 75% stenosis of the LAD / LMCA and the presence of left
ventricular dysfunction

Unstable angina

• Inverted U waves in a patient with unstable angina.

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Prinzmetal’s angina

• Inverted U waves in a patient with Prinzmetal’s angina.

NSTEMI

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 • Note the subtle U-wave inversion in the lateral leads (I, V5 and V6) in this patient with a
NSTEMI; these were the only abnormal findings on his ECG.
•

Osborn Wave (J Wave):

• The Osborn wave (J wave) is a positive deflection at the J point (negative in aVR and V1)
• It is usually most prominent in the precordial leads

Osborn Wave Causes

Characteristically seen in hypothermia (typically T<30C), but they are not pathognomonic.
J waves may be seen in a number of other conditions:
Normal variant
Hypercalcaemia
Medications
Neurological insults such as intracranial hypertension, severe head injury
and subarachnoid haemorrhage
Le syndrome d’Haïssaguerre (idiopathic VF)

Osborn Wave ECG examples

Example 1

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 Typical J Waves

Example 2

• Subtle J waves in mild hypothermia (temp 32.5°C)

• The height of the J wave is roughly proportional to the degree of hypothermia

Example 3

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 • J waves in moderate hypothermia (temp 30°C)

Example 4

• Marked J waves in severe hypothermia (temp < 27°C)

Delta Wave:
• The Delta wave is a slurred upstroke in the QRS complex often associated with a short
PR interval. It is most commonly associated with pre-excitation syndrome such as WPW.

The characteristic ECG findings in the Wolff-Parkinson-White syndrome are:

o Short PR interval (< 120ms)
o Broad QRS (> 100ms)
o A slurred upstroke to the QRS complex (the delta wave)

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ECG examples of Delta Waves
Delta wave

Negative delta waves (e.g. seen in lead aVR)

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

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ECG Examples of Epsilon Waves

Reproduced from ECGpedia.org.

Image reproduced from Wikimedia Commons.

Image reproduced from heartpearls.com.

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 Image reproduced from heartpearls.com.

Image reproduced from Perez Diez & Brugada.

Arrhythmogenic Right Ventricular Dysplasia

The ECG changes in ARVD include:

• Epsilon wave (most specific finding, seen in 30% of patients)

• T wave inversions in V1-3 (85% of patients)
• Prolonged S-wave upstroke of 55ms in V1-3 (95% of patients)
• Localised QRS widening of 110ms in V1-3
• Paroxysmal episodes of ventricular tachycardia with a LBBB morphology

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ECG Examples

Example 1

The following 12-lead ECG is a typical example of ARVD.

Image reproduced from heartpearls.com. Click for link.

Prolonged S-wave upstroke in ARVD

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Example 2

VT with LBBB morphology due to ARVD

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PR Interval:
• The PR interval is the time from the onset of the P wave to the start of the QRS complex.
• It reflects conduction through the AV node.
• The normal PR interval is between 120 – 200 ms duration (three to five small squares).
• If the PR interval is > 200 ms, first degree heart block is said to be present.
• PR interval < 120 ms suggests pre-excitation (the presence of an accessory pathway between
the atria and ventricles) or AV nodal (junctional) rhythm.

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Prolonged PR Interval – AV block (PR >200ms)

• Delayed conduction through the AV node

• May occur in isolation or co-exist with other blocks (e.g., second-degree AV block, tri fascicular
block)

First degree AV block

• Sinus rhythm with marked 1st degree heart block (PR interval 340ms)

Second degree AV block (Mobitz I) with prolonged PR interval

• Second degree heart block, Mobitz type I (Wenckeback phenomenon).

• Note how the baseline PR interval is prolonged, and then further prolongs with each successive
beat, until a QRS complex is dropped.
• The PR interval before the dropped beat is the longest (340ms), while the PR interval after the
dropped beat is the shortest (280ms).

Short PR interval (<120ms): A short PR interval is seen with:

• Pre excitation syndromes.

• AV nodal (junctional) rhythm.

Pre-excitation syndromes

• Wolff-Parkinson-White (WPW) and Lown-Ganong-Levine (LGL) syndromes.

• These involve the presence of an accessory pathway connecting the atria and ventricles.
• The accessory pathway conducts impulses faster than normal, producing a short PR interval.

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 • The accessory pathway also acts as an anatomical re-entry circuit, making patients susceptible
to re-entry tachyarrhythmias.
• Patients present with episodes of paroxsymal supraventricular tachycardia (SVT), specifically
atrioventricular re-entry tachycardia (AVRT), and characteristic features on the resting 12-lead
ECG.

Wolff-Parkinson-White syndrome

The characteristic features of Wolff-Parkinson-White syndrome are a short PR interval, broad

QRS and a slurred upstroke to the QRS complex, the delta wave.

Short PR (<120ms), broad QRS and delta waves in WPW syndrome

Lown-Ganong-Levine syndrome

The features of LGL syndrome are a very short PR interval with normal P waves and QRS
complexes and absent delta waves.

Short PR interval with normal QRS complexes in LGL syndrome

AV nodal (junctional) rhythm

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 • Junctional rhythms are narrow complex, regular rhythms arising from the AV node.
• P waves are either absent or abnormal (e.g. inverted) with a short PR interval (=retrograde P
waves).

Accelerated junctional rhythm demonstrating inverted P waves with a short PR interval

(retrograde P waves)

PR segment:

The PR segment is the flat, usually isoelectric segment between the end of the P wave and the
start of the QRS complex.

PR segment abnormalities occur in two main conditions:

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 • Pericarditis
• Atrial ischaemia

Pericarditis

The characteristic changes of acute pericarditis are:

• PR segment depression.
• Widespread concave (‘saddle-shaped’) ST elevation.
• Reciprocal ST depression and PR elevation in aVR and V1
• Absence of reciprocal ST depression elsewhere.

NB. PR segment changes are relative to the baseline formed by the T-P segment.

Typical ECG of acute pericarditis.

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 • PR segment depression in V5 due to acute pericarditis (note also some concave ST elevation)

• PR elevation in aVR due to acute pericarditis (note the reciprocal ST depression)

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Atrial ischaemia

• PR segment elevation or depression in patients with myocardial infarction indicates concomitant

atrial ischaemia or infarction.
• This finding has been associated with poor outcomes following MI, increased risk for the
development of atrioventricular block, supraventricular arrhythmias and cardiac free-wall
rupture.

Liu’s criteria for diagnosing atrial ischaemia / infarction include:

• PR elevation >0.5 mm in V5 & V6 with reciprocal PR depression in V1 & V2

• PR elevation >0.5 mm in lead I with reciprocal PR depression in leads II & III
• PR depression >1.5 mm in the precordial leads
• PR depression >1.2 mm in leads I, II, & III
• Abnormal P wave morphology: M-shaped,W-shaped,irregular,or notched (minor criteria)

PR depression in inferior STEMI indicating concomitant atrial infarction

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 • Profound PR-segment depression in inferior leads with (A) and without (B) clear-cut TP segment
in acute inferior myocardial infarction. Note also ST-segment elevation in inferior leads.
(Reproduced from Jim et al.)

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Measurement of PR depression

Measurement of PR-segment depression with (A) and with- out (B) clear-cut TP segment.

QT Interval:
• The QT interval is the time from the start of the Q wave to the end of the T wave.
• It represents the time taken for ventricular depolarization and repolarization.

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The QT interval is inversely proportional to heart rate:

• The QT shortens at faster heart rates

• The QT lengthens at slower heart rates
• An abnormally prolonged QT is associated with an increased risk of ventricular arrhythmias,
especially Torsades de Pointes.
• The recently described congenital short QT syndrome has been found to be associated with an
increased risk of paroxysmal atrial and ventricular fibrillation and sudden cardiac death.

How to measure QT

• The QT interval should be measured in either lead II or V5-6

• Several successive beats should be measured, with the maximum interval taken
• Large U waves (> 1mm) that are fused to the T wave should be included in the measurement
• Smaller U waves and those that are separate from the T wave should be excluded
• The maximum slope intercept method is used to define the end of the T wave (see below)

The QT interval is defined from the beginning of the QRS complex to the end of the T wave. The
maximum slope intercept method defines the end of the T wave as the intercept between the

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isoelectric lines with the tangent drawn through the maximum down slope of the T wave (left).
When notched T waves are present (right), the QT interval is measured from the beginning of
the QRS complex extending to the intersection point between the isoelectric line and the
tangent drawn from the maximum down slope of the second notch, T2

Corrected QT

• The corrected QT interval (QTc) estimates the QT interval at a heart rate of 60 bpm.
• This allows comparison of QT values over time at different heart rates and improves detection of
patients at increased risk of arrhythmias.

There are multiple formulas used to estimate QTc (see below). It is not clear which formula is
the most useful.

• Bazett’s formula: QTC = QT / √ RR

• Fredericia’s formula: QTC = QT / RR 1/3
• Framingham formula: QTC = QT + 0.154 (1 – RR)
• Hodges formula: QTC = QT + 1.75 (heart rate – 60)

NB. The RR interval is given in seconds (RR interval = 60 / heart rate).

• Bazett’s formula is the most commonly used due to its simplicity. It over-corrects at heart rates
> 100 bpm and under-corrects at heart rates < 60 bpm, but provides an adequate correction for
heart rates ranging from 60 – 100 bpm.
• At heart rates outside of the 60 – 100 bpm range, the Fredericia or Framingham corrections are
more accurate and should be used instead.
• If an ECG is fortuitously captured while the patient’s heart rate is 60 bpm, the absolute QT
interval should be used instead!

There are now multiple i-phone apps that will calculate QTc for you (e.g. MedCalc), and the
website MDCalc.com has a quick and easy QTc calculator that is free to use.

Normal QTc values

• QTc is prolonged if > 440ms in men or > 460ms in women

• QTc > 500 is associated with increased risk of torsades de pointes
• QTc is abnormally short if < 350ms
• A useful rule of thumb is that a normal QT is less than half the preceding RR interval

Causes of a prolonged QTc (>440ms)

• Hypokalaemia
• Hypomagnesaemia
• Hypocalcaemia
• Hypothermia
• Myocardial ischemia

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 • Post-cardiac arrest
• Raised intracranial pressure
• Congenital long QT syndrome
• DRUGS
Hypokalaemia

Apparent QTc 500ms – prominent U waves in precordial leads (hypokalaemia (K+ 1.9))

• Hypokalaemia causes apparent QTc prolongation in the limb leads (due to T-U fusion)
with prominent U waves in the precordial leads.

Hypomagnesaemia

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 QTc 510 ms secondary to hypomagnesaemia
Hypocalcaemia

QTc 510ms due to hypocalcaemia

• Hypocalcaemia typically prolongs the ST segment, leaving the T wave unchanged.

Hypothermia

QTc 620 ms due to severe hypothermia

• Severe hypothermia can cause marked QTc prolongation, often in association with
bradyarrhythmias (especially slow AF), Osborne waves and shivering artefact.

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Myocardial Ischaemia

QTc 495 ms due to hyperacute MI

• Myocardial ischemia tends to produce a modest increase in the QTc, in the 450-500 ms
range.
• This may be useful in distinguishing hyperacute MI from benign early
repolarization (both may produce similar hyperacute T waves, but BER will usually have
a normal QTc).

Raised ICP

QTc 630ms with widespread T wave inversion due to subarachnoid haemorrhage

• A sudden rise in intracranial pressure (e.g. due to subarachnoid haemorrhage) may produce
characteristic T wave changes (‘cerebral T waves’): widespread, deep T wave inversions with a
prolonged QTc.

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Congenital Long QT Syndrome

QTc 550ms due to congenital long QT syndrome

• There are several congenital disorders of ion channels that produce a long QT
syndrome and are associated with increased risk of torsades de pointes and sudden
cardiac death.

Causes of a short QTc (<350ms)

• Hypercalcaemia
• Congenital short QT syndrome
• Digoxin effect

Hypercalcaemia: Hypercalcaemia leads to shortening of the ST segment and may be associated

with the appearance of Osborne waves.

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 Marked shortening of the QTc (260ms) due to hypercalcaemia
Congenital short QT syndrome

Very short QTc (280ms) with tall, peaked T waves due to congenital short QT syndrome

• Congenital short QT syndrome (SQTS) is an autosomal-dominant inherited disorder of potassium

channels associated with an increased risk of paroxysmal atrial and ventricular fibrillation and
sudden cardiac death.
• The main ECG changes are very short QTc (<300-350ms) with tall, peaked T waves.

Short QT syndrome may be suggested by the presence of:

• Lone atrial fibrillation in young adults

• Family member with a short QT interval
• Family history of sudden cardiac death
• ECG showing QTc < 350 ms with tall, peaked T waves
• Failure of the QT interval to increase as the heart rate slows

Very short QT (< 300ms) with peaked T waves in two patients with SQTS

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Digoxin

Short QT interval due to digoxin (QT 260 ms, QTc 320ms approx)

• Digoxin produces a relative shortening of the QT interval, along with downward sloping
ST segment depression in the lateral leads (‘reverse tick’ appearance), widespread T-
wave flattening and inversion, and a multitude of arrhythmias (ventricular ectopy, atrial
tachycardia with block, sinus bradycardia, regularized AF, any type of AV block).

QT interval scale: Viskin (2009) proposes the use of a ‘QT interval scale’ to aid
diagnosis of patients with short and long QT syndromes (once reversible causes have
been excluded):

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Drug-induced QT-Prolongation and Torsades

In the context of acute poisoning with QT-prolonging agents, the risk of TdP is better
described by the absolute rather than corrected QT.
More precisely, the risk of TdP is determined by considering both the absolute QT
interval and the simultaneous heart rate (i.e. on the same ECG tracing).
These values are then plotted on the QT nomogram (below) to determine whether the
patient is at risk of TdP.
A QT interval-heart rate pair that plots above the line indicates that the patient is at risk
of TdP.
From the nomogram, you can see that QTc-prolonging drugs that are associated with a
relative tachycardia (e.g. quetiapine) are much less likely to cause TdP than those that
are associated with a relative bradycardia (e.g. amisulpride).

Polymorphic VT & Torsades de Pointes (TdP):

• 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.
• For TdP to be diagnosed, the patient has to have evidence of both PVT and QT
prolongation.
• Bidirectional VT is another type of polymorphic VT, most commonly associated with
digoxin toxicity.

Torsades de pointes

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Clinical Significance

• TdP is often short lived and self-terminating, however can be associated with
hemodynamic instability and collapse. TdP may also degenerate into ventricular
fibrillation (VF).
• QT prolongation may occur secondary to multiple drug effects, electrolyte
abnormalities and medical conditions; these may combine to produce TdP, e.g.
hypokalaemia may precipitate TdP in a patient with congenital long QT syndrome.
• Recognition of TdP and the risk of TdP allows the instigation of specific management
strategies (e.g. magnesium, isoprenaline, overdrive pacing, etc.)

Pathophysiology of TdP

• A prolonged QT reflects prolonged myocyte repolarisation due to ion channel

malfunction.
• This prolonged repolarisation period also gives rise to early after-depolarisations (EADs).
• EADs may manifest on the ECG as tall U waves; if these reach threshold amplitude they
may manifest as premature ventricular contractions (PVCs).
• TdP is initiated when a PVC occurs during the preceeding T wave, known as ‘R on T’
phenomenon.
• The onset of TdP is often preceded by a sequence of short-long-short R-R intervals, so
called “pause dependent” TDP, with longer pauses associated with faster runs of TdP.

Electrocardiographic Pearls
• During short runs of TdP or single lead recording the characteristic “twisting” morphology
may not be apparent.
• Bigeminy in a patient with a known long QT syndrome may herald imminent TdP.
• TdP with heart rates > 220 beats/min are of longer duration and more likely to degenerate
into VF.
• Presence of abnormal (“giant”) T-U waves may precede TdP
Drug-induced Torsades

• In the context of acute poisoning with QT-prolonging agents, the risk of TdP is better
described by the absolute rather than corrected QT.
• More precisely, the risk of TdP is determined by considering both the absolute QT
interval and the simultaneous heart rate (i.e. on the same ECG tracing).
• These values are then plotted on the QT nomogram (below) to determine whether the
patient is at risk of TdP.
• A QT interval-heart rate pair that plots above the line indicates that the patient is at risk of
TdP.

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ECG Examples

Example 1

Torsades de Pointes:

• Frequent PVCs with ‘R on T’ phenomenon trigger a run of polymorphic VT which

subsequently begins to degenerate to VF.
• QT is difficult to see because of artefact but appears slightly prolonged (QTc ~480ms),
making this likely to be TdP.
• This combination of mildly prolonged QTc and frequent PVCs / bigeminy is commonly
seen in acute myocardial ischaemia and is high-risk for deterioration to PVT / VF.

Example 2

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TdP secondary to hypokalaemia:

• Sinus rhythm with inverted T waves, prominent U waves and a long Q-U interval due to
severe hypokalaemia (K+ 1.7)
• A premature atrial complex (beat #9 of the rhythm strip) lands on the end of the T wave,
causing ‘R on T’ phenomenon and initiating a paroxysm of polymorphic VT.
• Because of the preceding long QU interval, this can be diagnosed as TdP.

Example 3

TdP secondary to hypokalaemia:

• Another ECG from the same patient (K+ still 1.7).

• A brief, self-terminating paroxysm of TdP is again precipitated by a PAC causing ‘R on
T’.

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Example 4

Torsades de Pointes:

• Sinus rhythm, or possibly ectopic atrial rhythm (biphasic / inverted P waves in lead II).
• Prolonged QTc interval of 540 ms (greater than half the R-R interval).
• Ventricular ectopics with ‘R-on-T’ phenomenon; the second PVC initiates a run of TdP.

NB. See how the arterial line pressure waveform (lower tracing) is affected by the
dysrhythmia. There is a reduced volume pulse during the first PVC as the heart has less
time to fill. Subsequently the cardiac output drops away to almost nothing during the run
of TdP – this is likely to result in syncope or cardiac arrest.

Example 5

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R on T phenomenon:

• There is sinus rhythm with frequent PVCs in a pattern of ventricular bigeminy.

• The QT interval is markedly prolonged (at least 600ms), with each PVC falling on the
preceding T wave (= ‘R on T’ phenomenon).
• This ECG is extremely high risk for TdP – in fact this patient had a TdP cardiac arrest shortly
after this ECG was taken.

Short QT Syndrome:
• Short QT syndrome is a recently-discovered arrhythmogenic disease associated with
paroxysmal atrial and ventricular fibrillation, syncope and sudden cardiac death.
• It is a genetically-inherited cardiac channelopathy on the same spectrum as other familial
arrhythmogenic diseases such as Long QT Syndrome (LQTS), Brugada Syndrome
and Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT).
• Patients are typically young and healthy, with no structural heart abnormalities; age at
first presentation ranges from a few months to the sixth decade of life (median age = 30
years).
• The most common initial presenting symptom is cardiac arrest (in one-third of cases);
other patients may present with palpitations or syncope due to rapid atrial fibrillation or
self-terminating ventricular arrhythmias.
• Witnessed cardiac arrest within the first year of life and unexplained infant deaths have
been observed in patients and families with SQTS, making it a possible cause of sudden
infant death syndrome (SIDS).
• SQTS is still a relatively new disease: It was first described in 2000, and elucidation of the
genetic, electrophysiological and clinical abnormalities associated with the disease has
only taken place over the past few years.

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Mechanism

Arrhythmogenesis in SQTS is thought to result from:

• Extremely short atrial and ventricular refractory periods (manifest on the ECG as a
short QT interval).
• Transmural dispersion of repolarizations, i.e., the different layers of the myocardium
(endocardium, epicardium and the mid-myocardial ‘M-cells’) repolarize at different rates.

Both these repolarisation abnormalities convey an increased susceptibility to re-entrant

atrial and ventricular arrhythmias.

Genetic Basis

• SQTS is a genetically heterogenous disease, with multiple mutations producing a similar

clinical picture. Five mutations have been characterized so far, all of which seem to be
inherited in an autosomal dominant fashion.
• SQTS genotypes 1-3 are produced by a gain-of-function mutation in myocardial potassium
channels (the opposite to LQTS), with increased potassium efflux during various stages
of the action potential leading to more rapid atrial and ventricular repolarization with
marked shortening of the QT interval (<320 ms).
• SQTS genotypes 4 and 5 are produced by a loss-of-function mutation in the L-type cardiac
channel, with reduced influx of calcium during the plateau phase of the action potential

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 leading to modest shortening of the QT interval (<360ms) associated with a Brugada-
syndrome-like QRS complex morphology.

Potassium fluxes in SQTS 1-3

A. Schematic representation of the normal action potential and the flux of ions. B.
With gain-of-function mutations in any of 3 different potassium channels (SQTS
1-3), the cardiac action potential shortens and the QT interval decreases.
(Reproduced from Brugada et al)

Classification of SQTS according to genotype

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Diagnosis
At present, there are no diagnostic criteria for SQTS. The diagnosis is based upon the patient’s
symptoms (e.g. syncope, palpitations), family history (of syncope, sudden death or atrial
fibrillation at an early age) and characteristic findings on the 12-lead ECG.
Clinical features

So far, there have only been a handful of cases of SQTS reported in the literature. The
true prevalence of the disease is unknown. The largest case series to date reported on
29 patients with the disease:

• The most common presenting symptom was cardiac arrest (in one-third of cases).
• Cardiac arrest occurred in the first months of life in two patients.
• Syncope was the presenting symptom in 24% of cases, thought to be secondary to self-
terminating episodes of ventricular fibrillation.
• Up to 31% of patients complained of palpitations, and 80% of patients had documented
episodes ofatrial fibrillation.
• All patients had a QT < 320ms and a QTc < 340ms with no evidence of structural
heart disease(NB. This case series did not include the more recently-described SQTS
genotypes 4 & 5)

ECG features

The main electrocardiographic abnormalities seen in SQTS are:

• Short QT interval
• Lack of the normal changes in QT interval with heart rate
• Peaked T waves, particularly in the precordial leads
• Short or absent ST segments
• Episodes of atrial or ventricular fibrillation

QT, ST and T-wave changes in SQTS

Short QT interval, peaked T waves and short ST segments in two patients with SQTS 1.

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 Reproduced from Crotti et al.
Short QT interval

There is currently no universally accepted lower limit of normal for the QT interval that
can be used to diagnose SQTS.

• Known patients with SQTS genotypes 1-3 all had QTc intervals < 300-320 ms
• Known patients with SQTS genotypes 4 & 5 all had QTc intervals < 360 ms

A recent review by Viskin suggested the following approach:

• QTc intervals < 330 ms in males or < 340 ms in females should be considered
diagnostic of SQTS
• QTc intervals < 360 ms in males or < 370 ms in females should only be considered
diagnostic of SQTS when supported by symptoms or family history

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 A ‘QT interval scale’ for diagnosing SQTS and LQTS. (Reproduced from Viskin)
Lack of the normal changes in QT with heart rate

• Patients with SQTS demonstrate fixed QT intervals which remain constant over a range
of heart rates.
• At fast heart rates, the calculated QTc may appear normal (= ”pseudonormal” QTc)
• However, as the heart rate slows, the QTc typically fails to prolong.
• Serial ECGs or Holter monitoring at rest may be used to try and capture short QT
intervals during periods of relative bradycardia (heart rate 60-80bpm).
• Exercise testing may demonstrate lack of adaptation of QT interval with different heart
rates.

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Holter strip from a patient with SQTS at heart rates of 68 and 119 bpm. QT interval
of 280 ms remains constant at both heart rates. (Reproduced from Short QT
Syndrome.org)
Electrophysiological Studies
Electrophysiological studies in SQTS demonstrate:

• Extremely short atrial and ventricular refractory periods

• High rates of inducible atrial and ventricular fibrillation
• Marked vulnerability to mechanical induction of ventricular fibrillation

The role of EP studies in diagnosing and risk-stratifying patients with SQTS has not yet
been established.

Treatment Options

At present, the only effective treatment is implantation of an ICD.

The main problem with this is T-wave oversensing and inappropriate shocks due to
the tall, narrow T waves seen in SQTS.
Efforts to find a suitable pharmacological treatment have focused on potassium blocking
anti-arrhythmic agents (classes Ia and III).
Class III agents ibutilide and sotalol, while having theoretical benefits in prolonging QT
and suppressing arrhythmias, have been shown to be ineffective due to reduced drug
binding to mutated potassium channels.
Class Ia agents quinidine and disopyramide have shown more promising effects.
Quinidine is currently the agent of choice, having been shown in SQTS 1 patients to
markedly prolong both the QT interval and ventricular refractory period, with normalisation
of ST segments and T waves and prevention of VF induction.

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The ST Segment:
• 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.

Causes of ST Segment Elevation

• Acute myocardial infarction

• Coronary vasospasm (Printzmetal’s angina)
• Pericarditis
• Benign early repolarization
• Left bundle branch block
• Left ventricular hypertrophy
• Ventricular aneurysm
• Brugada syndrome
• Ventricular paced rhythm
• Raised intracranial pressure

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Morphology of the Elevated ST segment
Myocardial Infarction

Acute STEMI may produce ST elevation with either concave, convex or obliquely
straight morphology.

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ST Segment Morphology in Other Conditions

Patterns of ST Elevation
Acute ST elevation myocardial infarction (STEMI)

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Causes ST segment elevation and Q-wave formation in contiguous leads, either:

• Septal (V1-2)
• Anterior (V3-4)
• Lateral (I + aVL, V5-6)
• Inferior (II, III, aVF)
• Right ventricular (V1, V4R)
• Posterior (V7-9)

There is usually reciprocal ST depression in the electrically opposite leads. For

example, STE in the high lateral leads I + aVL typically produces reciprocal ST
depression in lead III (see example below).

Follow the links above to find out more about the different STEMI patterns.

Anterolateral STEMI
Coronary Vasospasm (Prinzmetal’s angina)

• This causes a pattern of ST elevation that is very similar to acute STEMI — i.e. localized
ST elevation with reciprocal ST depression occurring during episodes of chest pain.
• However, unlike acute STEMI the ECG changes are transient, reversible with
vasodilators and not usually associated with myocardial necrosis.
• It may be impossible to differentiate these two conditions based on the ECG alone.

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Pericarditis

Pericarditis

Acute Pericarditis causes widespread concave (“saddleback”) ST segment elevation

with PR segment depression in multiple leads, typically involving I, II, III, aVF, aVL, and
V2-6. There is reciprocal ST depression and PR elevation in leads aVR and V1. Spodick’s
sign — a downward sloping TP segment — may also be seen.

• Concave “saddleback” ST elevation in leads I, II, III, aVF, V5-6 with depressed PR
segments.
• There is reciprocal ST depression and PR elevation in aVR.
• Spodick’s sign is present.

Benign Early Repolarization

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 Benign Early Repolarization

Benign Early Repolarization (BER) causes mild ST elevation with tall T-waves mainly in
the precordial leads. Is a normal variant commonly seen in young, healthy patients.
There is often notching of the J-point — the “fish-hook” pattern. The ST changes may
be more prominent at slower heart rates and disappear in the presence of tachycardia.

• There is slight concave ST elevation in the precordial and inferior leads with notching of
the J-point (the “fish-hook” pattern)

Left Bundle Branch Block

Left Bundle Branch Block

In Left bundle branch block (LBBB), the ST segments and T waves show “appropriate
discordance” — i.e. they are directed opposite to the main vector of the QRS complex.
This produces ST elevation and upright T waves in leads with a negative QRS complex
(dominant S wave), while producing ST depression and T wave inversion in leads with a
positive QRS complex (dominant R wave).

• Note the ST elevation in leads with deep S waves — most apparent in V1-3.
• Also note the ST depression in leads with tall R waves — most apparent in I and aVL.

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 Background

• In patients with left bundle branch block (LBBB) or ventricular paced rhythm, infarct diagnosis based on
the ECG can be difficult
• Abnormal depolarisation should be followed by abnormal repolarisation, manifesting as ST-segment and
T-wave deviations that do not necessarily indicate acute ischaemia (“appropriate discordance”)

The original three criteria used to diagnose infarction in patients with LBBB are:

• Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5)
• Concordant ST depression > 1 mm in V1-V3 (score 3)
• Excessively discordant ST elevation > 5 mm in leads with a -ve QRS complex (score 2)

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Left Ventricular Hypertrophy

Left Ventricular Hypertrophy

Left Ventricular Hypertrophy (LVH) causes a similar pattern of repolarization

abnormalities as LBBB, with ST elevation in the leads with deep S-waves (usually V1-3)
and ST depression/T-wave inversion in the leads with tall R waves (I, aVL, V5-6).

• Deep S waves with ST elevation in V1-3

• ST depression and T-wave inversion in the lateral leads V5-6
• Note in this this case there is also right axis deviation, which is unusual for LVH and may
be due to associated left posterior fascicular block.

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Ventricular Aneurysm

Ventricular Aneurysm

This is an ECG pattern of Ventricular Aneurysm – residual ST elevation and deep Q

waves seen in patients with previous myocardial infarction. It is associated with
extensive myocardial damage and paradoxical movement of the left ventricular wall
during systole.

• There is ST elevation with deep Q waves and inverted T waves in V1-3.

• This pattern suggests the presence of a left ventricular aneurysm due to a prior
anteroseptal MI.

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Brugada Syndrome

Brugada syndrome

Brugada Syndrome is an inherited channelopathy (a disease of myocardial sodium

channels) that leads to paroxysmal ventricular arrhythmias and sudden cardiac death in
young patients. The tell-tale sign on the resting ECG is the “Brugada sign” — ST
elevation and partial RBBB in V1-2 with a “coved” morphology.

• There is ST elevation and partial RBBB in V1-2 with a coved morphology — the
“Brugada sign”.

Ventricular Paced Rhythm

AV Sequential Pacing (PTO)

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Ventricular pacing (with a pacing wire in the right ventricle) causes ST segment
abnormalities identical to that seen in LBBB. There is appropriate discordance, with the
ST segment and T wave directed opposite to the main vector of the QRS complex.
Raised Intracranial Pressure

ST elevation due to traumatic brain injury

Raised Intracranial Pressure (ICP) (e.g. due to intracranial haemorrhage, traumatic brain
injury) may cause ST elevation or depression that simulates myocardial ischaemia or
pericarditis. More commonly, raised ICP is associated with widespread, deep T-wave
inversions (“cerebral T waves”).

• Widespread ST elevation with concave (pericarditis-like) morphology in a patient with

severe traumatic brain injury.

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, hypercalcaemia)
Following electrical cardioversion
Others: Cardiac tumour, myocarditis, pancreas or gallbladder disease

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 Transient ST elevation after DC cardioversion from VF

J waves in hypothermia simulating ST elevation

Causes of ST Depression
• Myocardial ischaemia / NSTEMI
• Reciprocal change in STEMI
• Posterior MI
• Digoxin effect
• Hypokalaemia
• Supraventricular tachycardia
• Right bundle branch block
• Right ventricular hypertrophy
• Left bundle branch block
• Left ventricular hypertrophy
• Ventricular paced rhythm
Morphology of 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.

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 • Up sloping 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: up sloping (A), down sloping (B), horizontal (C)

ST segment morphology in myocardial ischaemia

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Reciprocal change

ST segment morphology in posterior MI

Patterns of ST depression
Myocardial Ischaemia

ST depression due to subendocardial ischaemia may be present in a variable number of

leads and with variable morphology. It is often most prominent in the left precordial

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leads V4-6 plus leads I, II and aVL. Widespread ST depression with ST elevation in
aVR is seen in left main coronary artery occlusion and severe triple vessel disease.

LMCA Occlusion

NB. ST depression localized to the inferior or high lateral leads is more likely to represent
reciprocal change than subendocardial ischaemia. The corresponding ST elevation may be subtle
and difficult to see, but should be sought. This concept is discussed further here.

Reciprocal Change

ST elevation during acute STEMI is associated with simultaneous ST depression in the electrically
opposite leads:

• 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 (see below).

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 Reciprocal ST depression in aVL with inferior STEMI

Reciprocal ST Depression in III and aVF with high lateral STEMI

Posterior Myocardial Infarction

Acute posterior STEMI causes ST depression in the anterior leads V1-3, along with
dominant R waves (“Q-wave equivalent”) and upright T waves. There is ST elevation in
the posterior leads V7-9.

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 Posterior MI
De Winters T Waves

De Winter’s T waves: a pattern of up-sloping ST depression with symmetrically peaked

T waves in the precordial leads is considered to be a STEMI equivalent, and is highly
specific for an acute occlusion of the LAD.

De Winter’s T Waves

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Digoxin Effect

Digoxin Effect: Treatment with digoxin causes downsloping ST depression with a

“sagging” morphology, reminiscent of Salvador Dali’s moustache.

Digoxin reverse tick salvador dali moustache

Hypokalaemia

Hypokalaemia causes widespread downsloping ST depression with T-wave

flattening/inversion, prominent U waves and a prolonged QU interval.

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 Hypokalaemia
Right ventricular hypertrophy

Right ventricular hypertrophy (RVH) causes ST depression and T-wave inversion in the
right precordial leads V1-3.

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 Right ventricular hypertrophy
Right Bundle Branch Block

Right Bundle Branch Block (RBBB) may produce a similar pattern of repolarizations
abnormalities to RVH, with ST depression and T wave inversion in V1-3.

Right bundle branch block

Supraventricular tachycardia

Supraventricular tachycardia (e.g. AVNRT) typically causes widespread horizontal ST

depression, most prominent in the left precordial leads (V4-6). This rate-related ST
depression does not necessarily indicate the presence of myocardial ischaemia, provided
that it resolves with treatment.

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 AV-nodal re-entry tachycardia

Anterior Myocardial Infarction:

• Anterior STEMI results from occlusion of the left anterior descending artery (LAD).
• Anterior myocardial infarction carries the worst prognosis of all infarct locations, mostly
due to larger infarct size.
• A study comparing outcomes from anterior and inferior infarctions (STEMI + NSTEMI)
found that on average, patients with anterior MI had higher incidences of in-hospital
mortality (11.9 vs 2.8%), total mortality (27 vs 11%), heart failure (41 vs 15%) and
significant ventricular ectopic activity (70 vs 59%) and a lower ejection fraction on
admission (38 vs 55%) compared to patients with inferior MI.
• In addition to anterior STEMI, other high-risk presentations of anterior ischaemia
include left main coronary artery (LMCA) occlusion, Wellens’ syndrome and De Winter’s
T waves.

How to Recognise Anterior STEMI

• ST segment elevation with Q wave formation in the precordial leads (V1-6) ± the high
lateral leads (I and aVL).

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Resources:

Other resources:

• AFEM Presentation Bank

• Tintinalli
• Rosen
• Roberts and Hedges
• UpToDate
• LITFL
• Family Practice Notebook
• Cochrane Reviews
• https://litfl.com/ecg-library

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