ECG MASTERCLASS 4.

0
REVISION NOTES BY DR VG
BASIC ANATOMY OF HEART :

- Cardiac Chambers:

- The heart serves as the central organ in the circulatory system, pumping
blood throughout the body.

- Comprises two upper receiving chambers: the right atrium and left
atrium.

- Features two lower pumping muscular chambers: the right ventricle and
left ventricle

- Right Atrium:

- Receives venous blood from various body parts via the superior and
inferior vena cavae.

- Directs the received blood to the right ventricle.

- Right Ventricle:

- Pumps blood to the pulmonary artery for transportation to the lungs.

- Left Atrium:

- Receives oxygenated blood from the lungs through four separate

pulmonary veins.

- Delivers the received blood to the left ventricle.

Left Ventricle Pumps oxygenated blood to the aorta, facilitating delivery to

different parts of the body.
- BASIC ELECTROPHYSIOLOGY:

- Three types of cells in the heart with distinct electrophysiologic

properties:

- Muscle cells (atria and ventricles) for contraction.

- Conducting cells (His-Purkinje system) for rapid impulse conduction.

- Pacemaking cells (sinus node and His-Purkinje system) with

automaticity.

- Myocardial Cell Polarization:

- All myocardial cells electrically polarized.

- Inside of the cell more negative due to electrolyte concentration

difference.
- Action Potential Phases (Ventricular Muscle Cell):

The following is a simplified description of the steps involved in the

generation of an action potential in the heart

Phase 0 – Rapid depolarization (phase 0) occurs when the resting cell is

brought to threshold, leading sequentially to activation or opening of
voltage-dependent sodium channels, rapid sodium entry into the cells
down a favorable concentration gradient, and a cell interior positive
potential that can approach +45 mV.

The marked depolarization initiates voltage-dependent inactivation of

the sodium channels. Calcium channels also open during depolarization,
but the inward calcium flux is much slower.

Phase 1 – Phase 1 repolarization often inscribes a "notch" and is primarily

caused by activation of the transient outward potassium currents (Ito)
combined with a corresponding rapid decay of the sodium current.

The degree of repolarization in phase 1 is dependent on the density of

Ito and varies between cardiac chambers and regions within chambers.
Phase 2 – Following initial repolarization in phase 1, phase 2 represents a
plateau that lasts for hundreds of milliseconds and distinguishes the
cardiac action potential from nerve and skeletal muscle action
potentials, which are significantly shorter.

Late inactivating depolarizing calcium and sodium currents are balanced

by activating repolarizing potassium currents to maintain the plateau,
which is often down-sloping as repolarizing currents begin to dominate.

●Phases 3 and 4 – The final rapid repolarizing phase 3 is driven by the

decay of the calcium current and progressive activation of repolarizing
potassium currents (IKr, IKs).

Terminal repolarization toward the potassium equilibrium potential is

dominated in phase 3 by IK1, which then maintains the resting membrane
potential (phase 4).
- ACTION POTENTIAL OF SINUS NODE CELL (PACEMAKER CELL):
- Spontaneous depolarization during phase 4 due to slow entry of sodium
ions.

- Resting potential around -60 mV.

- Smaller overshoot (0 to 10 mV) during phase 0 compared to non-

pacemaker cells.

Action potential in slow response tissues — The SA and AV nodes represent slow
response tissues, which have different properties from the fast response
tissues

Phase 0 depolarization depends on an inward calcium (not sodium)

current via L-type calcium channels .
- Repolarization:

- Recovery process after depolarization.

- Longer than depolarization, includes phases 1, 2, and 3.

- Refractory Periods:

- Absolute Refractory Period:

- Phases 1 and 2, cell unable to respond to any stimulus.

- Effective Refractory Period:

- Small portion of phase 3, potential generated but too weak to

propagate.

- Relative Refractory Period:

- Partial repolarization, may respond if stimulus stronger than usual.

- Extends to threshold potential (~-70 mV).

- Supernormal Phase:

- Responds to less-than-normal stimulus.

- End of phase 3 when repolarization is almost complete.

MECHANISMS OF TACHYARRHYTHMIA FORMATION

(A) Enhanced automaticity

(B) Reentry: a schematic of a reentrant circuit with fast and slow
conduction adjacent to a fixed core. An example of reentrant arrhythmia
of ventricular tachycardia is shown below the figure.
(C) Triggered activity, DADs: Bidirectional ventricular tachycardia from a
catecholaminergic polymorphic ventricular tachycardia patient is
depicted and thought to initiate with DADs.
(D) Triggered activity, EADs: Typical short-long-short cycles initiate
torsade de pointes in a patient with drug-induced long QT syndrome.
Basic Anatomy and Electrophysiology

Basic Anatomy

- Sinus Node:

- Location: Superior and lateral border of the right atrium.

- Extends from epicardium at the junction of superior vena cava and right
atrium to subendocardial region.

- Contains pacemaker cells with automaticity, fastest rate of discharge.

- Supplied by sinus node artery (60-65% from right coronary artery, rest
from left circumflex coronary artery).

- Internodal Tracts:

- Three tracts (anterior, posterior, and middle) connect sinus node to AV

node.

- Significance uncertain as sinus impulse primarily conducted through

atria.

- AV Node:

- Smaller than sinus node, lower right atrium, above insertion of tricuspid
valve septal leaflet.

- Three regions: AN (atrionodal), N (nodal), NH (nodo-His).

- AV node primarily responsible for delaying AV conduction, where

acetylcholine is released.

- Blood supply: 90% from AV nodal artery (branch of right coronary artery),
10% from left circumflex coronary artery.

- His-Purkinje System:
 - AV node continues as His bundle, divides into right and left bundle
branches.

- Right bundle branch continues down right side of interventricular

septum.

- Left bundle branch fans into anterior, midseptal, and posterior fascicles,
ending in Purkinje fibers over both ventricles.

- Conduction across His-Purkinje system unaffected by autonomic

influences.

- Blood supply from anterior and posterior descending coronary arteries.

Normal Sinus Impulse and Electrical Activation

Normal Sinus Impulse

- Sinus node origin of normal electrical impulse, fastest rate of discharge,

pacemaker of the heart.

- Normal Sinus Rhythm: Impulse from sinus node, 60-100 bpm, may vary
based on metabolic needs.

- Sinus Bradycardia: 60 bpm, Sinus Tachycardia: 100 bpm, Sinus Arrhythmia:

Irregular sinus impulse.

Electrical Activation

- Activation of the Atria - The P Wave:

- Sinus impulse spreads from atria to ventricles in an orderly sequence.

- The P wave is the first deflection in the ECG, due to atrial activation.

- Configuration: Smooth and well-rounded, representing right atrium (first

half) and left atrium (second half).

- Duration: 2.5 small blocks (0.10 seconds), reflecting activation of both atria.

- Amplitude: 2.5 small blocks (0.25 mV).

- Activation of the Atrioventricular Node (AV Node):

- After atrial depolarization, the AV node delays conduction to ventricles,

resulting in a flat line.

- No electrical activity in ECG during AV node conduction.

- Intraventricular Conduction System:

- Impulse travels rapidly through His bundle, bundle branches, and fascicles
to Purkinje fibers.
 - Like the AV node, intraventricular conduction system doesn't cause
deflection in the ECG.

- Activation of the Ventricles - The QRS Complex:

- QRS complex represents ventricular activation, generating the largest

deflection.

- Spread of impulse from Purkinje fibers to myocardium results in the QRS

complex.

- Ventricular activation is from endocardium to epicardium, outward

direction.

- QRS Complex Identification:

- Various waves in QRS complex: Q, R, S, R', S', and additional waves if

present.

- Capital and small letters used for convenience, regardless of deflection

size.

- Q wave: First negative wave, R wave: First positive deflection, S wave:

Negative deflection after R.

- R' (R prime) and S' (S prime): Next positive and negative deflections after
R and S.

- Additional waves denoted as R'' and S'' if needed.

- QRS Complex Configuration:

- QRS complex identified regardless of the number of waves.

- Tall R wave without Q or S is still identified as a QRS complex.

The J Point, ST Segment, and T Wave

J Point, ST Segment, and T Wave

- J Point:

- Marks the end of the QRS complex and the beginning of the ST segment.

- Critical transition point in the electrocardiogram (ECG).

- ST Segment:
 - Flat or isoelectric segment starting from the J point to the beginning of
the T wave.

- Represents phase 2 (plateau phase) of ventricular action potential.

- Ventricular cells are depolarized, in sustained contraction, and refractory

during this phase.

- T Wave:

- Represents rapid ventricular repolarization, corresponding to phase 3 of

the action potential.

- Action potential abruptly returns to resting potential of -90 mV.

- Marks the completion of ventricular repolarization, preparing for the

next depolarization.

PR Interval, QRS Complex, and QT Interval

- PR Interval:

- Measured from the beginning of the P wave to the beginning of the QRS
complex.

- Normal duration: 0.12 to 0.20 seconds in adults.

- Reflects the time for the sinus impulse to travel from atria to ventricles.

- QRS Complex:

- Measured from the beginning of the first deflection to the end of the last
deflection.

- Normal duration: 0.06 to 0.10 seconds.

- Increased duration with ventricular hypertrophy, bundle branch block, or

premature ventricular excitation.

- QT Interval:

- Includes QRS complex, ST segment, and T wave (phases 0 to 3 of action

potential).

- Measured from the beginning of the QRS complex to the end of the T
wave.

- Affected by heart rate; corrected QT interval (QTc) is used.

- QTc (Corrected QT Interval):

- Corrects QT interval for heart rate.

- Calculated using the Bazett formula.

- Normal QTc: Should not exceed 0.42 seconds in men, 0.44 seconds in women.

- Prolonged QTc associated with increased risk, especially when exceeding

0.46 seconds in women and children.
Normal U Wave and T-Q Segment

The exact cause of this wave is uncertain, though data suggest it may
be from late repolarization of the mid-myocardial M cells, due to a longer
action potential duration compared with the endocardium or epicardium.

- Normal U Wave:

- Follows the T wave, usually small (one-tenth of the T wave size).

- Often recorded in anterior precordial leads (V2, V3).

- U waves best visible with a slow heart rate (≤ 65 bpm).

- Abnormal U Wave:

- Inverted or equal/exceeding T wave size, seen in hypokalemia.

- T-Q Segment:

- Measured from the end of the T wave to the Q wave of the next QRS
complex.

- Represents electrical diastole, corresponding to phase 4 of the action

potential.
Abnormal Waves:

- Delta Wave:

- Slow and slurred upstroke at the beginning of the QRS complex.

- Diagnostic of Wolff-Parkinson-White syndrome.

- Osborn Wave (J Wave):

- Exaggerated elevation of the J point, forming an H shape in the QRS

complex.

- Associated with hypothermia or hypercalcemia.

Epsilon Wave:

- Extra notch at the end of the QRS or early ST segment.

- Diagnostic of arrhythmogenic right ventricular dysplasia.

3 : The Lead System:

Transmission of Heart Impulses:

- Electrical impulses from the heart transmitted through body fluids and
chemicals.

- Recorded using electrodes on the body surface.

ECG Deflection Basics:

- Electrical impulses measured by placing electrodes; upright deflection for

current towards positive electrode (left arm), downward for current away.

- Deflection height corresponds to potential difference.

Bipolar Leads I, II, III:

- Bipolar leads connect positive and negative electrodes equidistant from

the heart.

- Leads I, II, and III illustrate bipolar leads with specific deflection directions.

Lead I:

- Constructed with left arm (positive) to right arm (negative).

- Upward deflection if impulse is leftward, downward if rightward.

Lead II:

- Constructed with left leg (positive) to right arm (negative).

- Positive deflection for leftward impulse, downward for rightward.

Lead III:

- Constructed with left leg (positive) to left arm (negative).

- Upward deflection for leftward impulse, downward for rightward.

Einthoven Triangle:

- Leads I, II, III form a triangle representing different axes.

- Leads can be superimposed for a triaxial reference system.

Unipolar Leads:

- One exploring electrode and one distant indifferent electrode.

- VR, VL, VF conventionally in right arm, left arm, left foot.

- Central terminal serves as the ground electrode with near-zero potential.

Exploring and Ground Electrodes:

- Flow towards exploring electrode yields upward deflection, away yields

downward.

- Ground electrode is neutral with near-zero potential.

Augmented Unipolar Leads (aVR, aVL, aVF):

- Originally VR, VL, VF renamed aVR, aVL, aVF with 50% increase in ECG
deflection size when disconnected from central terminal.

Lead aVR:

- Unipolar electrode over the right arm.

- Detects impulse towards the right shoulder.

- Location at –150.

Lead aVL:

- Unipolar electrode over the left arm.

- Detects potentials towards the left shoulder.

- Location at –30.

Lead aVF:

- Unipolar electrode over the left leg.

- Detects potentials towards the left groin.

- Location at 90.
Precordial Leads :

Precordial leads: Six precordial leads were later added to the six frontal
leads to complete the 12-lead ECG.
-
- Frontal Plane:

- Left/right and superior/inferior orientation

- Axis deviation describes QRS complex position: normal, left, right, or

northwest quadrant.

- Horizontal Plane:

- Represented by leads V1 to V6 (Fig. 4.1B).

- Includes left/right and anteroposterior orientation.

- Rotation of the heart can be normal, clockwise, or counterclockwise.

- Hexaxial Reference System:

- Divides frontal plane into four quadrants

- Normal quadrant (0-90), left upper quadrant (0-90) represents left axis
deviation.

- Right lower quadrant (90-180) represents right axis deviation.

- Right upper quadrant (–90-180) is extreme right or left axis deviation

(northwest axis).
- Normal QRS Axis:

- Depends on the patient's age.

- In newborns (up to 6 months): Normal axis is 90 (vertical axis).

- In adults: Normal axis extends horizontally from 90 to –30.

- Axis –1 to –30 in the left upper quadrant is considered left axis deviation
(Fig. 4.2).

- Newborns (Up to 6 Months):

- Normal QRS axis is 90 (vertical axis).

- With Increasing Age:

- Axis shifts horizontally leftward toward 0.

- Rare in Children:

- Horizontal axis is uncommon.

- In Adults:

- Normal axis extends horizontally from 90 to –30.

- Axis –1 to –30:

- Located in the left upper quadrant.

- Considered left axis deviation.

- Normal Axis Extension:

- Extends up to –30 in adults.

- Consideration for –1 to –30:

- Despite being in the left upper quadrant, it is considered part of the

normal axis (Fig. 4.2).

Interpretation of ECG Axis :

Since the left ventricle makes up most of the heart muscle under normal circumstances,
normal cardiac axis is directed downward and slightly to the left:

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

Abnormal axis deviation, indicating underlying pathology, is demonstrated by:

• 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:

• The Quadrant Method – (Lead I and aVF)

• Three Lead analysis – (Lead I, Lead II and aVF)

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 aVF are both positive, the axis
is between 0° and +90° (i.e. normal axis).
Now estimate the AXIS using the Lead I and aVF – Quadrant Method:

Example no.1
Example no.2

Example no.3
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 coloured 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
NOW ESTIMATE THE AXIS USING THREE LEAD ANALYSIS:
CAUSES OF AXIS DEVIATION
RIGHT AXIS DEVIATION
• 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

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

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

• Hyperkalaemia
• Severe right ventricular hypertrophy
BASICS OF ECG INTERPRETATION:

Understanding paper speeds

• Paper output speed is the rate at which the ECG machine produces
a trace
• Standard output is 25mm per second
• If a different paper speed is used, standard rate calculations will
have to be modified appropriately (see other examples below)

The standard paper speed is 25mm/sec:

• 1 SMALL square (1mm) = 0.04 sec (40ms)

• 5 SMALL squares (5mm) = 1 LARGE square = 0.2 sec (200ms)
• 5 LARGE squares = 1 second
At standard paper speed of 25mm/sec, the rhythm strip comprises of:

• 250 SMALL squares = 50 LARGE squares = 10 seconds

Before calculating rate in beats per minute (bpm), we should understand that a rhythm strip
recorded for 1 minute will therefore compromise:

• 1500 SMALL squares = 300 LARGE squares = 1 minute

CALCULATING RATE
There are three main methods of calculating ECG rate. There is no
specific best method, and preference varies between clinicians. However,
certain methods may be better suited for rhythms such
bradyarrhythmias or tachyarrhythmias.

1) LARGE SQUARE METHOD

• Recall above that 300 large squares is equal to 1 minute at a paper

speed of 25mm/sec
• We can thus calculate bpm by dividing 300 by the number of LARGE
squares between each R-R interval (space between two
consecutive R waves = one beat)
• For example, two large squares between each R-R interval implies
a rate of 150 bpm, three implies a rate of 100 bpm and so forth:

2) SMALL SQUARE METHOD

• Similar to above, except 1500 is divided by the number of SMALL

squares between consecutive R waves
• For example, 10 small squares between R-R interval implies a rate
of 150 bpm, 15 implies a rate of 100 bpm, and so forth:
3) R WAVE METHOD :

• Rate = Number of R waves (rhythm strip) X 6

• The number of complexes (count R waves) on the rhythm strip
gives the average rate over a ten-second period. This is multiplied
by 6 (10 seconds x 6 = 1 minute) to give the average beats per
minute (bpm)
• Useful for slow and/or irregular rhythms.

INTERPRETATION (ADULTS)
• Normal: 50 – 100 bpm
• Tachycardia: > 100 bpm
• Bradycardia: < 50 bpm

NORMAL HEART RATES IN CHILDREN

• Newborn: 110 – 150 bpm
• 2 years: 85 – 125 bpm
• 4 years: 75 – 115 bpm
• 6 years+: 60 – 100 bpm

OTHER PAPER SPEEDS: 50MM/SEC

Doubling the standard rate will cause the ECG to appear drawn out or
wider complex than 25mm/sec paper speeds

• 1mm (small square) = 0.02 sec (20ms)

• 5mm (large square) = 0.1 sec (100ms)
The rhythm strip will thus comprise 5 seconds total capture compared to
the standard 10 seconds.

WHY USE 50 MM/SECOND?

Doubling the standard rate can reveal subtle ECG findings hidden at the
slower rates, in particular atrial flutter waves in a 2:1 block:

7 STEP APPROACH TO ECG RHYTHM ANALYSIS

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
 o complete: atrial and ventricular activity is always
independent.
o incomplete: intermittent capture.

6. Onset and termination

• Abrupt: suggests re-entrant process.

• Gradual: suggests increased automaticity.

7. RESPONSE TO VAGAL MANOEUVRES

• Sinus tachycardia, ectopic atrial tachydysrhythmia: gradual slowing
during the vagal manoeuvre, but resumes on cessation.
• AVNRT or AVRT: abrupt termination or no response.
• Atrial fibrillation and atrial flutter: gradual slowing during the
manoeuvre.
• VT: no response.
ECG WAVES :

P WAVE OVERVIEW
The P wave is the first positive deflection on the ECG and
represents atrial depolarisation.

• The P wave is the first positive deflection on the ECG

• It represents atrial depolarisation
• Normal duration: < 0.12 s (< 120ms or 3 small squares)

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
• < 0.12 s (<120ms or 3 small squares)
AMPLITUDE
• < 2.5 mm (0.25mV) in the limb leads
• < 1.5 mm (0.15mV) in the precordial leads

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.

THE ATRIAL WAVEFORM – RELATIONSHIP TO THE P WAVE

• Atrial depolarisation proceeds sequentially from right to left, with

the right atrium activated before the left atrium
• The right and left atrial waveforms summate to form the P wave
• The first 1/3 of the P wave corresponds to right atrial activation,
the final 1/3 corresponds to left atrial activation; the middle 1/3 is
a combination of the two
• In most leads (e.g. lead II), the right and left atrial waveforms
move in the same direction, forming a monophasic P wave
• However, in lead V1 the right and left atrial waveforms move in
opposite directions. This produces a biphasic P wave with the initial
positive deflection corresponding to right atrial activation and the
subsequent negative deflection denoting left atrial activation
• This separation of right and left atrial electrical forces in lead V1
means that abnormalities affecting each individual atrial
waveform can be discerned in this lead. Elsewhere, the overall
shape of the P wave is used to infer the atrial abnormality.

• Normal P-wave Morphology – Lead II

• The right atrial depolarisation wave (brown) precedes that of the
left atrium (blue)
 • The combined depolarisation 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 depolarisation lasts longer

than normal and its waveform extends to the end of left atrial
depolarisation
• Although the amplitude of the right atrial depolarisation current
remains unchanged, its peak now falls on top of that of the left
atrial depolarisation 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)

LEFT ATRIAL ENLARGEMENT – LEAD II

• In left atrial enlargement, left atrial depolarisation 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.

LEFT ATRIAL ENLARGEMENT – V1
Left atrial enlargement causes widening (> 40ms wide) and deepening (>

1mm deep) in V1 of the terminal negative portion of the P wave.

COMMON 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, 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

P PULMONALE
The 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).

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

If ≥ 3 different P wave morphologies are seen and the rate is ≥ 100,

then multifocal atrial tachycardia(MAT) is diagnosed:

THE Q WAVE
A Q wave is any negative deflection that precedes an R wave

• The Q wave represents the normal left-to-right depolarisation of

the interventricular septum
• Small ‘septal’ Q waves are typically seen in the left-sided leads (I,

aVL, V5 and 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

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

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.

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

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

EXAMPLE 5

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

QRS COMPLEX MORPHOLOGY

Main features to consider:

• Width of the complexes: Narrow versus broad.

 • Voltage (height) of the complexes.
• Spot diagnoses: Specific morphology patterns that are important
to recognise.

QRS WIDTH
Normal QRS width is 70-100 ms (a duration of 110 ms is sometimes
observed in healthy subjects). The QRS width is useful in determining the
origin of each QRS complex (e.g. sinus, atrial, junctional or ventricular).

• Narrow complexes (QRS < 100 ms) are supraventricular in origin.

• Broad complexes (QRS > 100 ms) may be either ventricular in origin,

or due to aberrant conduction of supraventricular complexes (e.g.

due to bundle branch block, hyperkalaemia or sodium-channel
blockade).

Sinus rhythm with frequent ventricular ectopic beats (VEBs) in a pattern

of ventricular bigeminy. The narrow beats are sinus in origin, the broad
complexes are ventricular.

NARROW QRS COMPLEX MORPHOLOGY

Narrow (supraventricular) complexes arise from three main places:

• Sino-atrial node (= normal P wave)

• Atria (= abnormal P wave / flutter wave / fibrillatory wave)
• AV node / junction (= either no P wave or an abnormal P wave with

a PR interval < 120 ms)

BROAD QRS COMPLEX MORPHOLOGY
BROAD/WIDE QRS COMPLEXES
• A QRS duration > 100 ms is abnormal
• A QRS duration > 120 ms is required for the diagnosis of bundle
branch block or ventricular rhythm

Broad complexes may be ventricular in origin or due to aberrant

conduction secondary to:

• Bundle branch block (RBBB or LBBB)

• Hyperkalaemia
• Poisoning with sodium-channel blocking agents (e.g. tricyclic
antidepressants)
• Pre-excitation (i.e. Wolff-Parkinson-White syndrome)
• Ventricular pacing
• Hypothermia
• Intermittent aberrancy (e.g. rate-related aberrancy)

Example of a Broad Complex Rhythm:

VENTRICULAR VS SUPRAVENTRICULAR RHYTHMS

Differentiation between ventricular complexes and aberrantly conducted supraventricular
complexes may be difficult.
 • In general, aberrant conduction of sinus rhythm and atrial rhythms
(tachycardia, flutter, fibrillation) can usually be identified by the
presence of preceding atrial activity (P waves, flutter waves,
fibrillatory waves).

• However, aberrantly conducted junctional (AV nodal) complexes

may appear identical to ventricular complexes as both produce
broad QRS without any preceding atrial activity.

• In the case of ectopic beats, this distinction is not really important

(as occasional ectopic beats do not usually require treatment).

• However, in the case of sustained tachyarrhythmias, the

distinction between ventricular tachycardia and SVT with
aberrancy becomes more important. This topic is covered in more
detail here.

Fortunately, many causes of broad QRS can be identified by pattern recognition:

• Right bundle branch block produces an RSR’ pattern in V1 and deep

slurred S waves in the lateral leads.
• Left bundle branch block produces a dominant S wave in V1 with
broad, notched R waves and absent Q waves in the lateral leads.
• Hyperkalaemia is associated with a range of abnormalities
including peaked T waves
• Tricyclic poisoning is associated with sinus tachycardia and tall R’
wave in aVR
• Wolff-Parkinson White syndrome is characterised by a short PR
interval and delta waves
• Ventricular pacing will usually have visible pacing spikes
 • Hypothermia is associated with bradycardia, long QT, Osborn
waves and shivering artefact

HIGH VOLTAGE QRS MORPHOLOGY

• Increased QRS voltage is often taken to infer the presence of left
ventricular hypertrophy.
• However, high left ventricular voltage (HLVV) may be a normal
finding in patients less than 40-45 years of age, particularly slim or
athletic individuals.
• There are multiple “voltage criteria” for left ventricular
hypertrophy.
• Probably the most commonly used are the Sokolov-Lyon criteria (S
wave depth in V1 + tallest R wave height in V5-V6 > 35 mm).
• Voltage criteria must be accompanied by non-voltage criteria to be
considered diagnostic of left ventricular hypertrophy.

LOW VOLTAGE QRS MORPHOLOGY

The QRS is said to be low voltage when:

• The amplitudes of all the QRS complexes in the limb leads are < 5
mm; or
• The amplitudes of all the QRS complexes in the precordial leads are
< 10 mm

ELECTRICAL ALTERNANS
• This is when the QRS complexes alternate in height.
• The most important cause is massive pericardial effusion, in which
the alternating QRS voltage is due to the heart swinging back and
forth within a large fluid-filled pericardium.
SPOT DIAGNOSES

These cardiac diseases produce distinctive QRS morphologies that are important not to
miss:

• Brugada syndrome (partial RBBB with ST elevation in V1-2)

• Wolff-Parkinson White Syndrome (delta wave)
• Tricyclic poisoning (wide QRS with dominant R wave in aVR)

QT Interval :

DEFINITION

• Time from the start of the Q wave to the end of the T wave
• Represents time taken for ventricular depolarisation and
repolarisation, effectively the period of ventricular systole from
ventricular isovolumetric contraction to isovolumetric relaxation

The QT interval is inversely proportional to heart rate:

• The QT interval shortens at faster heart rates

• The QT interval lengthens at slower heart rates
• An abnormally prolonged QT is associated with an increased risk of
ventricular arrhythmias, especially Torsades de Pointes
• 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 the QT interval

• The QT interval is usually measured in either lead II or V5-6,

however the lead with the longest measurement should be used
 • 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 isoelectric line 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 to the intersection point
between the isoelectric line and the tangent drawn from the maximum
down slope of the second notch.

NORMAL QTC VALUES

• QTc is prolonged if > 440ms in men or > 460ms in women
• QTc > 500 is associated with an 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
• ROSC Post-cardiac arrest
• Raised intracranial pressure
• Congenital long QT syndrome
• Medications/Drugs
CAUSES OF A SHORT QTC (<350MS)
• Hypercalcaemia
• Congenital short QT syndrome
• Digoxin effect
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 (developed
by Chan et al) to determine whether the patient is at risk of TdP.
• The QT nomogram is a clinically relevant risk assessment tool that
predicts arrhythmogenic risk for drug-induced QT prolongation can
be used for risk stratification
• A QT interval-heart rate pair that plots above the line indicates the
patient is at risk of TdP.
THE J POINT

The J point is the the junction between the termination of the QRS
complex and the beginning of the ST segment.

The J (junction) point in the ECG is the point where the QRS complex
joins the ST segment.

It represents the approximate end of depolarization and the beginning of

repolarization as determined by the surface ECG. There is an overlap of
around 10ms.

The J point marks the end of the QRS complex, and is often situated
above the baseline, particularly in healthy young males.

The J point may deviate from the baseline in early repolarization,

epicardial or endocardial ischaemia or injury, pericarditis, RBBB, LBBB,
RVH, LVH or digitalis effect.

On most ECGs the determination of the J point as a demarcation

between QRS and the start of the ST is clear.

However with the advance of electrophysiological studies and scrutiny of

the cellular/ionic mechanisms at each stage of the ECG – these lines
become blurred.

For simplicity:

• J point is present in all ECGs and marks the transition of QRS

complex to ST segment
• J wave deflection occurs before the J point
• The position of the J point in relation to a slurred terminal QRS is
still debated.
ABNORMALITIES OF THE J POINT

• Elevation or depression of the J point is seen with the various

causes of ST segment abnormality.
• It may be elevated as a result of injury currents during acute
myocardial ischemia and pericarditis, as well as in various other
patterns of both normal and abnormal ECGs
• Elevation of the J point occurs with benign early repolarisation

• A positive deflection prior to the J point is termed a J wave

(Osborn wave) and is characteristically seen with hypothermia.
R WAVE OVERVIEW
The R wave is the first upward deflection after the P wave. The R wave
represents early ventricular depolarisation

1. DOMINANT R WAVE IN V1
Causes of Dominant R wave in V1

• Normal in children and young adults

• Right Ventricular Hypertrophy (RVH)
o Pulmonary Embolus
o Persistence of infantile pattern
o 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

EXAMPLES OF DOMINANT R WAVE IN V1

Normal paediatric ECG (2 yr old)

Right Ventricular Hypertrophy (RVH)
Right Bundle Branch Block (RBBB)
POSTERIOR MI
WOLFF-PARKINSON-WHITE (WPW) TYPE A

Lead V1 and V3 reversed :

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

MUSCULAR DYSTROPHY

2. 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:
o R wave height > 3mm
o R/S ratio > 0.7

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

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
3. POOR R WAVE PROGRESSION
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
NORMAL T WAVE CHARACTERISTICS

Which of the following statements accurately describes a characteristic of

a normal T wave on an electrocardiogram (ECG)?

a) The T wave is inverted in leads aVR and V1.

b) The T wave has an amplitude greater than 5mm in limb leads and
greater than 10mm in precordial leads.

c) The duration of the T wave is independent of the QT interval.

d) The T wave is typically taller in females compared to males.

 • Upright in all leads except aVR and V1
• Amplitude < 5mm in limb leads, < 10mm in precordial leads (10mm
males, 8mm females)
• Duration relates to QT interval

PEAKED T WAVES

Tall, narrow, symmetrically peaked T-waves are characteristically seen

in hyperkalaemia
HYPERACUTE T WAVES (HATW)

Broad, asymmetrically peaked or ‘hyperacute’ T-waves (HATW) are seen

in the early stages of ST-elevation MI (STEMI), and often precede the
appearance of ST elevation and Q waves.

Particular attention should be paid to their size in relation to the

preceding QRS complex, as HATW may appear ‘normal’ in size if the
preceding QRS complex is of a small amplitude.

They are also seen with Prinzmetal angina.

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
In which of the following conditions are inverted T waves commonly
observed on an electrocardiogram (ECG)?

a) Myocardial ischaemia and infarction (including Wellens Syndrome)

b) Bundle branch block

c) Sinus Arrhythmia

d) Pulmonary embolism

e) Hypertrophic cardiomyopathy

f) Raised intracranial pressure

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 (including Wellens Syndrome)
• Bundle branch block
• Ventricular hypertrophy (‘strain’ patterns)
• 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).

Inverted T-waves in the right precordial leads (V1-3) are a normal

finding in children, representing the dominance of right ventricular
forces

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

Inferior T wave inversion due to acute ischaemia

Inferior T wave inversion with Q waves – prior myocardial infarction

T wave inversion in the lateral leads due to acute ischaemia

Anterior T wave inversion with Q waves due to recent MI

BUNDLE BRANCH BLOCK

In bundle branch block, T-wave inversion is an expected finding, even in

the absence of ischaemia:

• Appropriate discordance refers to the fact that abnormal

depolarisation (such as in bundle branch block) should be followed
by abnormal repolarisation, which appears discordant to the
preceding QRS complex in the form of ST-depression and T-wave
inversion
LEFT BUNDLE BRANCH BLOCK

• Left bundle branch block produces T-wave inversion in the lateral

leads I, aVL and V5-6

RIGHT BUNDLE BRANCH BLOCK (RBBB)

• Right bundle branch block produces T-wave inversion in the right

precordial leads V1-3
• Ventricular Hypertrophy
• Left Ventricular Hypertrophy (LVH)
 • Left ventricular hypertrophy (LVH) 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

Right Ventricular Hypertrophy (RVH)

 • 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
SI QIII TIII

• Pulmonary embolism may also produce T-wave inversion in lead III

as part of the SI QIII TIII pattern

• S wave in lead I, Q wave in lead III, T-wave inversion in lead III

Acute massive PE with SI QIII TIII RBBB TWI V1-3
Hypertrophic Cardiomyopathy (HCM)

• Hypertrophic Cardiomyopathy is associated with deep T wave

inversions in all the precordial lead

RAISED INTRACRANIAL PRESSURE (ICP)

• 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

What are the two main causes of biphasic T waves on an electrocardiogram

(ECG)?

a) Myocardial infarction and atrial fibrillation

b) Myocardial ischaemia and hypokalaemia

c) Bundle branch block and pulmonary embolism

d) Ventricular hypertrophy and sinus tachycardia

There are two main causes of biphasic T waves:

• Myocardial ischaemia

• Hypokalaemia

The two waves go in opposite directions:

Biphasic T waves due to ischaemia – T waves go UP then DOWN

Biphasic T waves due to Hypokalaemia – T waves go DOWN then UP

Wellens Syndrome

Wellens syndrome is a pattern of inverted or biphasic T waves in V2-3 (in

patients presenting with/following ischaemic sounding 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 A = Biphasic T waves with the initial deflection positive and

the terminal deflection negative (25% of cases)

• Type B = T-waves are deeply and symmetrically inverted (75% of

cases)

Note: The T waves evolve over time from a Type A to a Type B pattern
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

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)

Hypokalaemia

Note global T-wave flattening in hypokalaemia associated with

prominent U waves in the anterior leads (V2 and V3).
U Wave Overview

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 repolarisation of Purkinje fibres

• Prolonged repolarisation of mid-myocardial “M-cells”

• After-potentials resulting from mechanical forces in the ventricular

wall

Abnormalities of the U wave

• Prominent U waves

• Inverted U waves
Prominent U waves

U waves are described as prominent if they are

• >1-2mm or 25% of the height of the T wave.

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
 1. Delta waves are associated with which of the following conditions?
a) Myocardial infarction
b) Atrial fibrillation
c) Bundle branch block
d) Wolff-Parkinson-White syndrome

• Epsilon waves are typically seen in patients with:

• a) Ventricular hypertrophy
• b) Atrial flutter
• c) Acute pericarditis
• d) Arrhythmogenic right ventricular dysplasia

The Osborn wave (J wave) is commonly associated with:

• Hyperkalemia
• Hypokalemia
• Myocardial infarction
• Pulmonary embolism
Osborn Wave (J Wave) Overview

The Osborn wave (J wave) is a positive deflection seen at the J point in

precordial and true limb leads.

It is most commonly associated with hypothermia. These changes will

appear as a reciprocal, negative deflection in aVR and V1.

The J point in the ECG is the point where the QRS complex joins the ST
segment. It represents the approximate end of depolarization and the
beginning of repolarization as determined by the surface ECG.

There is an overlap of around 10ms.

The J point may deviate from the baseline in early repolarization,

epicardial or endocardial ischemia or injury, pericarditis, RBBB, LBBB,
RVH, LVH or digitalis effect.
Delta Wave Overview

The Delta wave is a slurred upstroke in the QRS complex. It relates to

pre-excitation of the ventricles, and therefore often causes an
associated shortening of the PR interval. It is most commonly associated
with pre-excitation syndromes such as WPW.

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

• Short PR interval (< 120ms)

• Broad QRS (> 100ms)

• A slurred upstroke to the QRS complex (the delta wave)

Epsilon Wave Definition

• Small deflection (“blip” or “wiggle”) buried in the end of the QRS

complex

• On Standard 12-lead ECG (S-ECG), best seen in ST segment of V1

and V2, they are usually present in leads V1 through V4

• Caused by post-excitation of myocytes in the right ventricle

• Characteristic finding in patients with arrhythmogenic right

ventricular dysplasia(ARVD)

Epsilon wave in V1 due to RV conduction delay

Epsilon waves are the most specific and characteristic finding
in arrhythmogenic right ventricular dysplasia (ARVD).

In ARVD, myocytes are replaced by fat, producing islands of viable

myocytes in a sea of fat. This causes a delay in excitation of some of the
myocytes of the right ventricle, producing a small “blip” seen during the
ST segment of the ECG.

Epsilon waves have also been described in patients with:

1. Posterior myocardial infarction

2. Right ventricular infarction
3. Infiltrative disease
4. Sarcoidosis
Epsilon waves can be detected by:

1. S-ECG: Standard 12-lead electrocardiography (S-ECG)

2. R-ECG; Right-sided precordial lead electrocardiography (R-ECG)

3. F-ECG; Fontaine bipolar precordial lead electrocardiography (F-ECG)

Fontaine lead

Comparison of S-ECG versus F-ECG in the ability to detect epsilon waves

(arrows).
The Fontaine lead placement increases sensitivity of detecting epsilon
waves so that they are detected in three leads (FI, FII, FIII) rather than
one lead in the regular placement.
Myocardial infarction. :

- Edward Hyde (Before 1550BC): Earliest description of angina

in the Ebers Papyrus
- William Heberden (1768): Coined the term "angina pectoris"
and also referred to it as "Heberden's asthma."
- Edward Jenner (1776): Proposed that angina is a result of
coronary artery insufficiency.
- William Osler (1912): Termed angina as the "cramp of heart
muscle."
- Nikolay Anichkov (1950): Linked coronary artery disease as
the predominant cause of angina, marking the appearance of
ischemic heart disease in textbooks.
1970: Thrombus confirmed as the cause of myocardial
infarction through post-mortem examinations.
- Eugene Braunwald (20th Century): Contributed significantly
to the understanding of ischemic heart disease, advancing
knowledge on its pathophysiology and treatment strategies.

Coronary Artery Disease (CAD):

- Refers to luminal narrowing of a coronary artery, typically

caused by atherosclerosis.
- Leading contributor to ischemic heart disease (IHD).

Ischemic Heart Disease (IHD):

- Encompasses conditions such as angina pectoris, myocardial

infarction (MI), and silent myocardial ischemia.
- Represents a spectrum of cardiovascular disorders.

Cardiovascular Disease (CVD):

- Includes a broader range of conditions beyond IHD.

 - Encompasses cardiomyopathy, heart failure (HF), arrhythmia,
hypertension, cerebrovascular accident (CVA), diseases of the
aorta, peripheral vascular disease (PVD), valvular heart
disease, and congenital heart disease.

Stable Angina:

- Defined as angina symptoms or equivalent symptoms

reproducible with consistent levels of activity.
- Relief achieved through rest.

Definition of MI: UDMI 2018

Universal definition of myocardial injury summary :

First few definitions were based on clinical features and ECG

Then came CPK MB

Then came Trop I which was optional but now it’s compulsory
Gist of the definition :

1.Myocardial Injury

2. Troponin > 99th percentile

3. Acute MI 5 types
Myocardial injury:

Elevated cardiac Troponin with at least one value above 99th Percentile
of upper reference limit

Acute - Rise or/and fall in Troponin

Chronic - Elevated above Upper limit but no rise and fall

Causes of elevated trop I :
Approach to chest pain

Typical angina has three features:

(1) substernal chest discomfort with a characteristic quality and

duration that is

(2) provoked by stress or exertion and

(3) relieved by rest or nitroglycerin.

Atypical angina has two of these three characteristics. Non-cardiac chest

pain meets one or none of these characteristics.

Chronic stable angina is reproducibly precipitated in a predictable manner

by exertion or emotional stress and relieved within 5–10 minutes by
sublingual nitroglycerin or res

Chest pain history taking -

Blood supply of heart :
Myocardial Ischaemia Background

Non-ST-elevation acute coronary syndrome (NSTEACS) encompasses two

main entities:

Non-ST-elevation myocardial infarction (NSTEMI).

Unstable angina pectoris (UAP).

Which of the following ECG findings are associated with myocardial

ischemia, except:

A) ST segment depression

B) T wave flattening

C) Peaked T waves

D) U-wave inversion

E) None

Patterns of Myocardial Ischaemia

Two main ECG patterns associated with NSTEACS:

ST segment depression

T wave flattening or inversion

While there are numerous conditions that may simulate myocardial ischaemia
(e.g. left ventricular hypertrophy, digoxin effect), dynamic ST segment and T wave

changes (i.e. different from baseline ECG or changing over time) are strongly
suggestive of myocardial ischaemia.

Other ECG patterns of ischaemia

Hyperacute (peaked) T waves or pseudonormalisation of previously inverted T waves

(i.e. becoming upright) suggest hyperacute STEMI.

Another, less well-known ECG feature of myocardial ischaemia is U-wave inversion.

MORPHOLOGY OF ST DEPRESSION

Which of the following statements regarding ST depression on an ECG is

Wrong?

A) Upsloping ST depression is highly specific for myocardial ischemia.

B) ST depression ≥ 2 mm in ≥ 3 leads indicates a high probability of

NSTEMI with significant mortality.

C) Horizontal or down sloping ST depression ≥ 1 mm at the J-point in ≥ 2

contiguous leads suggest myocardial ischemia.

D) ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads may

indicate myocardial ischemia according to the 2007 Task Force Criteria.
ST depression can be either upsloping, downsloping, or horizontal
(see diagram below).

Horizontal or down sloping ST depression ≥ 0.5 mm at the J-point in ≥

2 contiguous leads indicates myocardial ischaemia (according to
the 2007 Task Force Criteria).

ST depression ≥ 1 mm is more specific and conveys a worse

prognosis.

ST depression ≥ 2 mm in ≥ 3 leads is associated with a high

probability of NSTEMI and predicts significant mortality (35%
mortality at 30 days).

Upsloping ST depression is non-specific for myocardial ischaemia.

Examples of ST segment morphology in myocardial ischaemia

T wave inversion

T wave inversion may be considered to be evidence of myocardial

ischaemia if:

At least 1 mm deep

Present in ≥ 2 continuous leads that have dominant R waves

(R/S ratio > 1)

Dynamic — not present on old ECG or changing over time

Widespread T wave inversion due to myocardial ischaemia (most prominent in the lateral leads)
 Myocardial Infarction on ECG

Which of the following criteria is NOT typically associated with ST elevation

myocardial infarction (STEMI)?

A) New ST elevation ≥ 1 mm in two contiguous leads

B) ST elevation ≥ 2 mm in V2-V3 in men above 40 years old or ≥ 2.5 mm in

men below 40 years old.

C) ST elevation ≥ 1.5 mm in leads V2-V3 in women.

D) ST elevation ≥ 1.5 mm in V2-V3 if age below 40 years and >2mm if age

is above 40 years
DYNAMIC ST-T WAVE CHANGES

What is the primary reason for the dynamic ST-T changes observed in
myocardial infarction (MI)?

A) Abnormalities in the P wave morphology

B) Alterations in ventricular hypertrophy

C) Ischemia-induced cellular changes and electrophysiological alterations

D) Changes in atrioventricular node conduction

Pathophysiology for Dynamic ST-T wave changes :

1. Ischemia-induced cellular changes: Ischemia disrupts cellular

metabolism and ion homeostasis in cardiac myocytes, leading to altered
ion channel function and membrane potentials.

2. Electrophysiological alterations: Ischemia affects the transmembrane

ion currents responsible for action potential generation and propagation,
particularly in phases 2 and 3 of the action potential. This disruption
manifests as ST segment deviation and T wave changes on the ECG.

3. Regional myocardial injury: The specific ECG changes observed in MI

depend on the location and extent of myocardial injury resulting from
reduced blood flow in a particular coronary artery territory.

4. Temporal evolution of changes: The dynamic nature of ST-T changes

reflects the evolving nature of ischemic injury, with ST segment
elevation indicating ongoing myocardial injury and potential reperfusion
or resolution leading to normalization or decrease in ST elevation.
ECG Features of Anterior STEMI

ST segment elevation with subsequent Q wave formation in precordial

leads (V1-6) +/- high lateral leads. These changes are often preceded by
hyperacute T waves

Reciprocal ST depression in inferior leads (mainly III and aVF)

NB: The magnitude of reciprocal change in inferior leads is determined by

the magnitude of ST elevation in I and aVL (as these leads are electrically
opposite III and aVF), and hence may be minimal or absent in anterior
STEMIs that do not involve high lateral leads.

Clinical Relevance of Anterior Myocardial Infarction

Anterior STEMI usually results from occlusion of the left anterior

descending artery (LAD).

Anterior myocardial infarction carries the poorest prognosis of all infarct

locations, due to the larger area of myocardium infarct size.
A study comparing outcomes from anterior and inferior infarctions
(STEMI + NSTEMI) found that compared with inferior MI, 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%)

Significant ventricular ectopic activity (70 vs 59%)

Lower ejection fraction on admission (38 vs 55%)

In addition to anterior STEMI, other high-risk presentations of anterior

ischaemia include left main coronary artery (LMCA) stenosis, Wellens
syndromeand De Winter T waves.

The precordial leads can be classified as follows:

• Septal leads = V1-2

• Anterior leads = V3-4
• Lateral leads = V5-6

The different infarct patterns are named according to the leads with maximal ST
elevation:

• Septal = V1-2
• Anterior = V2-5
• Anteroseptal = V1-4
• Anterolateral = V3-6, I + aVL
• Extensive anterior / anterolateral = V1-6, I + aVL

Clinically important

Other important ECG patterns to be aware of:

Anterior-inferior STEMI due to occlusion of a “wraparound” LAD

. This presents with simultaneous ST elevation in the precordial

and inferior leads, due to occlusion of a variant (“type III”) LAD
that wraps around the cardiac apex to supply both the anterior
and inferior walls of the left ventricle

Left main coronary artery stenosis: widespread ST depression with

ST elevation in aVR ≥ V1

Wellens syndrome: deep precordial T wave inversions or biphasic T waves

in V2-3, indicating critical proximal LAD stenosis (a warning sign of
imminent anterior infarction)

De Winter T waves: upsloping ST depression with symmetrically peaked T

waves in the precordial leads; a “STEMI equivalent” indicating acute LAD
occlusion.

ECG Examples

Example 1

Hyperacute Anteroseptal STEMI:

 • ST elevation and hyperacute T waves in V2-4
• ST elevation in I and aVL with reciprocal ST depression in lead III
• Q waves are present in the septal leads V1-2
• These features indicate a hyperacute anteroseptal STEMI

Example 2a

Hyperacute Anterior STEMI:

• There are hyperacute T-waves in V2-6 (most marked in V2 and V3) with loss of
R wave height.
• Normal sinus rhythm with 1st degree AV block
• There are premature atrial complexes (beat 4 on the rhythm strip) and
multifocal ventricular ectopy (PVCs of two different types), indicating an
“irritable” myocardium at risk of ventricular fibrillation
Example 2b :

Example 3

Example 4
Extensive Anterior STEMI (acute):

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

Example 5

Tombstoning of ST segment seen in Proximal LAD Occlusion

Example 6

Anterior-inferior STEMI

• ST elevation is present throughout the precordial and inferior leads

There are hyperacute T waves, most prominent in V1-3

Q waves are forming in V1-3, as well as leads III and aVF

This pattern is suggestive of occlusion occurring in “type III” or

“wraparound” LAD (i.e. one that wraps around the cardiac apex to supply
the inferior wall)
Territories

Prediction of the Site of LAD Occlusion

The site of LAD occlusion (proximal versus distal) predicts both infarct
size and prognosis.

Proximal LAD / LMCA occlusion has a significantly worse prognosis due

to larger infarct territory size and more severe haemodynamic
disturbance

The site of occlusion can be inferred from the pattern of ST changes in

leads corresponding to the two most proximal branches of the LAD:

the first septal branch (S1) and the first diagonal branch (D1)

• S1 supplies the basal part of the interventricular septum, including

the bundle branches (corresponding to leads aVR and V1)
• D1 supplies the high lateral region of the heart (leads I and aVL)
Occlusion proximal to S1

Signs of basal septal involvement:

ST elevation in aVR

ST elevation in V1 > 2.5 mm

Complete RBBB

ST depression in V5

This patient’s ECG shows several signs of a very proximal LAD occlusion (ostial LAD
occlusion septal STEMI):

Occlusion proximal to D1

Signs of high lateral involvement:

• ST elevation / Q-wave formation in aVL and I

• ST depression ≥ 1 mm in II, III or aVF (reciprocal to STE in aVL)

• There is a septal STEMI with ST elevation maximal in V1-2 (extending out to

V3).
• There is a new bifascicular block (RBBB + LAFB)
• Marked ST elevation (> 2.5 mm) in V1 plus STE in aVR — these features
suggest occlusion proximal to S1
MCQ
LATERAL STEMI
Clinical Significance of lateral STEMI

• The lateral wall of the LV is supplied by branches of the left anterior

descending (LAD) and left circumflex (LCx) arteries.

• Infarction of the lateral wall usually occurs as part of a larger territory

infarction, e.g. anterolateral STEMI.

• Isolated lateral STEMI is less common, but may be produced by occlusion of

smaller branch arteries that supply the lateral wall, e.g. the first diagonal
branch (D1) of the LAD, the obtuse marginal branch (OM) of the LCx, or
the ramus intermedius.

• Lateral STEMI is a stand-alone indication for emergent reperfusion.

• Lateral extension of an anterior, inferior or posterior MI indicates a larger

territory of myocardium at risk with consequent worse prognosis.

How to recognise a lateral STEMI

• ST elevation in the lateral leads (I, aVL, V5-6).

• Reciprocal ST depression in the inferior leads (III and aVF).
• ST elevation primarily localised to leads I and aVL is referred to as a high
lateral STEMI.
NB. Reciprocal change in the inferior leads is only seen when there is ST elevation in
leads I and aVL. This reciprocal change may be obliterated when there is concomitant
inferior ST elevation (i.e an inferolateral STEMI)
Patterns of lateral infarction

Three broad categories of lateral infarction:

• Anterolateral STEMI due to LAD occlusion.

• Inferior-posterior-lateral STEMI due to LCx occlusion.
• Isolated lateral infarction due to occlusion of smaller branch arteries such as
the D1, OM or ramus intermedius.

High Lateral STEMI

ST elevation is present in the high lateral leads (I and aVL).

There is also subtle ST elevation with hyperacute T waves in V5-6.

There is reciprocal ST depression in the inferior leads (III and aVF) with
associated ST depression in V1-3 (which could represent anterior
ischaemia or reciprocal change).

This pattern is consistent with an acute infarction localised to the

superior portion of the lateral wall of the left ventricle (high lateral
STEMI).

The culprit vessel in this case was an occluded first diagonal branch of
the LAD.
Example no.2

• There is subtle ST elevation in the high lateral leads (I and avL).

• There is a pathological Q wave in aVL plus inverted T waves in both I and aVL.
• This pattern is diagnostic of a recent (“completed”) high lateral MI.
• The patient in this case had a 90% occlusion of his obtuse marginal artery (= a
branch of the LCx supplying the lateral wall of the LV).

Example no.3

Anterolateral STEMI:

• ST elevation is present in the anterior (V2-4) and lateral leads (I, aVL, V5-6).
• Q waves are present in both the anterior and lateral leads, most prominently
in V2-4.
• There is reciprocal ST depression in the inferior leads (III and aVF).
• This pattern indicates an extensive infarction involving the anterior and lateral
walls of the left ventricle .
INFERIOR STEMI

Inferior myocardial infarction (MI) accounts for 40-50% of all MIs. It

generally has a more favourable prognosis than anterior
myocardial infarction (in-hospital mortality only 2-9%), however
certain associated features indicate a worse outcome

ECG DIAGNOSTIC CRITERIA

ST elevation in leads II, III, aVF

Hyperacute T waves may precede these changes

Reciprocal ST depression in aVL

Progressive development of Q waves in II, III, aVF

Associated features, all of which confer a worse prognosis, include:

• Concomitant right ventricular infarction (40% of patients);

these patients may develop severe hypotension in response to
nitrates
• Significant bradycardia due to second or third-degree AV
block (20%)
• Posterior infarction due to extension of infarct area
Don’t neglect Avl :

• aVL is the only lead truly reciprocal to the inferior wall, as it

is the only lead facing the superior part of the ventricle. It is
thus a sensitive marker for inferior infarction
• In patient cohorts with inferior occlusion myocardial
infarction (OMI), ST depression in aVL has been shown to be
more prevalent than STE in inferior leads
• 91% of “subtle” inferior STEMIs that do not meet STEMI
criteria but show occlusion on PCI demonstrate ST depression
in aVL
Which Artery is the Culprit?

Inferior STEMI can result from occlusion of any of the three main
coronary arteries:

• Dominant right coronary artery (RCA) in 80% of cases

• Dominant left circumflex artery (LCx) in 18%
• Occasionally, a “type III” or “wraparound” left anterior descending
artery (LAD), producing the unusual pattern of concomitant
inferior and anterior ST elevation.

RCA occlusion is suggested by:

• ST elevation in lead III > lead II

• Presence of reciprocal ST depression in lead I
• Signs of right ventricular infarction: STE in V1 and V4R

Circumflex occlusion is suggested by:

• ST elevation in lead II = lead III

• Absence of reciprocal ST depression in lead I

Signs of lateral infarction: ST elevation in the lateral leads I and

aVL or V5-6
WE MUST KNOW V4 R LEAD IN IWMI

Early inferior STEMI:

• Hyperacute (peaked) T waves in II, III and aVF with relative

loss of R wave height
• Early ST elevation and Q-wave formation in lead III
• Reciprocal ST depression and T wave inversion in aVL
• ST elevation in lead III > lead II suggests an RCA occlusion; the
subtle ST elevation in V4R would be consistent with this.
Reciprocal changes of iwmi in aVL

Example 3
Massive inferolateral STEMI:

• Marked ST elevation in II, III and aVF with a “tombstone”

morphology
• Reciprocal change in aVL
• ST elevation is also present in the lateral leads V5-6, indicating an
extensive infarct of the inferior and lateral walls

Inferior STEMI with sinus node dysfunction (either sinus arrest or

extreme sinus bradycardia) and a slow junctional escape rhythm.

• Bradycardia and AV Block in inferior STEMI

• Up to 20% of patients with inferior STEMI will develop either
second- or third-degree AV block. There are two presumed
mechanisms for this:
• Ischaemia of the AV node due to impaired blood flow via the
AV nodal artery. This artery arises from the RCA 80% of the
time, hence its involvement in inferior STEMI due to RCA
occlusion.
• Bezold-Jarisch reflex = increased vagal tone secondary to
ischaemia.
Right Ventricular Infarction
DIAGNOSTIC CRITERIA

In patients with inferior STEMI, right ventricular infarction is

suggested by:

• ST elevation in V1
• ST elevation in V1 and ST depression in V2 (highly specific for
RV infarction)
• Isoelectric ST segment in V1 with marked ST depression in V2
• ST elevation in III > II
• Diagnosis is confirmed by the presence of ST elevation in the
right-sided leads (V3R-V6R)

1. V1 is the only standard ECG lead that looks directly at the

right ventricle
2. Lead III is more rightward facing than lead II and hence more
sensitive to the injury current produced by the right ventricle
Example ECG

Example 1a

Inferior STEMI. Right ventricular infarction is suggested by:

• ST elevation in V1
• ST elevation in lead III > lead II

Example 1b

Repeat ECG of the same patient with V4R electrode position:

• There is ST elevation in V4R consistent with RV infarction

Example 2

Another example of right ventricular infarction in the context of inferior STEMI:

• ST elevation in lead III > lead II

• Isoelectric ST segment in V1 with marked ST depression in V2
• There is ST elevation in V4R
Posterior Myocardial Infarction
Clinical Significance of Posterior MI

Posterior infarction accompanies 15-20% of STEMIs, usually occurring in the context

of an inferior or lateral infarction.

• Isolated posterior MI is less common (3-11% of infarcts).

• Posterior extension of an inferior or lateral infarct implies a much
larger area of myocardial damage, with an increased risk of left
ventricular dysfunction and death.
• Isolated posterior infarction is an indication for emergent coronary
reperfusion. However, the lack of obvious ST elevation in this
condition means that the diagnosis is often missed

Be vigilant for evidence of posterior MI in any patient with an inferior or lateral

STEMI.
How to spot posterior infarction

As the posterior myocardium is not directly visualised by the standard

12-lead ECG, reciprocal changes of STEMI are sought in the anteroseptal
leads V1-3.

Posterior MI is suggested by the following changes in V1-3:

• Horizontal ST depression
• Tall, broad R waves (>30ms)
• Upright T waves
• Dominant R wave (R/S ratio > 1) in V2
• In patients presenting with ischaemic symptoms, horizontal ST
depression in the anteroseptal leads (V1-3) should raise the suspicion
of posterior MI

Typical appearance of posterior infarction in V2

Explanation of the ECG changes in V1-3

The anteroseptal leads are directed from the anterior precordium

towards the internal surface of the posterior myocardium.

Because posterior electrical activity is recorded from the anterior

side of the heart, the typical injury pattern of ST elevation and Q
waves becomes inverted:
ST elevation becomes ST depression

Q waves become R waves

Terminal T-wave inversion becomes an upright T wave

The progressive development of pathological R waves in posterior

infarction (the “Q wave equivalent”) mirrors the development of Q
waves in anteroseptal STEMI.
Posterior leads
Leads V7-9 are placed on the posterior chest wall in the following
positions (see diagram below):

• V7 – Left posterior axillary line, in the same horizontal plane as V6.

• V8 – Tip of the left scapula, in the same horizontal plane as V6.
• V9 – Left paraspinal region, in the same horizontal plane as V6.

POSTERIOR LEAD PLACEMENT V7, V8, V9

THE DEGREE OF ST ELEVATION SEEN IN V7-9 IS TYPICALLY MODEST –
NOTE THAT ONLY 0.5 MM OF ST ELEVATION IS REQUIRED TO MAKE THE
DIAGNOSIS OF POSTERIOR MI!
Example ECG

Example 1a

Inferolateral STEMI. Posterior extension is suggested by:

• Horizontal ST depression in V1-3

• Tall, broad R waves (> 30ms) in V2-3
• Dominant R wave (R/S ratio > 1) in V2
• Upright T waves in V2-3

Example 1b

The same patient, with posterior leads recorded:

• Marked ST elevation in V7-9 with Q-wave formation confirms involvement of

the posterior wall, making this an inferior-lateral-posterior STEMI (= big
territory infarct!).
Example 3a

Patient presenting with chest pain:

• The ST depression and upright T waves in V2-3 suggest posterior MI.

• There are no dominant R waves in V1-2, but it is possible that this ECG was
taken early in the course of the infarct, prior to pathological R-wave
formation.
• There are also some features suggestive of early inferior infarction, with
hyperacute T waves in II, III and aVF.

Example 3b

An ECG of the same patient taken 30 minutes later:

• There is now some ST elevation developing in V6.

• With the eye of faith there is perhaps also some early ST elevation in the
inferior leads (lead III looks particularly abnormal).
Example 3c

The same patient with posterior leads recorded:

• Posterior infarction is confirmed by the presence of ST elevation >0.5mm in

leads V7-9.

Example 4a

Patient presenting with central chest pain

• Inferior STEMI with posterior extension. Extensive territory

Example 4b

The same patient with posterior leads (V8,9) recorded:

STEMI EQUIVALENT :
Wellen’s syndrome
• The pattern is usually present in the pain free state — it may be
obscured during episodes of ischaemic chest pain, when there is
“pseudonormalisation” of T waves in V2-3
• Wellens syndrome is a key example of why all patients presenting
with chest pain must have serial ECGs

Clinical significance

• Patients may be pain free by the time the ECG is taken, and have
normal or minimally elevated cardiac enzymes. However, they are
at extremely high risk for extensive anterior wall MI within the
subsequent days to weeks

• Due to the critical LAD stenosis, these patients usually require

invasive therapy, do poorly with medical management, and may
suffer MI or cardiac arrest if inappropriately stress tested

Diagnostic criteria

Rhinehart et al (2002) describe the following diagnostic criteria for Wellens

syndrome:

• Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)

• ECG pattern present in pain-free state
• Isoelectric or minimally-elevated ST segment (< 1mm)
• No precordial Q waves
• Preserved precordial R wave progression
• Recent history of angina
• Normal or slightly elevated serum cardiac markers
There are two patterns of T-wave abnormality in Wellens syndrome:

Type A – Biphasic, with initial positivity and terminal negativity (25% of

cases)

Type B – Deeply and symmetrically inverted (75% of cases)

Biphasic T Waves (Type A) Deeply Inverted T Waves (Type B)

Wellens T wave evolution

T wave changes can evolve over time from Type A to Type B pattern (Smith et al).

Evolution of T-wave inversion [A-D] after coronary reperfusion in STEMI reperfusion

and in Wellens syndrome (NSTEMI). Modified from Smith et al. Evolution of T-wave
inversion. The ECG in acute MI, 2002
Example 5

This fantastic ECG series (submitted by paramedic Andrew Bishop) shows a stuttering
pattern of LAD occlusion, reperfusion and re-occlusion in a middle aged lady with
chest pain.

The ECGs are presented in chronological order, over a 45 minute period from the
prehospital environment to the cath lab:

(a) Patient experiencing chest pain and diaphoresis

• The ECG shows a clear anterolateral STEMI, with inferior reciprocal change
• The artery is occluded at this point
(b) Resolution of pain

• The ECG now shows a typical Wellens pattern of biphasic T waves in V2-3,
plus improvement in the anterolateral ST elevation
• This indicates spontaneous reperfusion of the LAD — i.e. the artery has re-
opened
(c) Recurrence of chest pain and diaphoresis

• With recurrence of pain there is pseudo-normalisation of the precordial T

waves: the previously biphasic T waves have become prominently upright (=
“hyperacute” T waves)
• This apparent normalisation of the T waves indicates re-occlusion of the LAD
artery
(d) Ongoing ischaemic symptoms

• Following re-occlusion of the artery, there is further evolution of the

anterolateral ST changes, with evolving anterior STEMI

(e) Symptoms improving

• Once again there is reperfusion of the artery, only this time the ST changes are
slower to resolve
•
(f) Now Pain Free

• Now the T waves are starting to become biphasic again (Wellens Pattern A)
Original Sgarbossa Criteria
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)

These criteria are specific, but not sensitive (36%) for myocardial infarction. A
total score of ≥ 3 is reported to have a specificity of 90% for diagnosing
myocardial infarction.

During right ventricular pacing the ECG also shows left bundle brach
block and the above rules also apply for the diagnosis of myocardial
infarction during pacing, however they are less specific.
ECG Examples

Example 1

Positive Sgarbossa criteria in a patient with LBBB and troponin-positive

myocardial infarction:

• This patient presented with chest pain and had elevated cardiac
enzymes.
• Previous ECG showed typical LBBB
• There is 1mm concordant ST elevation in aVL (= 5 points)
• Other features on this ECG that are abnormal in the context of
LBBB (but not considered “positive” Sgarbossa criteria) are the
pathological Q wave in lead I and the concordant ST depression in
the inferior leads III and aVF.
• This constellation of abnormalities suggests to the authors that
the patient was having a high lateral infarction
Example 2

E
Positive Sgarbossa criteria in a patient with a ventricular paced rhythm:

• There is concordant ST depression in V2-5 (= Sgarbossa positive).

• The morphology in V2-5 is reminiscent of posterior STEMI, with
horizontal ST depression and prominent upright T waves.
• This patient had a confirmed posterior infarction, requiring PCI to a
completely occluded posterolateral branch of the RCA.
PULMONARY EMBOLISM

1. What is the most common ECG finding in patients with pulmonary

embolism?

- A) Right axis deviation

- B) Right atrial

Saz a`7H ECG Features:

• Sinus tachycardia – the most common abnormality (seen in 44% of

patients with PE)
• Complete or incomplete RBBB (18%)
• Right ventricular strain pattern – T wave inversions in the right
precordial leads (V1-4) ± the inferior leads (II, III, aVF). This pattern
is associated with high pulmonary artery pressures (34%)
• Right axis deviation (16%). Extreme right axis deviation may occur,
with axis between zero and -90 degrees, giving the appearance of
left axis deviation (“pseudo left axis”)
• Dominant R wave in V1 – a manifestation of acute right ventricular
dilatation
• Right atrial enlargement (P pulmonale) – peaked P wave in lead II >
2.5 mm in height (9%)
• SI QIII TIII pattern – deep S wave in lead I, Q wave in III, inverted T
wave in III (20%). This “classic” finding is neither sensitive nor
specific for PE
• Clockwise rotation – shift of the R/S transition point towards V6
with a persistent S wave in V6 (“pulmonary disease pattern”),
implying rotation of the heart due to right ventricular dilatation
• Atrial tachyarrhythmias – AF, flutter, atrial tachycardia (8%)
• Non-specific ST segment and T wave changes, including ST
elevation and depression (50%)
 • Simultaneous T wave inversions in the inferior (II, III, aVF) and right
precordial leads (V1-4) is the most specific finding in favour of PE,
with reported specificities of up to 99% in one study.

ECG Examples

Example 1

Massive bilateral pulmonary embolus

• Sinus tachycardia
• RBBB
• T-wave inversions in the right precordial leads (V1-3) as well as lead III

Example 2
Massive bilateral pulmonary embolus

• RBBB
• Extreme right axis deviation (+180 degrees)
• S1 Q3 T3
• T-wave inversions in V1-4 and lead III
• Clockwise rotation with persistent S wave in V6

Example 3

Massive pulmonary embolus

• Sinus tachycardia.
• Simultaneous T-wave inversions in the anterior (V1-4) and inferior
leads (II, III, aVF).
• Non-specific ST changes – slight ST elevation in III and aVF.
ARRYTHMIA
QUESTION
Which of the following best defines a high-grade atrioventricular (AV)
block?

a) Intermittent atrial conduction to the ventricle with no delay in

ventricular activation.
b) Complete absence of atrial impulses conducting to the ventricle.
c) Intermittent atrial conduction to the ventricle with two or more
consecutive blocked P waves but without complete AV block.
d) Regular pattern of intermittent atrial conduction with varying PR
intervals.

Heart block :

OVERVIEW

Abnormalities may occur at any part of the conduction system

Atrioventricular (AV) block is defined as a delay or interruption in the

transmission of an impulse from the atria to the ventricles due to an
anatomical or functional impairment in the conduction system.

The conduction disturbance can be transient or permanent, with

conduction that is delayed, intermittent, or absent. Commonly used
terminology includes:

●First-degree AV block – Delayed conduction from the atrium to the

ventricle (defined as a prolonged PR interval of >200 milliseconds) without
interruption in atrial to ventricular conduction.

●Second-degree AV block – Intermittent atrial conduction to the ventricle,

often in a regular pattern (eg, 2:1, 3:2, or other pattern), which are further
classified into Mobitz type I (Wenckebach) and Mobitz type II second
degree AV block.

●Third-degree (complete AV) block – No atrial impulses conduct to the

ventricle.

●High-grade AV block – Intermittent atrial conduction to the ventricle

with two or more consecutive blocked P waves but without complete AV
block.

TYPES

1st degree block

prolongation of PR interval (>0.2s)

2nd degree Mobitz type I (Wenckebach) block

progressive lengthening of PR interval with eventual dropped ventricular

conduction

2nd degree Mobitz type II (Hay) block

• Intermittent dropping of ventricular conduction

2nd degree (2:1 type) block
• alternate p-wave not conducted to ventricles
3rd degree block (complete heart block)

• complete dissociation between atria and ventricular

Left Anterior Fascicular Block (LAFB) (Left anterior hemiblock)

LAD, Q waves in I and aVL, small R in III (and absence of LVH)

ECG criteria

• Left axis deviation (usually -45 to -90 degrees)

• qR complexes in leads I, aVL

• rS complexes in leads II, III, aVF

• Prolonged R wave peak time in aVL > 45ms
Left Posterior Fascicular Block (LPFB) (Left posterior hemiblock)

• RAD, small R in I, small Q in III (and absence of RVH)

ECG Criteria

• Right axis deviation (RAD) (> +90 degrees)

• rS complexes in leads I and aVL
• qR complexes in leads II, III and aVF
• Prolonged R wave peak time in aVF

• Note: The diagnosis of LFPB can only be made after excluding other
causes of RAD. There should be:
• No evidence of right ventricular hypertrophy
• No evidence of any other cause for right axis deviation
Right bundle branch block (RBBB)
• RSR in V1 (‘M’), and ‘W’ in V6 (MARROW), normal axis

Left bundle branch block (LBBB)

 • septal depolarisation reversed so there is a change in initial direction of QRS
(WILLIAM), normal axis

Bifascicular block
• RBBB + block of either left anterior or posterior fascicle.
• RBBB + left anterior fascicle block -> LAD
• RBBB + left posterior fascicle block -> RAD

Trifascicular block – 3 types:

• Prolonged PR interval + RBBB + LAD
• LBBB + RAD
• AF + RBBB + LAD
MANAGEMENT
By diagnosis

1st degree
– nothing unless symptomatic and other causes of symptoms excluded

2nd degree (Mobitz type I)

– nothing unless symptomatic and other causes of symptoms excluded

2nd degree (Mobitz type II)

– pacemaker

3rd degree
– pacemaker

Branch blocks
– nothing unless progresses or symptomatic -> pacemaker
— if sympatomatic -> pacemaker
— trifascicular block -> pacemaker

may need temporary pacing wire or external pacing

also if rates too slow and unresponsive to drugs -> pace

Emergency management of bradycardia

• check blood pressure

• atropine 25microgram/kg or glycopyrolate 0.2mg
• isoprenaline 1-10mcg/min
• adrenaline 0.1-1.0mcg/kg/min
• temporary pacing – tranthoracic, transoesophageal, transvenous
Tachycardia:

Normal heart rates in children

 • Newborn: 110 – 150 bpm
• 2 years: 85 – 125 bpm
• 4 years: 75 – 115 bpm
• 6 years+: 60 – 100 bpm

Causes

Sinus tachycardia is usually a secondary condition. Inappropriate sinus tachycardia is

a primary condition diagnosed in patients with symptomatic-persisting sinus
tachycardia in which the below causes have been excluded.

Non-pharmacological

• Exercise
• Pain
• Anxiety
• Hypovolaemia
• Hypoxia, hypercarbia
• Acidaemia
• Sepsis, pyrexia
• Anaemia
• Pulmonary embolism
• Cardiac tamponade
• Hyperthyroidism
• Alcohol withdrawal

Pharmacological

• Beta-agonists: adrenaline, isoprenaline, salbutamol, dobutamine

• Sympathomimetics: amphetamines, cocaine, methylphenidate
• Antimuscarinics: antihistamines, TCAs, carbamazepine, atropine
• Others: caffeine, theophylline, marijuana

Example ECG
Sinus tachycardia:

• Heart rate 150 bpm.

• P waves are hidden within each preceding T wave.

Handy Tip

With very fast heart rates the P waves may be hidden in the preceding T wave,
producing a ‘camel hump’ appearance.

DEFINITION
• Focal atrial tachycardia (FAT) is a form of supraventricular
tachycardia (SVT) originating from a single ectopic focus within
the atria but outside of the sinus node
 • Focal atrial tachycardia (FAT): Consistent, abnormal P wave
morphology indicating an ectopic focus
• The term FAT is commonly used synonymously with atrial
tachycardia, a broader term referring to any form of SVT
originating within the atria but outside of the sinus node
• FAT, atrial flutter and multifocal atrial tachycardia(MAT) are all
forms of atrial tachycardia
• Management of the three types varies and thus distinguishing
between them is clinically important

Pathophysiology of FAT

• Due to a single ectopic focus

• The underlying mechanism can involve increased automaticity,
triggered activity or reentry
• May be paroxysmal or sustained
• Multiple causes including:
• Digoxin toxicity
• Atrial scarring due to ischaemic heart disease
• Catecholamine excess
• Stimulants including cocaine, caffeine
• Alcohol
• Congenital abnormalities
• Idiopathic
• Sustained atrial tachycardia may rarely be seen and can progress
to tachycardia-induced cardiomyopathy
Supraventricular Tachycardia

• It is often used synonymously with AV nodal re-entry tachycardia (AVNRT), a

form of SVT

• In the absence of aberrant conduction (e.g. bundle branch block), the ECG will
demonstrate a narrow complex tachycardia

• Paroxysmal SVT (pSVT) describes an SVT with abrupt onset and offset –
characteristically seen with re-entrant tachycardias involving the AV node
such as AVNRT or atrioventricular re-entry tachycardia (AVRT)

Supraventricular tachycardia (SVT): Rhythm strip demonstrating a regular, narrow-

complex tachycardia

Classification

• SVTs can be classified based on:

o Site of origin (atria or AV node) or;
o Regularity (regular or irregular)
• Classification based on QRS width is unhelpful as this is also influenced by the
presence of pre-existing bundle branch block, rate-related aberrant
conduction, or presence of accessory pathways.
Classification of SVT by site of origin and regularity

Regular Atrial

• Sinus tachycardia
• Atrial tachycardia
• Atrial flutter
• Inappropriate sinus tachycardia
• Sinus node reentrant tachycardia

Irregular Atrial

• Atrial fibrillation
• Atrial flutter (variable block)
• Multifocal atrial tachycardia

Regular Atrioventricular

• AVRT
• AVNRT
• Automatic junctional tachycardia
AV Nodal Re-entry Tachycardia (AVNRT)

• This is the commonest cause of palpitations in

patients with structurally normal hearts
• AVNRT is typically paroxysmal and may occur
spontaneously or upon provocation with exertion,
caffeine, alcohol, beta-agonists (salbutamol) or
sympathomimetics (amphetamines)
• It is more common in women than men (~ 75% of
cases occurring in women) and may occur in young
and healthy patients as well as those suffering
chronic heart disease
• Patients will typically complain of the sudden onset
of rapid, regular palpitations. Other associated
symptoms may include:
• Presyncope or syncope due to a transient fall in blood
pressure
• Chest pain, especially in the context of underlying
coronary artery disease
• Dyspnoea
• Anxiety
• Rarely, polyuria due to elevated atrial pressures
causing release of atrial natriuretic peptide
• The tachycardia typically ranges between 140-280
bpm and is regular in nature. It may self-resolve or
 continue indefinitely until medical treatment is
sought
• The condition is generally well tolerated and is rarely
life threatening in patients with pre-existing heart
disease

Pathophysiology

In comparison to AVRT, which involves an anatomical re-entry circuit

(Bundle of Kent), in AVNRT there is a functional re-entry circuit within
the AV node.

Alrternate re-entry loops: Functional circuit in AVNRT

(left), anatomical circuit in AVRT (right)

Functional pathways within the AV node

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.
 • Mechanism of re-entry in “slow-fast” AVNRT:
1) A premature atrial contraction (PAC) arrives while the fast
pathway is still refractory, and is directed down the slow pathway
2) The ERP in the fast pathway ends, and the PAC impulse travels
retrogradely up the fast pathway
3) The impulse continually cycles around the two pathways

Initiation of re-entry

• During normal sinus rhythm, electrical impulses travel down both

pathways simultaneously. The impulse transmitted down the fast
pathway enters the distal end of the slow pathway and the two
impulses cancel each other out

• However, 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, and the impulse
is permitted to recycle retrogradely up the fast pathway

• This creates a circus movement whereby the impulse continually

cycles around the two pathways, activating the Bundle of His
anterogradely and the atria retrogradely

• The short cycle length is responsible for the rapid heart rate

• This most common type of re-entrant circuit is termed Slow-Fast

AVNRT

• Similar mechanisms exist for the other types of AVNRT

Electrocardiographic Features

ECG features of AVNRT

• Regular tachycardia ~140-280 bpm

• Narrow QRS complexes (< 120ms) unless there is co-existing
bundle branch block, accessory pathway, or rate-related
aberrant conduction
• P waves if visible exhibit retrograde conduction with P-wave
inversion in leads II, III, aVF. They may be buried within,
visible after, or very rarely visible before the QRS complex

Associated features include:

 • Rate-related ST depression, which may be seen with or
without underlying coronary artery disease
• QRS alternans – phasic variation in QRS amplitude associated
with AVNRT and AVRT, distinguished from electrical
alternans by a normal QRS amplitude

Subtypes of AVNRT

Different subtypes vary in terms of the dominant pathway, and the R-P
interval, which is the time between anterograde ventricular activation (R
wave) and retrograde atrial activation (P wave).

1. Slow-Fast AVNRT (80-90%)

2. Fast-Slow AVNRT (10%)
3. Slow-Slow AVNRT (1-5%)

1. Slow-Fast AVNRT (common type)

• Accounts for 80-90% of AVNRT

• Associated with slow AV nodal pathway for anterograde
conduction and fast AV nodal pathway for retrograde conduction
• The retrograde P wave is obscured in the corresponding QRS or occurs
at the end of the QRS complex as pseudo R’ or S waves

ECG features:

• P waves are often hidden – being embedded in the QRS complexes

• Pseudo R’ wave may be seen in V1 or V2
• Pseudo S waves may be seen in leads II, III or aVF
 • In most cases this results in a ‘typical’ SVT appearance with absent
P waves and tachycardia

Top strip: Normal sinus rhythm. Absence of pseudo-R waves

Bottom strip: Paroxysmal SVT. The P wave is seen as a pseudo-R wave
(circled) in lead V1 during tachycardia. This very short ventriculo-atrial
time is frequently seen in typical Slow-Fast AVNRT

2. Fast-Slow AVNRT (Uncommon AVNRT)

• Accounts for 10% of AVNRT

• Associated with Fast AV nodal pathway for anterograde conduction and Slow
AV nodal pathway for retrograde conduction
• Due to the relatively long ventriculo-atrial interval, the retrograde P wave is
more likely to be visible after the corresponding QRS

ECG features:

• QRS-P-T complexes
• Retrograde P waves are visible between the QRS and T wave

3. Slow-Slow AVNRT (Atypical AVNRT)

• 1-5% AVNRT
• Associated with Slow AV nodal pathway for anterograde conduction and Slow
left atrial fibres as the pathway for retrograde conduction.
ECG features:

• Tachycardia with a P-wave seen in mid-diastole, effectively appearing “before”

the QRS complex.
• May be misinterpreted as sinus tachycardia

Summary of AVNRT subtypes

• No visible P waves? –> Slow-Fast

• P waves visible after the QRS complexes? –> Fast-Slow
• P waves visible before the QRS complexes? –> Slow-Slow

Management of AVNRT

•May respond to vagal maneuvers with reversion to sinus rhythm.

• The mainstay of treatment is adenosine
• Other agents which may be used include calcium-channel blockers, beta-
blockers and amiodarone
• DC cardioversion is rarely required
• Catheter ablation may be considered in recurrent episodes not amenable to
medical treatment
Example 1
.

This is ??
Atrioventricular Re-entry Tachycardia
(AVRT)
Atrioventricular Re-entry Tachycardia (AVRT) is a form of paroxysmal
supraventricular tachycardia that occurs in patients with accessory pathways, usually
due to formation of a re-entry circuit between the AV node and accessory pathway.

ECG features depend on the direction of conduction, which can

be orthodromic or antidromic.

• In orthodromic AVRT, anterograde conduction is via the AV node,

producing a regular narrow complex rhythm (in the absence of pre-
existing bundle branch block)
• In antidromic AVRT, anterograde conduction is via the accessory
pathway (AP), producing a regular wide complex rhythm. This can
be difficult to distinguish from ventricular tachycardia (VT)
• Often triggered by premature atrial or premature ventricular beats
• In both forms, the features of pre-excitation are lost
Orthodromic AVRT, or just AVNRT?

This rhythm can appear very similar to AVNRT, but the RP interval can assist us to
differentiate:

• In typical AVNRT, retrograde P waves occur early, so we either

don’t see them (buried in QRS) or partially see them (pseudo R’
wave at terminal portion of QRS complex)

• In AVRT, retrograde P waves occur later, with a long RP interval >

70 msec

In the above example, look closely at V1 — P waves are evident as a small notch at
the beginning of the T wave, with a long RP interval, indicating this is likely
orthodromic AVRT.

Fortunately, treatment is fairly similar for both.

Treatment of orthodromic AVRT

• As always, patients that are unstable due to this rhythm require urgent DC
cardioversion
• The anterograde portion of conduction is typically the “weak link” of the re-
entry circuit. Management options in the stable patient therefore target
slowing conduction through the AV node
• A stepwise approach similar to AVNRT can be employed, beginning with vagal
manoeuvres followed by adenosine and/or verapamil

Note that with administration of any AV nodal blocking drug, there is a very small but
significant risk of inducing AF.

If verapamil is used, patients should be observed for at least 4 hours to ensure AF does not
develop as a consequence of AV nodal blockade
See what happened when our patient above was given adenosine

• The patient reverts to sinus rhythm after treatment with

adenosine
• Wolff-Parkinson-White (WPW) pattern is now evident on the
baseline ECG; this confirms that the initial rhythm was
orthodromic AVRT
• Tall R waves in right precordial leads (V1-3) indicate a left-sided AP

Antidromic AVRT

• Antidromic AVRT is rare, and makes up only 5% of

tachyarrhythmias in patients with WPW. As the name suggests, it
involves anterograde conduction via the AP. Retrograde conduction
is usually via the AV node, but can also be via another AP. The
abnormal direction of ventricular depolarisation results in a broad
complex tachycardia, which can be easily mistaken for VT.
ECG features of AVRT with antidromic conduction:

Rate usually 200-300 bpm

Wide QRS complexes due to abnormal ventricular depolarisation via AP

Antidromic AVRT: Regular broad complex tachycardia

Treatment of antidromic AVRT

• This rhythm can be difficult to distinguish from VT, and if there is any doubt,
we should presume a diagnosis of VT and treat accordingly
• In stable patients, drug therapy should be targeted at the AP
• Procainamide (class I) would be our first line antiarrhythmic. Ibutilide (class III)
and amiodarone are second-line options, but their effectiveness is less
established
• DC cardioversion may still be required if drug therapy fails

APs can be left-sided or right-sided, and ECG features will vary depending on this:
 • Left-sided AP: produces a positive delta wave in all precordial leads, with R/S
> 1 in V1. Sometimes referred to as a type A WPW pattern

• Right-sided AP: produces a negative delta wave in leads V1 and V2. Sometimes
referred to as a type B WPW pattern

Note that the features of pre-excitation may be subtle, or present only intermittently.
Pre-excitation may be more pronounced with increased vagal tone e.g. during
Valsalva manoeuvres, or with AV blockade e.g. drug therapy.

Tachyarrhythmias in WPW

There are only two main forms of tachyarrhythmias that occur in patients with WPW
— these are discussed separately:

• Atrial fibrillation or flutter. Due to direct conduction from atria to ventricles

via an AP, bypassing the AV node
• Atrioventricular re-entry tachycardia(AVRT). Due to formation of a re-entry
circuit involving the AP
Re-entry circuit during AVRT (retrograde conduction via Bundle of Kent)

ECG Examples

Sinus Rhythm – Type A Pattern

Example 1

• Sinus rhythm with a very short PR interval (< 120 ms)

• Broad QRS complexes with a slurred upstroke to the QRS complex — the delta
wave
 • Dominant R wave in V1 suggests a left-sided AP, and is sometimes referred
to as “Type A” WPW
• Tall R waves and inverted T waves in V1-3 mimicking right ventricular
hypertrophy (RVH) — these changes are due to WPW and do not indicate
underlying RVH
• Negative delta wave in aVL simulating the Q waves of lateral infarction — this
is referred to as the “pseudo-infarction” pattern

Sinus rhythm – Type B Pattern

Example 3
• Sinus rhythm with very short PR interval (< 120 ms)
• Broad QRS complexes with a slurred upstroke to the QRS complexes —
the delta wave
• Dominant S wave in V1 indicates a right-sided AP — sometimes referred to
as “Type B” WPW
• Tall R waves and inverted T waves in the inferior leads and V4-6 mimic the
appearance of left ventricular hypertrophy (LVH) — again, this is due to WPW
and does not indicate underlying LVH
Atrial Flutter
ECG features of atrial flutter

• Narrow complex tachycardia

• Regular atrial activity at ~300 bpm
• Loss of the isoelectric baseline
• “Saw-tooth” pattern of inverted flutter waves in leads II, III, aVF
• Upright flutter waves in V1 that may resemble P waves
• Ventricular rate depends on AV conduction ratio (see below)
Note: the above pattern of inverted flutter waves in inferior leads and upright flutter
waves in V1 occurs in atrial flutter due to anticlockwise reentry, which makes up
90% of cases.

Fixed AV conduction ratio (“AV block”)

Ventricular rate is a fraction of the atrial rate, for example:

• 2:1 block = 150 bpm

• 3:1 block = 100 bpm
• 4:1 block = 75 bpm

Variable AV conduction ratio

• The ventricular response is irregular and may mimic atrial fibrillation (AF)
• On closer inspection, there may be a pattern of alternating 2:1, 3:1 and 4:1
conduction ratios

Atrial flutter with a 3:1 block

Pathophysiology of atrial flutter

Atrial flutter is a form of supraventricular tachycardia caused by a re-entry circuit

within the right atrium. The length of the re-entry circuit corresponds to the size of
the right atrium, resulting in a fairly predictable atrial rate of around 300 bpm (range
200-400)

• Ventricular rate is determined by the AV conduction ratio (“degree of AV

block”). The most common AV ratio is 2:1, resulting in a ventricular rate of
~150 bpm
• Higher-degree blocks can occur — usually due to medications or underlying
heart disease — resulting in lower rates of ventricular conduction, e.g. 3:1 or
4:1 block.
• Atrial flutter with 1:1 conduction can occur due to sympathetic stimulation, or
in the presence of an accessory pathway. The administration of AV-nodal
blocking agents to a patient with Wolff-Parkinson-White syndrome can
precipitate this
• Atrial flutter with 1:1 conduction is associated with severe haemodynamic
instability and progression to ventricular fibrillation
Atrial Fibrillation

ECG Features of Atrial Fibrillation

• Irregularly irregular rhythm

• No P waves
• Absence of an isoelectric baseline
• Variable ventricular rate
• QRS complexes usually < 120ms, unless pre-existing bundle branch block,
accessory pathway, or rate-related aberrant conduction
• Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm)
or coarse (amplitude > 0.5mm)
• Fibrillatory waves may mimic P waves leading to misdiagnosis

Atrial fibrillation: Irregularly irregular ventricular rate without visible P waves

Causes of Atrial Fibrillation

• Ischaemic heart disease

• Hypertension
• Valvular heart disease (esp. mitral stenosis / regurgitation)
• Acute infections
• Electrolyte disturbance (hypokalaemia, hypomagnesaemia)
• Thyrotoxicosis
• Drugs (e.g. sympathomimetics)
• Alcohol
• Pulmonary embolus
• Pericardial disease
• Acid-base disturbance
• Pre-excitation syndromes
• Cardiomyopathies: dilated, hypertrophic.
• Phaeochromocytoma

Atrial Fibrillation in Wolff-Parkinson-White Syndrome

• Atrial fibrillation can occur in up to 20% of patients with Wolff-Parkinson-

White Syndrome(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

ECG features of Atrial Fibrillation in WPW:

• 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, unlikely polymorphic VT
Treatment

• Treatment with AV nodal blocking drugs e.g. adenosine, calcium-channel

blockers, beta-blockers may increase conduction via the accessory pathway
with a resultant increase in ventricular rate and possible degeneration
into VT or VF
• In a haemodynamically unstable patient urgent synchronised DC cardioversion
is required.
• Medical treatment options in a stable patient include procainamide or
ibutilide, although DC cardioversion may be preferred

Accelerated Junctional Rhythm Overview

Accelerated junctional rhythm (AJR) occurs when the rate of an AV junctional

pacemaker exceeds that of the sinus node. This situation arises when there
is increased automaticity in the AV node coupled with decreased automaticity in the
sinus node.

ECG Features of AJR

• Narrow complex rhythm; QRS duration < 120ms (unless pre-existing bundle
branch block or rate-related aberrant conduction)
• Ventricular rate usually 60 – 100 bpm
• Retrograde P waves may be present and can appear before, during or after
the QRS complex. They are usually inverted in inferior leads (II, III, aVF),
upright in aVR + V1
• AV dissociation may be present with the ventricular rate usually greater than
the atrial rate
• There may be associated ECG features of digoxin effect or digoxin toxicity

Rhythm strip in AJR: Narrow complex rhythm; inverted retrograde P waves seen
before the QRS complex
Ventricular Tachycardia – Monomorphic
VT

ECG features of monomorphic VT

• Regular, broad complex tachycardia

• Uniform QRS complexes within each lead — each QRS is identical (except for
fusion/capture beats)

Monomorphic VT: Regular, broad complex tachycardia

Below are some examples of positive and negative concordance, and Brugada’s and
Josephson’s sign. For more examples of the other suggestive features, see VT versus
SVT.
Positive concordance: Predominantly positive QRS complexes throughout precordial leads

Negative concordance: Predominantly negative QRS complexes throughout precordial leads

Josephson’s sing (left): Notching near nadir of S wave

Brugada’s sign (right): R-S interval > 100 ms
Causes of Monomorphic VT

1. Ischaemic Heart Disease

2. Dilated cardiomyopathy

3. Hypertrophic cardiomyopathy
4. Chaga’s Disease

Clinical Significance

VT may impair cardiac output with consequent hypotension, collapse, and acute

cardiac failure. This is due to extreme heart rates and loss of coordinated atrial
contraction (“atrial kick”)

The presence of pre-existing poor ventricular function is strongly associated with

cardiovascular compromise

Decreased cardiac output may result in decreased myocardial perfusion with

degeneration into VF

Prompt recognition and initiation of treatment (e.g. electrical cardioversion) is

required in all cases of VT

ECG Examples – Monomorphic VT

Example 1
Monomorphic VT:

• Classic monomorphic VT with uniform QRS complexes

• Indeterminate axis
• Very broad QRS (~200 ms)
• Notching near the nadir of the S wave in lead III = Josephson’s sign

Monomorphic VT alternating with ventricular bigeminy.

The ventricular complexes have the following features:

• Very broad QRS duration (> 160 bpm)

• Positive concordance in the precordial leads (dominant R waves in V1-6)
• Brugada’s sign – time from onset of QRS to nadir of S wave > 100 ms; best
seen in leads aVR and aVL
Polymorphic VT

Definitions

Polymorphic ventricular tachycardia (PVT)is a form of ventricular tachycardia in

which there are multiple ventricular foci with the resultant QRS complex varying in
amplitude, axis, and duration. The most common cause of PVT is myocardial
ischaemia/infarction.

Torsades de pointes (TdP) is a specific form of PVT occurring in the context of QT

prolongation — it has a characteristic morphology in which the QRS complexes
“twist” around the isoelectric line.

Torsades de pointes
• For TdP to be diagnosed, the patient must have evidence of both PVT and QT
prolongation
• Bidirectional VT is another specific type of of PVT, most commonly associated
with digoxin toxicity
• TdP is often short lived and self terminating, however can be associated with
haemodynamic 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.

Ventricular Fibrillation :

ECG findings in Ventricular Fibrillation (VF)

 • Chaotic irregular deflections of varying amplitude
• No identifiable P waves, QRS complexes, or T waves
• Rate 150 to 500 per minute
• Amplitude decreases with duration (coarse VF –> fine VF)

Ventricular fibrillation (rhythm strip): Chaotic irregular deflections without

identifiable P-QRS-T waves

Clinical significance of VF

Ventricular fibrillation (VF) is 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, ultimately degenerating into asystole due to
progressive depletion of myocardial energy stores
Quiz :

HR and Dx
Q.2
Q.3
ECG 3

25-year-old with exertional dizziness.

ECG 4

17-year-old noticed “high” heart rate on Apple watch.

ECG 5

75-year old with atypical chest pain.

ECG 6

30-year old with palpitations.

ECG 7

30-year old with shortness of breath.

ECG 8
ECG 9
ECG 10
ECG 11
ECG Features of AIVR

• Regular rhythm
• Rate typically 50-120 bpm
• Three or more ventricular complexes; QRS duration > 120ms
• Fusion and capture beats

Pathophysiology

• Proposed mechanism is enhanced automaticity of ventricular pacemaker,

although triggered activity may play a role, particularly
in ischaemia and digoxin toxicity
• AIVR is classically seen in the reperfusion phase of an acute STEMI, e.g. post
thrombolysis
• Usually a well-tolerated, benign, self-limiting arrhythmia
ECG 12
ECG 13
ECG 14
ECG 15
ECG 16
ECG 17
ECG Features demonstrating the Digoxin Effect

Digoxin effect refers to the presence on the ECG of:

• Downsloping ST depression with a characteristic “reverse tick” or “Salvador

Dali sagging” appearance
• Flattened, inverted, or biphasic T waves
• Shortened QT interval

Digoxin
effect: Sagging ST segments resemble a “reverse tick”
ECG 18
ECG 19
ECG 20